FN Thomson Reuters Web of Science™ VR 1.0 PT J AU LEE, MG TANG, A SHARROW, SO UDEY, MC AF LEE, MG TANG, A SHARROW, SO UDEY, MC TI MURINE DENDRITIC EPIDERMAL T-CELLS (DETC) EXPRESS THE HOMOPHILIC ADHESION MOLECULE E-CADHERIN SO EPITHELIAL CELL BIOLOGY LA English DT Article DE ADHESION; CADHERIN; DENDRITIC EPIDERMAL T CELLS (DETC); EPIDERMIS; LEUKOCYTES; THYMOCYTES ID DELTA-ANTIGEN RECEPTORS; MONOCLONAL-ANTIBODY; LANGERHANS CELLS; SKIN; IDENTIFICATION; PRECURSORS; DIVERSITY; SYSTEM AB Cadherins mediate homotypic intercellular adhesion in epidermis and other epithelia. E-cadherin is also involved in interactions between murine epidermal Langerhans cells (LC) and keratinocytes (KC). Dendritic epidermal T cells (DETC) comprise another subpopulation of epidermal leukocytes. Using flow cytometry, we determined that DETC expressed levels of E-cadherin similar to those expressed by LC and KC. DETC also adhered similar to three-fold better to KC and E-cadherin-transfected fibroblasts than to normal fibroblasts. Treatment of DETC with trypsin in the absence of calcium caused a loss of E-cadherin and resulted in an similar to 80% decrease in DETC-KC adhesion whereas treatment of DETC with trypsin in the presence of calcium did not significantly affect E-cadherin expression or DETC-KC binding. Thus, E-cadherin may be involved in adhesion of DETC to KC. DETC are derived from TCR V gamma 3(+) thymocytes that transiently populate embryonic murine thymus. We determined that TCR V gamma 3(+) thymocytes as well as other early (fetal day 16) TCR gamma/delta(+) thymocytes expressed E-cadherin; TCR gamma/delta(+) (TCR V gamma 3(-)) thymocytes that developed later did not. These results indicate that cells of the T cell lineage can express E-cadherin, and suggest that E-cadherin may play a role in adhesion of DETC (and/or DETC precursors) to KC. C1 NCI, DERMATOL BRANCH, BETHESDA, MD 20892 USA. NCI, EXPTL IMMUNOL BRANCH, BETHESDA, MD 20892 USA. NR 31 TC 11 Z9 11 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0940-9912 J9 EPITHELIAL CELL BIOL JI Epithelial Cell Biol. PY 1994 VL 3 IS 4 BP 149 EP 155 PG 7 WC Cell Biology SC Cell Biology GA RJ266 UT WOS:A1994RJ26600002 PM 7550606 ER PT S AU CRAGG, GM BOYD, MR CARDELLINA, JH NEWMAN, DJ SNADER, KM MCCLOUD, TG AF CRAGG, GM BOYD, MR CARDELLINA, JH NEWMAN, DJ SNADER, KM MCCLOUD, TG BE Chadwick, DJ Marsh, J TI ETHNOBOTANY AND DRUG DISCOVERY - THE EXPERIENCE OF THE US NATIONAL-CANCER-INSTITUTE SO ETHNOBOTANY AND THE SEARCH FOR NEW DRUGS SE CIBA FOUNDATION SYMPOSIA LA English DT Article; Proceedings Paper CT Symposium on Ethnobotany and the Search for New Drugs CY NOV 30-DEC 02, 1993 CL FORTALEZA, BRAZIL SP CIBA FDN ID INHIBITORY NATURAL-PRODUCTS; PLANTS; ALKALOIDS; HIV-1 AB Between 1960 and 1981 the National Cancer Institute (NCI) screened 114 000 extracts of 35 000 plants, mainly collected in temperate regions. Of the three clinically active anticancer drugs so far discovered in that programme, none was isolated from a plant collected on an ethnobotanical basis, though various Taxus species, which are the source of taxol, are reported to have been used medicinally. Since 1986, the NCI has focused its collections in tropical and subtropical regions worldwide; collections cover a broad taxonomic range, though priority is given to medicinal plants when relevant information is available. As of August 1993, 21 881 extracts derived from over 10 500 samples had been tested in a screen for activity against the human immunodeficiency virus (HIV); 2320 of these extracts were of medicinal plant origin. Approximately 18% of both the total number of extracts and the medicinal plant-derived extracts showed significant anti-HIV activity; in each instance about 90% of the active extracts were aqueous. The activity of the aqueous extracts has been attributed mainly to the presence of polysaccharides or tannins. Four plant-derived compounds are in preclinical development at the NCI; only one of the four source plants, obtained from a non-contract source, was collected on an ethnobotanical basis. At this stage the results indicate that the current NCI collection policy offers the best chances for the discovery and development of agents for the treatment of AIDS (acquired immune deficiency syndrome) and cancer. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. RP CRAGG, GM (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892, USA. NR 30 TC 77 Z9 80 U1 3 U2 11 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, ENGLAND PO19 7UD SN 0300-5208 BN 0-471-95024-6 J9 CIBA F SYMP PY 1994 VL 185 BP 178 EP 190 PG 13 WC Plant Sciences; Medicine, General & Internal; Pharmacology & Pharmacy SC Plant Sciences; General & Internal Medicine; Pharmacology & Pharmacy GA BB81W UT WOS:A1994BB81W00012 PM 7736854 ER PT J AU ULLMER, EJ AF ULLMER, EJ TI MEDIA AND LEARNING - ARE THERE 2 KINDS OF TRUTH SO ETR&D-EDUCATIONAL TECHNOLOGY RESEARCH AND DEVELOPMENT LA English DT Article ID INSTRUCTIONAL-DESIGN AB This article examines the assumptions and methods of conventional instructional media research to gauge its sufficiency as a basis for issuing the controversial finding that media do not influence learning and as an inquiry model for documenting media's educational effects generally. Examples of complex media effects are given and emerging media application paradigms are identified to support the argument that both a new conceptualization of the media and learning question and new approaches to its study are needed. An alternative values framework for guiding research on the effects of modern interactive technologies in complex learning environments is offered. RP ULLMER, EJ (reprint author), NIH,BETHESDA,MD 20892, USA. NR 49 TC 10 Z9 10 U1 0 U2 1 PU ASSOC EDUC COMMUNICATIONS & TECHNOLOGY PI WASHINGTON PA 1025 VERMONT AVE NW, SUITE 820, WASHINGTON, DC 20005 SN 1042-1629 J9 ETR&D-EDUC TECH RES JI ETR&D-Educ. Tech. Res. Dev. PY 1994 VL 42 IS 1 BP 21 EP 32 DI 10.1007/BF02298168 PG 12 WC Education & Educational Research SC Education & Educational Research GA NM706 UT WOS:A1994NM70600002 ER PT J AU HIRSCH, A SLAMA, K ALBERISIO, A FOWLER, G LAGRUE, G MALVEZZI, I MANLEY, M MOLIMARD, R TONNESEN, P AF HIRSCH, A SLAMA, K ALBERISIO, A FOWLER, G LAGRUE, G MALVEZZI, I MANLEY, M MOLIMARD, R TONNESEN, P TI SMOKING CESSATION METHODS - RECOMMENDATIONS FOR HEALTH-PROFESSIONALS - ADVISORY GROUP OF THE EUROPEAN SCHOOL OF ONCOLOGY SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID NICOTINE CHEWING-GUM; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND TRIAL; GENERAL-PRACTICE; PATCH; THERAPY; PRACTITIONERS; INTERVENTION; PHYSICIANS; TOBACCO AB Smoking is the leading preventable cause of death. Approximately 40% of Europeans now smoke. Many smokers want to stop but do not make the attempt, and of those who try, most are unsuccessful. Primary care health providers can help their patients to stop by using brief behavioural and pharmacological interventions. Specialised smoking cessation clinics can support selected patients referred by primary care providers. This report reviews intervention techniques for health care providers, which, in combination with effective legislative and educational interventions, can significantly reduce the prevalence of smoking. C1 IST NAZL RIC CANC,RESPONSABILE SERV PSICOL,I-16132 GENOA,ITALY. UNIV OXFORD,RADCLIFFE INFIRM,DEPT COMMUNITY MED & GEN PRACTICE,OXFORD OX2 6HE,ENGLAND. HOP HENRI MONDOR,INSERM,U139,F-94010 CRETEIL,FRANCE. LEGA ITALIANA LOTTO CONTRO & TUMORI,I-20133 MILAN,ITALY. NCI,BETHESDA,MD 20892. UER BIOMED SAINTS PERES,F-75006 PARIS,FRANCE. RUDOLPH BERGHS GADEZO,DK-2100 COPENHAGEN 0,DENMARK. RP HIRSCH, A (reprint author), HOP ST LOUIS,SERV PNEUMOL,1 AV CLAUDE VELLEFAUX,F-75475 PARIS 10,FRANCE. NR 64 TC 9 Z9 10 U1 2 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 2 BP 253 EP 263 DI 10.1016/0959-8049(94)90104-X PG 11 WC Oncology SC Oncology GA NA106 UT WOS:A1994NA10600035 PM 8155401 ER PT J AU WARENIUS, HM BROWNING, PGW BRITTEN, RA PEACOCK, JA RAPP, UR AF WARENIUS, HM BROWNING, PGW BRITTEN, RA PEACOCK, JA RAPP, UR TI C-RAF-1 PROTOONCOGENE EXPRESSION RELATES TO RADIOSENSITIVITY RATHER THAN RADIORESISTANCE SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID DOUBLE-STRAND BREAKS; CELL LUNG-CANCER; NIH 3T3 CELLS; BIOLOGICAL-ACTIVITY; IONIZING-RADIATION; RAS ONCOGENE; H-RAS; REPAIR; HETEROGENEITY; TRANSFECTION AB The transfection of several oncogenes, particularly c-raf-1, into mammalian in vitro cell lines has been reported to be associated with increased radioresistance. We have thus investigated (by scanning photodensitometry of western blots) the phenotypic expression of the c-raf-1, c-myc and c-ras protein products in 19 human in vitro cell lines, whose intrinsic cellular sensitivity to 4 MeV photon irradiation has also been determined. High levels of c-raf-1 proto-oncogene product expression did not correlate with increased cellular radioresistance, but rather showed a significant correlation with intrinsic cellular radiosensitivity to photon irradiation for alpha (r = 0.664, P = 0.002), and SF2 (r = -0.655, P = 0.002). There was no significant correlation for the ras family, c-myc or actin. These results conflict with those of previous studies in which transfection of the activated forms of the c-raf-1 oncogene were associated with increased radioresistance, and suggest the possibility that the full length proto-oncogene may influence cellular radiosensitivity in a different manner from that of the activated oncogene. C1 INST CANC RES,RADIOTHERAPY RES UNIT,SUTTON SM2 5PX,SURREY,ENGLAND. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD. RP WARENIUS, HM (reprint author), UNIV LIVERPOOL,DEPT MED,CRC,ONCOL RES UNIT,POB 147,LIVERPOOL L69 3BX,MERSEYSIDE,ENGLAND. NR 30 TC 20 Z9 21 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 3 BP 369 EP 375 DI 10.1016/0959-8049(94)90258-5 PG 7 WC Oncology SC Oncology GA NF756 UT WOS:A1994NF75600020 PM 8204361 ER PT J AU KOC, ON MCFEE, M REED, E GERSON, SL AF KOC, ON MCFEE, M REED, E GERSON, SL TI DETECTION OF PLATINUM DNA-ADDUCTS IN CORD-BLOOD LYMPHOCYTES FOLLOWING IN-UTERO PLATINUM EXPOSURE SO EUROPEAN JOURNAL OF CANCER LA English DT Letter ID CHEMOTHERAPY; CANCER; CISPLATIN C1 CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. UNIV CLEVELAND HOSP,CLEVELAND,OH 44106. NIH,BETHESDA,MD 20892. NR 7 TC 23 Z9 23 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 5 BP 716 EP 717 PG 2 WC Oncology SC Oncology GA NP813 UT WOS:A1994NP81300036 PM 8080694 ER PT J AU SETH, A PALLI, D MARIANO, JM METCALF, R VENANZONI, MC BIANCHI, S KOTTARIDIS, SD PAPAS, TS AF SETH, A PALLI, D MARIANO, JM METCALF, R VENANZONI, MC BIANCHI, S KOTTARIDIS, SD PAPAS, TS TI P53 GENE-MUTATIONS IN WOMEN WITH BREAST-CANCER AND A PREVIOUS HISTORY OF BENIGN BREAST DISEASE SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE BREAST CANCER; BENIGN BREAST DISEASE; P53 TUMOR SUPPRESSOR GENE; MUTATIONS ID MEDICAL PROGRESS; CARCINOMAS AB Mutations of the p53 tumour suppressor gene are the most common genetic lesions in human cancers and have been reported in breast cancer as part of the Li-Fraumeni syndrome. In the present study, we determined frequencies and types of the p53 mutations in breast cancer tissues in women with a history of benign breast disease (BBD) identified in Florence, Italy, with (n = 6) or without (n = 10) a family history of breast cancer. Among the cases with a family history of breast cancer and BBD, 2 out of 6 had p53 gene mutations in cancer samples. 1 patient had a mutation at codon 248 and the other had double mutations at codons 243 and 241. In these cases, the p53 gene was also analysed in the tissue samples from previous BBD lesions; however, no mutations were observed (0 out of 6). These results suggest that the p53 mutations occur during advanced stages of tumour progression. In sporadic breast cancer cases with a history of BBD, p53 point mutations were observed in four samples (4 out of 10). Two of these mutations turned out to be silent changes and one of the samples showed triple mutations at amino acid positions 267, 277 and 296. No p53 gene mutations were found in the breast tumour tissues of 10 additional women from the same area with a family history of breast cancer, but no previous BBD (0 out of 10). Family history of breast cancer does not appear to affect the frequency of p53 mutations in women with a previous history of BBD. C1 CSPO,EPIDEMIOL UNIT,FLORENCE,ITALY. US FDA,CTR BIOL EVALUAT & RES,MOLEC MED GENET LAB,BETHESDA,MD 20892. UNIV FLORENCE,DEPT PATHOL,FLORENCE,ITALY. PAPANIKOLAOU RES CTR ONCOL & EXPTL SURG,HELLENIC ANTICANC INST,ATHENS,GREECE. RP SETH, A (reprint author), NCI,MOLEC ONCOL LAB,POB B,FREDERICK,MD 21702, USA. OI PALLI, Domenico/0000-0002-5558-2437 NR 24 TC 9 Z9 10 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 6 BP 808 EP 812 DI 10.1016/0959-8049(94)90297-6 PG 5 WC Oncology SC Oncology GA NW063 UT WOS:A1994NW06300017 PM 7917542 ER PT J AU VANDENBRULE, FA BERCHUCK, A BAST, RC LIU, FT GILLET, C SOBEL, ME CASTRONOVO, V AF VANDENBRULE, FA BERCHUCK, A BAST, RC LIU, FT GILLET, C SOBEL, ME CASTRONOVO, V TI DIFFERENTIAL EXPRESSION OF THE 67-KD LAMININ RECEPTOR AND 31-KD HUMAN LAMININ-BINDING PROTEIN IN HUMAN OVARIAN CARCINOMAS SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE OVARIAN CANCER; LAMININ RECEPTORS ID MESSENGER-RNA; HUMAN COLON; CELLS; MACROPHAGES AB The expression of the 67-kD laminin receptor (67LR) and the 31-kD human laminin-binding protein (HLBP31), two proteins involved in cancer cell laminin interaction, was evaluated on 30 ovarian cancer specimens. Expression of the 67LR was increased (up to 2.5-fold, in 87% of the patients), while HLBP31 expression was downregulated in cancer cells compared with the normal tissue, as detected by northern blotting and immunohistochemistry. The immunohistochemical study demonstrated that the 67LR was significantly overexpressed (P < 0.05) in the group of patients whose cytoreductive surgery was suboptimal, and those with poor clinical outcome. No correlation was observed between HLBP31 expression and clinicopathological features. Increased expression of the 67LR appears to correlate with the invasive phenotype of ovarian cancer cells and suggests a role of the latter in ovarian cancer invasion. C1 NCI,MOLEC PATHOL SECT,PATHOL LAB,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DURHAM,NC 27710. SCRIPPS CLIN & RES FDN,LA JOLLA,CA 92037. RP VANDENBRULE, FA (reprint author), UNIV LIEGE,METASTASIS RES LAB,TOUR PATHOL 3,B23,SART TILMAN,B-4000 LIEGE,BELGIUM. RI Bast, Robert/E-6585-2011 OI Bast, Robert/0000-0003-4621-8462 NR 20 TC 100 Z9 101 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 8 BP 1096 EP 1099 DI 10.1016/0959-8049(94)90464-2 PG 4 WC Oncology SC Oncology GA PH327 UT WOS:A1994PH32700013 PM 7654437 ER PT J AU BLAESE, RM ISHIIMORITA, H MULLEN, C RAMSEY, J RAM, Z OLDFIELD, E CULVER, K AF BLAESE, RM ISHIIMORITA, H MULLEN, C RAMSEY, J RAM, Z OLDFIELD, E CULVER, K TI IN-SITU DELIVERY OF SUICIDE GENES FOR CANCER-TREATMENT SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID THYMIDINE KINASE GENES; BRAIN-TUMORS; CYTOSINE DEAMINASE; GLIOMA-CELLS; 5-FLUOROCYTOSINE; INVIVO C1 NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. IOWA METHODIST HOSP,INST HUMAN GENE THERAPY,DES MOINES,IA. RP BLAESE, RM (reprint author), NATL CTR HUMAN GENOME RES,CLIN GENE THERAPY BRANCH,BETHESDA,MD, USA. NR 18 TC 31 Z9 31 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 8 BP 1190 EP 1193 DI 10.1016/0959-8049(94)90482-0 PG 4 WC Oncology SC Oncology GA PH327 UT WOS:A1994PH32700031 PM 7654455 ER PT J AU CLERICI, M FERRARIO, E TRABATTONI, D VIVIANI, S BONFANTI, V VENZON, DJ CLERICI, E SHEARER, GM VILLA, ML AF CLERICI, M FERRARIO, E TRABATTONI, D VIVIANI, S BONFANTI, V VENZON, DJ CLERICI, E SHEARER, GM VILLA, ML TI MULTIPLE DEFECTS OF T-HELPER CELL-FUNCTION IN NEWLY-DIAGNOSED PATIENTS WITH HODGKINS-DISEASE SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE HODGKINS LYMPHOMA; IMMUNOLOGY; T HELPER; INTERLEUKIN-2 ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; SOLUBLE INTERLEUKIN-2 RECEPTORS; KAPOSIS-SARCOMA; AIDS; LYMPHOMA; INFECTION; PROLIFERATION; THERAPY; HIV; LYMPHOCYTES AB T helper cell(TH) function, as assessed by interleukin-2 (IL-2) production and [H-3]thymidine incorporation, was studied in 47 newly diagnosed untreated patients with Hodgkin's disease (HD) and 34 healthy controls. Three different stimuli were used to stimulate in vitro peripheral blood mononuclear cells (PBMC): influenza A vaccine (FLU), HLA alloantigens (ALLO) and phytohaemagglutinin (PHA). Four different patterns of TH function were observed in HD patients: (1) IL-2 production in response to all of the stimuli (40%); (2) IL-2 production in response to ALLO and PHA but not to FLU (26%); (3) IL-2 production in response to PHA alone (19%); and (4) failure to respond by IL-2 production to any of the three of the stimuli (15%). Thus, defective in vitro TH function was detected in the majority of these patients (60%). Defective TH function was observed in none of the 34 controls. Severely compromised TH function (patterns 3 and 4) tended to be associated with more advanced clinical presentation and more compromised haematological parameters (P < 0.05). The IL-2 production assay was more sensitive than the proliferative assay as only 30% of the HD patients failed to proliferate in response to FLU, and none failed to proliferate in response to either ALLO or PHA; this assay can detect subtle, multiple patterns of immune dysregulation in untreated HD patients. Our results suggest that HD is associated with a fundamental dysregulation in TH function, illustrate the complexity of such dysregulation, and raise the possibility that HD progression will be associated with a type-1-type-2 switch in immunoregulatory cytokine production. C1 IST NAZL TUMORI,I-20133 MILAN,ITALY. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP CLERICI, M (reprint author), UNIV MILAN,CATTEDRA IMMUNOL,I-20133 MILAN,ITALY. RI Venzon, David/B-3078-2008; Trabattoni, Daria/G-7424-2012 NR 44 TC 34 Z9 34 U1 2 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 10 BP 1464 EP 1470 DI 10.1016/0959-8049(94)00305-O PG 7 WC Oncology SC Oncology GA PP467 UT WOS:A1994PP46700013 PM 7833103 ER PT J AU STEIN, U WALTHER, W WUNDERLICH, V AF STEIN, U WALTHER, W WUNDERLICH, V TI POINT MUTATIONS IN THE MDR1 PROMOTER OF HUMAN OSTEOSARCOMAS ARE ASSOCIATED WITH IN-VITRO RESPONSIVENESS TO MULTIDRUG-RESISTANCE RELEVANT DRUGS SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE SARCOMAS; MULTIDRUG RESISTANCE; MDR1 GENE; PROMOTER; MUTATION ID P-GLYCOPROTEIN GENE; HUMAN-CELLS; EXPRESSION; P53; ACTIVATION; MODULATION; CARCINOMA; PROTEIN; REGION AB Among human sarcomas, osteosarcomas usually display high intrinsic mdr1 expression while malignant fibrous histiocytomas (MFH) do not. A comparative polymerase chain reaction (PCR)-based sequence analysis of the mdr1 promoter revealed point mutations in seven out of nine osteosarcomas at nucleotides + 103 (2 cases T-->C) and +137 (5 cases G-->T). No changes were seen in eight MFHs. When COS cells transfected with CAT constructs containing the T-->C chloramphenicol acetyltransferase mutant mdr1 promoters were treated with vincristine or doxorubicin, expression of the CAT gene was enhanced to a higher extent than with constructs containing wild-type or G-->T-mutant mdr1 promoters. We suggest that there is a correlation between the type of mdr1 promoter mutation and responsiveness to MDR relevant drugs. C1 HUMBOLDT UNIV BERLIN,BIOL SECT,BERLIN,GERMANY. RP STEIN, U (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DRUG DISCOVERY RES & DEV LAB,DEV THERAPEUT PROGRAM,BLDG 1052,FREDERICK,MD 21702, USA. NR 22 TC 42 Z9 45 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 10 BP 1541 EP 1545 DI 10.1016/0959-8049(94)00287-F PG 5 WC Oncology SC Oncology GA PP467 UT WOS:A1994PP46700025 PM 7833115 ER PT J AU MCVICAR, DW MASON, AT BERE, EW ORTALDO, JR AF MCVICAR, DW MASON, AT BERE, EW ORTALDO, JR TI ACTIVATION OF PERIPHERAL LARGE GRANULAR LYMPHOCYTES WITH THE SERINE/THREONINE PHOSPHATASE INHIBITOR, OKADAIC ACID SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE OKADAIC ACID; INTERFERON-GAMMA; NATURAL KILLER; PROTEIN PHOSPHATASE; KINASE RENATURATION ID MEDIATED CYTO-TOXICITY; PROTEIN-KINASE; PHORBOL ESTER; CELLS; PHOSPHORYLATION; CYTOTOXICITY; SIGNAL; TOXIN; S6 AB The murine polyether fatty acid, okadaic acid, is a potent inhibitor of serine/threonine phosphatases in eukaryotic cells. This compound inhibits both protein phosphatase 1 (PP1) and phosphatase 2A (PP2A). Here we have examined the potential of okadaic acid as an activator of fresh peripheral CD3(-) large granular lymphocytes (LGL). We demonstrate that overnight exposure of LGL to as little as 1 nM okadaic acid induced an increase in natural killing against the K562 cell line, but does not induce LAK activity Optimal cytotoxic activation (2-fold) occurred at 0.01-1.0 nM okadaic acid, with a return to baseline levels at 10-20 nM, and inhibition, likely due to toxicity, at 40 nM. In addition, okadaic acid at doses greater than or equal to 20 nM induced LGL but not T cells to produce interferon-gamma. Similar to phorbol esters, overnight incubation with okadaic acid causes a dose-dependent reduction in expression of the low-affinity receptor for the Fc portion of IgG (CD16). However, unlike phorbol ester, short-term (5 min) okadaic acid treatment did not block CD16-mediated Ca2+ mobilization in LGL. To address the underlying biochemical mechanisms of okadaic acid activities, the levels of several as-yet-unidentified serine/threonine kinases were assayed after renaturation. Under these conditions, okadaic acid induced similar increases in kinase levels in both T cells and LGL. Taken together: these data suggest an important role for PP1 and PP2A in LGL physiology, and define okadaic acid as a potentially important biological response modifier for the study of LGL and T cell biochemistry, signal transduction, and transcriptional regulation. RP MCVICAR, DW (reprint author), NCI,FCRDR,DIV CANC TREATMENT,EXPTL IMMUNOL LAB,BIOL RESPONSE MODIFIERS PROGRAM,BLDG 560,RM 31-93,FREDERICK,MD 21702, USA. RI McVicar, Daniel/G-1970-2015 NR 31 TC 8 Z9 8 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 1994 VL 24 IS 1 BP 165 EP 170 DI 10.1002/eji.1830240125 PG 6 WC Immunology SC Immunology GA MT838 UT WOS:A1994MT83800024 PM 8020552 ER PT J AU RAUSCHECKER, JP KNIEPERT, U AF RAUSCHECKER, JP KNIEPERT, U TI AUDITORY LOCALIZATION BEHAVIOR IN VISUALLY DEPRIVED CATS SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE HEARING; SOUND LOCALIZATION; AUDITORY SPACE PERCEPTION; VISUAL DEPRIVATION; BLINDNESS; AUDITORY COMPENSATION; CROSS-MODAL; PLASTICITY ID ANTERIOR ECTOSYLVIAN SULCUS; SOUND-LOCALIZATION; SUPERIOR COLLICULUS; SPATIAL LOCALIZATION; BRAIN-STEM; PATHWAYS; BLIND; ORGANIZATION; DEPRIVATION; KITTENS AB The ability to localize sounds in azimuth was tested in five cats that had been binocularly deprived of vision from birth for several months and in three normal age-matched controls. Brief tone bursts were presented in an eight-choice apparatus along 360 degrees of the azimuthal plane at constant elevation. Using positive reinforcement techniques, the cats were trained to walk from the centre of the 3 m diameter circular enclosure to the hidden loudspeakers. The distribution of sound localization error from 55 trials per cat at each speaker position was measured, and its standard deviation was used to assess the precision of sound localization. All cats localized tones straight ahead of them most precisely; performance at lateral and rear positions was gradually less precise. When the sound localization ability of normal and binocularly deprived cats was compared across speakers, a significantly enhanced precision was found for binocularly deprived cats overall (P < 0.002; two-way analysis of variance). An improvement was found at each individual speaker position, but it was greatest at lateral and rear positions. In two sets of control experiments normal cats were retested (i) in the dark with the aid of an infrared camera and (ii) after 3 months of binocular lid suture. Normal cats in the dark did not show any differences in their sound localization behaviour. Late-deprived cats showed a tendency for better performance, which fell short of statistical significance. Our results in visually deprived cats agree well with some reports on the sound localization ability of blind humans, but disagree with others. Our data provide support for a hypothesis of compensatory plasticity, in which sensory functions get sharpened with the loss of another modality. They seem to rule out the necessity for vision to play a role in the postnatal calibration of auditory space. C1 MAX PLANCK INST BIOL CYBERNET,W-7400 TUBINGEN,GERMANY. RP RAUSCHECKER, JP (reprint author), NIMH,NEUROPHYSIOL LAB,POB 608,POOLESVILLE,MD 20837, USA. RI Rauschecker, Josef/A-4120-2013 NR 62 TC 91 Z9 92 U1 0 U2 10 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PD JAN 1 PY 1994 VL 6 IS 1 BP 149 EP 160 DI 10.1111/j.1460-9568.1994.tb00256.x PG 12 WC Neurosciences SC Neurosciences & Neurology GA MT048 UT WOS:A1994MT04800015 PM 8130930 ER PT J AU HASHIMOTO, K MANTIONE, CR SPADA, MR NEUMEYER, JL LONDON, ED AF HASHIMOTO, K MANTIONE, CR SPADA, MR NEUMEYER, JL LONDON, ED TI FURTHER CHARACTERIZATION OF [H-3] IFENPRODIL BINDING IN RAT-BRAIN SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION LA English DT Article DE [H-3] IFENPRODIL BINDING; POLYAMINES; NMDA RECEPTOR (N-METHYL-D-ASPARTATE) A RECEPTOR; BRAIN (RAT) ID D-ASPARTATE RECEPTOR; POLYAMINE-SENSITIVE SITE; ANTI-ISCHEMIC AGENTS; NMDA RECEPTOR; GLYCINE SITE; PHARMACOLOGICAL CHARACTERIZATION; I-125 IFENPRODIL; SIGMA-RECEPTORS; H-3 IFENPRODIL; MOUSE-BRAIN AB The present study was undertaken to characterize [H-3]ifenprodil binding in rat brain. [H-3]ifenprodil showed saturable, high-affinity binding at 4 degrees C. Specific binding, defined with 10 mu M ifenprodil as a competitor, was inhibited biphasically by the s receptor ligands, GBR 12909, 1,3-di-o-tolylguanidine (DTG), and (+)-3-(3-hydroxyphenyl)-N-propylpiperidine ((+)3-PPP). At 4 degrees C, 3 mu M GBR 12909, which inhibited about 50% of specific binding of [H-3]ifenprodil, was used to mask a receptors. Under these conditions, specific binding of [H-3]ifenprodil was inhibited potently by ifenprodil, SL 82.0715, poly(L-arginine), poly(L-lysine), neomycin, ruthenium red, spermine, arcaine and spermidine. In the presence of 3 mu M GBR 12909, Zn2+ and Mg2+ partially inhibited specific binding of [H-3]ifenprodil at 4 degrees C. In contrast, in the absence of GBR 12909, at 37 degrees C specific binding of [H-3]ifenprodil was partially inhibited by Zn2+, but not by Mg2+. The anatomical distribution of [3H]ifenprodil binding at 4 degrees C (GBR 12909 included) in rat brain closely paralleled that of [3H]MK-801 (dizocilpine) binding (r=0.971, P<0.005). Without GBR 12909, specific [H-3]ifenprodil binding at 37 degrees C was inhibited potently by a ligands. In the presence of 3 mu M GBR 12909, [H-3]ifenprodil binding at 4 degrees C was highest in synaptosomal and myelin fractions; however, without GBR 12909, [H-3]ifenprodil binding at 37 degrees C was highest in microsomal and myelin fractions, consistent with the subcellular distribution of a receptors. The results suggest that, in the presence of 3 mu M GBR 12909, at 4 degrees C, [H-3]ifenprodil binds to sites that are sensitive to polyamines and related compounds; and that without GBR 12909, at 37 degrees C, [H-3]ifenprodil interacts with a receptors in rat brain. C1 NIDA, ADDICT RES CTR, NEUROSCI BRANCH, NEUROIMAGING & DRUG ACT SECT, BALTIMORE, MD 21224 USA. RES BIOCHEM INC, NATICK, MA 01706 USA. JOHNS HOPKINS MED INST, DEPT RADIOL, BALTIMORE, MD 21205 USA. UNIV MARYLAND, SCH MED, DEPT PHARMACOL & EXPTL THERAPEUT, BALTIMORE, MD 21201 USA. NR 44 TC 56 Z9 56 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0922-4106 J9 EUR J PHARM-MOLEC PH JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect. PD JAN 1 PY 1994 VL 266 IS 1 BP 67 EP 77 DI 10.1016/0922-4106(94)90211-9 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MR471 UT WOS:A1994MR47100010 PM 7907988 ER PT S AU LUCIER, GW AF LUCIER, GW BE Fracchia, GN TI ISSUES IN TOXICITY TESTING FOR ENVIRONMENTAL CHEMICALS AND PHARMACEUTICALS SO EUROPEAN MEDICINES RESEARCH: PERSPECTIVES IN PHARMACOTOXICOLOGY AND PHARMACOVIGILANCE SE BIOMEDICAL AND HEALTH RESEARCH LA English DT Proceedings Paper CT Conference on European Medicines Research: Perspectives in Pharmacotoxicology and Pharmacovigilance CY OCT 06, 1993 CL BRUSSELS, BELGIUM C1 NIEHS,BIOCHEM RISK ANAL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU I O S PRESS PI AMSTERDAM PA VAN DIEMENSTRAAT 94, 1013 CN AMSTERDAM, NETHERLANDS SN 0929-6743 BN 90-5199-154-1 J9 BIOM HLTH R PY 1994 VL 7 BP 51 EP 57 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA BA69N UT WOS:A1994BA69N00008 ER PT B AU FEDOROVA, OV BAGROV, AY AUSTINLANE, JL ANDERSON, DE AF FEDOROVA, OV BAGROV, AY AUSTINLANE, JL ANDERSON, DE BE Haunso, S Kjeldsen, K TI NA, K-ATPASE INHIBITION DURING PRESSOR RESPONSE TO HYPOVENTILATION SO EUROPEAN SECTION MEETING - INTERNATIONAL SOCIETY FOR HEART RESEARCH LA English DT Proceedings Paper CT XV European-Section Meeting of the International-Society-for-Heart-Research CY JUN 08-11, 1994 CL COPENHAGEN, DENMARK SP INT SOC HEART RES, EUROPEAN SECT C1 NIA,BEHAV SCI LAB,BALTIMORE,MD 21224. 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 88-323-0608-5 PY 1994 BP 385 EP 388 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA BB91T UT WOS:A1994BB91T00056 ER PT B AU GAMBASSI, G AF GAMBASSI, G BE Haunso, S Kjeldsen, K TI FUNCTIONAL ASPECTS OF ALPHA-1 ADRENERGIC RECEPTORS IN MYOCARDIAL CELLS SO EUROPEAN SECTION MEETING - INTERNATIONAL SOCIETY FOR HEART RESEARCH LA English DT Proceedings Paper CT XV European-Section Meeting of the International-Society-for-Heart-Research CY JUN 08-11, 1994 CL COPENHAGEN, DENMARK SP INT SOC HEART RES, EUROPEAN SECT C1 NIA,CARDIOVASC SCI LAB,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 88-323-0608-5 PY 1994 BP 501 EP 505 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA BB91T UT WOS:A1994BB91T00080 ER PT J AU CLARK, GC TAYLOR, MJ AF CLARK, GC TAYLOR, MJ TI TUMOR-NECROSIS-FACTOR INVOLVEMENT IN THE TOXICITY OF TCDD - THE ROLE OF ENDOTOXIN IN THE RESPONSE SO EXPERIMENTAL AND CLINICAL IMMUNOGENETICS LA English DT Article DE TUMOR NECROSIS FACTOR; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN; DIOXIN; ENDOTOXIN; LIPOPOLYSACCHARIDE; CACHEXIA; C3H/HEJ MICE; C57BL/6J MICE ID AH LOCUS; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN; EXPOSURE; DIOXIN; MICE; DEXAMETHASONE; HAMSTER; RAT AB We have previously demonstrated that tumor necrosis factor is involved in the acute toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), since therapies designed to attenuate the effects of tumor necrosis factor resulted in reduced mortality and toxicity in mice exposed to an LD(75) dose of TCDD. The current study addresses whether endotoxin may be a contributing factor in the cachexia and mortality resulting from TCDD exposure. Endotoxin-nonresponsive C3H/HeJ mice and endotoxin-responsive C57BL/6 mice were treated with 350 mu g/kg TCDD and body weight and mortality were recorded. C3H/HeJ mice showed no trend in body weight loss (p = 0.554), while C57BL/6 mice demonstrated a statistically significant (p < 0.01) linear decline in body weight of -0.23 g/day, resulting in a net loss of 3.5 g over 15 days preceding mortality. Mortality was observed in the C57BL/6 mice beginning on day 16 with 100% of the mice dying by the 23rd day while no mortality was observed in C3H/HeJ mice until the 24th day of the study with only 22% mortality observed. These data further demonstrate that endotoxin is a contributing factor to the cachexia and lethality of TCDD. RP CLARK, GC (reprint author), NIEHS,POB 12233,MAIL DROP D4-04,RES TRIANGLE PK,NC 27709, USA. NR 29 TC 13 Z9 13 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-9670 J9 EXP CLIN IMMUNOGENET JI Exp. Clin. Immunogenet. PY 1994 VL 11 IS 2-3 BP 136 EP 141 PG 6 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology GA PL327 UT WOS:A1994PL32700010 PM 7826662 ER PT J AU KUTTY, G DUNCAN, T NICKERSON, JM SI, JS VANVEEN, T CHADER, GJ WIGGERT, B AF KUTTY, G DUNCAN, T NICKERSON, JM SI, JS VANVEEN, T CHADER, GJ WIGGERT, B TI LIGHT DEPRIVATION PROFOUNDLY AFFECTS GENE-EXPRESSION OF INTERPHOTORECEPTOR RETINOID-BINDING PROTEIN IN THE MOUSE EYE SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE INTERPHOTORECEPTOR RETINOID-BINDING PROTEIN; IRBP; LIGHT DEPRIVATION; GENE EXPRESSION; MOUSE EYE ID MESSENGER-RNA; DEVELOPMENTAL EXPRESSION; PHOTORECEPTOR NEURONS; 48-KDA PROTEIN; VITAMIN-A; IRBP; RD; RHODOPSIN; SECRETION; MATRIX C1 NEI,BETHESDA,MD 20892. EMORY UNIV,DEPT OPHTHALMOL,ATLANTA,GA 30322. GOTHENBURG UNIV,DEPT ZOOL,S-40031 GOTHENBURG,SWEDEN. NR 35 TC 18 Z9 18 U1 0 U2 3 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JAN PY 1994 VL 58 IS 1 BP 65 EP 75 DI 10.1006/exer.1994.1195 PG 11 WC Ophthalmology SC Ophthalmology GA MX141 UT WOS:A1994MX14100007 PM 8157102 ER PT J AU RAO, CM ZIGLER, JS AF RAO, CM ZIGLER, JS TI ON THE INTRACELLULAR STABILITY OF LENS CRYSTALLINS - REPLY SO EXPERIMENTAL EYE RESEARCH LA English DT Letter C1 NEI,BETHESDA,MD 20892. RP RAO, CM (reprint author), CTR CELLULAR & MOLEC BIOL,HYDERABAD 500007,INDIA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JAN PY 1994 VL 58 IS 1 BP 127 EP 128 PG 2 WC Ophthalmology SC Ophthalmology GA MX141 UT WOS:A1994MX14100015 ER PT J AU ROTH, GS INGRAM, DK BAKER, GT AF ROTH, GS INGRAM, DK BAKER, GT TI THE NATHAN-W-SHOCK-MEMORIAL-LECTURESHIP SO EXPERIMENTAL GERONTOLOGY LA English DT Editorial Material C1 SHOCK AGING RES FDN,BALTIMORE,MD. RP ROTH, GS (reprint author), NIA,MOLEC PHYSIOL & GENET SECT,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PD JAN-FEB PY 1994 VL 29 IS 1 BP 1 EP 1 DI 10.1016/0531-5565(94)90057-4 PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA MX873 UT WOS:A1994MX87300001 ER PT J AU BURKE, EM HORTON, WE PEARSON, JD CROW, MT MARTIN, GR AF BURKE, EM HORTON, WE PEARSON, JD CROW, MT MARTIN, GR TI ALTERED TRANSCRIPTIONAL REGULATION OF HUMAN INTERSTITIAL COLLAGENASE IN CULTURED SKIN FIBROBLASTS FROM OLDER DONORS SO EXPERIMENTAL GERONTOLOGY LA English DT Article DE METALLOPROTEINASES; INTERSTITIAL COLLAGENASE; TIMP-1; AGING; WOUND HEALING ID TISSUE INHIBITOR; ACTIVE FORMS; CELL-LINES; GENE; EXPRESSION; METALLOPROTEINASES; INTERLEUKIN-1; PURIFICATION; INDUCTION; PRECURSOR AB Primary human dermal fibroblasts isolated from the medial aspect of the proximal forearm of young and old donors were compared for the expression of interstitial collagenase, 72 kDa type IV collagenase, the tissue inhibitor of metalloproteinase type 1, and pro-alpha 2 (I) collagen mRNA at basal levels and after stimulation with the tumor promotor 12-O-tetradecanoyl-phorbol-13-acetate. Higher basal and induced steady-state mRNA levels of interstitial collagenase were found in the cells from older donors. Ratios of basal and induced steady-state mRNA levels of interstitial collagenase to pro-alpha 2 (I) collagen, and interstitial collagenase to the tissue inhibitor of metalloproteinases type 1 were also higher in the cells from older donors. Seventy-two kiloDalton type IV collagenase and pro-alpha 2 (I) collagen mRNA showed similar levels of expression in the cells from young and old donors and were not altered by treatment with 12-O-tetradecanoyl-phorbol-13-acetate. Transient transfection assays with the interstitial collagenase promoter linked to a reporter gene showed increased activity of the reporter in cell strains with high interstitial collagenase mRNA levels. Mobility shift assays demonstrated increased binding activity to the specific 12-O-tetradecanoyl-phorbol-13-acetate response element in nuclear extracts from the cell strains with higher induced collagenase mRNA levels and higher reporter gene activity. These findings are consistent with the observed phenotype of interstitial collagenase and its specific tissue inhibitor in the senescent fibroblast aging model. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV GERIATR MED,BALTIMORE,MD 21224. RP BURKE, EM (reprint author), NIA,GERONTOL RES CTR,MOLEC GENET LAB,RM 2E15,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 54 TC 36 Z9 36 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PD JAN-FEB PY 1994 VL 29 IS 1 BP 37 EP 53 DI 10.1016/0531-5565(94)90061-2 PG 17 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA MX873 UT WOS:A1994MX87300005 PM 8187840 ER PT S AU TAKAMI, H BURBELO, PD FUKUDA, K CHANG, HS PHILLIPS, SL YAMADA, Y AF TAKAMI, H BURBELO, PD FUKUDA, K CHANG, HS PHILLIPS, SL YAMADA, Y BE Koide, H Hayashi, T TI MOLECULAR-ORGANIZATION AND GENE-REGULATION OF TYPE-IV COLLAGEN SO EXTRACELLULAR MATRIX IN THE KIDNEY SE CONTRIBUTIONS TO NEPHROLOGY LA English DT Proceedings Paper CT 6th International Symposium on Basement Membrane: Extracellular Matrix in the Kidney CY MAY 29-JUN 01, 1993 CL SHIZUOKA, JAPAN C1 UNIV PITTSBURGH,SCH MED,DEPT MOLEC GENET & BIOCHEM,PITTSBURGH,PA 15261. KAGOSHIMA UNIV,SCH MED,DEPT OTOLARYNGOL,KAGOSHIMA 890,JAPAN. RP TAKAMI, H (reprint author), NIDR,DEV BIOL LAB,BLDG 30,BETHESDA,MD 20892, USA. RI Burbelo, Peter/B-1027-2009 NR 0 TC 8 Z9 8 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0302-5144 BN 3-8055-5833-3 J9 CONTRIB NEPHROL JI Contrib.Nephrol. PY 1994 VL 107 BP 36 EP 46 PG 11 WC Urology & Nephrology SC Urology & Nephrology GA BA03T UT WOS:A1994BA03T00006 PM 8004973 ER PT S AU STRIKER, GE PETEN, EP YANG, CW STRIKER, LJ AF STRIKER, GE PETEN, EP YANG, CW STRIKER, LJ BE Koide, H Hayashi, T TI GLOMERULOSCLEROSIS - STUDIES OF ITS PATHOGENESIS IN HUMANS AND ANIMALS SO EXTRACELLULAR MATRIX IN THE KIDNEY SE CONTRIBUTIONS TO NEPHROLOGY LA English DT Proceedings Paper CT 6th International Symposium on Basement Membrane: Extracellular Matrix in the Kidney CY MAY 29-JUN 01, 1993 CL SHIZUOKA, JAPAN RP STRIKER, GE (reprint author), NIDDK,DIV KIDNEY UROL & HEMATOL DIS,RENAL CELL BIOL SECT,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0302-5144 BN 3-8055-5833-3 J9 CONTRIB NEPHROL JI Contrib.Nephrol. PY 1994 VL 107 BP 124 EP 131 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA BA03T UT WOS:A1994BA03T00017 PM 8004958 ER PT S AU KOPP, JB RAY, PE ADLER, SH BRUGGEMAN, LA MANGURIAN, CV OWENS, JW ECKHAUS, MA BRYANT, JL KLOTMAN, PE AF KOPP, JB RAY, PE ADLER, SH BRUGGEMAN, LA MANGURIAN, CV OWENS, JW ECKHAUS, MA BRYANT, JL KLOTMAN, PE BE Koide, H Hayashi, T TI NEPHROPATHY IN HIV-TRANSGENIC MICE SO EXTRACELLULAR MATRIX IN THE KIDNEY SE CONTRIBUTIONS TO NEPHROLOGY LA English DT Proceedings Paper CT 6th International Symposium on Basement Membrane: Extracellular Matrix in the Kidney CY MAY 29-JUN 01, 1993 CL SHIZUOKA, JAPAN C1 NIDR,ANIM CARE UNIT,BETHESDA,MD 20892. NIH,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,BETHESDA,MD 20892. HOWARD HUGHES MED INST NIH RES SCHOLARS PROGRAM,BETHESDA,MD. RP KOPP, JB (reprint author), NIDR,DEV BIOL LAB,BLDG 30,ROOM 430,BETHESDA,MD 20892, USA. OI Kopp, Jeffrey/0000-0001-9052-186X NR 0 TC 14 Z9 14 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0302-5144 BN 3-8055-5833-3 J9 CONTRIB NEPHROL JI Contrib.Nephrol. PY 1994 VL 107 BP 194 EP 204 PG 11 WC Urology & Nephrology SC Urology & Nephrology GA BA03T UT WOS:A1994BA03T00027 PM 8004968 ER PT J AU LOPEZ, MLL DATILES, MB PODGOR, MJ VIVINO, MA MAHURKAR, AA LASA, SM AF LOPEZ, MLL DATILES, MB PODGOR, MJ VIVINO, MA MAHURKAR, AA LASA, SM TI REPRODUCIBILITY STUDY OF POSTERIOR SUBCAPSULAR OPACITIES ON THE NEI RETROILLUMINATION IMAGE-ANALYSIS SYSTEM SO EYE LA English DT Article DE CATARACT QUANTIFICATION; IMAGE ANALYSIS; POSTERIOR SUBCAPSULAR CATARACT; REPRODUCIBILITY; RETROILLUMINATION ID LENS OPACITIES; LOCS-II; PHOTOGRAPHS; CATARACTS AB We developed a semi-automated retroillumination image analysis system which combines speed, ease of operation and interactive analysis. The system measures cataract area and integral of cataract density (ID). For system reproducibility evaluation, 20 eyes with posterior subcapsular opacities were captured twice by two photographers. Variability was estimated under a random effects analysis of variance model. Measurement errors for area and for ID were each small contributors to total variability (the sum of variability between study eyes plus measurement error), being 0.4% and 0.1% respectively. The largest contributor to area measurement error was image analysis variability (97%). For ID measurement error, the variability in images (44%) and in image analysis (46%) were major contributors. The reproducibility is comparable to previously described retroillumination analysis systems. This easy to use system may therefore be useful in clinical research studies including possible clinical trials of anti-cataract drugs. C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,CATARACT & CORNEA SECT,BETHESDA,MD 20892. NIH,DIV COMP RES & TECHNOL,COMPUTAT BIOSCI & ENGN LAB,BETHESDA,MD 20892. OI Datiles, Manuel III B./0000-0003-4660-1664 NR 22 TC 2 Z9 2 U1 0 U2 0 PU ROYAL COLL OPHTHALMOLOGISTS PI LONDON PA 17 CORNWALL TERRACE, LONDON, ENGLAND NW1 4QW SN 0950-222X J9 EYE JI Eye PY 1994 VL 8 BP 657 EP 661 PN 6 PG 5 WC Ophthalmology SC Ophthalmology GA PY776 UT WOS:A1994PY77600011 PM 7867822 ER PT S AU SALEM, N PAWLOSKY, RJ AF SALEM, N PAWLOSKY, RJ BE Galli, C Simopoulos, AP Tremoli, E TI HEALTH POLICY ASPECTS OF LIPID NUTRITION AND EARLY DEVELOPMENT SO FATTY ACIDS AND LIPIDS: BIOLOGICAL ASPECTS SE WORLD REVIEW OF NUTRITION AND DIETETICS LA English DT Proceedings Paper CT 1st International Congress of the International-Society-for-the-Study-of-Fatty-Acids-and-Lipids (ISSFAL) CY JUN 30-JUL 03, 1993 CL LUGANO, SWITZERLAND SP INT SOC STUDY FATTY ACIDS & LIPIDS RP SALEM, N (reprint author), NIAAA,DIV INTRAMURAL CLIN & BIOL RES,LMBB,ROOM 55C,12501 WASHINGTON AVE,ROCKVILLE,MD 20852, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0084-2230 BN 3-8055-5959-3 J9 WORLD REV NUTR DIET JI World Rev.Nutr.Diet. PY 1994 VL 75 BP 46 EP 51 PG 6 WC Medicine, Research & Experimental; Nutrition & Dietetics SC Research & Experimental Medicine; Nutrition & Dietetics GA BC15M UT WOS:A1994BC15M00010 PM 7871832 ER PT S AU SALEM, N PAWLOSKY, RJ AF SALEM, N PAWLOSKY, RJ BE Galli, C Simopoulos, AP Tremoli, E TI ARACHIDONATE AND DOCOSAHEXAENOATE BIOSYNTHESIS IN VARIOUS SPECIES AND COMPARTMENTS INVIVO SO FATTY ACIDS AND LIPIDS: BIOLOGICAL ASPECTS SE WORLD REVIEW OF NUTRITION AND DIETETICS LA English DT Proceedings Paper CT 1st International Congress of the International-Society-for-the-Study-of-Fatty-Acids-and-Lipids (ISSFAL) CY JUN 30-JUL 03, 1993 CL LUGANO, SWITZERLAND SP INT SOC STUDY FATTY ACIDS & LIPIDS RP SALEM, N (reprint author), NIAAA,DIV INTRAMURAL CLIN & BIOL RES,LMBB,ROOM 55C,12501 WASHINGTON AVE,ROCKVILLE,MD 20852, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0084-2230 BN 3-8055-5959-3 J9 WORLD REV NUTR DIET JI World Rev.Nutr.Diet. PY 1994 VL 75 BP 114 EP 119 PG 6 WC Medicine, Research & Experimental; Nutrition & Dietetics SC Research & Experimental Medicine; Nutrition & Dietetics GA BC15M UT WOS:A1994BC15M00021 PM 7871811 ER PT S AU MIELE, L PERI, A CORDELLAMIELE, E MUKHERJEE, AB AF MIELE, L PERI, A CORDELLAMIELE, E MUKHERJEE, AB BE Simpson, JL Elias, S TI DEVELOPMENT OF NOVEL, SENSITIVE, NONRADIOACTIVE, QUANTITATIVE ELISA-PCR METHODS POTENTIALLY APPLICABLE TO THE DETECTION OF FETAL CELLS IN MATERNAL CIRCULATION SO FETAL CELLS IN MATERNAL BLOOD: PROSPECTS FOR NONINVASIVE PRENATAL DIAGNOSIS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Fetal Cells in Maternal Blood: Prospects for a Noninvasive Prenatal Diagnosis CY SEP 27-29, 1993 CL ARLINGTON, VA SP NEW YORK ACAD SCI ID CHAIN-REACTION PRODUCTS; HYBRIDIZATION RP MIELE, L (reprint author), NICHHD,HUMAN GENET BRANCH,GENET DEV SECT,NIH BLDG 10,ROOM 9S242,BETHESDA,MD 20892, USA. NR 9 TC 1 Z9 1 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-888-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 731 BP 246 EP 247 DI 10.1111/j.1749-6632.1994.tb55777.x PG 2 WC Cell Biology; Hematology; Multidisciplinary Sciences; Obstetrics & Gynecology SC Cell Biology; Hematology; Science & Technology - Other Topics; Obstetrics & Gynecology GA BB36A UT WOS:A1994BB36A00037 PM 7944128 ER PT S AU CONWAY, JF DUDA, RL CHENG, N HENDRIX, RW STEVEN, AC AF CONWAY, JF DUDA, RL CHENG, N HENDRIX, RW STEVEN, AC BE Bailey, GW GarrattReed, AJ TI BACTERIOPHAGE HK97 - STRUCTURAL TRANSITIONS ALONG THE CAPSID ASSEMBLY PATHWAY SO FIFTY-SECOND ANNUAL MEETING - MICROSCOPY SOCIETY OF AMERICA/TWENTY-NINTH ANNUAL MEETING - MICROBEAM ANALYSIS SOCIETY, PROCEEDINGS SE PROCEEDINGS - ANNUAL MEETING OF THE MICROSCOPY SOCIETY OF AMERICA LA English DT Proceedings Paper CT 52nd Annual Meeting of the Microscopy-Society-of-America/29th Annual Meeting of the Microbeam-Analysis-Society CY JUL 31-AUG 05, 1994 CL NEW ORLEANS, LA SP MICROSCOPY SOC AMER, MICROBEAM ANAL SOC C1 NIAMS,STRUCT BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SAN FRANCISCO PRESS INC PI SAN FRANCISCO PA BOX 426800, SAN FRANCISCO, CA 94142-6800 SN 0424-8201 J9 PROC ANN MEET MSA PY 1994 BP 112 EP 113 PG 2 WC Instruments & Instrumentation SC Instruments & Instrumentation GA BC03U UT WOS:A1994BC03U00056 ER PT S AU TRUS, BL DAVISON, AJ BOOY, FP STEVEN, AC AF TRUS, BL DAVISON, AJ BOOY, FP STEVEN, AC BE Bailey, GW GarrattReed, AJ TI CAPSID STRUCTURE OF CHANNEL CATFISH VIRUS, AN EVOLUTIONARILY DISTANT HERPESVIRUS, BY CRYO-ELECTRON MICROSCOPY SO FIFTY-SECOND ANNUAL MEETING - MICROSCOPY SOCIETY OF AMERICA/TWENTY-NINTH ANNUAL MEETING - MICROBEAM ANALYSIS SOCIETY, PROCEEDINGS SE PROCEEDINGS - ANNUAL MEETING OF THE MICROSCOPY SOCIETY OF AMERICA LA English DT Proceedings Paper CT 52nd Annual Meeting of the Microscopy-Society-of-America/29th Annual Meeting of the Microbeam-Analysis-Society CY JUL 31-AUG 05, 1994 CL NEW ORLEANS, LA SP MICROSCOPY SOC AMER, MICROBEAM ANAL SOC C1 NIAMS,STRUCT BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SAN FRANCISCO PRESS INC PI SAN FRANCISCO PA BOX 426800, SAN FRANCISCO, CA 94142-6800 SN 0424-8201 J9 PROC ANN MEET MSA PY 1994 BP 114 EP 115 PG 2 WC Instruments & Instrumentation SC Instruments & Instrumentation GA BC03U UT WOS:A1994BC03U00057 ER PT S AU CHENG, NQ GRONENBORN, AM CLORE, GM STEVEN, AC AF CHENG, NQ GRONENBORN, AM CLORE, GM STEVEN, AC BE Bailey, GW GarrattReed, AJ TI PH-DEPENDENT POLYMORPHISM OF ASSEMBLIES OF CYTOKINE HMIP-1 beta SO FIFTY-SECOND ANNUAL MEETING - MICROSCOPY SOCIETY OF AMERICA/TWENTY-NINTH ANNUAL MEETING - MICROBEAM ANALYSIS SOCIETY, PROCEEDINGS SE PROCEEDINGS - ANNUAL MEETING OF THE MICROSCOPY SOCIETY OF AMERICA LA English DT Proceedings Paper CT 52nd Annual Meeting of the Microscopy-Society-of-America/29th Annual Meeting of the Microbeam-Analysis-Society CY JUL 31-AUG 05, 1994 CL NEW ORLEANS, LA SP MICROSCOPY SOC AMER, MICROBEAM ANAL SOC C1 NIAMS,STRUCT BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SAN FRANCISCO PRESS INC PI SAN FRANCISCO PA BOX 426800, SAN FRANCISCO, CA 94142-6800 SN 0424-8201 J9 PROC ANN MEET MSA PY 1994 BP 434 EP 435 PG 2 WC Instruments & Instrumentation SC Instruments & Instrumentation GA BC03U UT WOS:A1994BC03U00217 ER PT J AU RESTIFO, NP MINEV, BR TAGGARSE, AS MCFARLAND, BJ WANG, M IRVINE, KR AF RESTIFO, NP MINEV, BR TAGGARSE, AS MCFARLAND, BJ WANG, M IRVINE, KR TI ENHANCING THE RECOGNITION OF TUMOR-ASSOCIATED ANTIGENS SO FOLIA BIOLOGICA LA English DT Article ID CYTOLYTIC T-LYMPHOCYTES; COMPLEX CLASS-I; VACCINIA VIRUS-VACCINE; INTERFERON-GAMMA; INFILTRATING LYMPHOCYTES; CARCINOEMBRYONIC ANTIGEN; GENE-EXPRESSION; MELANOMA-CELLS; ADOPTIVE IMMUNOTHERAPY; ENDOGENOUS ANTIGENS AB Activated CD8+ T cells (T-CD8+) can directly recognize malignant cells because processed fragments of tumour associated antigens (TAA), 8-10 amino acids in length and complexed with MHC class I molecules, are displayed on tumour cell surfaces. Tumour cells have been genetically modified is a variety of ways ill efforts to enhance the immune recognition of TAA. An alternative strategy is the expression of TAA in recombinant or synthetic form. This has been made possible by the recent cloning of TAA recognized by T-CD8+. In this communication we review recent work in our own laboratory on the expression of TAA as synthetic peptide, by ''naked'' plasmid DNA injected intramuscularly or transdermally, and by recombinant viruses including vaccinia (rVV), fowlpox (rFV) and adenovirus (rAd). The expression of TAA in recombinant and synthetic forms allows increased control over the quantity, location, and kinetics of TAA presentation and can result in powerful, Specific, anti-tumour immune responses. RP RESTIFO, NP (reprint author), NCI,DIV CANC TREATMENT,SURG BRANCH,RECOMBINANT & SYNTHET VACCINE GRP,BETHESDA,MD 20892, USA. RI Restifo, Nicholas/A-5713-2008; OI Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z01 BC010763-01, Z99 CA999999, Z99 TW999999] NR 69 TC 17 Z9 18 U1 0 U2 1 PU INST MOLECULAR GENETICS PI PRAGUE 6 PA FOLIA BIOLOGICA(PRAHA) FLEMINGOVO N.2, PRAGUE 6, CZECH REPUBLIC 166 37 SN 0015-5500 J9 FOLIA BIOL-PRAGUE JI Folia Biol.-Prague PY 1994 VL 40 IS 1-2 BP 74 EP 88 PG 15 WC Biochemistry & Molecular Biology; Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Oncology; Cell Biology GA PC660 UT WOS:A1994PC66000007 PM 7958066 ER PT J AU BAKER, PJ HRABA, T AF BAKER, PJ HRABA, T TI T-CELL MEDIATED IMMUNOSUPPRESSION AND ITS IMPLICATIONS FOR THE DEVELOPMENT OF PROTECTIVE IMMUNITY SO FOLIA BIOLOGICA LA English DT Article ID III PNEUMOCOCCAL POLYSACCHARIDE; MONOPHOSPHORYL LIPID-A; LOW-DOSE PARALYSIS; ANTIBODY-RESPONSE; BACTERIAL LIPOPOLYSACCHARIDES; SUPPRESSOR CELLS; B-CELLS; IMMUNOLOGICAL-UNRESPONSIVENESS; CAPSULAR POLYSACCHARIDE; PEYERS PATCHES AB The mechanisms by which regulatory CD4(-) CD8(+) suppressor T cells (Ts) and CD4(+) CD8(-) amplifier T cells (Ta) influence the magnitude of the antibody response to the capsular polysaccharide antigen of type III Streptococcus pneumoniae are reviewed in detail. This represents the best-characterized experimental model system available for demonstrating how subsets of T cells act in a negative and positive manner to control the magnitude of an antibody response. The fact that transferred Ts and Ta elicit their effects in athymic immunized mice affirms, that such regulatory T cells are antigen-specific and act on immune B cells to produce the effects observed. The ability of the lipid A and the inner core-region oligosaccharide fractions of bacterial lipopolysaccharide to abolish and increase the expression of Ts function, respectively, is examined with respect to its immunomodulatory potential and its possible role in enhancing the virulence of Gram-negative bacteria. C1 ACAD SCI CZECH REPUBL,INST MOLEC GENET,CR-16637 PRAGUE 6,CZECH REPUBLIC. RP BAKER, PJ (reprint author), NIAID,DIV MICROBIOL & INFECT DIS,SOLAR BLDG,ROOM 3A36,BETHESDA,MD 20892, USA. NR 50 TC 4 Z9 4 U1 0 U2 0 PU INST MOLECULAR GENETICS PI PRAGUE 6 PA FOLIA BIOLOGICA(PRAHA) FLEMINGOVO N.2, PRAGUE 6, CZECH REPUBLIC 166 37 SN 0015-5500 J9 FOLIA BIOL-PRAGUE JI Folia Biol. PY 1994 VL 40 IS 6 BP 349 EP 358 PG 10 WC Biochemistry & Molecular Biology; Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Oncology; Cell Biology GA QB563 UT WOS:A1994QB56300005 PM 7589694 ER PT J AU WESTERGAARD, GC SUOMI, SJ AF WESTERGAARD, GC SUOMI, SJ TI ASYMMETRICAL MANIPULATION IN THE USE OF TOOLS BY TUFTED CAPUCHIN MONKEYS (CEBUS-APELLA) SO FOLIA PRIMATOLOGICA LA English DT Note DE BIMANUAL MANIPULATION; CAPUCHIN MONKEY; SKILL; TOOL USE; CEBUS APELLA; PROBING BEHAVIOR ID CHIMPANZEES C1 NICHHD,COMPARAT ETHOL LAB,POOLESVILLE,MD. NR 10 TC 12 Z9 12 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 1994 VL 63 IS 2 BP 96 EP 98 PG 3 WC Zoology SC Zoology GA PX903 UT WOS:A1994PX90300008 PM 7813980 ER PT S AU WEBB, TE STROMBERG, PC ABOUISSA, H MOESCHBERGER, M PIERSON, HF CURLEY, RW AF WEBB, TE STROMBERG, PC ABOUISSA, H MOESCHBERGER, M PIERSON, HF CURLEY, RW BE Huang, MT Osawa, T Ho, CT Rosen, RT TI CHEMOPREVENTIVE PHYTOCHEMICALS IN SOY AND LICORICE DIETS AFFECTING KEY RAT ENZYME-SYSTEMS SO FOOD PHYTOCHEMICALS FOR CANCER PREVENTION I: FRUITS AND VEGETABLES SE ACS SYMPOSIUM SERIES LA English DT Article; Proceedings Paper CT Symposium on Food Phytochemicals for Cancer Prevention I: Fruits and Vegetables, at the 204th National Meeting of the American-Chemical-Society CY AUG 23-28, 1992 CL WASHINGTON, DC SP AMER CHEM SOC, DIV AGR & FOOD CHEM ID GLYCYRRHETINIC ACID; PRODUCTS; CANCER AB As a component of a feeding study of the possible chemopreventive diet additives soybean meal and licorice root extract, simplified extraction and HPLC methods were developed for the analysis of the soy isoflavones genistein and daidzein and the licorice triterpenoids glycyrrhizic acid and glycyrrhetinic acid. In the diet containing 25% soybean meal, genistein and daidzein were present at about 2-5 mu g/g of diet although some variability suggests these isoflavones, especially genistein, may not be stable in frozen diet extracts. Markers glycyrrhizic acid and glycyrrhetinic acid showed the 3% licorice extract containing diet to be uniformly mixed and stable with final concentrations of 300 and 20 mu g/g of diet each respectively. Of these markers, only glycyrrhetinic acid was reliably detected in the plasma of rats fed the appropriate diet with an observed concentration of 5.83 mu g/ml. C1 OHIO STATE UNIV,COLL VET MED,DEPT VET PATHOBIOL,COLUMBUS,OH 43210. OHIO STATE UNIV,COLL MED,DEPT SURG,COLUMBUS,OH 43210. OHIO STATE UNIV,COLL MED,DEPT PREVENT MED,COLUMBUS,OH 43210. NCI,BETHESDA,MD 20892. OHIO STATE UNIV,COLL PHARM,DIV MED CHEM & PHARMACOGNOSY,COLUMBUS,OH 43210. RP WEBB, TE (reprint author), OHIO STATE UNIV,COLL VET MED,DEPT BIOCHEM MED,COLUMBUS,OH 43210, USA. NR 17 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 SN 0097-6156 BN 0-8412-2768-3 J9 ACS SYM SER PY 1994 VL 546 BP 361 EP 371 PG 11 WC Chemistry, Multidisciplinary; Chemistry, Analytical; Food Science & Technology; Public, Environmental & Occupational Health; Medicine, Research & Experimental; Nutrition & Dietetics SC Chemistry; Food Science & Technology; Public, Environmental & Occupational Health; Research & Experimental Medicine; Nutrition & Dietetics GA BA14P UT WOS:A1994BA14P00030 ER PT S AU LAROSA, JH AF LAROSA, JH BE Sechzer, JA Griffin, A Pfafflin, SM TI OFFICE OF RESEARCH ON WOMENS HEALTH - NATIONAL-INSTITUTES-OF-HEALTH AND THE WOMENS HEALTH AGENDA SO FORGING A WOMEN'S HEALTH RESEARCH AGENDA: POLICY ISSUES FOR THE 1990S SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Symposium on Forging a Womens Health Research Agenda - Policy Issues for the 1990s CY OCT 23, 1992 CL NEW YORK, NY SP New York Acad Sci, Women Sci Sect ID MYOCARDIAL-INFARCTION; DRUG TRIALS; UNDERREPRESENTATION RP LAROSA, JH (reprint author), NIH,OFF RES WOMENS HLTH,BLDG 1,ROOM 203,BETHESDA,MD 20892, USA. NR 30 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-893-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 736 BP 196 EP 204 DI 10.1111/j.1749-6632.1994.tb12832.x PG 9 WC Public, Environmental & Occupational Health; Multidisciplinary Sciences; Women's Studies SC Public, Environmental & Occupational Health; Science & Technology - Other Topics; Women's Studies GA BD10N UT WOS:A1994BD10N00018 PM 7710206 ER PT B AU LEVIN, IW LEWIS, EN AF LEVIN, IW LEWIS, EN BE Yu, NT Li, XY TI Vibrational spectroscopic imaging microscopy: Chemical and biophysical applications SO FOURTEENTH INTERNATIONAL CONFERENCE ON RAMAN SPECTROSCOPY LA English DT Proceedings Paper CT 14th International Conference on Raman Spectroscopy CY AUG 22-26, 1994 CL HONG KONG, HONG KONG SP Hong Kong Univ Sci & Technol C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, WEST SUSSEX, ENGLAND PO19 1UD BN 0-471-95216-8 PY 1994 BP 864 EP 865 PG 2 WC Multidisciplinary Sciences; Spectroscopy SC Science & Technology - Other Topics; Spectroscopy GA BD55D UT WOS:A1994BD55D00402 ER PT J AU CAO, G CUTLER, RG AF CAO, G CUTLER, RG TI NEW APPROACHES FOR MEASURING PLASMA OR SERUM ANTIOXIDANT CAPACITY - A METHODOLOGICAL NOTE - REPLY SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Letter RP CAO, G (reprint author), NIA,GERONTOL RES CTR,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 4 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 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD JAN PY 1994 VL 16 IS 1 BP 136 EP 137 DI 10.1016/0891-5849(94)90252-6 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MM363 UT WOS:A1994MM36300038 ER PT S AU HAHN, SM KRISHNA, CM MITCHELL, JB AF HAHN, SM KRISHNA, CM MITCHELL, JB BE Armstrong, D TI NEW DIRECTIONS FOR FREE RADICAL CANCER RESEARCH AND MEDICAL APPLICATIONS SO FREE RADICALS IN DIAGNOSTIC MEDICINE: A SYSTEMS APPROACH TO LABORATORY TECHNOLOGY, CLINICAL CORRELATIONS, AND ANTIOXIDANT THERAPY SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT International Symposium on Free Radicals in Diagnostic Medicine: A Systems Approach to Laboratory Technology CY OCT 07-09, 1993 CL BUFFALO, NY SP MARION MERRELL DOW, INST RECH INT SERVIER & SERVIER INT FRANCE, EASTMAN KODAK CO, CLIN PROD DIV, LA HAYE LABS INC, DDI PHARM INC, UPJOHN LABS, CLIN RES DIV, RES INST ADDICT, SANOFI WINTHROP PHARM, ROCHE DIAGNOST SYST INC, PFIZER PHARM CO, OTSUKA AMER PHARM CO, ONO PHARM CO JAPAN, MERCK & CO INC, HUMAN HLTH DIV, HOFFMAN LA ROCHE INC, HENKEL CORP, FINE CHEM DIV, HAMAMATSU PHOTON SYSTS JAPAN, EISAI CO LTD, JAPAN, CAYMAN CHEM CO, BOEHRINGER MANNHEIM CORP, 3M PHARM, MILLARD FILLMORE HOSP, CLINICO PHARMACOKINET LAB, EMPIRE IMAGING SYST, FRESA BIOMED LABS INC, JM SCI INC, MILES INC, DIAGNOST DIV, SHIMADZU SCI INSTRUMENTS INC, SLM, AMER INSTRUMENTS & MILTON ROY CO, ROSWELL PARK CANC INST, VERIS VITAMIN E RES & INFORMAT SCI C1 NCI,RADIAT BIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 10 Z9 11 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 0-306-44981-1 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1994 VL 366 BP 241 EP 251 PG 11 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA BC72J UT WOS:A1994BC72J00017 PM 7771256 ER PT S AU ABUGO, O RIFKIND, JM AF ABUGO, O RIFKIND, JM BE Asada, K Yoshikawa, T TI THE PRODUCTION OF SUPEROXIDE BY HEMOGLOBIN UNDER HYPOXIA SO FRONTIERS OF REACTIVE OXYGEN SPECIES IN BIOLOGY AND MEDICINE SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Conference on Superoxide and Superoxide Dismutase CY OCT 11-15, 1993 CL KYOTO, JAPAN C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 1 Z9 1 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 0-444-81778-6 J9 INT CONGR SER PY 1994 VL 1058 BP 51 EP 52 PG 2 WC Biochemistry & Molecular Biology; Chemistry, Organic; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Chemistry; Research & Experimental Medicine GA BA69C UT WOS:A1994BA69C00018 ER PT J AU GOLDSWORTHY, TL RECIO, L BROWN, K DONEHOWER, LA MIRSALIS, JC TENNANT, RW PURCHASE, IFH AF GOLDSWORTHY, TL RECIO, L BROWN, K DONEHOWER, LA MIRSALIS, JC TENNANT, RW PURCHASE, IFH TI TRANSGENIC ANIMALS IN TOXICOLOGY SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID TUMOR-DEVELOPMENT; LIVER NEOPLASIA; P53 MUTATIONS; HA-RAS; MICE; ONCOGENE; CANCER; GENES; HETEROZYGOSITY; MUTAGENICITY C1 BEATSON INST CANC RES,GLASGOW G61 1BD,SCOTLAND. BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. SRI INT,MENLO PK,CA 94025. NIEHS,RES TRIANGLE PK,NC 27709. ZENECA CENT TOXICOL LAB,MACCLESFIELD SK10 4TJ,CHESHIRE,ENGLAND. RP GOLDSWORTHY, TL (reprint author), CHEM IND INST TOXICOL,6 DAVIS DR,POB 12137,RES TRIANGLE PK,NC 27709, USA. NR 49 TC 47 Z9 47 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1994 VL 22 IS 1 BP 8 EP 19 DI 10.1006/faat.1994.1002 PG 12 WC Toxicology SC Toxicology GA MT496 UT WOS:A1994MT49600002 PM 7907301 ER PT J AU GRIZZLE, TB GEORGE, JD FAIL, PA SEELY, JC HEINDEL, JJ AF GRIZZLE, TB GEORGE, JD FAIL, PA SEELY, JC HEINDEL, JJ TI REPRODUCTIVE EFFECTS OF 4-VINYLCYCLOHEXENE IN SWISS MICE ASSESSED BY A CONTINUOUS BREEDING PROTOCOL SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID TOXICOLOGICAL EVALUATION; OVARIAN TOXICITY; B6C3F1 MICE; DOSE LEVELS; EPOXIDATION; RATS C1 PATHCO INC,RES TRIANGLE PK,NC 27709. NIEHS,NATL TOXICOL PROGRAM,DEV & REPROD TOXICOL GRP,RES TRIANGLE PK,NC 27709. RP GRIZZLE, TB (reprint author), RES TRIANGLE INST,POB 12194,RES TRIANGLE PK,NC 27709, USA. FU NIEHS NIH HHS [N01-ES-65141] NR 35 TC 11 Z9 11 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1994 VL 22 IS 1 BP 122 EP 129 DI 10.1006/faat.1994.1015 PG 8 WC Toxicology SC Toxicology GA MT496 UT WOS:A1994MT49600015 PM 8125205 ER PT J AU POLLOCK, PL GERMOLEC, DR COMMENT, CE ROSENTHAL, GJ LUSTER, MI AF POLLOCK, PL GERMOLEC, DR COMMENT, CE ROSENTHAL, GJ LUSTER, MI TI DEVELOPMENT OF HUMAN LYMPHOCYTE-ENGRAFTED SCID MICE AS A MODEL FOR IMMUNOTOXICITY ASSESSMENT SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID SEVERE COMBINED IMMUNODEFICIENCY; IMMUNE-DEFICIENT MICE; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN TCDD; HU MOUSE; HUMAN HEMATOPOIESIS; CYCLOSPORIN-A; STEM-CELLS; TRANSPLANTATION; DIFFERENTIATION; INFECTION RP POLLOCK, PL (reprint author), NIEHS,ENVIRONM IMMUNOL & NEUROBIOL SECT,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 40 TC 17 Z9 17 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1994 VL 22 IS 1 BP 130 EP 138 DI 10.1006/faat.1994.1016 PG 9 WC Toxicology SC Toxicology GA MT496 UT WOS:A1994MT49600016 PM 8125206 ER PT J AU LEE, JH DIBISCEGLIE, AM BAKER, BL ZELDIS, JB AF LEE, JH DIBISCEGLIE, AM BAKER, BL ZELDIS, JB TI THE DEVELOPMENT OF A MUTATION IN THE PRECORE REGION OF THE HEPATITIS-B VIRUS IN A CHRONICALLY INFECTED INDIVIDUAL SO GASTROENTEROLOGY LA English DT Article ID HBE POSITIVE CARRIERS; CHRONIC LIVER-DISEASE; E-ANTIGEN; FULMINANT-HEPATITIS; ACTIVE HEPATITIS; DNA; REPLICATION; MUTANTS; SERUM; REACTIVATION C1 UNIV CALIF DAVIS,MED CTR,DIV GASTROENTEROL,SACRAMENTO,CA 95816. NIDDKD,HEPATITUS STUDIES SECT,BETHESDA,MD. NR 22 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JAN PY 1994 VL 106 IS 1 BP 243 EP 247 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MP419 UT WOS:A1994MP41900031 PM 8276188 ER PT J AU LORI, F LISZIEWICZ, J SMYTHE, J CARA, A BUNNAG, TA CURIEL, D GALLO, RC AF LORI, F LISZIEWICZ, J SMYTHE, J CARA, A BUNNAG, TA CURIEL, D GALLO, RC TI RAPID PROTECTION AGAINST HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 (HIV-1) REPLICATION MEDIATED BY HIGH-EFFICIENCY NON-RETROVIRAL DELIVERY OF GENES INTERFERING WITH HIV-1 TAT AND GAG SO GENE THERAPY LA English DT Article ID ADENOVIRUS; EXPRESSION; DNA; THERAPY; PROTEIN; ACTIVATION; COMPLEXES; CELLS; AIDS AB Efficient transduction of inhibitory genes is a critical requirement in the development of a gene therapy strategy against human immunodeficiency virus type 1 (HIV-1). Commonly used systems based on retrovirus-mediated gene delivery are characterized by low efficiency gene transfer into the target cell. Genes were transduced in the absence of cell selection into 60-90% of human CD4(+) cells by using a novel technique that allows high efficiency gene transfer mediated by adenoviruses coupled with DNA-polylysine complexes. Protection of these cells against HIV-1 acute infection was evaluated by transducing them with three different inhibitory genes which interfere with HIV-1 replication at separate levels (polymeric Tat activation response element [TAR] decoy, dominant-negative mutant of the gag gene and antisense sequences of the gag gene) and subsequent challenging with HIV-1 replication over 95%. Both the dominant-negative mutant and the antisense sequence of the gag gene were less potent inhibitors than the polymeric-TAR decoy. Combinations of either polymeric-TAR with dominant-negative mutant or antisense of the gag gene synergistically enhanced the inhibitory effects of the single genes. These data suggest that the combination of a highly efficient transduction technique with effective HIV-1 inhibitory genes confers rapid protection against HIV-1 acute infection in vitro. C1 UNIV ALABAMA,CTR COMPREHENS CANC,BIRMINGHAM,AL 35201. RP LORI, F (reprint author), NCI,TUMOR CELL BIOL LAB,BLDG 37,BETHESDA,MD 20892, USA. RI Cara, Andrea/M-4865-2015 OI Cara, Andrea/0000-0003-4967-1895 NR 19 TC 21 Z9 21 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0969-7128 J9 GENE THER JI Gene Ther. PD JAN PY 1994 VL 1 IS 1 BP 27 EP 31 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA PT945 UT WOS:A1994PT94500004 PM 7584056 ER PT S AU HUBER, BE LAZO, JS KELLEY, WM LEDLEY, FD LOTAN, R GITLIN, S JUENGST, ET AF HUBER, BE LAZO, JS KELLEY, WM LEDLEY, FD LOTAN, R GITLIN, S JUENGST, ET BE Huber, BE Lazo, JS TI THE BEGINNING - STRATEGY AND ETHICS - GENERAL DISCUSSION SO GENE THERAPY FOR NEOPLASTIC DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Discussion CT Conference on Gene Therapy for Neoplastic Diseases CY JUN 26-29, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI C1 NCI,BETHESDA,MD. NATL CTR HUMAN GENOME RES,BETHESDA,MD. UNIV PITTSBURGH,PITTSBURGH,PA. UNIV PENN,MED CTR,PHILADELPHIA,PA 19104. BAYLOR COLL MED,HOUSTON,TX 77030. MD ANDERSON CANC CTR,HOUSTON,TX. RP HUBER, BE (reprint author), WELLCOME RES LABS,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 20 EP 22 PG 3 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00004 ER PT S AU BRODY, SL CRYSTAL, RG AF BRODY, SL CRYSTAL, RG BE Huber, BE Lazo, JS TI ADENOVIRUS-MEDIATED IN-VIVO GENE-TRANSFER SO GENE THERAPY FOR NEOPLASTIC DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Gene Therapy for Neoplastic Diseases CY JUN 26-29, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI ID CYSTIC-FIBROSIS GENE; ALPHA-1-ANTITRYPSIN DEFICIENCY; ARTERIAL-WALL; INVIVO; EXPRESSION; THERAPY; VECTORS; MICE; CELLS; IDENTIFICATION C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. CORNELL UNIV,MED CTR,NEW YORK HOSP,DEPT MED,DIV PULM & CRIT CARE,NEW YORK,NY 10021. NR 69 TC 149 Z9 150 U1 0 U2 4 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 90 EP 103 DI 10.1111/j.1749-6632.1994.tb21705.x PG 14 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00009 PM 7517653 ER PT S AU GOTTESMAN, MM GERMANN, UA AKSENTIJEVICH, I SUGIMOTO, Y CARDARELLI, CO PASTAN, I AF GOTTESMAN, MM GERMANN, UA AKSENTIJEVICH, I SUGIMOTO, Y CARDARELLI, CO PASTAN, I BE Huber, BE Lazo, JS TI GENE-TRANSFER OF DRUG-RESISTANCE GENES - IMPLICATIONS FOR CANCER-THERAPY SO GENE THERAPY FOR NEOPLASTIC DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Gene Therapy for Neoplastic Diseases CY JUN 26-29, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI ID BACTERIAL TRANSPORT PROTEINS; CONFERS MULTIDRUG RESISTANCE; P-GLYCOPROTEIN GENE; BONE-MARROW; RETROVIRAL TRANSFER; TRANSGENIC MICE; COMPLEMENTARY-DNA; HUMAN MDR1; EXPRESSION; CELLS C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. RP GOTTESMAN, MM (reprint author), NCI,CELL BIOL LAB,BLDG 37,ROOM IB22,BETHESDA,MD 20892, USA. NR 43 TC 34 Z9 34 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 126 EP 139 DI 10.1111/j.1749-6632.1994.tb21708.x PG 14 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00012 PM 7912913 ER PT S AU HUBER, BE GITLIN, S BLAESE, RM LU, B GOTTESMAN, MM LAZO, JS JOLLY, D SIKORA, K AF HUBER, BE GITLIN, S BLAESE, RM LU, B GOTTESMAN, MM LAZO, JS JOLLY, D SIKORA, K BE Huber, BE Lazo, JS TI ENGINEERING DRUG-SENSITIVITY AND DRUG-RESISTANCE - IMPLICATIONS IN CANCER-THERAPY SO GENE THERAPY FOR NEOPLASTIC DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Discussion CT Conference on Gene Therapy for Neoplastic Diseases CY JUN 26-29, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI C1 ROYAL POSTGRAD MED SCH,LONDON,ENGLAND. ALBERT EINSTEIN COLL MED,BRONX,NY. UNIV PITTSBURGH,PITTSBURGH,PA. VIAGENE INC,SAN DIEGO,CA. NCI,BETHESDA,MD 20892. RP HUBER, BE (reprint author), WELLCOME RES LABS,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 140 EP 143 PG 4 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00013 ER PT S AU PRIMUS, FJ FINCH, MD WETZEL, SA MASCI, AM SCHLOM, J KASHMIRI, SVS AF PRIMUS, FJ FINCH, MD WETZEL, SA MASCI, AM SCHLOM, J KASHMIRI, SVS BE Huber, BE Lazo, JS TI MONOCLONAL-ANTIBODY GENE-TRANSFER - IMPLICATIONS FOR TUMOR-SPECIFIC CELL-MEDIATED CYTOTOXICITY SO GENE THERAPY FOR NEOPLASTIC DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Gene Therapy for Neoplastic Diseases CY JUN 26-29, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI ID NATURAL-KILLER CELLS; T-CELLS; NECROSIS FACTOR; CYTO-TOXICITY; TNF-ALPHA; INDUCTION; RESPONSES; D612; IMMUNOTHERAPY; MACROPHAGES C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. RP PRIMUS, FJ (reprint author), CITY HOPE NATL MED CTR,BECKMAN RES INT,DIV IMMUNOL,DUARTE,CA 91010, USA. FU NCI NIH HHS [CA33572] NR 32 TC 4 Z9 4 U1 1 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 154 EP 166 DI 10.1111/j.1749-6632.1994.tb21710.x PG 13 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00015 PM 8024192 ER PT S AU HWU, P ROSENBERG, SA AF HWU, P ROSENBERG, SA BE Huber, BE Lazo, JS TI THE USE OF GENE-MODIFIED TUMOR-INFILTRATING LYMPHOCYTES FOR CANCER-THERAPY SO GENE THERAPY FOR NEOPLASTIC DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Gene Therapy for Neoplastic Diseases CY JUN 26-29, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI ID T-CELL-RECEPTOR; NECROSIS-FACTOR-ALPHA; CARCINOMA-ASSOCIATED ANTIGENS; ANTIBODY-TYPE-SPECIFICITY; HIGH-DOSE INTERLEUKIN-2; METASTATIC MELANOMA; MONOCLONAL-ANTIBODIES; FUNCTIONAL RECEPTORS; MURINE TUMORS; FACTOR TNF RP HWU, P (reprint author), NCI,SURG BRANCH,BLDG 10,ROOM 2B42,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 42 TC 15 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 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 188 EP 199 DI 10.1111/j.1749-6632.1994.tb21712.x PG 12 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00017 PM 8024194 ER PT S AU NABEL, GJ HUBER, BE JOLLY, D LEDLEY, FD HWU, P LAZO, JS DRANOFF, G AF NABEL, GJ HUBER, BE JOLLY, D LEDLEY, FD HWU, P LAZO, JS DRANOFF, G BE Huber, BE Lazo, JS TI IMMUNOMODULATION THROUGH GENE-THERAPY - IMPLICATIONS FOR NEOPLASTIC-DISEASE - GENERAL DISCUSSION SO GENE THERAPY FOR NEOPLASTIC DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Discussion CT Conference on Gene Therapy for Neoplastic Diseases CY JUN 26-29, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI C1 VIAGENE INC,SAN DIEGO,CA. BAYLOR COLL MED,HOUSTON,TX. NCI,BETHESDA,MD. UNIV PITTSBURGH,PITTSBURGH,PA. WHITEHEAD INST,CAMBRIDGE,MA. WELLCOME RES LABS,RES TRIANGLE PK,NC 27709. RP NABEL, GJ (reprint author), UNIV MICHIGAN,ANN ARBOR,MI 48109, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 200 EP 203 PG 4 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00018 ER PT S AU BRENNER, MK RILL, DR MOEN, RC KRANCE, RA HESLOP, HE MIRRO, J ANDERSON, WF IHLE, JN AF BRENNER, MK RILL, DR MOEN, RC KRANCE, RA HESLOP, HE MIRRO, J ANDERSON, WF IHLE, JN BE Huber, BE Lazo, JS TI MARKING AND AUTOLOGOUS BONE-MARROW TRANSPLANTATION SO GENE THERAPY FOR NEOPLASTIC DISEASES SE Annals of the New York Academy of Sciences LA English DT Article ID MEDIATED GENE-TRANSFER; ACUTE MYELOGENOUS LEUKEMIA; ACUTE MYELOID-LEUKEMIA; ADENOSINE-DEAMINASE; 1ST REMISSION; CELLS; EXPRESSION; LYMPHOMA; RELAPSE; 4-HYDROPEROXYCYCLOPHOSPHAMIDE C1 GENET THERAPY INC, CLIN LABS, GAITHERSBURG, MD 20878 USA. CHILDRENS HOSP PITTSBURGH, DIV HEMATOL ONCOL, PITTSBURGH, PA 15213 USA. NHLBI, BETHESDA, MD 20892 USA. ST JUDE CHILDRENS RES HOSP, DEPT BIOCHEM, MEMPHIS, TN 38105 USA. UNIV TENNESSEE, COLL MED, DEPT PEDIAT, MEMPHIS, TN 38163 USA. UNIV TENNESSEE, COLL MED, DEPT MED, MEMPHIS, TN 38163 USA. RP BRENNER, MK (reprint author), ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL ONCOL, DIV BONE MARROW TRANSPLANTAT, MEMPHIS, TN 38105 USA. FU NCI NIH HHS [CA 21765, CA 58211] NR 37 TC 26 Z9 29 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 204 EP 215 DI 10.1111/j.1749-6632.1994.tb21713.x PG 12 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00019 PM 8024195 ER PT S AU DUNBAR, CE BODINE, DM SORRENTINO, B DONAHUE, R MCDONAGH, K COTTLERFOX, M OSHAUGHNESSY, J COWAN, K CARTER, C DOREN, S CASSELL, A NIENHUIS, AW AF DUNBAR, CE BODINE, DM SORRENTINO, B DONAHUE, R MCDONAGH, K COTTLERFOX, M OSHAUGHNESSY, J COWAN, K CARTER, C DOREN, S CASSELL, A NIENHUIS, AW BE Huber, BE Lazo, JS TI GENE-TRANSFER INTO HEMATOPOIETIC-CELLS - IMPLICATIONS FOR CANCER-THERAPY SO GENE THERAPY FOR NEOPLASTIC DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Gene Therapy for Neoplastic Diseases CY JUN 26-29, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI ID BONE-MARROW CELLS; HUMAN MDR1; TRANSPLANTATION; SUPPORT; CULTURE C1 NIH,CTR CLIN,DEPT TRANSFUS MED,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. RP DUNBAR, CE (reprint author), NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892, USA. NR 17 TC 22 Z9 22 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 216 EP 224 DI 10.1111/j.1749-6632.1994.tb21714.x PG 9 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00020 PM 7517651 ER PT S AU BRENNER, MK PETERS, WP HUBER, BE LAZO, JS DUNBAR, CE MCGRATH, IT AF BRENNER, MK PETERS, WP HUBER, BE LAZO, JS DUNBAR, CE MCGRATH, IT BE Huber, BE Lazo, JS TI IMPLICATIONS OF GENE-THERAPY IN BONE-MARROW TRANSPLANTATION AND HEMATOPOIETIC-CELLS - DISCUSSION SO GENE THERAPY FOR NEOPLASTIC DISEASES SE Annals of the New York Academy of Sciences LA English DT Discussion C1 DUKE UNIV, MED CTR, DURHAM, NC USA. WELLCOME RES LABS, RES TRIANGLE PK, NC 27709 USA. UNIV PITTSBURGH, PITTSBURGH, PA USA. NHLBI, BETHESDA, MD 20892 USA. NCI, BETHESDA, MD 20892 USA. RP BRENNER, MK (reprint author), ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN USA. NR 0 TC 2 Z9 3 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-850-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 716 BP 225 EP 227 PG 3 WC Genetics & Heredity; Multidisciplinary Sciences; Pathology SC Genetics & Heredity; Science & Technology - Other Topics; Pathology GA BA67E UT WOS:A1994BA67E00021 ER PT J AU WELLS, KB NORQUIST, G BENJAMIN, B ROGERS, W KAHN, K BROOK, R AF WELLS, KB NORQUIST, G BENJAMIN, B ROGERS, W KAHN, K BROOK, R TI QUALITY OF ANTIDEPRESSANT MEDICATIONS PRESCRIBED AT DISCHARGE TO DEPRESSED ELDERLY PATIENTS IN GENERAL MEDICAL HOSPITALS BEFORE AND AFTER PROSPECTIVE PAYMENT SYSTEM SO GENERAL HOSPITAL PSYCHIATRY LA English DT Article ID OLD-AGE; THERAPY; CARE AB This study describes the quality of antidepressant medication use at hospital discharge for depressed elderly inpatients and compares quality of care before and after implementation of Medicare's Prospective Payment System (PPS). The study reviewed data from medical records of 2746 depressed, elderly, hospitalized patients in acute-care general medical hospitals in five U. S. states (pre-PPS period 1981-82; post-PPS period 1985-86). The majority were discharged on antidepressant medication both pre-PPS and post-PPS. After PPS' implementation, sedating medications were used less often in all treatment settings. In general medical wards, a higher percentage post-PPS (24%) than pre-PPS (14%) were discharged 48 hours or less after first starting an antidepressant medication. In both time periods, one-third of patients receiving antidepressant medications were prescribed daily dosages at discharge below recommended, minimum, therapeutic levels, whether treated in general medical wards or psychiatric units. Otherwise, patients previously treated in psychiatric units received higher quality of medication management than those treated in general medical wards. Over time, patients discharged on antidepressant medication were less likely to use sedating medication, suggesting improved quality of care. In general medical wards, however, patients were discharged more rapidly after starting medication, possibly suggesting lower quality of care. A substantial percentage of patients received subtherapeutic dosages of medication or sedating medications, suggesting that improved management of discharge antidepressant medication in the elderly is needed in general medical hospitals, C1 UNIV CALIF LOS ANGELES, NEUROPSYCHIAT INST & HOSP, DEPT PSY PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. NIMH, BETHESDA, MD 20892 USA. UNIV CALIF LOS ANGELES, CTR HLTH SCI, HLTH SERV, LOS ANGELES, CA USA. RP WELLS, KB (reprint author), RAND CORP, 1700 MAIN ST, POB 2138, SANTA MONICA, CA 90406 USA. FU AHRQ HHS [R01 HS06802-02]; NIMH NIH HHS [R01 MH44260-02]; PHS HHS [18-C-9885319-03] NR 31 TC 19 Z9 19 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD JAN PY 1994 VL 16 IS 1 BP 4 EP 15 DI 10.1016/0163-8343(94)90081-7 PG 12 WC Psychiatry SC Psychiatry GA NL441 UT WOS:A1994NL44100002 PM 8039682 ER PT J AU GALLEGO, MI ZIMONJIC, DB POPESCU, NC DIPAOLO, JA LAZO, PA AF GALLEGO, MI ZIMONJIC, DB POPESCU, NC DIPAOLO, JA LAZO, PA TI INTEGRATION SITE OF HUMAN PAPILLOMAVIRUS TYPE-18 DNA IN CHROMOSOME BAND-8Q22.1 OF C4-1 CERVICAL-CARCINOMA - DNASE-I HYPERSENSITIVITY AND METHYLATION OF CELLULAR FLANKING SEQUENCES SO GENES CHROMOSOMES & CANCER LA English DT Article ID FRAGILE SITES; HELA-CELLS; PREFERENTIAL INTEGRATION; ADENOASSOCIATED VIRUS; CHROMATIN STRUCTURE; VIRAL INTEGRATION; GENES; LOCALIZATION; EXPRESSION; LINES AB The C4-1 cell line derived from a non-keratinizing squamous cell carcinoma of the uterine cervix contains integrated human papillomavirus-18 DNA. Fluorescence in situ hybridization of C4-1 cells demonstrated a single viral integration site at 8q22.1 on a derivative chromosome originating from an 8q;12q translocation. 8q22 is a site of chromosome fragility and is also recombinogenic in several human malignancies. DNase I hypersensitivity of the integration site was studied with a cellular flanking probe. A hypersensitive site was detected within 3 kb from viral DNA. The integration sites are undermethylated in C4-1 and HeLa cells and fully methylated in tumor cell lines of other origin, such as lymphoid cells. (C) 1994 Wiley-Uss, Inc. C1 INST SALUD CARLOS III,CTR NACL BIOL CELULAR & RETROVIRUS,UNIDAD GENET MOLEC,E-28220 MAJADAHONDA,SPAIN. NCI,DIV CANC ETIOL,BIOL LAB,BETHESDA,MD 20892. RI Lazo, Pedro /M-6435-2014 OI Lazo, Pedro /0000-0001-8997-3025 NR 32 TC 16 Z9 16 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 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD JAN PY 1994 VL 9 IS 1 BP 28 EP 32 DI 10.1002/gcc.2870090106 PG 5 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA MM704 UT WOS:A1994MM70400005 PM 7507697 ER PT J AU MARSH, J AF MARSH, J TI KINETIC DETERMINATION OF CELLULAR LACZ EXPRESSION SO GENETIC ANALYSIS-BIOMOLECULAR ENGINEERING LA English DT Article ID COLI BETA-GALACTOSIDASE; MAMMALIAN-CELLS; RECOMBINANT RETROVIRUS; GENE-TRANSFER; TRANSCRIPTION; LINEAGE; CULTURE; ASSAY AB A kinetic assay for the expression of beta-galactosidase in cells transfected with the LacZ gene was developed using a 96-well-plate for mat. The assay involves solubilization of the cells followed by measuring hydrolytic rates of o-nitrophenyl beta-D-galactoside on a standard 96-well-plate reader without other manipulations. The protocol requires only that reagent be added sequentially to the wells at ambient temperatures, thus permitting a semiautomated or fully automated determination of reporter expression. The rates of chromophore development were found to be linear over a 6-log enzyme concentration range, from 0.001 to 100 mU. Additionally, the use of kinetic data avoids the complications of non-enzymatic, background optical density. RP MARSH, J (reprint author), NIMH,MOLEC BIOL LAB,LYMPHOCYTE FUNCT UNIT,BLDG 336,ROOM 1B08,BETHESDA,MD 20892, USA. NR 24 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1050-3862 J9 GENET ANAL-BIOMOL E JI Genet. Anal.-Biomol. Eng. PY 1994 VL 11 IS 1 BP 20 EP 23 DI 10.1016/1050-3862(94)90005-1 PG 4 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA NM740 UT WOS:A1994NM74000004 PM 8060677 ER PT J AU LAING, AE AMOS, CI DEMEESTER, C DIEP, A XIA, YR ELSTON, RC SRINIVASAN, SR BERENSON, GS LUSIS, AJ AF LAING, AE AMOS, CI DEMEESTER, C DIEP, A XIA, YR ELSTON, RC SRINIVASAN, SR BERENSON, GS LUSIS, AJ TI LINKAGE BETWEEN THE APO-B GENE AND SERUM APO-B LEVELS IN A LARGE PEDIGREE FROM THE BOGALUSA HEART-STUDY SO GENETIC EPIDEMIOLOGY LA English DT Article DE APOLIPOPROTEIN B; GENETICS; LINKAGE; HAPLOTYPES ID APOLIPOPROTEIN-B-GENE; FRAGMENT LENGTH POLYMORPHISMS; PROTEIN CETP LOCUS; LIPASE LPL GENE; DNA POLYMORPHISMS; LIPOPROTEIN CHOLESTEROL; A-I; ATHEROSCLEROSIS; DISEASE; LIPIDS AB Maximum likelihood linkage analyses were performed to test for linkage between serum apoB levels and several candidate gene markers including apolipoprotein B, lipoprotein lipase, hepatic lipase, cholesterol ester transfer protein, and apolipoprotein AI in a large pedigree. Parameters of general Mendelian inheritance derived from maximum likelihood segregation analysis of the serum apoB levels were used in the linkage analysis. The highest two-point lod score between the quantitative trait and a marker defined by a single restriction digest was 1.86 at recombination fraction (theta) = 0. This was observed for linkage between serum apoB levels and the presence or absence of a PvuII digestion site in the apoB gene. Linkage between serum apoB levels and polymorphisms of the apoB gene defined by the two restriction digests EcoR1 and PvuII was supported by a lod score of 3.30, while inclusion of VNTR typings led to a lod score of 2.33. None of the other candidate genes gave positive evidence of linkage. (C) 1994 Wiley-Liss, Inc. C1 HOWARD UNIV,CTR CANC,DIV BIOSTAT,WASHINGTON,DC 20059. NIAMS,GENET STUDIES SECT,BETHESDA,MD. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,MED CTR,CTR MOLEC & HUMAN GENET,NEW ORLEANS,LA 70112. TULANE UNIV,MED CTR,DEPT APPL HLTH SCI,NEW ORLEANS,LA 70118. FU NCRR NIH HHS [RR03655]; NHLBI NIH HHS [HL42488, HL28481] NR 56 TC 6 Z9 6 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1994 VL 11 IS 1 BP 29 EP 40 DI 10.1002/gepi.1370110104 PG 12 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA NB032 UT WOS:A1994NB03200003 PM 7912214 ER PT J AU SEMINARA, D OBRAMS, GI AF SEMINARA, D OBRAMS, GI TI GENETIC EPIDEMIOLOGY OF CANCER - A MULTIDISCIPLINARY APPROACH SO GENETIC EPIDEMIOLOGY LA English DT Article DE ENVIRONMENT; PHENOTYPE; GENETIC DETERMINANTS; GENOTYPE ID OVARIAN-CANCER; BREAST-CANCER; LUNG-CANCER; MENDELIAN INHERITANCE; SEGREGATION ANALYSIS; PROSTATE-CANCER; RAS ONCOGENE; WILMS-TUMOR; LINKAGE; MODELS RP SEMINARA, D (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL BIOSTAT PROGRAM,EXTRAMURAL PROGRAMS BRANCH,6130 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 68 TC 15 Z9 16 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1994 VL 11 IS 3 BP 235 EP 254 DI 10.1002/gepi.1370110303 PG 20 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA NN135 UT WOS:A1994NN13500002 PM 8088505 ER PT J AU JARVIK, GP AUSTIN, MA FABSITZ, RR AUWERX, J REED, T CHRISTIAN, JC DEEB, S AF JARVIK, GP AUSTIN, MA FABSITZ, RR AUWERX, J REED, T CHRISTIAN, JC DEEB, S TI GENETIC INFLUENCES ON AGE-RELATED CHANGE IN TOTAL CHOLESTEROL, LOW-DENSITY LIPOPROTEIN-CHOLESTEROL, AND TRIGLYCERIDE LEVELS - LONGITUDINAL APOLIPOPROTEIN-E GENOTYPE EFFECTS SO GENETIC EPIDEMIOLOGY LA English DT Article DE APOLIPOPROTEIN E; LONGITUDINAL; CHOLESTEROL; TRIGLYCERIDE; AGING; GENOTYPE; POLYMORPHISM ID CORONARY-ARTERY DISEASE; E POLYMORPHISM; SERUM-CHOLESTEROL; PLASMA-LIPIDS; E PHENOTYPE; NHLBI TWIN; METABOLISM; RISK; FREQUENCIES; ALLELE AB This study addressed the possible influence of apolipoprotein E (ape E) genotype on age-related changes in total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), and triglyceride (TG) levels in older males. Apo E is a component of LDL, is a ligand for the LDL receptor, and apo E genotype has been consistently associated with variation in mean levels of TC and LDL-C, and also appears to influence TG levels. Using male twins followed longitudinally between mean ages of 48 and 63 years, the change in TC, LDL-C, and TG over time for individuals with the epsilon 3 epsilon 3 and the epsilon 3 epsilon 4 genotypes was contrasted. At exam 1 mean TC and LDL-C levels were lower in the epsilon 3 epsilon 3 group than in the epsilon 3 epsilon 4 group, but at exam 3 mean TC and LDL-C levels were significantly higher in the epsilon 3 epsilon 3 group than in the epsilon 3 epsilon 4 group. The rate of change in TC and LDL-C with age differed significantly between epsilon 3 epsilon 3 and epsilon 3 epsilon 4 groups. Results for TG were not statistically significantly. These findings suggest that the apo E genotype effects on risk of coronary artery disease may be age-dependent. This study demonstrates the value of longitudinal studies in refining models for genetic risk factors for disease. (C) 1994 Wiley-Liss, Inc. C1 UNIV WASHINGTON,SCH PUBL HLTH & COMMUNITY MED,DEPT MED,DIV MED GENET,SEATTLE,WA 98195. UNIV WASHINGTON,SCH PUBL HLTH & COMMUNITY MED,DEPT EPIDEMIOL,SEATTLE,WA 98195. NIH,BETHESDA,MD 20892. CTR BIOCHIM,BIOL REGULAT CHEZ EUCARYOTES LAB,NICE,FRANCE. INDIANA UNIV,MED CTR,DEPT MOLEC & MED GENET,INDIANAPOLIS,IN. RI Jarvik, Gail/N-6476-2014 OI Jarvik, Gail/0000-0002-6710-8708 FU NHLBI NIH HHS [HC-55028, N01 HC-55023, HC-55027] NR 47 TC 49 Z9 49 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1994 VL 11 IS 4 BP 375 EP 384 DI 10.1002/gepi.1370110407 PG 10 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA PJ558 UT WOS:A1994PJ55800006 PM 7813899 ER PT B AU LESHNER, AI AF LESHNER, AI BE Frankel, MS Teich, AH TI GENETIC AND ENVIRONMENTAL-INFLUENCES ON BEHAVIOR SO GENETIC FRONTIER: ETHICS, LAW AND POLICY LA English DT Proceedings Paper CT Conference on The Genetic Frontier: Ethics, Law and Policy CY JUN, 1992 CL LOS ALAMOS NATL LAB, LOS ALAMOS, NM SP AMER ASSOC ADV SCI, AMER BAR ASSOC, NIH, US DOE HO LOS ALAMOS NATL LAB C1 NIMH,ROCKVILLE,MD 20857. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1333 H STREET NW, WASHINGTON, DC 20005 BN 0-87168-526-4 PY 1994 BP 103 EP 104 PG 2 WC Law; Social Sciences, Biomedical SC Government & Law; Biomedical Social Sciences GA BZ99E UT WOS:A1994BZ99E00008 ER PT J AU PARALKAR, V WISTOW, C AF PARALKAR, V WISTOW, C TI CLONING THE HUMAN GENE FOR MACROPHAGE-MIGRATION INHIBITORY FACTOR (MIF) SO GENOMICS LA English DT Article ID PROTEIN; CELLS AB Macrophage migration inhibitory factor (MH) was originally identified as a lymphokine. However, recent work strongly suggests a wider role for MIF beyond the immune system. It is expressed specifically in the differentiating cells of the immunologically privileged eye lens and brain, is a delayed early response gene in fibroblasts, and is expressed in many tissues. Here, we report the structure of the remarkably small gene for human MIF that has three exons separated by introns of only 189 and 95 bp and covers less than 1 kb. The cloned sequence also includes 1 kb of 5' flanking region. Primer extension and 5' rapid amplification of cDNA ends (RACE) of human brain RNA both indicate the presence of a single transcription start site in a TATA-less promoter. Northern blot analysis shows a single size of MIF mRNA (about 800 nt) in all human tissues examined. In contrast to previous reports, we find no evidence for multiple genes for MLF in the human genome. (C) 1994 Academic Press, Inc. C1 NEI, MOLEC STRUCT & FUNCT SECT, BETHESDA, MD 20892 USA. NR 20 TC 89 Z9 95 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 EI 1089-8646 J9 GENOMICS JI Genomics PD JAN 1 PY 1994 VL 19 IS 1 BP 48 EP 51 DI 10.1006/geno.1994.1011 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NA601 UT WOS:A1994NA60100010 PM 8188240 ER PT J AU HUPPI, K SIWARSKI, D GOODNIGHT, J MISCHAK, H AF HUPPI, K SIWARSKI, D GOODNIGHT, J MISCHAK, H TI ASSIGNMENT OF THE PROTEIN-KINASE-C-DELTA POLYPEPTIDE GENE (PRKCD) TO HUMAN-CHROMOSOME-3 AND MOUSE CHROMOSOME-14 SO GENOMICS LA English DT Note ID FAMILY; EXPRESSION; MEMBER AB The protein kinase C (pkc) enzymes are a family of serine-threonine protein kinases, each encoded by a distinct and separate gene. The chromosomal locations of human PRKCA, PRKCB, and PRKCG have previously been established. We now report that PRKCD, a novel member of the pkc gene family, maps to human chromosome 3. The chromosomal location of Pkcd has also been determined in the mouse by analysis of recombination frequency in an interspecific panel of backcross mice. We find that the locus encoding pkcd resides proximal to nucleoside phosphorylase (Np-2) and Tcra on mouse chromosome 14 in a region syntenic with human 3p. (C) 1994 Academic Press, Inc. RP HUPPI, K (reprint author), NCI,GENET LAB,MOLEC GENET SECT,BETHESDA,MD 20892, USA. RI Mischak, Harald/E-8685-2011 NR 9 TC 21 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1994 VL 19 IS 1 BP 161 EP 162 DI 10.1006/geno.1994.1028 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NA601 UT WOS:A1994NA60100027 PM 8188219 ER PT J AU BUTLER, RN AHRONHEIM, J FILLIT, H RAPOPORT, SI TATEMICHI, TK AF BUTLER, RN AHRONHEIM, J FILLIT, H RAPOPORT, SI TATEMICHI, TK TI VASCULAR DEMENTIA - AN UPDATED APPROACH TO PATIENT-MANAGEMENT - A ROUND-TABLE DISCUSSION .3. SO GERIATRICS LA English DT Discussion ID MULTI-INFARCT DEMENTIA; STROKE AB A new clinical approach to the prevention and treatment of vascular dementia is evolving. The physician has numerous options to consider when the patient is in an asymptomatic ''brain-at-risk'' stage. These include treatment of hypertension, elevated cholesterol, and atrial fibrillation, as well as smoking cessation, exercise, and dietary changes. When there are early signs of cerebrovascular disease, such as TIAs and subtle cognitive changes, more aggressive therapy may be warranted, including carotid endarterectomy, anticoagulants, aspirin, and ticlopidine. For patients with vascular dementia, treatment focuses on preventing further cerebrovascular damage and managing related symptoms, such as depression. C1 MT SINAI MED CTR,GERIATR CONSULTAT & LIAISON SERV,NEW YORK,NY 10029. NIA,NEUROSCI LAB,BETHESDA,MD 20892. COLUMBIA UNIV COLL PHYS & SURG,STROKE & AGING RES PROJECT,NEW YORK,NY 10032. RP BUTLER, RN (reprint author), CUNY MT SINAI SCH MED,DEPT GERIATR & ADULT DEV,NEW YORK,NY 10029, USA. NR 19 TC 2 Z9 2 U1 0 U2 0 PU ADVANSTAR COMMUNICATIONS PI DULUTH PA 131 W FIRST ST, DULUTH, MN 55802 SN 0016-867X J9 GERIATRICS JI Geriatrics PD JAN PY 1994 VL 49 IS 1 BP 39 EP & PG 0 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA MR451 UT WOS:A1994MR45100006 ER PT B AU NASH, TE AF NASH, TE BE Thompson, RCA Reynoldson, JA Lymbery, AJ TI IMMUNOLOGY - THE ROLE OF THE PARASITE SO GIARDIA: FROM MOLECULES TO DISEASE LA English DT Proceedings Paper CT 2nd International Meeting on Giardia: From Molecules to Disease and Beyond CY 1992 CL FREMANTLE, AUSTRALIA C1 NIH,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU UNIV ARIZONA PRESS PI TUCSON PA 1615 E SPEEDWAY, TUCSON, AZ 85706 BN 0-85198-840-7 PY 1994 BP 139 EP 154 PG 16 WC Immunology; Microbiology; Pathology SC Immunology; Microbiology; Pathology GA BA65F UT WOS:A1994BA65F00008 ER PT J AU PETERKOFSKY, B GOSIEWSKA, A KIPP, DE SHAH, V WILSON, S AF PETERKOFSKY, B GOSIEWSKA, A KIPP, DE SHAH, V WILSON, S TI CIRCULATING INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEINS (IGFBP)-1 AND (IGFBP)-2 INDUCED IN VITAMIN-C-DEFICIENT OR FASTED GUINEA-PIGS INHIBIT IGF-I ACTION IN CULTURED-CELLS SO GROWTH FACTORS LA English DT Article DE COLLAGEN; MITOGENESIS; INSULIN-LIKE GROWTH FACTORS; ASCORBATE; NUTRITION ID COLLAGEN-SYNTHESIS; SOMATOMEDIN; CARTILAGE; SERUM; RATS; HYDROXYLATION; PROTEOGLYCAN; STIMULATION; FIBROBLASTS; PROCOLLAGEN AB Collagen gene expression and proteoglycan synthesis are decreased in vitamin C-deficient guinea pigs losing weight and in fasted guinea pigs receiving ascorbate. Sera from such guinea pigs contain an insulin-like growth factor (IGF)-I-reversible inhibitor of collagen, proteoglycan and DNA synthesis and elevated levels of 29 and 35-kDa IGF binding proteins (IGFBPs). We now have identified the induced proteins as IGFBPs 1 and 2 and investigated their role as inhibitors. Guinea pig sera were treated with antibodies to IGFBPs 1 and 2 and antibody-IGFBP complexes were removed by passage through a Protein A-Sepharose column. Inhibitor content of fasted and scorbutic sera, and Protein A pass-through fractions derived from them, was assessed by their level of stimulation of DNA and collagen synthesis in 3T3 cells, compared to analogously treated normal guinea pig serum. Removal of IGFBP-1 from scorbutic serum reversed inhibition of collagen and DNA synthesis by more than half but removal of IGFBP-2 was less effective. Removal of both IGFBPs reversed inhibition almost completely. Similar results were obtained with fasted guinea pig serum. Conversely, purified rat IGFBPs 1 and 2 inhibited DNA and collagen synthesis in cells cultured in normal guinea pig serum or IGF-I-stimulated DNA synthesis, with IGFBP-1 being more potent. Thus, IGFBP-1 and, to a lesser extent IGFBP-2, cause inhibition of IGF-I action by sera from fasted and scorbutic guinea pigs and may inhibit collagen gene expression in vivo. RP NCI, BIOCHEM LAB, BLDG 37, ROOM 4C-18, BETHESDA, MD 20892 USA. NR 35 TC 20 Z9 20 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0897-7194 EI 1029-2292 J9 GROWTH FACTORS JI Growth Factors PY 1994 VL 10 IS 4 BP 229 EP 241 DI 10.3109/08977199409010989 PG 13 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA PD827 UT WOS:A1994PD82700001 PM 7528515 ER PT J AU SEIGEL, GM TOMBRANTINK, J BECERRA, SP CHADER, GJ DILORETO, DA DELCERRO, C LAZAR, ES DELCERRO, M AF SEIGEL, GM TOMBRANTINK, J BECERRA, SP CHADER, GJ DILORETO, DA DELCERRO, C LAZAR, ES DELCERRO, M TI DIFFERENTIATION OF Y79 RETINOBLASTOMA CELLS WITH PIGMENT EPITHELIAL-DERIVED FACTOR AND INTERPHOTORECEPTOR MATRIX WASH - EFFECTS ON TUMORIGENICITY SO GROWTH FACTORS LA English DT Article DE RETINAL TRANSPLANTATION; NEURITE OUTGROWTH; RETINA; HUMAN TUMORS; TISSUE CULTURE ID NEUROTROPHIC ACTIVITY; TRANSPLANTATION; EXPRESSION; EYES AB We investigated the in vivo differentiation potential of Y79 human retinoblastoma cells following pre-treatment with two novel neurotrophic agents: PEDF (human recombinant pigmented-epithelial derived factor) or IPM (interphotoreceptor matrix) wash. These agents were able to induce a significant degree of morphological differentiation in vitro. However, 48 days after subretinal transplantation of pre-treated cells, massive tumor formation was apparent. In contrast, Y79 cells pre-treated with retinoic acid/sodium butyrate, which attain a lesser degree of morphological differentiation, did not produce tumors over a 30 to 60 day-survival time (del Cerro et al., Brain Research, 12-22, 1992). We conclude that for PEDF and IPM, the degree of in vitro differentiation and the degree of mitotic arrest are independent features. C1 UNIV ROCHESTER,SCH MED,ROCHESTER,NY 14642. NIH,BETHESDA,MD 20892. FU PHS HHS [5262] NR 16 TC 32 Z9 34 U1 0 U2 2 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 1994 VL 10 IS 4 BP 289 EP 297 DI 10.3109/08977199409010995 PG 9 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA PD827 UT WOS:A1994PD82700007 PM 7803045 ER PT B AU ROSENWALD, AG KAHN, RA AF ROSENWALD, AG KAHN, RA BE Corda, D Hamm, H Luini, A TI ROLES FOR ARF IN MEMBRANE TRAFFIC SO GTPASE-CONTROLLED MOLECULAR MACHINES SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT Serono Symposium on GTPase-Controlled Molecular Machines CY SEP, 1993 CL SANTA MARIA IMBAR, ITALY SP SERONO SYMP RP ROSENWALD, AG (reprint author), NCI,DIV CANC TREATMENT,BIOL CHEM LAB,BLDG 37,ROOM 5D02,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-27-9 J9 CHALL MOD MED PY 1994 VL 6 BP 143 EP 155 PG 13 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA BA79X UT WOS:A1994BA79X00013 ER PT B AU MOSS, J VAUGHAN, M AF MOSS, J VAUGHAN, M BE Corda, D Hamm, H Luini, A TI ADP-RIBOSYLATION FACTORS, 20-KDA GUANINE-NUCLEOTIDE-BINDING PROTEIN ACTIVATORS OF CHOLERA-TOXIN AND COMPONENTS OF THE VESICULAR TRANSPORT-SYSTEM SO GTPASE-CONTROLLED MOLECULAR MACHINES SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT Serono Symposium on GTPase-Controlled Molecular Machines CY SEP, 1993 CL SANTA MARIA IMBAR, ITALY SP SERONO SYMP RP MOSS, J (reprint author), NHLBI,CELLULAR METAB LAB,BLDG 10,ROOM 5N307,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-27-9 J9 CHALL MOD MED PY 1994 VL 6 BP 157 EP 173 PG 17 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA BA79X UT WOS:A1994BA79X00014 ER PT S AU HASCALL, VC CALABRO, A MIDURA, RJ YANAGISHITA, M AF HASCALL, VC CALABRO, A MIDURA, RJ YANAGISHITA, M BE Lennarz, WJ Hart, GW TI ISOLATION AND CHARACTERIZATION OF PROTEOGLYCANS SO GUIDE TO TECHNIQUES IN GLYCOBIOLOGY SE Methods in Enzymology LA English DT Review ID HEPARAN-SULFATE PROTEOGLYCANS; OVARIAN GRANULOSA-CELLS; CHONDROITIN SULFATE; KERATAN SULFATE; CORE PROTEINS; FIBROBLASTS; MEMBRANE; SURFACE; LINE; OLIGOSACCHARIDES C1 UNIV IOWA, DEPT ORTHOPED SURG, IOWA CITY, IA 52242 USA. RP HASCALL, VC (reprint author), NIDR, BONE RES BRANCH, BETHESDA, MD 20892 USA. NR 46 TC 78 Z9 82 U1 0 U2 2 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 0-12-443665-X; 0-12-182131-5 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1994 VL 230 BP 390 EP 417 PG 28 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88M UT WOS:A1994BA88M00024 PM 8139509 ER PT J AU DONNELLEY, S MCCARTHY, CR SINGLETON, R BALK, R BURGHARDT, GM ELLIS, GB JENNINGS, B JOHNSON, N KLEINIG, J NELSON, JL NOLAN, K ROWAN, AN RUSSOW, LM WACHBROIT, R AF DONNELLEY, S MCCARTHY, CR SINGLETON, R BALK, R BURGHARDT, GM ELLIS, GB JENNINGS, B JOHNSON, N KLEINIG, J NELSON, JL NOLAN, K ROWAN, AN RUSSOW, LM WACHBROIT, R TI THE BRAVE-NEW-WORLD OF ANIMAL BIOTECHNOLOGY SO HASTINGS CENTER REPORT LA English DT Article ID PLANTS; MODEL C1 GEORGETOWN UNIV,WASHINGTON,DC. KENNEDY INST,LONDON W6 7DW,ENGLAND. UNIV DELAWARE,NEWARK,DE. ROYAL VICTORIA HOSP,MONTREAL H3A 1A1,PQ,CANADA. UNIV TENNESSEE,KNOXVILLE,TN. NIH,OFF PROTECT RES RISKS,BETHESDA,MD. WORLD RESOURCES INST,WASHINGTON,DC 20006. CUNY,JOHN J COLL CRIMINAL JUSTICE,NEW YORK,NY 10021. ZEN MT MONASTERY,MT TREMPER,NY. TUFTS UNIV,CTR ANIM & PUBL POLICY,MEDFORD,MA. PURDUE UNIV,W LAFAYETTE,IN 47907. UNIV MARYLAND,INST PHILOSOPHY & PUBL POLICY,BALTIMORE,MD 21201. RP DONNELLEY, S (reprint author), HASTINGS CTR,HASTINGS ON HUDSON,NY 10706, USA. RI Burghardt, Gordon/E-4501-2010 OI Burghardt, Gordon/0000-0003-4943-8145 NR 79 TC 0 Z9 0 U1 0 U2 1 PU HASTINGS CENTER PI BRIARCLIFF MANOR PA 255 ELM ROAD, BRIARCLIFF MANOR, NY 10510 SN 0093-0334 J9 HASTINGS CENT REP JI Hastings Cent. Rep. PD JAN-FEB PY 1994 VL 24 IS 1 BP S1 EP S31 DI 10.2307/3562392 PG 31 WC Ethics; Health Care Sciences & Services; Medical Ethics; Social Sciences, Biomedical SC Social Sciences - Other Topics; Health Care Sciences & Services; Medical Ethics; Biomedical Social Sciences GA MW658 UT WOS:A1994MW65800011 PM 11654088 ER PT B AU KOHN, MC LUCIER, GW PORTIER, CJ AF KOHN, MC LUCIER, GW PORTIER, CJ BE Andrews, JS Frumkin, H Johnson, BL Mehlman, MA Xintaras, C Bucsela, JA TI RECEPTOR MECHANISMS AND DIOXIN RISK ASSESSMENT SO HAZARDOUS WASTE AND PUBLIC HEALTH: INTERNATIONAL CONGRESS ON THE HEALTH EFFECTS OF HAZARDOUS WASTE LA English DT Proceedings Paper CT International Congress on the Health Effects of Hazardous Waste - Hazardous Waste and Public Health CY MAY 03-06, 1993 CL ATLANTA, GA SP AGCY TOX SUBST & DIS REGISTRY, ASSOC OCCUPAT & ENVIRONM CLIN, ASSOC SCH PUBLIC HLTH, CTR DIS CONTROL & PREVENT, NATL CTR ENVIRONM HLTH, CTR DIS CONTROL & PREVENT, NATL INST OCCUPAT SAFETY & HLTH, CHEM MANUFACTURERS ASSOC, EMORY UNIV, CARTER CTR, EMORY UNIV, SCH PUBLIC HLTH, INT LABOUR ORG, UN, ENVIRONM PROGRAMME, WHO, INT PROGRAMME CHEM SAFETY, INT LIFE SCI INST, INT SOC ENVIRONM EPIDEMIOL, INT SOC EXPOSURE ANAL, NIH, NIEHS, PAN AMER HLTH ORG, SIERRA CLUB, US EPA RP KOHN, MC (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PRINCETON SCIENTIFIC PUBL CO PI PRINCETON PA PO BOX 2155, PRINCETON, NJ 08543 BN 0-911131-52-3 PY 1994 BP 421 EP 432 PG 12 WC Environmental Sciences; Environmental Studies; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA BC34E UT WOS:A1994BC34E00058 ER PT J AU EDMUNDSON, EW LUTON, SC MCGRAW, SA KELDER, SH LAYMAN, AK SMYTH, MH BACHMAN, KJ PEDERSEN, SA STONE, EJ AF EDMUNDSON, EW LUTON, SC MCGRAW, SA KELDER, SH LAYMAN, AK SMYTH, MH BACHMAN, KJ PEDERSEN, SA STONE, EJ TI CATCH - CLASSROOM PROCESS EVALUATION IN A MULTICENTER TRIAL SO HEALTH EDUCATION QUARTERLY LA English DT Article ID HEART-HEALTH-PROGRAM; SCHOOL-AGE CHILDREN; PHYSICAL-ACTIVITY; RISK-FACTORS; PROMOTION; BEHAVIOR; TRACKING; FITNESS; YOUTH; DIET AB The purpose of this paper is to describe the process evaluation model for the classroom curricula of the Child and Adolescent Trial for Cardiovascular Health (CATCH) Project. The process evaluation plan specifically targets how much each curriculum was implemented, to what degree it was implemented as designed, and the barriers to implementation. Additionally, the rationale for each of the process evaluation measures and the instrument development process are presented. Data resulting from these measures will be essential in order to answer questions regarding the internal validity of the main outcomes of the project. Specific examples and sample results are provided from the CATCH third-grade classroom curriculum, which was implemented the first year of CATCH. A discussion also is presented of how the findings from a sample of these measures were used to gain additional insight on the salient features of the curriculum, and how those features may be related to student outcomes. C1 NEW ENGLAND RES INST,WATERTOWN,MA. UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. TULANE UNIV,DEPT PUBL HLTH & TROP MED,NEW ORLEANS,LA 70118. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NHLBI,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. RP EDMUNDSON, EW (reprint author), UNIV TEXAS,DEPT KINESIOL & HLTH EDUC,AUSTIN,TX 78712, USA. NR 49 TC 4 Z9 4 U1 0 U2 1 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0195-8402 J9 HEALTH EDUC QUART JI Health Educ. Q. PY 1994 SU 2 BP S27 EP S50 PG 24 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MP436 UT WOS:A1994MP43600003 ER PT J AU ELDER, JP MCGRAW, SA STONE, EJ REED, DB HARSHA, DW GREENE, T WAMBSGANS, KC AF ELDER, JP MCGRAW, SA STONE, EJ REED, DB HARSHA, DW GREENE, T WAMBSGANS, KC TI CATCH - PROCESS EVALUATION OF ENVIRONMENTAL-FACTORS AND PROGRAMS SO HEALTH EDUCATION QUARTERLY LA English DT Article ID HEALTH PROMOTION; CARDIOVASCULAR HEALTH; SCHOOL AB The Child and Adolescent Trial for Cardiovascular Health (CATCH) is a multicenter trial designed to test the effectiveness of school and family-based cardiovascular health promotion for preadolescents. CATCH interventions target multiple cardiovascular health behaviors such as dietary intake of fat and sodium, physical activity, and tobacco use. Evaluation includes physiological, psychosocial, behavioral, and process measures. An important aspect of the process evaluation is the assessment of environmental factors and ''secular events'' in both intervention and control schools that may affect outcomes independently of the CATCH interventions. With such information, CATCH investigators are able to isolate the impact of the CATCH intervention from competing (non-CATCH) factors as well as ''track'' proximal (i.e., immediate and short term) changes related to the intervention that may in turn lead to ''distal'' (long-term) behavior change. The School Health Questionnaire, the major process evaluation tool for monitoring secular and environmental changes in the schools, is described in detail, and data describing tobacco-related environmental factors and secular events are presented. C1 NEW ENGLAND RES INST,WATERTOWN,MA. SE UNIV LOUISIANA,HAMMOND,LA. TULANE UNIV,MED CTR,SCH PUBL HLTH & TROP MED,NEW ORLEANS,LA 70118. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. UNIV CALIF SAN DIEGO,SCH MED,LA JOLLA,CA 92093. NHLBI,BETHESDA,MD 20892. RP ELDER, JP (reprint author), SAN DIEGO STATE UNIV,COLL HLTH & HUMAN SERV,GRAD SCH PUBL HLTH,SAN DIEGO,CA 92182, USA. NR 15 TC 2 Z9 2 U1 1 U2 4 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0195-8402 J9 HEALTH EDUC QUART JI Health Educ. Q. PY 1994 SU 2 BP S107 EP S127 PG 21 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MP436 UT WOS:A1994MP43600007 ER PT J AU JOHNSON, CC OSGANIAN, SK BUDMAN, SB LYTLE, LA BARRERA, EP BONURA, SR WU, MC NADER, PR AF JOHNSON, CC OSGANIAN, SK BUDMAN, SB LYTLE, LA BARRERA, EP BONURA, SR WU, MC NADER, PR TI CATCH - FAMILY PROCESS EVALUATION IN A MULTICENTER TRIAL SO HEALTH EDUCATION QUARTERLY LA English DT Article ID CARDIOVASCULAR HEALTH PROMOTION; BEHAVIOR; CHILDREN; PROGRAM; WEIGHT AB The Child and Adolescent Trial for Cardiovascular Health (CATCH) is an elementary school cardiovascular health education field trial in progress in San Diego, California, New Orleans, Louisiana, Minneapolis, Minnesota, and Austin, Texas. Because a significant part of a child's health behaviors are shaped within the home, CATCH is evaluating whether the effects of the school-based program are enhanced by the inclusion of a home-based program. A 7 x 7 x 10 randomized design with 7 school-only and 7 school-plus-family intervention schools, along with 10 control schools is implemented at each site. The CATCH family intervention is implemented during Grades 3 through 5 and consists of home-based curricula and Family Fun Nights focusing on healthier eating and increased physical activity during Grades 3 and 4, along with a smoking prevention curriculum in Grade 5. CATCH is examining the effectiveness of family (household) involvement through changes in students' dietary intake of fat and sodium. This paper describes the process evaluation methods used to document the extent of participation in the family program. Data reported for the third-grade Family Fun Nights held in the 28 family schools across all sites reflected an average student participation rate of 67%. The average family member to student ratio was approximately 2:1. Participation by all third-grade teachers and the majority of physical education specialists was observed. C1 UNIV MINNESOTA, MINNEAPOLIS, MN 55455 USA. NEW ENGLAND RES INST, WATERTOWN, MA USA. UNIV MINNESOTA, MINNEAPOLIS, MN 55455 USA. UNIV TEXAS, HLTH SCI CTR, HOUSTON, TX 77225 USA. NHLBI, BETHESDA, MD 20892 USA. UNIV CALIF SAN DIEGO, SAN DIEGO, CA 92103 USA. RP JOHNSON, CC (reprint author), TULANE UNIV, MED CTR, SCH PUBL HLTH & TROP MED, 1501 CANAL ST, ROOM 1205, NEW ORLEANS, LA 70112 USA. NR 32 TC 0 Z9 0 U1 1 U2 1 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0195-8402 J9 HEALTH EDUC QUART JI Health Educ. Q. PY 1994 SU 2 BP S91 EP S106 PG 16 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MP436 UT WOS:A1994MP43600006 ER PT J AU MCGRAW, SA STONE, EJ OSGANIAN, SK ELDER, JP PERRY, CL JOHNSON, CC PARCEL, GS WEBBER, LS LUEPKER, RV AF MCGRAW, SA STONE, EJ OSGANIAN, SK ELDER, JP PERRY, CL JOHNSON, CC PARCEL, GS WEBBER, LS LUEPKER, RV TI DESIGN OF PROCESS EVALUATION WITHIN THE CHILD AND ADOLESCENT TRIAL FOR CARDIOVASCULAR HEALTH (CATCH) SO HEALTH EDUCATION QUARTERLY LA English DT Article ID PROMOTION; PROGRAM AB Process evaluation complements outcome evaluation by providing data to describe how a program was implemented, how well the activities delivered fit the original design, to whom services were delivered, the extent to which the target population was reached, and factors external to the program that may compete with the program effects. The process evaluation system used in the Child and Adolescent Trial for Cardiovascular Health (CATCH) is presented in this paper. The conceptual model underlying the CATCH process evaluation system is described, and process measures and data collection protocols are reviewed. Functions of process evaluation data in the trial include: (1) describing the implementation of the program, (2) quality control and monitoring, and (3) explaining program effects. The importance of incorporating process evaluation into final outcome analyses and assessments of program impact is emphasized. C1 NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,SCH MED,SAN DIEGO STATE UNIV,LA JOLLA,CA 92093. UNIV MINNESOTA,SCH PUBL HLTH,MINNEAPOLIS,MN 55455. TULANE UNIV,SCH PUBL HLTH & TROP MED,NEW ORLEANS,LA 70118. UNIV TEXAS,HLTH SCI CTR,CTR HLTH PROMOT RES & DEV,HOUSTON,TX 77225. RP MCGRAW, SA (reprint author), NEW ENGLAND RES INST,WATERTOWN,MA 02171, USA. NR 25 TC 0 Z9 0 U1 1 U2 3 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0195-8402 J9 HEALTH EDUC QUART JI Health Educ. Q. PY 1994 SU 2 BP S5 EP S26 PG 22 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MP436 UT WOS:A1994MP43600002 ER PT J AU MCKENZIE, TL STRIKMILLER, PK STONE, EJ WOODS, SE EHLINGER, SS ROMERO, KA BUDMAN, ST AF MCKENZIE, TL STRIKMILLER, PK STONE, EJ WOODS, SE EHLINGER, SS ROMERO, KA BUDMAN, ST TI CATCH - PHYSICAL-ACTIVITY PROCESS EVALUATION IN A MULTICENTER TRIAL SO HEALTH EDUCATION QUARTERLY LA English DT Article ID PUBLIC-HEALTH PERSPECTIVE; CHILDREN; FITNESS AB This paper presents the process evaluation model for the physical activity intervention component of the Child and Adolescent Trial for Cardiovascular Health (CATCH) and describes the major procedures used to monitor CATCH PE, the physical education intervention. The paper focuses on CATCH PE teacher training and in-service support as well as on the curriculum implementation. Monitoring training and support included assessing the in-service training workshops and the follow-up on-site assistance provided by staff. Monitoring the implementation included assessing the quantity and quality of CATCH PE instruction in terms of student physical activity engagement and lesson context, the fidelity of the curricular implementation, and the opportunities for other physical activity by children throughout the school day. C1 TULANE UNIV,SCH PUBL HLTH & TROP MED,NEW ORLEANS,LA 70118. NHLBI,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NEW ENGLAND RES INST,BOSTON,MA. RP MCKENZIE, TL (reprint author), SAN DIEGO STATE UNIV,DEPT PHYS EDUC,SAN DIEGO,CA 92182, USA. NR 20 TC 1 Z9 1 U1 1 U2 1 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0195-8402 J9 HEALTH EDUC QUART JI Health Educ. Q. PY 1994 SU 2 BP S73 EP S89 PG 17 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MP436 UT WOS:A1994MP43600005 ER PT J AU RAIZMAN, DJ MONTGOMERY, DH OSGANIAN, SK EBZERY, MK EVANS, MA NICKLAS, TA ZIVE, MM HANN, BJ SNYDER, MP CLESI, AL AF RAIZMAN, DJ MONTGOMERY, DH OSGANIAN, SK EBZERY, MK EVANS, MA NICKLAS, TA ZIVE, MM HANN, BJ SNYDER, MP CLESI, AL TI CATCH - FOOD-SERVICE PROGRAM PROCESS EVALUATION IN A MULTICENTER TRIAL SO HEALTH EDUCATION QUARTERLY LA English DT Article ID HEALTHFUL DIET; INTERVENTION AB Process evaluation is an essential element of a multicenter trial in order to explain study outcomes and monitor intervention progress. This paper presents the process evaluation model for the Eat Smart School Nutrition Program, the food service intervention component of the Child and Adolescent Trial for Cardiovascular Health (CATCH), and describes the process evaluation strategies developed to assess this program. The paper details (1) measures of program implementation including training, support visits, and program promotion, (2) food service staff characteristics, and (3) measures of mediating variables including secular trends and school meal participation. C1 TUFTS UNIV NEW ENGLAND MED CTR,FRANCES STERN NUTR CTR,BOSTON,MA. UNIV TEXAS,HLTH SCI CTR,CTR HLTH PROMOT RES & DEV,HOUSTON,TX 77225. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. TULANE UNIV,SCH PUBL HLTH & TROP MED,NEW ORLEANS,LA 70118. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. UNIV MINNESOTA,SCH PUBL HLTH,MINNEAPOLIS,MN 55455. NEW ENGLAND RES INST,9 GALEN ST,WATERTOWN,MA 02172. NR 19 TC 1 Z9 1 U1 1 U2 1 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0195-8402 J9 HEALTH EDUC QUART JI Health Educ. Q. PY 1994 SU 2 BP S51 EP S71 PG 21 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MP436 UT WOS:A1994MP43600004 ER PT J AU STONE, EJ AF STONE, EJ TI PROCESS EVALUATION IN THE MULTICENTER CHILD AND ADOLESCENT TRIAL FOR CARDIOVASCULAR HEALTH (CATCH) - FOREWORD SO HEALTH EDUCATION QUARTERLY LA English DT Editorial Material RP STONE, EJ (reprint author), NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,PREVENT & DEMOSTRAT RES BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0195-8402 J9 HEALTH EDUC QUART JI Health Educ. Q. PY 1994 SU 2 BP S3 EP S4 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MP436 UT WOS:A1994MP43600001 ER PT J AU MACALLAN, L NARAYAN, V AF MACALLAN, L NARAYAN, V TI KEEPING THE HEART BEAT IN GRAMPIAN - A CASE-STUDY IN COMMUNITY PARTICIPATION AND OWNERSHIP SO HEALTH PROMOTION INTERNATIONAL LA English DT Article DE COMMUNITY OWNERSHIP; HEART HEALTH ID NORTH-KARELIA PROJECT; HEALTH-PROGRAM; DISEASE AB In the Grampian Region of Scotland, a new 10 year heart health initiative, 'Keeping the heart Beat in Grampian' was launched in October 1991. Although this programme is based on a number of well-tested health promotion principles it is unique in a number of aspects. The concepts of community ownership, corporate identity and people empowerment have been extended to a much greater degree. The programme is registered as a private company with charitable status so that management, decision-making and budgetary control are vested totally in the community. C1 NIH,PHOENIX EPIDEMIOL & CLIN RES BRANCH,PHOENIX,AZ. RP MACALLAN, L (reprint author), GRAMPIAN AREA HLTH BOARD,DIV HLTH PROMOT,1 ALBYN PL,ABERDEEN AB9 8QP,SCOTLAND. NR 25 TC 6 Z9 6 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0957-4824 J9 HEALTH PROMOT INT JI Health Promot. Int. PY 1994 VL 9 IS 1 BP 13 EP 19 DI 10.1093/heapro/9.1.13 PG 7 WC Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA NE790 UT WOS:A1994NE79000003 ER PT J AU PEI, XF GREIG, NH FLIPPENANDERSON, JL BI, S BROSSI, A AF PEI, XF GREIG, NH FLIPPENANDERSON, JL BI, S BROSSI, A TI TOTAL SYNTHESIS OF RACEMIC AND OPTICALLY-ACTIVE COMPOUNDS RELATED TO PHYSOSTIGMINE AND RING-C HETEROANALOGUES FROM 3-[2'-(DIMETHYLAMINO)ETHYL]-2,3-DIHYDRO-5-METHOXY-1,3-DIMETHY-1H-INDOL-2 -OL SO HELVETICA CHIMICA ACTA LA English DT Article ID CARBAMATE ANALOGS; ANTICHOLINESTERASE ACTIVITY; (+)-PHYSOSTIGMINE; (+)-PHYSOVENINE; (-)-PHYSOVENOL; INHIBITORS; ALKALOIDS AB Oxindole 11, obtained on 3-[2'-(dimethylamino)ethyl]alkylation of oxindole 12, yielded, on stereoselective reduction with sodium dihydridobis(2-methoxyelhoxy)aluminate, aminoalcohol 8 (Scheme 2). The quaternary methiodide 10, obtained from 8 with Mel, gave, in nucleophilic displacements concurring with a Hofmann elimination, (+/-)-esermethole 6, (+/-)-5-O-methylphysovenol (14),(+/-)-5-O-methyl-1-thiaphysovenol (15), and (+/-)-1-benzyl-1-demethylesermethole (16). Syntheses of(+/-)-1-benzyl-1-demethylphenserine (18), (+/-)-1-demethylphenserine (19), and (+/-)-phenserine (4) from 6 and 16 are described. Optically active 8a and 8b, obtained by chemical resolution, similarly gave the enantiomers 6a and 14a-16a of the (3aS)-series (prepared earlier from physostigmine (1a)) and their (3R)-enantiomers. The anticholinesterase activity of(+/-)-4, (+/-)-18, and (+/-)-19 was compared with that of their optically active enantiomers. C1 USN,RES LAB,STRUCT MATTER LAB,WASHINGTON,DC 20375. GEORGETOWN UNIV,DEPT CHEM,WASHINGTON,DC 20057. NIH,BETHESDA,MD 20892. RP PEI, XF (reprint author), NIA,NEUROSCI LAB,BLDG 10,BETHESDA,MD 20892, USA. NR 22 TC 22 Z9 22 U1 0 U2 1 PU NEW SWISS CHEMICAL SOC PI BASEL PA VERLAG HELVETICA CHIMICA ACTA, MALZGASSE 21, POSTFACH 313, CH-4010 BASEL, SWITZERLAND SN 0018-019X J9 HELV CHIM ACTA JI Helv. Chim. Acta PY 1994 VL 77 IS 5 BP 1412 EP 1422 DI 10.1002/hlca.19940770519 PG 11 WC Chemistry, Multidisciplinary SC Chemistry GA PC189 UT WOS:A1994PC18900018 ER PT J AU RIFKIND, JM ABUGO, O LEVY, A HEIM, J AF RIFKIND, JM ABUGO, O LEVY, A HEIM, J TI DETECTION, FORMATION, AND RELEVANCE OF HEMICHROMES AND HEMOCHROMES SO HEMOGLOBINS, PT B SE METHODS IN ENZYMOLOGY LA English DT Review ID ELECTRON-PARAMAGNETIC-RESONANCE; MOLLUSK SCAPHARCA-INAEQUIVALVIS; DRUG-INDUCED OXIDATION; ERYTHROCYTE-MEMBRANE; CYTOCHROME-C; METHEMOGLOBIN DERIVATIVES; HEMOGLOBIN DENATURATION; MOSSBAUER-SPECTROSCOPY; TETRAMERIC HEMOGLOBINS; UNSTABLE HEMOGLOBINS C1 NATL CTR RES RESOURCES,BETHESDA,MD 20014. RP RIFKIND, JM (reprint author), NIA,GERONTOL RES CTR,MOLEC & CELLULAR BIOL LAB,BALTIMORE,MD 21224, USA. NR 117 TC 75 Z9 76 U1 2 U2 2 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 1994 VL 231 BP 449 EP 480 PG 32 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88N UT WOS:A1994BA88N00028 PM 8041268 ER PT J AU HOFRICHTER, J ANSARI, A JONES, CM DUETSCH, RM SOMMER, JH HENRY, ER AF HOFRICHTER, J ANSARI, A JONES, CM DUETSCH, RM SOMMER, JH HENRY, ER TI LIGAND-BINDING AND CONFORMATIONAL-CHANGES MEASURED BY TIME-RESOLVED ABSORPTION-SPECTROSCOPY SO HEMOGLOBINS, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID INTERSUBUNIT COMMUNICATION; GEMINATE RECOMBINATION; TRANSIENT ABSORPTION; HUMAN-HEMOGLOBIN; MYOGLOBIN; PICOSECOND; BACTERIORHODOPSIN; PHOTOLYSIS; PHOTOCYCLE; DYNAMICS C1 UNIV ILLINOIS,DEPT PHYS,CHICAGO,IL 60680. UNIV SO ALABAMA,DEPT CHEM,MOBILE,AL 36688. RP HOFRICHTER, J (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 2,BETHESDA,MD 20892, USA. RI Henry, Eric/J-3414-2013 OI Henry, Eric/0000-0002-5648-8696 NR 47 TC 16 Z9 16 U1 0 U2 1 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 1994 VL 232 BP 387 EP 415 PG 29 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88P UT WOS:A1994BA88P00018 PM 8057870 ER PT J AU VANDEGRIFF, KD SHRAGER, RI AF VANDEGRIFF, KD SHRAGER, RI TI HEMOGLOBIN-OXYGEN EQUILIBRIUM BINDING - RAPID-SCANNING SPECTROPHOTOMETRY AND SINGULAR-VALUE DECOMPOSITION SO HEMOGLOBINS, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID COOPERATIVITY; TRANSITIONS; RESOLUTION; SPECTRA C1 NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892. RP VANDEGRIFF, KD (reprint author), UNIV CALIF SAN DIEGO,VET AFFAIRS MED CTR,DEPT MED,SAN DIEGO,CA 92161, USA. NR 33 TC 14 Z9 15 U1 4 U2 6 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 1994 VL 232 BP 460 EP 485 PG 26 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88P UT WOS:A1994BA88P00022 PM 8057875 ER PT J AU WINSLOW, RM MURRAY, A GIBSON, CC AF WINSLOW, RM MURRAY, A GIBSON, CC TI OXYGEN EQUILIBRIUM CURVE OF CONCENTRATED HEMOGLOBIN SO HEMOGLOBINS, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID BLOOD SUBSTITUTE C1 LETTERMAN ARMY INST RES,DIV BLOOD RES,SAN FRANCISCO,CA 94129. NIH,BETHESDA,MD 20892. RP WINSLOW, RM (reprint author), UNIV CALIF SAN DIEGO,VET AFFAIRS MED CTR,DEPT MED,SAN DIEGO,CA 92161, USA. NR 16 TC 3 Z9 3 U1 1 U2 1 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 1994 VL 232 BP 486 EP 495 PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88P UT WOS:A1994BA88P00023 PM 8057876 ER PT J AU BERGER, RL DAVIDS, N PERRELLA, M AF BERGER, RL DAVIDS, N PERRELLA, M TI SIMULATION OF HEMOGLOBIN KINETICS USING FINITE-ELEMENT NUMERICAL-METHODS SO HEMOGLOBINS, PT C SE METHODS IN ENZYMOLOGY LA English DT Review C1 PENN STATE UNIV,SCH ENGN,DEPT ENGN SCI & MECH,UNIVERSITY PK,PA 16802. UNIV MILAN,SCH MED,DEPT SCI & TECHNOL,I-20133 MILAN,ITALY. RP BERGER, RL (reprint author), NHLBI,BIOPHYS CHEM LAB,BLDG 10,BETHESDA,MD 20892, USA. NR 14 TC 5 Z9 5 U1 0 U2 1 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 1994 VL 232 BP 517 EP 558 PG 42 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88P UT WOS:A1994BA88P00025 PM 8057878 ER PT J AU DOYLE, ML MYERS, DW ACKERS, GK SHRAGER, RI AF DOYLE, ML MYERS, DW ACKERS, GK SHRAGER, RI TI WEIGHTED NONLINEAR-REGRESSION ANALYSIS OF HIGHLY COOPERATIVE OXYGEN EQUILIBRIUM CURVES SO HEMOGLOBINS, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID HEMOGLOBIN CONCENTRATION; RESOLVABILITY; VARIABLES; CONSTANTS; ERRORS C1 WASHINGTON UNIV,SCH MED,DEPT BIOCHEM & MOLEC BIOPHYS,ST LOUIS,MO 63110. DUKE UNIV,MED CTR,DEPT BIOCHEM,DURHAM,NC 27710. NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892. RP DOYLE, ML (reprint author), SMITHKLINE BEECHAM PHARMACEUT,DEPT MACROMOLEC SCI,KING OF PRUSSIA,PA 19406, USA. NR 33 TC 4 Z9 4 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 1994 VL 232 BP 576 EP 597 PG 22 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88P UT WOS:A1994BA88P00027 PM 8057881 ER PT S AU JHON, DY PARK, D RHEE, SG AF JHON, DY PARK, D RHEE, SG BE Iyengar, R TI PURIFICATION OF PHOSPHOLIPASE C-BETA-3 FROM RAT-BRAIN SO HETEROTRIMERIC G-PROTEIN EFFECTORS SE Methods in Enzymology LA English DT Review ID BOVINE BRAIN; C ISOZYMES; ACTIVATION; CLONING; EXPRESSION; FORMS RP NHLBI, BIOCHEM LAB, BLDG 3, BETHESDA, MD 20892 USA. NR 14 TC 6 Z9 6 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 0-12-182139-0 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1994 VL 238 BP 219 EP 227 PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BB62M UT WOS:A1994BB62M00017 PM 7799787 ER PT J AU LEE, CW LEE, KH RHEE, SG AF LEE, CW LEE, KH RHEE, SG TI CHARACTERIZATION OF PHOSPHOLIPASE-C ISOZYMES IN BOVINE RETINA - PURIFICATION OF PHOSPHOLIPASE C-BETA-4 SO HETEROTRIMERIC G-PROTEIN EFFECTORS SE METHODS IN ENZYMOLOGY LA English DT Review ID ROD OUTER SEGMENTS; LIGHT-MEDIATED BREAKDOWN; INOSITOL-TRISPHOSPHATE; PHOSPHATIDYLINOSITOL-4,5-BISPHOSPHATE; PHOTORECEPTOR; EXCITATION; ADAPTATION; ACTIVATION; CLONING; BRAIN RP LEE, CW (reprint author), NHLBI,BIOCHEM LAB,BLDG 3,BETHESDA,MD 20892, USA. NR 21 TC 2 Z9 2 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 1994 VL 238 BP 227 EP 237 PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BB62M UT WOS:A1994BB62M00018 PM 7799788 ER PT J AU DEMAUREX, N RAWLINGS, SR KRAUSE, KH JACONI, MEE LEW, PD SCHLEGEL, W AF DEMAUREX, N RAWLINGS, SR KRAUSE, KH JACONI, MEE LEW, PD SCHLEGEL, W TI COMBINATION OF MICROFLUORIMETRIC MONITORING OF CYTOSOLIC CALCIUM AND PH WITH PATCH-CLAMP ELECTROPHYSIOLOGICAL RECORDINGS IN NEUTROPHIL GRANULOCYTES SO HETEROTRIMERIC G-PROTEIN EFFECTORS SE METHODS IN ENZYMOLOGY LA English DT Review ID CELLS; EXOCYTOSIS; CA-2+ C1 UNIV HOSP GENEVA,DIV INFECT DIS,CH-1211 GENEVA 4,SWITZERLAND. UNIV GENEVA,DEPT MED,FDN MED RES,CH-1211 GENEVA 4,SWITZERLAND. MAYO CLIN & MAYO FDN,DEPT PHARMACOL,ROCHESTER,MN 55905. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RP DEMAUREX, N (reprint author), HOSP SICK CHILDREN,DIV CELL BIOL,555 UNIV AVE,TORONTO M5G 1X8,ON,CANADA. RI Krause, Karl-Heinz/E-8030-2011; Jaconi, Marisa/J-4392-2013 NR 11 TC 3 Z9 3 U1 0 U2 1 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 1994 VL 238 BP 308 EP 320 PG 13 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BB62M UT WOS:A1994BB62M00026 PM 7799797 ER PT S AU MOSS, J HAUN, RS TSAI, SC WELSH, CF LEE, FJS PRICE, SR VAUGHAN, M AF MOSS, J HAUN, RS TSAI, SC WELSH, CF LEE, FJS PRICE, SR VAUGHAN, M BE Iyengar, R TI ACTIVATION OF CHOLERA-TOXIN BY ADP-RIBOSYLATION FACTORS - 20-KDA GUANINE-NUCLEOTIDE-BINDING PROTEINS SO HETEROTRIMERIC G PROTEINS SE Methods in Enzymology LA English DT Review ID LIGATION-INDEPENDENT CLONING; AMINO-ACID-SEQUENCE; ADENYLATE-CYCLASE; RIBOSYLTRANSFERASE ACTIVITY; ESCHERICHIA-COLI; SACCHAROMYCES-CEREVISIAE; REGULATORY COMPONENT; BOVINE BRAIN; FACTORS ARFS; HUMAN GENE C1 EMORY UNIV HOSP, DIV RENAL, ATLANTA, GA 30322 USA. UNIV MIAMI, DEPT CELL BIOL & ANAT, MIAMI, FL 33136 USA. RP NHLBI, CELLULAR METAB LAB, BETHESDA, MD 20892 USA. NR 58 TC 8 Z9 8 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 0-12-182138-2 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1994 VL 237 BP 44 EP 63 PG 20 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88T UT WOS:A1994BA88T00005 PM 7935017 ER PT J AU LEE, E LINDER, ME GILMAN, AG AF LEE, E LINDER, ME GILMAN, AG TI EXPRESSION OF G-PROTEIN ALPHA-SUBUNITS IN ESCHERICHIA-COLI SO HETEROTRIMERIC G PROTEINS SE METHODS IN ENZYMOLOGY LA English DT Review ID LIPID MODIFICATIONS; BINDING C1 WASHINGTON UNIV,SCH MED,DEPT CELL BIOL & PHYSIOL,ST LOUIS,MO 63110. UNIV TEXAS,SW MED CTR,DEPT PHARMACOL,DALLAS,TX 75235. RP LEE, E (reprint author), NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892, USA. FU NIGMS NIH HHS [GM34497, GM07062] NR 20 TC 229 Z9 229 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 1994 VL 237 BP 146 EP 164 PG 19 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88T UT WOS:A1994BA88T00012 PM 7934993 ER PT J AU GEJMAN, PV WEINSTEIN, LS AF GEJMAN, PV WEINSTEIN, LS TI DETECTION OF MUTATIONS AND POLYMORPHISMS OF G(S)ALPHA, SUBUNIT GENE BY DENATURING GRADIENT GEL-ELECTROPHORESIS SO HETEROTRIMERIC G PROTEINS SE METHODS IN ENZYMOLOGY LA English DT Review ID SINGLE-BASE SUBSTITUTIONS; STIMULATORY G-PROTEIN; MCCUNE-ALBRIGHT SYNDROME; HUMAN PITUITARY-TUMORS; ALPHA-SUBUNIT; DNA FRAGMENTS; HEREDITARY OSTEODYSTROPHY; ADENYLYL CYCLASE; NUCLEIC-ACIDS; GENOMIC DNA C1 NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892. RP GEJMAN, PV (reprint author), NIMH,CLIN NEUROSCI BRANCH,MOLEC CLIN INVEST UNIT,BETHESDA,MD 20892, USA. RI Weinstein, Lee/I-5575-2015 NR 46 TC 7 Z9 7 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 1994 VL 237 BP 308 EP 320 PG 13 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88T UT WOS:A1994BA88T00024 PM 7935007 ER PT B AU ACCILI, D AF ACCILI, D BE Andreoli, M Shields, M TI GENE MANIPULATION BY HOMOLOGOUS RECOMBINATION - IMPACT ON ENDOCRINE RESEARCH SO HIGHLIGHTS IN MOLECULAR AND CLINICAL ENDOCRINOLOGY SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT 25th National Congress of the Italian-Society-of-Endocrinology CY MAY 22-25, 1994 CL ROME, ITALY RP ACCILI, D (reprint author), NIDDKD,DIABET BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-24-4 J9 FRONT ENDOCRINOL PY 1994 VL 9 BP 9 EP 16 PG 8 WC Cell Biology; Electrochemistry SC Cell Biology; Electrochemistry GA BC27X UT WOS:A1994BC27X00003 ER PT B AU MIGLIACCIO, S NEWBOLD, RR CENTANNI, M MCLACHLAN, JA ANDREOLI, M KORACH, KS AF MIGLIACCIO, S NEWBOLD, RR CENTANNI, M MCLACHLAN, JA ANDREOLI, M KORACH, KS BE Andreoli, M Shields, M TI TRANSIENT DEVELOPMENTAL EXPOSURE OF FEMALE MICE TO DIETHYLSTILBESTROL AFFECTS ADULT BONE DENSITY SO HIGHLIGHTS IN MOLECULAR AND CLINICAL ENDOCRINOLOGY SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT 25th National Congress of the Italian-Society-of-Endocrinology CY MAY 22-25, 1994 CL ROME, ITALY RP MIGLIACCIO, S (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-24-4 J9 FRONT ENDOCRINOL PY 1994 VL 9 BP 319 EP 322 PG 4 WC Cell Biology; Electrochemistry SC Cell Biology; Electrochemistry GA BC27X UT WOS:A1994BC27X00060 ER PT J AU ARAI, R JACOBOWITZ, DM DEURA, S AF ARAI, R JACOBOWITZ, DM DEURA, S TI HETEROGENEITY IN CALBINDIN-D28K EXPRESSION IN OXYTOCIN-CONTAINING MAGNOCELLULAR NEURONS OF THE RAT HYPOTHALAMUS SO HISTOCHEMISTRY LA English DT Article ID CORTICOTROPIN-RELEASING-FACTOR; C-FOS IMMUNOREACTIVITY; NERVOUS-SYSTEM; NUCLEI; CHOLECYSTOKININ; COLOCALIZATION; LOCALIZATION; COEXISTENCE; PROTEINS; GALANIN AB We have used a double-labeling immunofluorescence method to examine whether oxytocin-containing magnocellular neurons possess a calcium-binding protein, calbindin-D28k, in the hypothalamus of the rat. In the supraoptic nucleus, most oxytocin-immunoreactive cells were also stained for calbindin-D28k. However, in the magnocellular part of the paraventricular nucleus nearly all oxytocin-labeled cells were devoid of calbindin-D28k. In the anterior commissural nucleus, approximately one-third of oxytocin-stained cells were also calbindin-D28k-immunoreactive, but the other cells were negative for calbindin-D28k. This study indicates that there may be distinct chemical features between oxytocin-containing magnocellular neurons of the supraoptic nucleus compared to those of the paraventricular nucleus. C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. RP ARAI, R (reprint author), FUJITA HLTH UNIV,SCH MED,DEPT ANAT,TOYOAKE,AICHI 47011,JAPAN. NR 28 TC 10 Z9 10 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-5564 J9 HISTOCHEMISTRY JI Histochemistry PD JAN PY 1994 VL 101 IS 1 BP 9 EP 12 DI 10.1007/BF00315825 PG 4 WC Cell Biology SC Cell Biology GA NC653 UT WOS:A1994NC65300002 PM 7517930 ER PT B AU VITKOVIC, L DACUNHA, A TYOR, WR AF VITKOVIC, L DACUNHA, A TYOR, WR BE Price, RW Perry, SW TI CYTOKINE EXPRESSION AND PATHOGENESIS IN AIDS BRAIN SO HIV, AIDS, AND THE BRAIN SE RESEARCH PUBLICATIONS : ASSOCIATION FOR RESEARCH IN NERVOUS AND MENTAL DISEASE LA English DT Proceedings Paper CT 72nd Annual ARNMD Meeting CY DEC, 1992 CL NEW YORK, NY SP ASSOC RES NERVOUS & MENTAL DIS C1 NIMH,DIV NEUROSCI & BEHAV SCI,ROCKVILLE,MD 20857. NR 0 TC 46 Z9 46 U1 0 U2 1 PU RAVEN PRESS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 BN 0-7817-0063-9 J9 RES P ARNMD PY 1994 VL 72 BP 203 EP 222 PG 20 WC Immunology; Clinical Neurology; Neurosciences; Pathology; Virology SC Immunology; Neurosciences & Neurology; Pathology; Virology GA BZ44J UT WOS:A1994BZ44J00011 PM 8115714 ER PT B AU SCHULTZ, AM AF SCHULTZ, AM BE Nicolosi, A TI OBSTACLES IN THE PURSUIT OF AN AIDS VACCINE SO HIV EPIDEMIOLOGY: MODELS AND METHODS LA English DT Proceedings Paper CT Workshop on Models and Methods of Epidemiologic Research on HIV Infection CY SEP, 1992 CL ITALY SP ITALIAN NATL RES COUNCIL RP SCHULTZ, AM (reprint author), NIAID,BRDP,DIV AIDS,VACCINE RES & DEV BRANCH,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 0-7817-0118-X PY 1994 BP 175 EP 185 PG 11 WC Public, Environmental & Occupational Health; Immunology; Virology SC Public, Environmental & Occupational Health; Immunology; Virology GA BZ45Z UT WOS:A1994BZ45Z00014 ER PT B AU VERMUND, SH AF VERMUND, SH BE Nicolosi, A TI THE EFFICACY OF HIV VACCINES - METHODOLOGICAL ISSUES IN PREPARING FOR CLINICAL-TRIALS SO HIV EPIDEMIOLOGY: MODELS AND METHODS LA English DT Proceedings Paper CT Workshop on Models and Methods of Epidemiologic Research on HIV Infection CY SEP, 1992 CL ITALY SP ITALIAN NATL RES COUNCIL RP VERMUND, SH (reprint author), NIAID,DIV AIDS,VACCINE TRIALS & EPIDEMIOL BRANCH,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 0-7817-0118-X PY 1994 BP 187 EP 209 PG 23 WC Public, Environmental & Occupational Health; Immunology; Virology SC Public, Environmental & Occupational Health; Immunology; Virology GA BZ45Z UT WOS:A1994BZ45Z00015 ER PT B AU GAIL, MH ROSENBERG, PS AF GAIL, MH ROSENBERG, PS BE Nicolosi, A TI BACK-CALCULATION MODELS THAT TAKE TREATMENT INTO ACCOUNT SO HIV EPIDEMIOLOGY: MODELS AND METHODS LA English DT Proceedings Paper CT Workshop on Models and Methods of Epidemiologic Research on HIV Infection CY SEP, 1992 CL ITALY SP ITALIAN NATL RES COUNCIL RP GAIL, MH (reprint author), NCI,EPIDEMIOL METHODS SECT,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 BN 0-7817-0118-X PY 1994 BP 345 EP 358 PG 14 WC Public, Environmental & Occupational Health; Immunology; Virology SC Public, Environmental & Occupational Health; Immunology; Virology GA BZ45Z UT WOS:A1994BZ45Z00024 ER PT J AU ENGEL, BT AF ENGEL, BT TI BEHAVIORAL MEDICINE - WHERES THE BEHAVIOR - WHERES THE MEDICINE SO HOMEOSTASIS IN HEALTH AND DISEASE LA English DT Article; Proceedings Paper CT CIANS-ISBM Satellite Conference on the Occasion of the 2nd International Congress of Behavioral Medicine CY JUL 12-14, 1992 CL HANNOVER MED UNIV, HANNOVER, GERMANY SP COLLEGIUM INT ACTIVITATIS NERVOSAE SUPERIORIS, INT SOC BIOPHYS MED HO HANNOVER MED UNIV RP ENGEL, BT (reprint author), NIA,GERONTOL RES CTR,BEHAV SCI LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU CIANS-HOMEOSTASIS PI PRAGUE 10 PA C/O NATL INST PUBLIC HEALTH, SROBAROVA 48, PRAGUE 10, CZECH REPUBLIC CZ 100 42 SN 0960-7560 J9 HOMEOSTASIS HLTH DIS JI Homeost. Health Dis. PY 1994 VL 35 IS 1-2 BP 3 EP 5 PG 3 WC Behavioral Sciences; Cardiac & Cardiovascular Systems SC Behavioral Sciences; Cardiovascular System & Cardiology GA PF922 UT WOS:A1994PF92200004 ER PT J AU ENGEL, BT AF ENGEL, BT TI BIOFEEDBACK AND RELAXATION IN THE TREATMENT OF HYPERTENSION - NOT JUST REGRESSION TO THE MEAN SO HOMEOSTASIS IN HEALTH AND DISEASE LA English DT Article; Proceedings Paper CT CIANS-ISBM Satellite Conference CY JUL 12-14, 1992 CL HANNOVER, GERMANY SP COLLEGIUM INT ACTIVITATIS NERVOSAE SUPER, INT SOC BIOPHYS MED RP ENGEL, BT (reprint author), NIH,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CIANS-HOMEOSTASIS PI PRAGUE 10 PA C/O NATL INST PUBLIC HEALTH, SROBAROVA 48, PRAGUE 10, CZECH REPUBLIC CZ 100 42 SN 0960-7560 J9 HOMEOSTASIS HLTH DIS JI Homeost. Health Dis. PY 1994 VL 35 IS 3 BP 136 EP 136 PG 1 WC Behavioral Sciences; Cardiac & Cardiovascular Systems SC Behavioral Sciences; Cardiovascular System & Cardiology GA PU521 UT WOS:A1994PU52100006 ER PT J AU KIM, SJ ROMEO, D YOO, YD PARK, K AF KIM, SJ ROMEO, D YOO, YD PARK, K TI TRANSFORMING GROWTH-FACTOR-BETA - EXPRESSION IN NORMAL AND PATHOLOGICAL CONDITIONS SO HORMONE RESEARCH LA English DT Article; Proceedings Paper CT 36th International Henri-Pierre Klotz Symposium of Hormonal Resistance Syndromes - Growth Factors in Endocrinology: Recent Advances, Therapeutic Prospects CY MAY 06-07, 1993 CL PARIS, FRANCE DE TRANSCRIPTION; POST-TRANSCRIPTION; TUMOR SUPPRESSOR GENE; EXPRESSION; GROWTH FACTOR ID RETINOBLASTOMA-SUSCEPTIBILITY GENE; FACTOR-BETA-1 GENE; RETINOIC ACID; TRANSCRIPTION; KERATINOCYTES; PRODUCT; TGF-BETA-1; SECRETION; REGION; CELLS AB Expression of the various isoforms of transforming growth factor-beta (TGF-beta) is differentially controlled both in vivo and in vitro. Characterization of the molecular mechanisms governing expression of TGF-beta isoforms now provides a basis for understanding the selective regulation of expression of the TGF-beta s by a variety of factors including oncogenes and tumor suppressor genes. In addition to transcriptional control, data suggest that expression of TGF-beta s is also regulated posttranscriptionally. Regulation of TGF-beta s by steroids and retinoids appears to involve predominantly posttranscriptional mechanisms. Identification of these mechanisms may contribute to the understanding of the regulatory events controlling cellular proliferation and differentiation by TGF-beta s and steroids/retinoids. RP KIM, SJ (reprint author), NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892, USA. NR 24 TC 32 Z9 32 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 1994 VL 42 IS 1-2 BP 5 EP 8 DI 10.1159/000184136 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PB056 UT WOS:A1994PB05600001 PM 7959634 ER PT J AU LEROITH, D DIMARCHI, RD AF LEROITH, D DIMARCHI, RD TI SYMPOSIUM - INSULIN, IGFS AND GROWTH-HORMONE FROM BASIC RESEARCH TO NOVEL CLINICAL-APPLICATIONS - INTRODUCTION SO HORMONE RESEARCH LA English DT Editorial Material C1 LILLY RES LABS,DIV DIABET RES,INDIANAPOLIS,IN. RP LEROITH, D (reprint author), NIDDK,DIABET BRANCH,BETHESDA,MD, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 1994 VL 41 SU 2 BP 49 EP 50 DI 10.1159/000183960 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NV615 UT WOS:A1994NV61500013 ER PT J AU LEROITH, D SAMPSON, PC ROBERTS, CT AF LEROITH, D SAMPSON, PC ROBERTS, CT TI HOW DOES THE MITOGENIC INSULIN-LIKE GROWTH-FACTOR-I RECEPTOR DIFFER FROM THE METABOLIC INSULIN-RECEPTOR SO HORMONE RESEARCH LA English DT Article; Proceedings Paper CT XIIth Annual Lilly International Symposium on Endocrinology and Development - Insulin, IGFs and Growth Hormone: From Basic Research to Novel Clinical Applications CY OCT 01-02, 1993 CL INTERLAKEN, SWITZERLAND SP ELI LILLY & CO DE INSULIN RECEPTOR; INSULIN-LIKE GROWTH FACTOR I RECEPTOR; LIGAND-RECEPTOR INTERACTIONS; INSULIN-LIKE GROWTH FACTOR BINDING PROTEINS; SUBUNIT STRUCTURE ID IGF BINDING-PROTEINS; PHOSPHATIDYLINOSITOL 3'-KINASE; IRS-1; OVEREXPRESSION; SPECIFICITY; CELLS AB Under normal physiological conditions, insulin regulates intermediary metabolism by interacting with insulin receptors in liver, fat and muscle cells. The insulin-like growth factors (IGF-I and IGF-II), on the other hand, are primarily involved in the regulation of growth and development of the whole organism and interact with IGF receptors expressed by most, if not all, tissues of the body. As the insulin and IGF-I receptors are both structurally and functionally similar, one of the fundamental questions in this area of research has been the basis for the distinct pathways of hormone action elicited by insulin and the IGFs. Several features are involved in the divergence of the signalling pathways of insulin and the IGFs. The insulin receptor binds insulin with high affinity, and this specificity is determined by domains lying to the N-terminal and C-terminal sides of the cysteine-rich region in the alpha-subunit. The high-affinity IGF binding by the IGF-I receptor is determined by its cysteine-rich domain. Secondly, the IGF-binding proteins (IGFBPs), of which six have been characterized, bind the IGFs with an affinity higher than that of the IGF receptors. They bind all the circulating IGFs, protect them from degradation and deliver them to the IGF receptors in the target tissues, where they modulate IGF action. As they have no affinity for insulin, insulin is free to interact with its own receptor. Finally, structural differences in the beta-subunits of the insulin and IGF-I receptors may result in divergence of the signal pathways. Although both receptors have similar tyrosine kinase domains, their C-terminal domains, for example, differ. Recent studies have suggested that these structural differences may be causally related to their different signalling pathways. RP LEROITH, D (reprint author), NIDDK,DIABET BRANCH,BETHESDA,MD 20892, USA. OI Roberts, Charles/0000-0003-1756-5772 NR 19 TC 32 Z9 32 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 1994 VL 41 SU 2 BP 74 EP 79 DI 10.1159/000183964 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NV615 UT WOS:A1994NV61500017 PM 8088708 ER PT J AU ZIEDONIS, DM RAYFORD, BS BRYANT, KJ ROUNSAVILLE, BJ AF ZIEDONIS, DM RAYFORD, BS BRYANT, KJ ROUNSAVILLE, BJ TI PSYCHIATRIC COMORBIDITY IN WHITE AND AFRICAN-AMERICAN COCAINE ADDICTS SEEKING SUBSTANCE-ABUSE TREATMENT SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Article ID OPIATE ADDICTS; DISORDERS; DEPENDENCE; DIAGNOSIS; BLACK AB Objective: Few diagnostic studies have reported rates of psychiatric comorbidity among cocaine addicts according to race. This study examines psychiatric comorbidity in African-American and white cocaine addicts. Methods: Rates of psychiatric comorbidity were assessed in 263 cocaine addicts seeking substance abuse treatment. The sample included 163 non-Hispanic whites and 100 African Americans. Diagnoses were based on patient interviews using the Schedule for Affective Disorders and Schizophrenia-Lifetime Version (SADS-L). The SADS-L was supplemented to include DSM-III-R criteria for substance abuse or dependence and other psychiatric diagnoses and DSM-III criteria for attention deficit disorder. Results: Overall, 55.7 percent of the cocaine addicts met Research Diagnostic Criteria for a current psychiatric diagnosis, and 73.5 percent met criteria for a lifetime psychiatric diagnosis. Whites and African Americans did not differ significantly in overall psychiatric comorbidity. however, whites had significantly higher rates of lifetime major depression, alcohol dependence, attention deficit disorder, and conduct disorder. African-American addicts, particularly women, were more likely to meet criteria for a current diagnosis of phobia. Conclusions: Psychiatric comorbidity is common among cocaine addicts, and the rates for specific disorders vary by race. Differences in current and lifetime rates should be noted. Cocaine addicts seeking treatment should be assessed for comorbid alcohol dependence and other psychiatric disorders, including anxiety, affective, and personality disorders. C1 NIAAA,ROCKVILLE,MD 20852. RP ZIEDONIS, DM (reprint author), YALE UNIV,SCH MED,DEPT PSYCHIAT,904 HOWARD AVE,NEW HAVEN,CT 06519, USA. FU NIDA NIH HHS [P50-DA04060, R01-DA04029, R01-DA05592] NR 19 TC 55 Z9 55 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD JAN PY 1994 VL 45 IS 1 BP 43 EP 49 PG 7 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA MP418 UT WOS:A1994MP41800010 PM 8125458 ER PT J AU CHAN, KC MUSCHIK, GM ISSAQ, HJ SNADER, KM AF CHAN, KC MUSCHIK, GM ISSAQ, HJ SNADER, KM TI SEPARATION OF TAXOL AND RELATED-COMPOUNDS BY MICELLAR ELECTROKINETIC CHROMATOGRAPHY SO HRC-JOURNAL OF HIGH RESOLUTION CHROMATOGRAPHY LA English DT Note DE TAXOL; MICELLAR ELECTROKINETIC CHROMATOGRAPHY ID TAXUS-BREVIFOLIA; PHASE-II; CANCER; DRUG; BARK C1 NCI,DCT,DTP,NAT PROD BRANCH,FREDERICK,MD 21702. RP CHAN, KC (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21702, USA. NR 18 TC 5 Z9 5 U1 1 U2 1 PU DR ALFRED HUTHIG VERLAG GMBH PI HEIDELBERG 1 PA POSTFACH 102869, W-69018 HEIDELBERG 1, GERMANY SN 0935-6304 J9 HRC-J HIGH RES CHROM JI HRC-J. High Resolut. Chromatogr. PD JAN PY 1994 VL 17 IS 1 BP 51 EP 52 PG 2 WC Chemistry, Analytical SC Chemistry GA MX711 UT WOS:A1994MX71100011 ER PT S AU ROMERO, R MAZOR, M MUNOZ, H GOMEZ, R GALASSO, M SHERER, DM AF ROMERO, R MAZOR, M MUNOZ, H GOMEZ, R GALASSO, M SHERER, DM BE Bulletti, C Gurpide, E Flamigni, C TI THE PRETERM LABOR SYNDROME SO HUMAN ENDOMETRIUM SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 2nd Conference on the Endometrium CY SEP 20-22, 1993 CL BOLOGNA, ITALY SP Univ Bologna, Mt Sinai Sch Med New York ID PREGNANT RHESUS-MONKEY; TUMOR-NECROSIS-FACTOR; AMNIOTIC-FLUID CONCENTRATIONS; LOW-BIRTH-WEIGHT; HUMAN PARTURITION; ARACHIDONIC-ACID; UTERINE ACTIVITY; LATE GESTATION; GAP-JUNCTIONS; INTRAAMNIOTIC INFECTION C1 BEN GURION UNIV NEGEV,SOROKA MED CTR,IL-84105 BEER SHEVA,ISRAEL. NICHHD,PERINATOL BRANCH,BETHESDA,MD 20892. RP ROMERO, R (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,DEPT OBSTET & GYNECOL,4707 ST ANTOINE BLVD,DETROIT,MI 48201, USA. NR 173 TC 224 Z9 229 U1 1 U2 7 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-870-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 734 BP 414 EP 429 DI 10.1111/j.1749-6632.1994.tb21771.x PG 16 WC Cell Biology; Multidisciplinary Sciences; Obstetrics & Gynecology SC Cell Biology; Science & Technology - Other Topics; Obstetrics & Gynecology GA BD10M UT WOS:A1994BD10M00043 PM 7978942 ER PT J AU WAHBA, ZZ MILLER, MS WAALKES, MP AF WAHBA, ZZ MILLER, MS WAALKES, MP TI ABSENCE OF CHANGES IN METALLOTHIONEIN RNA IN THE RAT TESTES MADE REFRACTORY TO CADMIUM TOXICITY BY ZINC PRETREATMENT SO HUMAN & EXPERIMENTAL TOXICOLOGY LA English DT Note ID WISTAR CRL-(WI)BR RATS; DOSE-RESPONSE ANALYSIS; TUMOR-INDUCTION; INJECTION SITE; CARCINOGENESIS; DEFICIENCY; TOLERANCE; PROSTATE; METALS; LIVER AB Testicular toxicity and interstitial cell tumours induced by cadmium are prevented by zinc or by low dose cadmium pretreatments. The mechanism of this tolerance is unknown, though metallothionein (MT) is thought to play a role in tissue resistance to cadmium toxicity. Thus, the possible involvement of the testicular MT gene in metal-induced tolerance to cadmium toxicity was studied. Rats were pretreated with zinc (1.0 mmol kg-1, s.c.). Histological examination of the testes indicated such pretreatments prevented the necrotizing effects of subsequent doses of cadmium (20 mumol kg-1, s.c.) administered 24 h later. RNA was extracted from testes or liver 24 h after zinc pretreatment, and analysed by the slot blot technique using the p2A10 cDNA probe to the MT gene. Zinc pretreatment had little effect on MT RNA in the testes, and such pretreatments did not alter testicular cadmium-binding protein capacity. In contrast, RNAs derived from livers of zinc pretreated rats showed marked increases in MT RNA and MT protein. Hence, the testicular MT gene does not appear to play a major role in the induced tolerance to cadmium toxicity and carcinogenesis generated by zinc. C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,BLDG 538,ROOM 205E,FREDERICK,MD 21702. NR 21 TC 20 Z9 20 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0144-5952 J9 HUM EXP TOXICOL JI Hum. Exp. Toxicol. PD JAN PY 1994 VL 13 IS 1 BP 65 EP 67 PG 3 WC Toxicology SC Toxicology GA MR166 UT WOS:A1994MR16600010 PM 7515252 ER PT J AU KOTANI, H NEWTON, PB ZHANG, SY CHIANG, YWL OTTO, E WEAVER, L BLAESE, RM ANDERSON, WF MCGARRITY, GJ AF KOTANI, H NEWTON, PB ZHANG, SY CHIANG, YWL OTTO, E WEAVER, L BLAESE, RM ANDERSON, WF MCGARRITY, GJ TI IMPROVED METHODS OF RETROVIRAL VECTOR TRANSDUCTION AND PRODUCTION FOR GENE-THERAPY SO HUMAN GENE THERAPY LA English DT Article ID T-CELL LYMPHOMA; VIRUS; LINES; IMMUNOTHERAPY; GENERATION; EXPRESSION; PRIMATES; HUMANS AB To facilitate clinical applications of retroviral-mediated human gene transfer, retroviral vectors must be of high titer and free of detectable replication-competent retroviruses. The purpose of this study was to optimize methods of retroviral vector production and transduction. Studies were conducted using 22 retroviral vector producer cell lines. Inactivation of retroviral vectors was greater at 37 degrees C than at 32 degrees C. A 5- to 15-fold increase of vectors was produced at 32 degrees C compared to 37 degrees C; the vector increase at 34 degrees C was intermediate. For example, PA317/G1Na.40 grew to a titer of 1.8 x 10(7) cfu/ml at 32 degrees C, compared to 5.0 x 10(5) cfu/ml at 37 degrees C. The production of retroviral vectors was scalable achieving similar results in flasks, roller bottles, or a CellCube Bioreactor. Retroviral vectors were concentrated 15-24 times with vector recovery ranging from 91 to 96% in a Pellicon tangential flow filtration system. Retroviral supernatants were successfully lyophilized, The combination of glucose or sorbitol with gelatin resulted in recovery rates of 64-83%. In studies on transduction by retroviral vectors, centrifugation of vector supernatants onto target cells significantly increased transduction efficiency as measured by vector titration for G418 resistance, fluorescence-activated cell sorting (FACS), and polymerase chain reaction (PCR) analyses. The combination of the above methods has significantly increased the growth and transduction by this vector system. C1 NCI,METAB BRANCH,BETHESDA,MD 20892. UNIV SO CALIF,DEPT BIOCHEM & PEDIAT,LOS ANGELES,CA 90033. RP KOTANI, H (reprint author), GENET THERAPY INC,19 FIRSTFIELD RD,GAITHERSBURG,MD 20878, USA. NR 34 TC 329 Z9 346 U1 1 U2 7 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD JAN PY 1994 VL 5 IS 1 BP 19 EP 28 DI 10.1089/hum.1994.5.1-19 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA MT853 UT WOS:A1994MT85300004 PM 8155767 ER PT J AU MITSUDOMI, T FRIEDMAN, E GEJMAN, PV MCCORMICK, F GAZDAR, AF AF MITSUDOMI, T FRIEDMAN, E GEJMAN, PV MCCORMICK, F GAZDAR, AF TI GENETIC-ANALYSIS OF THE CATALYTIC DOMAIN OF THE GAP GENE IN HUMAN LUNG-CANCER CELL-LINES SO HUMAN GENETICS LA English DT Article ID GRADIENT GEL-ELECTROPHORESIS; POLYMERASE CHAIN-REACTION; GTPASE-ACTIVATING PROTEIN; RAS ONCOGENE ACTIVATION; SINGLE-BASE CHANGES; MOLECULAR-CLONING; P53 GENE; MUTATIONS; DNA; NEUROFIBROMATOSIS AB Cell lines of non-small cell lung cancer (non-SCLC) have been shown to contain activating mutation of the K-ms oncogene in about 30% of cases, whereas no small cell lung cancer (SCLC) cell lines displayed these mutations. Biochemically, these mutations result in the ras gene product (p21) being constitutively activated in its GTP-bound form and insensitive to the hydrolytic action of the ms-specific GTPase-activating protein (ras GAP). We hypothesized that, if tumor development is related to the p21 ms being in the active GTP-bound state, then a similar malignant phenotype may result from an inactivating mutation in the ms GAP gene in the region that inter acts with ms p21 (so-called catalytic domain). To test this hypothesis, we screened a panel of SCLC and non-SCLC eel lines for major genetic alterations in the catalytic domain of the GAP gene with the Sothern blot technique, and for minor genetic abnormalities (e.g., point mutations) with denaturing gradient gel electrophoresis and single-strand conformation polymorphism. Mutations in the catalytic domain of the GAP gene could not be demonstrated by any technique in any cell line examined. We conclude that mutational inactivation of the catalytic domain of the CAP gene probably does not contribute to the development of lung cancer. C1 NCI, NAVY MED ONCOL BRANCH, BETHESDA, MD 20889 USA. NATL NAVAL MED CTR, BETHESDA, MD 20889 USA. NIDDKD, MOLEC PATHOPHYSIOL BRANCH, BETHESDA, MD 20892 USA. KAROLINSKA HOSP, DEPT CLIN GENET, S-10401 STOCKHOLM, SWEDEN. NIMH, CLIN NEUROGENET BRANCH, BETHESDA, MD 20892 USA. ONYX CORP, EMERYVILLE, CA 94608 USA. UNIV TEXAS, SW MED CTR, SIMMONS CANC CTR, DALLAS, TX 75235 USA. UNIV TEXAS, SW MED CTR, DEPT PATHOL, DALLAS, TX 75235 USA. RP MITSUDOMI, T (reprint author), UNIV OCCUPAT & ENVIRONM HLTH, DEPT SURG 2, YAHATANISHI KU, ISEIGAOKA 1-1, KITAKYUSHU, FUKUOKA 807, JAPAN. OI Mitsudomi, Tetsuya/0000-0001-9860-8505 NR 32 TC 6 Z9 6 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD JAN PY 1994 VL 93 IS 1 BP 27 EP 31 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA MP224 UT WOS:A1994MP22400006 PM 8270251 ER PT J AU CROSSEY, PA FOSTER, K RICHARDS, FM PHIPPS, ME LATIF, F TORY, K JONES, MH BENTLEY, E KUMAR, R LERMAN, MI ZBAR, B AFFARA, NA FERGUSONSMITH, MA MAHER, ER AF CROSSEY, PA FOSTER, K RICHARDS, FM PHIPPS, ME LATIF, F TORY, K JONES, MH BENTLEY, E KUMAR, R LERMAN, MI ZBAR, B AFFARA, NA FERGUSONSMITH, MA MAHER, ER TI MOLECULAR-GENETIC INVESTIGATIONS OF THE MECHANISM OF TUMORIGENESIS IN VON HIPPEL-LINDAU DISEASE - ANALYSIS OF ALLELE LOSS IN VHL TUMORS SO HUMAN GENETICS LA English DT Article ID RENAL-CELL CARCINOMA; LINKAGE ANALYSIS; SMALL REGION; SHORT ARM; CHROMOSOME-3; MUTATION; HETEROZYGOSITY; TRANSLOCATION; POLYMORPHISM; HEREDITARY AB Von Hippel-Lindau (VHL) disease is a dominantly inherited familial cancer syndrome characterised by the development of retinal and central nervous system haemangioblastomas, renal cell carcinoma (RCC), phaeochromocytoma and pancreatic tumours. The VHL disease gene maps to chromosome 3p25-p26. To investigate the mechanism of tumourigenesis in VHL disease, we analysed 24 paired blood/tumour DNA samples from 20 VHL patients for allele loss on chromosome 3p and in the region of tumour suppressor genes on chromosomes 5, 11, 13, 17 and 22. Nine out of 24 tumours showed loss of heterozygosity (LOH) at at least one locus on chromosome 3p and in each case the LOH included the region to which the VHL gene has been mapped. Chromosome 3p allele loss was found in four tumour types (RCC, haemangioblastoma, phaeochromocytoma and pancreatic tumour) suggesting a common mechanism of tumourigenesis in all types of tumour in VHL disease. The smallest region of overlap was between D3S1038 and D3S18, a region that corresponds to the target region for the VHL gene from genetic linkage studies. The parental origin of the chromosome 3p25-p26 allele loss could be determined in seven tumours from seven familial cases; in each tumour, the allele lost had been inherited from the unaffected parent. Our results suggest that the VHL disease gene functions as a recessive tumour suppressor gene and that inactivation of both alleles of the VHL gene is the critical event in the pathogenesis of VHL neoplasms. Four VHL tumours showed LOH on other chromosomes (5q21, 13q, 17q) indicating that homozygous VHL gene mutations may be required but may not be sufficient for tumourigenesis in VHL disease. C1 UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE,ENGLAND. NCI,IMMUNOBIOL LAB,FREDERICK,MD 21701. CANC INST,TOKYO,TOKYO,JAPAN. RI MAHER, EAMONN/A-9507-2008 OI MAHER, EAMONN/0000-0002-6226-6918 NR 30 TC 101 Z9 103 U1 1 U2 6 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD JAN PY 1994 VL 93 IS 1 BP 53 EP 58 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA MP224 UT WOS:A1994MP22400011 PM 8270255 ER PT J AU MAEKAWA, M SUDO, K NAGURA, K LI, SSL KANNO, T AF MAEKAWA, M SUDO, K NAGURA, K LI, SSL KANNO, T TI POPULATION SCREENING OF LACTATE-DEHYDROGENASE DEFICIENCIES IN FUKUOKA PREFECTURE IN JAPAN AND MOLECULAR CHARACTERIZATION OF 3 INDEPENDENT MUTATIONS IN THE LACTATE DEHYDROGENASE-B(H) GENE SO HUMAN GENETICS LA English DT Note ID SUBUNIT DEFICIENCIES; DNA; VARIANT; AMPLIFICATION AB Screening for lactate dehydrogenase (LDH) subunit deficiencies was performed on 2880 blood samples from healthy individuals in the Fukuoka Prefecture in Japan by means of electrophoresis. The frequencies of heterozygotes with either LDH-A or LDH-B deficiency were found to be 0.104% at each locus. These estimated frequencies of either LDH-A or LDH-B deficiencies were slightly lower than, but not significantly different from, those found previously in Shizuoka Prefecture. The genetic mutations in individuals heterozygous for LDH-B deficiency were analyzed by the polymerase chain reaction and DNA conformation polymorphism. Abnormal migration patterns were observed in individuals heterozygous for LDH-B deficiency. Subsequent sequence determination of the mutant alleles revealed three novel mutations: an eight-base duplication in exon 3, a four-base duplication in exon 4, and a one-base deletion in exon 7 of the LDH-B gene. These three mutations result in frameshift translation and premature termination. In addition, the mutations resulting in the duplication of eight or four nucleotides appear to cause a decrease in the levels of LDH-B mRNA. C1 JIKEI UNIV, DAISAN HOSP, SCH MED, DEPT LAB MED, KOMAE, TOKYO 201, JAPAN. NIEHS, GENET LAB, RES TRIANGLE PK, NC 27709 USA. RP MAEKAWA, M (reprint author), HAMAMATSU UNIV SCH MED, DEPT LAB MED, HANDA CHO 3600, HAMAMATSU, SHIZUOKA 43131, JAPAN. NR 21 TC 10 Z9 10 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD JAN PY 1994 VL 93 IS 1 BP 74 EP 76 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA MP224 UT WOS:A1994MP22400015 PM 8270259 ER PT J AU CARRINGTON, M DEAN, M AF CARRINGTON, M DEAN, M TI A POLYMORPHIC DINUCLEOTIDE REPEAT IN THE 3RD INTRON OF TAP1 SO HUMAN MOLECULAR GENETICS LA English DT Note ID CLASS-II REGION C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. RP CARRINGTON, M (reprint author), DYNCORP,PRI,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 NR 3 TC 30 Z9 30 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD JAN PY 1994 VL 3 IS 1 BP 218 EP 218 DI 10.1093/hmg/3.1.218 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA MU617 UT WOS:A1994MU61700059 PM 8162046 ER PT J AU JARES, P FERNANDEZ, PL BLAY, M AIZA, G STETLERSTEVENSON, WG CARDESA, A CAMPO, E AF JARES, P FERNANDEZ, PL BLAY, M AIZA, G STETLERSTEVENSON, WG CARDESA, A CAMPO, E TI TAQI POLYMORPHISM OF THE HUMAN TISSUE INHIBITOR OF METALLO-PROTEINASES-2 (TIMP2) GENE SO HUMAN MOLECULAR GENETICS LA English DT Note ID METALLOPROTEINASES-2 C1 UNIV BARCELONA,HOSP CLIN,DEPT ANAT PATHOL,E-08036 BARCELONA,SPAIN. UNIV LLEIDA,SCH MED,DEPT BASIC MED SCI,LLEIDA,SPAIN. NCI,PATHOL LAB,BETHESDA,MD 20892. RI Blay, Mayte/B-1680-2009; Stetler-Stevenson, William/H-6956-2012 OI Blay, Mayte/0000-0002-6256-9847; Stetler-Stevenson, William/0000-0002-5500-5808 NR 3 TC 1 Z9 1 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD JAN PY 1994 VL 3 IS 1 BP 218 EP 218 DI 10.1093/hmg/3.1.218-a PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA MU617 UT WOS:A1994MU61700058 PM 7909251 ER PT J AU PUCK, JM AF PUCK, JM TI MOLECULAR-BASIS FOR 3 X-LINKED IMMUNE DISORDERS SO HUMAN MOLECULAR GENETICS LA English DT Article ID SEVERE COMBINED IMMUNODEFICIENCY; RECEPTOR GAMMA-CHAIN; HYPER-IGM SYNDROME; CD40 LIGAND GENE; CHROMOSOME INACTIVATION; DEFECTIVE EXPRESSION; FUNCTIONAL COMPONENT; CLOSE LINKAGE; T-CELLS; AGAMMAGLOBULINEMIA AB Gene defects causing three X-linked human immunodeficiencies, agammaglobulinemia (XLA), hyper-IgM syndrome (HIGM), and X-linked severe combined immunodeficiency (SCID), have been identified. These represent the first human disease phenotypes associated with three gene families already recognized to be important in lymphocyte development and signaling: XLA is caused by mutations of a B-cell specific intracellular tyrosine kinase; HIGM by mutations in the tumor necrosis factor-related CD40 ligand, through which T cells deliver helper signals by direct contact with B-cell CD40; and SCID by mutations in the gamma chain of the lymphocyte receptor for interleukin-2. The great variety of patient mutations in all three genes represent both a challenge for genetic diagnosis and a resource for dissecting molecular domains and physiologic functions of the gene products. RP PUCK, JM (reprint author), NATL CTR HUMAN GENOME RES,IMMUNOL GENET SECT,GENE TRANSFER LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 40 TC 12 Z9 12 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PY 1994 VL 3 SI SI BP 1457 EP 1461 PG 5 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA PJ827 UT WOS:A1994PJ82700003 PM 7849738 ER PT J AU TUGENDREICH, S BASSETT, DE MCKUSICK, VA BOGUSKI, MS HIETER, P AF TUGENDREICH, S BASSETT, DE MCKUSICK, VA BOGUSKI, MS HIETER, P TI GENES CONSERVED IN YEAST AND HUMANS SO HUMAN MOLECULAR GENETICS LA English DT Article ID EXPRESSED SEQUENCE TAGS; HUMAN GENOME PROJECT; GTP-BINDING PROTEIN; CELL-CYCLE GENE; SACCHAROMYCES-CEREVISIAE; HUMAN HOMOLOG; FUNCTIONAL COMPLEMENTATION; MOLECULAR-CLONING; HUMAN CDNA; CDC28 MUTATION AB Evolutionary conservation of homologous gene products from distantly related organisms provides an information resource of great value for elucidating protein structure and function. Sequence similarities also serve as molecular cross-references between diverse organisms that offer different, or complementary, experimental approaches for analyzing gene expression and biochemistry in normal and abnormal states. There are now countless examples of information about a protein from one species contributing to the understanding of biological phenomena or disease in another species. Such connections are often unanticipated and surprising, but there is an opportunity to make them more systematically as concerted genome sequencing projects progress. In the present review we focus on connections between yeast and human proteins and their functional implications. We present several 'case studies' as well as survey results derived from comprehensive sequence comparisons among all yeast and human proteins currently present in the public databases. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,CTR MED GENET,BALTIMORE,MD 21205. NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. FU NCI NIH HHS [CA16519, 5T32CA09139]; NHGRI NIH HHS [HG00971-01] NR 65 TC 61 Z9 61 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PY 1994 VL 3 SI SI BP 1509 EP 1517 PG 9 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA PJ827 UT WOS:A1994PJ82700011 PM 7849746 ER PT J AU SIDRANSKY, E BOTTLER, A STUBBLEFIELD, B GINNS, EI AF SIDRANSKY, E BOTTLER, A STUBBLEFIELD, B GINNS, EI TI DNA MUTATIONAL ANALYSIS OF TYPE-1 AND TYPE-3 GAUCHER PATIENTS - HOW WELL DO MUTATIONS PREDICT PHENOTYPE SO HUMAN MUTATION LA English DT Article DE GAUCHER DISEASE; MUTATION ANALYSIS; GENOTYPE; NEUROLOGIC INVOLVEMENT ID ACID BETA-GLUCOSIDASE; HIGH-FREQUENCY; DISEASE; HETEROGENEITY; DIAGNOSIS; GENOTYPE AB The wide spectrum of clinical manifestations resulting from glucocerebrosidase deficiency complicates genetic counseling for Gaucher disease. The identification of mutations in the glucocerebrosidase gene has enabled studies of genotype-phenotype correlation However, a genotypic analysis of 60 type 1 and type 3 Gaucher patients reveals that the 5 most common Gaucher mutations, N370S, L444P, R463C, 84insG, and IVS2 + 1 C-->A, can be found both in patients with and without neurologic manifestations. Moreover, although some generalizations can be made about mutations that are more frequently encountered in particular patient populations, Gaucher patients sharing identical genotypes can exhibit considerable clinical heterogeneity. Thus in considering rationale for population screening one cannot rely solely on PCR determined DNA mutation analysis to reliably predict prognosis in Gaucher disease. (C) 1994 Wiley-Liss,Inc. RP SIDRANSKY, E (reprint author), NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892, USA. NR 22 TC 49 Z9 49 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 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1994 VL 3 IS 1 BP 25 EP 28 DI 10.1002/humu.1380030105 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA MQ975 UT WOS:A1994MQ97500004 PM 8118463 ER PT J AU ZENG, FY RODGERS, GP HUANG, SZ SCHECHTER, AN SALAMAH, M PERRINE, S BERG, PE AF ZENG, FY RODGERS, GP HUANG, SZ SCHECHTER, AN SALAMAH, M PERRINE, S BERG, PE TI SEQUENCE OF THE -530-REGION OF THE BETA-GLOBIN GENE OF SICKLE-CELL-ANEMIA PATIENTS WITH THE ARABIAN HAPLOTYPE SO HUMAN MUTATION LA English DT Note ID MUTATION; THALASSEMIA; EXPRESSION; DISEASE; CARRIER C1 UNIV MARYLAND,SCH MED,DEPT PEDIAT HEMATOL ONCOL,BALTIMORE,MD 21201. NIDDKD,CHEM BIOL LAB,BETHESDA,MD 20892. CHILDRENS HOSP OAKLAND,OAKLAND,CA 94609. DHAHRAN HLTH CTR,DHAHRAN,SAUDI ARABIA. OI Schechter, Alan N/0000-0002-5235-9408 NR 16 TC 7 Z9 7 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 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1994 VL 3 IS 2 BP 163 EP 165 DI 10.1002/humu.1380030213 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA MY694 UT WOS:A1994MY69400012 PM 8199597 ER PT J AU RAVNIKGLAVAC, M GLAVAC, D CHERNICK, M DISANTAGNESE, P DEAN, M AF RAVNIKGLAVAC, M GLAVAC, D CHERNICK, M DISANTAGNESE, P DEAN, M TI SCREENING FOR CF MUTATIONS IN ADULT CYSTIC-FIBROSIS PATIENTS WITH A DIRECTED AND OPTIMIZED SSCP STRATEGY SO HUMAN MUTATION LA English DT Article DE CYSTIC FIBROSIS; ADULT PATIENTS; CFTR GENE; MUTATION SCREENING; OPTIMIZED SSCP ID POLYMERASE CHAIN-REACTION; GRADIENT GEL-ELECTROPHORESIS; CONDUCTANCE REGULATOR GENE; NUCLEOTIDE-BINDING FOLD; SINGLE-BASE CHANGES; FRAMESHIFT MUTATION; CHLORIDE CHANNELS; SWEAT GLANDS; IDENTIFICATION; DNA AB Twenty adolescent and adult cystic fibrosis (CF) patients have been studied for the presence of mutations in the CFTR gene. Mutations other than deltaF508 have been detected by comparison to the single stranded conformation polymorphism (SSCP) pattern of known mutations in eight exons, in which 80% of the more common mutations are present. Each mutation was confirmed by direct sequencing. For each of the analyzed exons, optimal SSCP conditions have been determined that allow all available known mutations in that exon to be distinguished from each other. This approach allowed mutations to be defined in 75% of the non deltaF508 alleles and 92% of all CF alleles in this cohort. (C) 1994 Wiley-Liss, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV C,FREDERICK,MD 21702. NIDDKD,PEDIAT METAB BRANCH,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 NR 63 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 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1994 VL 3 IS 3 BP 231 EP 238 DI 10.1002/humu.1380030309 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA ND558 UT WOS:A1994ND55800008 PM 7517265 ER PT J AU ANGELICHEVA, D BOTEVA, K JORDANOVA, A SAVOV, A KUFARDJIEVA, A TOLUN, A TELATAR, M AKARSUBASI, A KOPRUBASI, F AYDOGDU, S DEMIRKOL, M KURDOGLU, G CONSTANTINOUDELTAS, CD GEORGIOU, C DEAN, M IVASCHENKO, T BARANOV, V KALAYDJIEVA, L AF ANGELICHEVA, D BOTEVA, K JORDANOVA, A SAVOV, A KUFARDJIEVA, A TOLUN, A TELATAR, M AKARSUBASI, A KOPRUBASI, F AYDOGDU, S DEMIRKOL, M KURDOGLU, G CONSTANTINOUDELTAS, CD GEORGIOU, C DEAN, M IVASCHENKO, T BARANOV, V KALAYDJIEVA, L TI CYSTIC-FIBROSIS PATIENTS FROM THE BLACK-SEA REGION - THE 1677DELTA MUTATION SO HUMAN MUTATION LA English DT Article DE CYSTIC FIBROSIS; MUTATION; POPULATION GENETICS OF CF; GENOTYPE PHENOTYPE CORRELATION ID CFTR GENE; IDENTIFICATION; DNA; EXON-10 AB A 2 bp deletion in exon 10 of the CFTR gene, 1677delTA, which is very rare among CF chromosomes worldwide, was found to be a relatively common cause of cystic fibrosis in countries located in the region of the Black Sea. The frequency of the mutation was compared among cystic fibrosis patients from several populations, namely Bulgarians, Turks, Greek-Cypriots, Georgians, and Russians. The deletion is most common among Georgian CF patients and gradually declines in frequency in neighbouring populations. It is invariably related to a common polymorphic haplotype which is rare among normal chromosomes in Bulgaria but was found to be common in Turkey. The geographic gradient in the frequency of the mutation, along with findings on polymorphic haplotype distribution, suggest that the mutation is relatively young in evolutionary terms and spread as the result of west and south-bound migrations originating from Georgia. The 1677delTA mutation is related to a severe clinical phenotype with a high early mortality rate among homozygotes and possibly to an increased risk of meconium ileus. (C) 1994 Wiley-Liss, Inc. C1 NIH,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. ST PETERSBURG OBSTET & GYNAECOL INST,MOLEC GENET LAB,ST PETERSBURG,RUSSIA. UNIV SOFIA,HOSP OBSTET & GYNACOL,MOLEC PATHOL LAB,BU-1431 SOFIA,BULGARIA. UNIV SOFIA,CHILDRENS HOSP,BU-1126 SOFIA,BULGARIA. BOGAZICI UNIV,DEPT BIOL,ISTANBUL,TURKEY. AGGEAN UNIV,SCH MED,DEPT PEDIAT,IZMIR,TURKEY. ISTANBUL MED SCH,INST PEDIAT,ISTANBUL,TURKEY. CYPRUS INST NEUROL & GENET,MOLEC GENET LAB,NICOSIA,CYPRUS. ARCHBISHOP MAKARIOS III HOSP,DEPT PEDIAT,NICOSIA,CYPRUS. RI Dean, Michael/G-8172-2012; Deltas, Constantinos/J-9345-2013; Demirkol, Mubeccel/B-3660-2014; Jordanova, Albena/H-8323-2015; Deltas, Constantinos/A-4936-2013 OI Dean, Michael/0000-0003-2234-0631; Deltas, Constantinos/0000-0001-5549-9169; Demirkol, Mubeccel/0000-0002-6817-4715; Jordanova, Albena/0000-0002-3833-3754; Deltas, Constantinos/0000-0001-5549-9169 NR 16 TC 12 Z9 12 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 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1994 VL 3 IS 4 BP 353 EP 357 DI 10.1002/humu.1380030405 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA NT133 UT WOS:A1994NT13300004 PM 8081388 ER PT S AU LEVINE, RJ AF LEVINE, RJ BE Campbell, KL Wood, JW TI MALE FACTORS CONTRIBUTING TO THE SEASONALITY OF HUMAN-REPRODUCTION SO HUMAN REPRODUCTIVE ECOLOGY: INTERACTIONS OF ENVIRONMENT, FERTILITY, AND BEHAVIOR SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Human Reproductive Ecology: Interactions of Environment, Fertility, and Behavior CY MAY 21-24, 1993 CL RESEARCH TRIANGLE PARK, NC SP NEW YORK ACAD SCI ID SEMEN QUALITY; CIRCANNUAL RHYTHMS; MEN; TESTOSTERONE; SUMMER; DETERIORATION; PARAMETERS; HORMONES RP LEVINE, RJ (reprint author), NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,EPIDEMIOL BRANCH,BLDG 6100,ROOM 7B03,BETHESDA,MD 20892, USA. NR 47 TC 38 Z9 39 U1 0 U2 5 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-841-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 709 BP 29 EP 45 DI 10.1111/j.1749-6632.1994.tb30386.x PG 17 WC Ecology; Multidisciplinary Sciences; Reproductive Biology SC Environmental Sciences & Ecology; Science & Technology - Other Topics; Reproductive Biology GA BA04D UT WOS:A1994BA04D00003 PM 8154722 ER PT S AU BAIRD, DD WEINBERG, CR SCHWINGL, P WILCOX, AJ AF BAIRD, DD WEINBERG, CR SCHWINGL, P WILCOX, AJ BE Campbell, KL Wood, JW TI SELECTION BIAS ASSOCIATED WITH CONTRACEPTIVE PRACTICE IN TIME-TO-PREGNANCY STUDIES SO HUMAN REPRODUCTIVE ECOLOGY: INTERACTIONS OF ENVIRONMENT, FERTILITY, AND BEHAVIOR SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Human Reproductive Ecology: Interactions of Environment, Fertility, and Behavior CY MAY 21-24, 1993 CL RESEARCH TRIANGLE PARK, NC SP NEW YORK ACAD SCI ID CIGARETTE-SMOKING; CONCEPTION; WOMEN; FERTILITY C1 NIEHS,STAT & BIOMATH BRANCH,RES TRIANGLE PK,NC 27709. FAMILY HLTH INT,RES TRIANGLE PK,NC 27709. RP BAIRD, DD (reprint author), NIEHS,EPIDEMIOL BRANCH,MD A3-05,POB 12233,RES TRIANGLE PK,NC 27709, USA. OI Wilcox, Allen/0000-0002-3376-1311; Baird, Donna/0000-0002-5544-2653 NR 15 TC 25 Z9 26 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-841-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 709 BP 156 EP 164 DI 10.1111/j.1749-6632.1994.tb30395.x PG 9 WC Ecology; Multidisciplinary Sciences; Reproductive Biology SC Environmental Sciences & Ecology; Science & Technology - Other Topics; Reproductive Biology GA BA04D UT WOS:A1994BA04D00012 PM 8154699 ER PT S AU WEINBERG, CR BAIRD, DD WILCOX, AJ AF WEINBERG, CR BAIRD, DD WILCOX, AJ BE Campbell, KL Wood, JW TI BIAS IN RETROSPECTIVE STUDIES OF SPONTANEOUS-ABORTION BASED ON THE OUTCOME OF THE MOST RECENT PREGNANCY SO HUMAN REPRODUCTIVE ECOLOGY: INTERACTIONS OF ENVIRONMENT, FERTILITY, AND BEHAVIOR SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Human Reproductive Ecology: Interactions of Environment, Fertility, and Behavior CY MAY 21-24, 1993 CL RESEARCH TRIANGLE PARK, NC SP NEW YORK ACAD SCI C1 NIEHS,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC 27709. RP WEINBERG, CR (reprint author), NIEHS,STAT & BIOMATH BRANCH,MD A3-03,POB 12233,RES TRIANGLE PK,NC 27709, USA. OI Wilcox, Allen/0000-0002-3376-1311; Baird, Donna/0000-0002-5544-2653 NR 10 TC 16 Z9 16 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 0-89766-841-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 709 BP 280 EP 286 DI 10.1111/j.1749-6632.1994.tb30416.x PG 7 WC Ecology; Multidisciplinary Sciences; Reproductive Biology SC Environmental Sciences & Ecology; Science & Technology - Other Topics; Reproductive Biology GA BA04D UT WOS:A1994BA04D00033 PM 8154720 ER PT S AU POTTS, M CAMPBELL, KL EVANS, VJ FRIEDLAENDER, J ROBINSON, JA SPIELER, J AF POTTS, M CAMPBELL, KL EVANS, VJ FRIEDLAENDER, J ROBINSON, JA SPIELER, J BE Campbell, KL Wood, JW TI FUNDING CONSIDERATIONS IN HUMAN REPRODUCTIVE ECOLOGY - SUMMARY OF AN EVENING PANEL DISCUSSION ON SOURCES AND RESOURCES SO HUMAN REPRODUCTIVE ECOLOGY: INTERACTIONS OF ENVIRONMENT, FERTILITY, AND BEHAVIOR SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Human Reproductive Ecology: Interactions of Environment, Fertility, and Behavior CY MAY 21-24, 1993 CL RESEARCH TRIANGLE PARK, NC SP NEW YORK ACAD SCI C1 UNIV MASSACHUSETTS,DEPT BIOL,BOSTON,MA 02125. UNIV CALIF BERKELEY,SCH PUBL HLTH SOCIAL ADM & HLTH SCI,DEPT POPULAT FAMILY PLANNING & HLTH,BERKELEY,CA 94720. NICHHD,POPULAT RES CTR,DEMOG & BEHAV SCI BRANCH,BETHESDA,MD. NATL SCI FDN,ANTHROPOL SECT,WASHINGTON,DC 20550. NIEHS,DIV EXTRAMURAL RES & TRAINING,ORGAN SYST TOXICOL BRANCH,BETHESDA,MD. US AGCY INT DEV,OFF POPULAT RES,DIV RES,WASHINGTON,DC 20523. NR 7 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-841-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 709 BP 347 EP 354 DI 10.1111/j.1749-6632.1994.tb30421.x PG 8 WC Ecology; Multidisciplinary Sciences; Reproductive Biology SC Environmental Sciences & Ecology; Science & Technology - Other Topics; Reproductive Biology GA BA04D UT WOS:A1994BA04D00038 PM 8154726 ER PT J AU TELL, GS RUTAN, GH KRONMAL, RA BILD, DE POLAK, JF WONG, ND BORHANI, NO BURKE, GL ETTINGER, WH ELSTER, A FURBERG, CD HAPONIK, E KITZMAN, D HEISS, G KLOPFENSTEIN, HS LEFKOWITZ, DS LYLES, MF MITTELMARK, MB RILEY, W TOOLE, JF NUNN, C TUCKER, B LAMB, M BOMMER, W LEE, M ROBBINS, J SCHENKER, M BRYAN, RN BUSH, TL CHABOT, J COMSTOCK, GW FRIED, LP GERMAN, PS HILL, J KITTNER, SJ KUMANYIKA, S POWE, NR PRICE, TR ROCK, R SZKLO, M BONK, J KNEPPER, L IVES, DG JUNGREIS, CA KULLER, LH MCDONALD, RH MEILAHN, E MEYER, P NEWMAN, A SCHULZ, R SMITH, VE WOLFSON, SK ANTONCULVER, H GARDIN, JM KNOLL, M KUROSAKI, T WONG, N OLEARY, DH FUNK, L BOVILL, E CORNELL, E HOWARD, P TRACY, RP ENRIGHT, P CALHOUN, K CALHOUN, H FESER, B RAUTAHARJU, P RAUTAHARJU, F FITZPATRICK, AL HERMANSON, BK PSATY, BM SISCOVICK, DS SHEMANSKI, L FISHER, L LONGSTRETH, W RAGUNATHAN, T WAHL, PW YANEZ, D MANOLIO, TA SAVAGE, PJ SMITH, P AF TELL, GS RUTAN, GH KRONMAL, RA BILD, DE POLAK, JF WONG, ND BORHANI, NO BURKE, GL ETTINGER, WH ELSTER, A FURBERG, CD HAPONIK, E KITZMAN, D HEISS, G KLOPFENSTEIN, HS LEFKOWITZ, DS LYLES, MF MITTELMARK, MB RILEY, W TOOLE, JF NUNN, C TUCKER, B LAMB, M BOMMER, W LEE, M ROBBINS, J SCHENKER, M BRYAN, RN BUSH, TL CHABOT, J COMSTOCK, GW FRIED, LP GERMAN, PS HILL, J KITTNER, SJ KUMANYIKA, S POWE, NR PRICE, TR ROCK, R SZKLO, M BONK, J KNEPPER, L IVES, DG JUNGREIS, CA KULLER, LH MCDONALD, RH MEILAHN, E MEYER, P NEWMAN, A SCHULZ, R SMITH, VE WOLFSON, SK ANTONCULVER, H GARDIN, JM KNOLL, M KUROSAKI, T WONG, N OLEARY, DH FUNK, L BOVILL, E CORNELL, E HOWARD, P TRACY, RP ENRIGHT, P CALHOUN, K CALHOUN, H FESER, B RAUTAHARJU, P RAUTAHARJU, F FITZPATRICK, AL HERMANSON, BK PSATY, BM SISCOVICK, DS SHEMANSKI, L FISHER, L LONGSTRETH, W RAGUNATHAN, T WAHL, PW YANEZ, D MANOLIO, TA SAVAGE, PJ SMITH, P TI CORRELATES OF BLOOD-PRESSURE IN COMMUNITY-DWELLING OLDER ADULTS - THE CARDIOVASCULAR-HEALTH-STUDY SO HYPERTENSION LA English DT Article DE BLOOD PRESSURE; AGED; EPIDEMIOLOGY; RISK FACTORS ID TRANSCAPILLARY ESCAPE RATE; CORONARY HEART-DISEASE; CAROTID ATHEROSCLEROSIS; ESSENTIAL HYPERTENSION; RISK-FACTORS; POPULATION; MORTALITY; ALBUMIN; ALCOHOL; ASSOCIATIONS AB Although elevated blood pressure is an important predictor of cardiovascular disease and stroke in the elderly, little information exists on the distribution and risk factor correlates of brood pressure in this group. As part of the Cardiovascular Health Study, a population-based cohort study of 5201 men and women aged 65 to 101 years, we investigated correlates of systolic and diastolic blood pressure. Multiple regression analyses were conducted for all participants and a subgroup of 2482 without coronary heart disease and not on antihypertensive therapy (the ''healthier'' subgroup). In the total group, independent predictors of diastolic blood pressure included heart rate, aortic root dimension, creatinine, hematocrit, alcohol use, and black race (positive associations) and internal carotid artery wall thickness, mitral early/late peak how velocity, white blood cell count, cigarette smoking, and age (negative associations). Positive predictors of systolic blood pressure included mitral late peak flow velocity, left ventricular mass, common carotid artery wall thickness, serum albumin, factor VII, diabetes, alcohol use, and age; negative predictors were coronary heart disease, uric acid, height, and smoking. In the healthier subgroup, positive predictors of diastolic blood pressure included heart rate, hematocrit, serum albumin, creatinine, and body weight, whereas mitral early/late peak flow velocity, serum potassium, smoking, and age inversely related to diastolic pressure. For the same group, common carotid artery wall thickness, left ventricular mass, serum albumin, factor VII, high-density lipoprotein cholesterol, and age were directly related to systolic blood pressure, whereas serum potassium was inversely related. Both systolic and diastolic pressures Varied considerably by geographic site. Thus, in the elderly blood pressure is associated with a variety of factors as previously reported in younger populations and also with cardiovascular disease status, subclinical disease, and several blood chemistry variables not previously reported. C1 VET AFFAIRS MED CTR,MEMPHIS,TN. UNIV WASHINGTON,CHS,COORDINATING CTR,SEATTLE,WA. JOHNS HOPKINS UNIV,HAGERSTOWN,MD. UNIV PITTSBURGH,PITTSBURGH,PA. UNIV CALIF IRVINE,CTR ECHOCARDIOG READING,IRVINE,CA. GEISINGER MED CTR,CTR ULTRASOUND READING,DANVILLE,PA. UNIV VERMONT,CENT BLOOD ANAL LAB,BURLINGTON,VT. UNIV ARIZONA,TUCSON,AZ. UNIV ALBERTA,CTR ELECTROCARDIOG READING,EDMONTON,AB,CANADA. UNIV CALIF DAVIS,SACRAMENTO,CA. UNIV CALIF IRVINE,DEPT MED,IRVINE,CA 92717. BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. NHLBI,PROJECT OFF,BETHESDA,MD 20892. RP TELL, GS (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,EPIDEMIOL SECT,MED CTR BLVD,WINSTON SALEM,NC 27157, USA. RI Tell, Grethe/G-5639-2015; Newman, Anne/C-6408-2013 OI Tell, Grethe/0000-0003-1386-1638; Newman, Anne/0000-0002-0106-1150 FU NHLBI NIH HHS [N01-HC-85081, N01-HC-85079, N01-HC-85080] NR 44 TC 65 Z9 66 U1 1 U2 6 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1994 VL 23 IS 1 BP 59 EP 67 PG 9 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MQ695 UT WOS:A1994MQ69500010 PM 8282331 ER PT J AU SANDBERG, K JI, H CATT, KJ AF SANDBERG, K JI, H CATT, KJ TI REGULATION OF ANGIOTENSIN-II RECEPTORS IN RAT-BRAIN DURING DIETARY-SODIUM CHANGES SO HYPERTENSION LA English DT Article; Proceedings Paper CT 10th Scientific Meeting of the Inter-American-Society-of-Hypertension CY APR 25-29, 1993 CL LA JOLLA, CA SP INTER AMER SOC HYPERTENS DE ANGIOTENSIN; RECEPTORS, ANGIOTENSIN; DIET, SODIUM-RESTRICTED; BRAIN ID SPONTANEOUSLY HYPERTENSIVE RATS; HUMAN PERIPHERAL PLASMA; EXPRESSION; SUBTYPE; SYSTEM; RADIOIMMUNOASSAY; ALDOSTERONE; CLONING; RNA AB Activation of the renin-angiotensin system by sodium deficiency is associated with reciprocal changes in the expression of angiotensin II receptors in adrenal glomerulosa and vascular smooth muscle cells. The effects of dietary sodium changes on the expression of brain angiotensin receptor subtype 1 (AT(1)) mRNAs were examined in rats maintained on normal, low, and high sodium intake for 3 weeks. Plasma aldosterone and renin activity were elevated in rats maintained on a low salt diet compared with normal rats and were reduced in rats maintained on a high salt diet. These results are consistent with previous findings on the effects of altered dietary sodium on the renin-angiotensin system. The expression of AT(1A) and AT(1B) receptor subtype mRNAs was determined by quantitative reverse transcriptase-polymerase chain reaction during changes in sodium intake. The results revealed that sodium deprivation enhanced the expression of AT(1B) receptors in decorticated brains by 164% compared with high sodium intake. Conversely, high sodium diet increased the expression of AT(1A) receptors by 155% in the brain compared with low sodium intake. These data suggest that AT(1B) and AT(1B) receptors play reciprocal roles in central mechanisms for the control of fluid homeostasis. Further analysis of the molecular biology of angiotensin II receptor regulation in the brain may provide new insights into the interplay between the renin-angiotensin system and brood pressure regulation and also into the role of angiotensin II in the pathogenesis of essential hypertension. RP SANDBERG, K (reprint author), NICHHD,ERRB,ROOM 6A-36,BLDG 49,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 33 TC 3 Z9 3 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1994 VL 23 IS 1 SU S BP I137 EP I141 PG 5 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MR843 UT WOS:A1994MR84300030 PM 7506698 ER PT B AU YAROSLAVSKY, LP AF YAROSLAVSKY, LP GP IEEE TI LOCAL CRITERIA - A UNIFIED APPROACH TO LOCAL ADAPTIVE LINEAR AND RANK FILTERS FOR IMAGE RESTORATION AND ENHANCEMENT SO ICIP-94 - PROCEEDINGS, VOL II LA English DT Proceedings Paper CT 1994 IEEE International Conference on Image Processing (ICIP-94) CY NOV 13-16, 1994 CL AUSTIN, TX SP IEEE, SIGNAL PROC SOC C1 NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU I E E E, COMPUTER SOC PRESS PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, LOS ALAMITOS, CA 90720 BN 0-8186-6952-7 J9 IEEE IMAGE PROC PY 1994 BP 517 EP 521 PG 5 WC Computer Science, Software Engineering; Optics SC Computer Science; Optics GA BC13D UT WOS:A1994BC13D00106 ER PT B AU UNSER, M NEIMARK, MA LEE, CH AF UNSER, M NEIMARK, MA LEE, CH GP IEEE TI AFFINE TRANSFORMATIONS OF IMAGES - A LEAST SQUARES FORMULATION SO ICIP-94 - PROCEEDINGS, VOL III LA English DT Proceedings Paper CT 1994 IEEE International Conference on Image Processing (ICIP-94) CY NOV 13-16, 1994 CL AUSTIN, TX SP IEEE, SIGNAL PROC SOC C1 NIH,NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU I E E E, COMPUTER SOC PRESS PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, LOS ALAMITOS, CA 90720 BN 0-8186-6952-7 J9 IEEE IMAGE PROC PY 1994 BP 558 EP 561 PG 4 WC Computer Science, Artificial Intelligence; Computer Science, Software Engineering; Engineering, Biomedical; Optics SC Computer Science; Engineering; Optics GA BC13E UT WOS:A1994BC13E00115 ER PT B AU BRENNAN, MB AF BRENNAN, MB BE Hochgeschwender, U Gardiner, K TI INTRODUCTION - 7 BLIND MEN AND AN ELEPHANT SO IDENTIFICATION OF TRANSCRIBED SEQUENCES LA English DT Proceedings Paper CT 3rd International Workshop on the Identification of Transcribed Sequences CY OCT 02-04, 1993 CL NEW ORLEANS, LA SP US DOE, NATL CTR HUMAN GENOME RES, AMGEN Inc C1 NIMH,GENOM UNIT,BETHESDA,MD 20892. 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 BN 0-306-44835-1 PY 1994 BP 1 EP 4 PG 4 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA BB84Q UT WOS:A1994BB84Q00001 ER PT B AU SCHWABE, W LAWRENCE, BJ ROBB, AS HOPFINGER, RM HOCHGESCHWENDER, U BRENNAN, MB AF SCHWABE, W LAWRENCE, BJ ROBB, AS HOPFINGER, RM HOCHGESCHWENDER, U BRENNAN, MB BE Hochgeschwender, U Gardiner, K TI DIRECT CDNA SCREENING OF GENOMIC REFERENCE LIBRARIES - A RAPID METHOD FOR THE IDENTIFICATION OF TRANSCRIBED SEQUENCES IN LARGE GENOMIC REGIONS SO IDENTIFICATION OF TRANSCRIBED SEQUENCES LA English DT Proceedings Paper CT 3rd International Workshop on the Identification of Transcribed Sequences CY OCT 02-04, 1993 CL NEW ORLEANS, LA SP US DOE, NATL CTR HUMAN GENOME RES, AMGEN Inc C1 NIMH,GENOM UNIT,BETHESDA,MD 20892. 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 BN 0-306-44835-1 PY 1994 BP 139 EP 155 PG 17 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA BB84Q UT WOS:A1994BB84Q00014 ER PT B AU CLAVERIE, JM AF CLAVERIE, JM BE Hochgeschwender, U Gardiner, K TI SHALLOW SHOTGUN SEQUENCING AS A STRATEGY FOR FINDING CODING EXONS SO IDENTIFICATION OF TRANSCRIBED SEQUENCES LA English DT Proceedings Paper CT 3rd International Workshop on the Identification of Transcribed Sequences CY OCT 02-04, 1993 CL NEW ORLEANS, LA SP US DOE, NATL CTR HUMAN GENOME RES, AMGEN Inc C1 NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44835-1 PY 1994 BP 229 EP 237 PG 9 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA BB84Q UT WOS:A1994BB84Q00020 ER PT B AU HENDERSON, E SEAMANS, JR AF HENDERSON, E SEAMANS, JR BE Titus, HC Waks, A TI IMAGE ACQUISITION OF MICROSCOPIC SLIDES SO IMAGE ACQUISITION AND SCIENTIFIC IMAGING SYSTEMS SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Image Acquisition and Scientific Imaging Systems CY FEB 09-10, 1994 CL SAN JOSE, CA SP SOC IMAGING SCI & TECHNOL, SOC PHOTO OPT INSTRUMENTAT ENGINEERS C1 NATL LIB MED,LISTER HILL NATL CTR BIOMED COMMUN,BETHESDA,MD 20894. 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 0-8194-1468-9 J9 P SOC PHOTO-OPT INS PY 1994 VL 2173 BP 21 EP 27 PG 7 WC Optics; Imaging Science & Photographic Technology SC Optics; Imaging Science & Photographic Technology GA BA43N UT WOS:A1994BA43N00003 ER PT B AU YAROSLAVSKY, L EDEN, M AF YAROSLAVSKY, L EDEN, M BE Loew, MH TI CORRELATIONAL ACCUMULATION AS A METHOD FOR SIGNAL RESTORATION SO IMAGE PROCESSING: MEDICAL IMAGING 1994 SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Image Processing CY FEB 15-18, 1994 CL NEWPORT BEACH, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS, AMER ASSOC PHYSICISTS MED, BIOMED OPT SOC, FDA, CTR DEVICES & RADIOL HLTH, NATL ELECT MANUFACTURERS ASSOC, DIAGNOST IMAGING & THERAPY SYST DIV, SOC IMAGING SCI & TECHNOL, RADIOL INFORMAT SYST CONSORTIUM, RADIOL SOC N AMER, SOC COMP APPLICAT RADIOL C1 NIH,BEIP,NCRR,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 0-8194-1462-X J9 P SOC PHOTO-OPT INS PY 1994 VL 2167 BP 353 EP 364 DI 10.1117/12.175069 PG 12 WC Engineering, Biomedical; Optics; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Optics; Radiology, Nuclear Medicine & Medical Imaging GA BB27L UT WOS:A1994BB27L00032 ER PT B AU VRHEL, MJ UNSER, M AF VRHEL, MJ UNSER, M BE Schulz, TJ Snyder, DL TI MULTICHANNEL DECONVOLUTION - THE GENERALIZED SAMPLING APPROACH SO IMAGE RECONSTRUCTION AND RESTORATION SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Image Reconstruction and Restoration CY JUL 25-26, 1994 CL SAN DIEGO, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS DE RESTORATION; RECONSTRUCTION; PROJECTORS; MULTICHANNEL; WIENER FILTER C1 NIH,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 1 Z9 2 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1626-6 J9 P SOC PHOTO-OPT INS PY 1994 VL 2302 BP 188 EP 199 DI 10.1117/12.188040 PG 12 WC Optics SC Optics GA BB57U UT WOS:A1994BB57U00018 ER PT J AU ARROYO, J DIEZOREJAS, R ALVAREZ, AM SHAW, S SANCHEZPEREZ, M AF ARROYO, J DIEZOREJAS, R ALVAREZ, AM SHAW, S SANCHEZPEREZ, M TI MOLECULAR ANALYSIS OF AN HLA-DP MUTANT-CELL LINE SELECTED FOR ITS RESISTANCE TO KILLING BY HLA-DPW2-SPECIFIC T-CELL CLONES SO IMMUNOGENETICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-II MOLECULES; SURFACE EXPRESSION; INTRACELLULAR-TRANSPORT; LYMPHOBLASTOID-CELLS; POSSIBLE INVOLVEMENT; ANTIGEN PRESENTATION; GENE-PRODUCTS; SB ANTIGENS; RECOGNITION AB A collection of HLA-DP mutants was generated, using ICR 191 as the mutagenic agent and resistance to lysis mediated by HLA-DPw2 allospecific cytotoxic T lymphocytes (CTLs) as the selection criterion. These mutants were derived from the HLA haploid lymphoblastoid cell line 45.1. Loss of HLA-DPw2 surface expression accounted for the lack of HLA-DPw2 CTL recognition in all the mutants. However, one of them, 45.EM19, binds to DPw2-specific monoclonal antibodies (mAb) after cell permeabilization. HLA-DPA1 and DPB1 mRNA expression studies permitted the classification of the mutants in four categories: 1) DPA1-negative, DPB1-positive; 2) DPA1-positive, DPB1-negative; 3) DPA1- and DPB1-negative, and 4) DPA1- and DPB1-positive mutants. Mutant 45.EM19 is included in the last group. The cloning and sequencing of the full-length DPA1 (DPA1*0103) and DPB1 (DPB1*02012) cDNAs from this mutant showed no changes in the DPA1 sequence compared to the wild-type sequence. However, a frame-shift mutation in the DPB1 gene exon coding for the transmembrane region was detected. The insertion of a guanine nucleotide provokes an extension of the open reading frame, increasing the length of the C-terminal domain and changing the hydropathicity pattern of the transmembrane domain. This change should be responsible for the phenotype of the 45.EM19 mutant. C1 UNIV COMPLUTENSE MADRID,FAC FARM,DEPT MICROBIOL 2,E-28040 MADRID,SPAIN. UNIV COMPLUTENSE MADRID,CTR CITOMETRIA FLUJO,E-28040 MADRID,SPAIN. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RI Arroyo, Javier/E-9308-2016 OI Arroyo, Javier/0000-0002-1971-1721 NR 41 TC 4 Z9 4 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JAN PY 1994 VL 39 IS 1 BP 40 EP 47 PG 8 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA MD187 UT WOS:A1994MD18700006 PM 8225437 ER PT J AU HUFFMAN, LC BRYAN, YE PEDERSEN, FA LESTER, BM NEWMAN, JD DELCARMEN, R AF HUFFMAN, LC BRYAN, YE PEDERSEN, FA LESTER, BM NEWMAN, JD DELCARMEN, R TI INFANT CRY ACOUSTICS AND MATERNAL RATINGS OF TEMPERAMENT SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article DE CRY; ACOUSTICS; TEMPERAMENT; INFANCY ID DIFFICULTNESS; PERCEPTIONS; BEHAVIOR; FEATURES; CRIES AB Amount of crying or fussiness has been associated with the concept of difficult temperament. In this study, we explored the associations between cry acoustics and temperament characteristics across the first 12 weeks of life in a group of healthy full-term infants. Maternal ratings of 12-week temperament, particularly negative emotional reactivity, were significantly related to both neonatal and 12-week cry acoustics. In addition, two acoustic variables, duration of cry utterance and fundamental frequency, were stable over the first 12 weeks of life. C1 PURDUE UNIV,W LAFAYETTE,IN 47907. UNIV DELAWARE,NEWARK,DE 19718. BROWN UNIV,BRADLEY HOSP,PROVIDENCE,RI 02912. WOMEN & INFANTS HOSP RHODE ISL,PROVIDENCE,RI 02908. NICHHD,BETHESDA,MD 20892. RP HUFFMAN, LC (reprint author), NIMH,BEHAV COGNIT & SOCIAL PROC RES BRANCH,PARKLAWN BLDG,ROOM 11C-10,ROCKVILLE,MD 20857, USA. NR 31 TC 8 Z9 8 U1 0 U2 1 PU ABLEX PUBL CORP PI NORWOOD PA 355 CHESTNUT ST, NORWOOD, NJ 07648 SN 0163-6383 J9 INFANT BEHAV DEV JI Infant Behav. Dev. PD JAN-MAR PY 1994 VL 17 IS 1 BP 45 EP 53 DI 10.1016/0163-6383(94)90021-3 PG 9 WC Psychology, Developmental SC Psychology GA NN435 UT WOS:A1994NN43500006 ER PT J AU ROCKEY, DD ROSQUIST, JL AF ROCKEY, DD ROSQUIST, JL TI PROTEIN ANTIGENS OF CHLAMYDIA-PSITTACI PRESENT IN INFECTED-CELLS BUT NOT DETECTED IN THE INFECTIOUS ELEMENTARY BODY SO INFECTION AND IMMUNITY LA English DT Article ID OUTER-MEMBRANE PROTEIN; LISTERIA-MONOCYTOGENES; TOXOPLASMA-GONDII; GUINEA-PIGS; PARASITOPHOROUS VACUOLE; PHAGOLYSOSOME FUSION; GENITAL-INFECTION; TRACHOMATIS; CONJUNCTIVITIS; PURIFICATION AB Ocular infection of guinea pigs with the guinea pig inclusion conjunctivitis (GPIC) strain of Chlamydia psittaci produces a clinical condition representative of acute chlamydial conjunctivitis in humans. Guinea pigs which had recovered from two challenges with GPIC were used as a source of sera for the identification of antigens present in GPIC-infected tissue culture cells but absent in the infectious elementary body (EB). Immunoblots of lysates of infected HeLa cells probed with the convalescent-phase sera identified protein antigens of 22, 34, and 52 kDa (p22, p34, and p52, respectively) that were not detected in lysates of purified EB or in uninfected HeLa cells. Protein p22 was also not detected in lysates of purified reticulate bodies. Immunoblotting of lysates of HeLa cells infected with other chlamydiae demonstrated that the antigenicity of p22 and p34 was subspecies specific. Immunoblotting was also used to detect p22 and p34 in lysates of the conjunctivae of infected guinea pigs. Adsorption of convalescent-phase sera with GPIC EB produced a reagent with dominant reactivity toward p22, p34, and a 28-kDa EB protein. Immunofluorescent staining of GPIC-infected HeLa cells demonstrated that these adsorbed sera labeled the inclusion and inclusion membrane, with no apparent reactivity toward EB or reticulate bodies. Collectively, these data identify non-EB chlamydial components which may be released into the inclusion during intracellular growth. RP ROCKEY, DD (reprint author), NIAID,ROCKY MT LABS,INTRACELLULAR PARASITES LAB,HAMILTON,MT 59840, USA. NR 32 TC 42 Z9 45 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1994 VL 62 IS 1 BP 106 EP 112 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MN488 UT WOS:A1994MN48800016 PM 8262615 ER PT J AU POLOTSKY, VY ROBBINS, JB BRYLA, D SCHNEERSON, R AF POLOTSKY, VY ROBBINS, JB BRYLA, D SCHNEERSON, R TI COMPARISON OF CONJUGATES COMPOSED OF LIPOPOLYSACCHARIDE FROM SHIGELLA-FLEXNERI TYPE-2A DETOXIFIED BY 2 METHODS AND BOUND TO TETANUS TOXOID SO INFECTION AND IMMUNITY LA English DT Article ID O-SPECIFIC POLYSACCHARIDE; SERUM ANTIBODIES; CHOLERA-TOXIN; IMMUNOGENICITY; CARRIER; VACCINES; ANTIGENS; IMMUNITY; SONNEI; MICE AB Shigella flexneri type 2a lipopolysaccharide (LPS) nas detoxified with acetic acid (O-SP) or with hydrazine (DeALPS). DeALPS, but not O-SP, retained part of its lipid A. Both gave an identical line of precipitation with typing antiserum by double immunodiffusion, and both had low levels of LPS activity by the Limulus amoebocyte lysate assay. O-SP had an M(r); of similar to 17,000. DeALPS had two components of MS similar to 30,00 (major) and similar to 10,000 (minor). Adipic acid hydrazide derivatives of O-SP and DeALPS were conjugated to tetanus toxoid (TT), purified by gel filtration through CL-6B Sepharose, and designated O-SP-TT and DeALPS-TT, respectively. Saccharide (2.5 mu g) as O-SP, DeALPS, or their conjugates was injected subcutaneously into 5-week-old mice three times 2 weeks apart. The mice were bled before the second injection and 7 days after the second and third. O-SP alone did not elicit immunoglobulin M (IgM) or IgG LPS antibodies. DeALPS elicited low levels of IgM LPS antibodies after the third injection only. Two of three lots of O-SP-TT induced significant levels of IgM LPS antibodies after the third injection. One O-SP-TT lot elicited IgG LPS antibodies after the second injection, and all three lots elicited significant levels of IgG after the third. DeALPS-TT induced low levels of anti-LPS IgM and IgG only after the third injection. The geometric mean antibody titers of both immunoglobulin classes induced by O-SP-TT were higher than those induced by DeALPS-TT. By these criteria, O-SP provided a more immunogenic saccharide than DeALPS for S. flexneri type 2a conjugates. C1 NICHHD,DEV & MOLEC IMMUN LAB,BETHESDA,MD 20892. NICHHD,BIOMETRY & MATH STAT BRANCH,BETHESDA,MD 20892. NR 31 TC 10 Z9 10 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1994 VL 62 IS 1 BP 210 EP 214 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MN488 UT WOS:A1994MN48800030 PM 8262629 ER PT J AU COLEMAN, JL ROGERS, RC ROSA, PA BENACH, JL AF COLEMAN, JL ROGERS, RC ROSA, PA BENACH, JL TI VARIATIONS IN THE OSPB GENE OF BORRELIA-BURGDORFERI RESULT IN DIFFERENCES IN MONOCLONAL-ANTIBODY REACTIVITY AND IN PRODUCTION OF ESCAPE VARIANTS SO INFECTION AND IMMUNITY LA English DT Note ID LYME-DISEASE SPIROCHETE; MEMBRANE-PROTEINS; SURFACE PROTEIN; COMPONENTS; SELECTION; ANTIGENS AB An escape variant of Borrelia burgdorferi, selected with a monoclonal antibody to OspB, expressed a truncated form of OspB, the result of point mutations in the ospB gene leading to a premature termination codon. A single amino acid position in the C terminus of OspB was critical for monoclonal antibody recognition. The variations in the ospB gene suggest a mechanism for the evasion of the immune response by these organisms and may also have implications for current diagnostic and vaccine efforts. C1 SUNY STONY BROOK,HLTH SCI CTR T9,DEPT PATHOL,STONY BROOK,NY 11794. SUNY STONY BROOK,STATE NEW YORK DEPT HLTH,STONY BROOK,NY 11794. NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNC LAB,HAMILTON,MT 59840. FU NIAID NIH HHS [AI 27044] NR 24 TC 37 Z9 37 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1994 VL 62 IS 1 BP 303 EP 307 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MN488 UT WOS:A1994MN48800043 PM 7505260 ER PT J AU MOCK, BA HOLIDAY, DL CERRETTI, DP DARNELL, SC OBRIEN, AD POTTER, M AF MOCK, BA HOLIDAY, DL CERRETTI, DP DARNELL, SC OBRIEN, AD POTTER, M TI CONSTRUCTION OF A SERIES OF CONGENIC MICE WITH RECOMBINANT CHROMOSOME-1 REGIONS SURROUNDING THE GENETIC-LOCI FOR RESISTANCE TO INTRACELLULAR PARASITES (ITY, LSH, AND BCG), DNA-REPAIR RESPONSES (REP-1), AND THE CYTOSKELETAL PROTEIN VILLIN (VIL) SO INFECTION AND IMMUNITY LA English DT Note ID SALMONELLA-TYPHIMURIUM; MOUSE CHROMOSOME-1; INNATE RESISTANCE; MACROPHAGES; PERITONEAL; INFECTION; MAP AB The interval of mouse chromosome 1 extending from Idh-1 to Pep-3 harbors the natural resistance gene Ity/Lsh/Bcg; it controls the outcome of infection with Salmonella typhimurium, Leishmania donovani, and several Mycobacterium species. This region also contains a DNA repair gene, Rep-1, which determines the rapidity with which double-strand breaks in chromatin are repaired, BALB/cAnPt and DBA/2N mice differ in their phenotypic expression of these genes. To generate appropriate strains of mice for the study of these genes, a series of 10 C.D2 congenic strains recombinant across a 28-centimorgan interval of mouse chromosome 1 extending from Idh-1 to Pep-3 were derived from crosses of the C.D2-ldh-1 Pep-3 congenic strain back to BALB/cAn. Analyses of these recombinant strains will allow the correlation of biological-immunological phenotypes with defined genetic regions. C1 IMMUNEX CORP,SEATTLE,WA 98101. UNIFORMED SERV UNIV HLTH SCI,DEPT MICROBIOL,BETHESDA,MD 20814. RP MOCK, BA (reprint author), NATL CANC INST,GENET LAB,BLDG 37,ROOM 2B-08,BETHESDA,MD 20892, USA. NR 20 TC 17 Z9 17 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1994 VL 62 IS 1 BP 325 EP 328 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MN488 UT WOS:A1994MN48800048 PM 8262646 ER PT J AU WILLY, ME KOZIOL, DE FLEISHER, T KOO, S MCFARLAND, H SCHMITT, J WESLEY, R HURWITZ, ES HENDERSON, DK AF WILLY, ME KOZIOL, DE FLEISHER, T KOO, S MCFARLAND, H SCHMITT, J WESLEY, R HURWITZ, ES HENDERSON, DK TI MEASLES IMMUNITY IN A POPULATION OF HEALTH-CARE WORKERS SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article ID UNITED-STATES; SCHOOL POPULATION; VACCINE FAILURES; EPIDEMIC MEASLES; TRANSMISSION; OUTBREAK; ANTIBODY; RUBELLA; SUSCEPTIBILITY; IMMUNIZATION AB OBJECTIVES: To evaluate measles seroprevalence among cohorts of new employees and to evaluate vaccine responses of susceptible adult healthcare workers. DESIGN: New employees were screened for measles susceptibility as part of employee evaluations. Anti-IgG measles antibody tests were completed on 2,473 workers. Demographic, measles history, and measles vaccination information was collected using a short questionnaire. Susceptible workers were vaccinated and screened for vaccine responses following vaccination. RESULTS: Ninety-three workers (4(%) were seronegative, and 56 (2%) were equivocal. Individuals in the youngest cohort (born after 1956) were significantly more likely to be susceptible than those in the middle cohort (born 1951 to 1956) and those in the oldest cohort (born before 1951) (P<0.01). The middle cohort included eight (5%) of the 149 seronegative or equivocal workers. Among the members of the youngest cohort, those from the United States were more likely to be susceptible (P<0.01) than those from outside the United States. Of the 106 vaccinated susceptible workers whose follow-up serologies were determined, 90 (85%) developed positive IgG serologies, six had equivocal results, and 10 were seronegative. Eleven of the 16 non- or hyporesponders were revaccinated and re-evaluated; nine developed low positive IgG antimeasles levels, one exhibited an equivocal response, and one failed to respond. CONCLUSIONS: A small but important proportion of healthcare workers are susceptible to measles. Whenever feasible, measles immunity programs for healthcare workers should include workers born before 1957. Of workers born after 1956, those from outside the United States are more likely to be immune than workers from inside the United States. Using the currently available vaccine, revaccination of initial non- or hyporesponders appears to be effective. C1 NIH,WARREN G MAGNUSON CLIN CTR,BLDG 10,ROOM 2C146,BETHESDA,MD 20892. NIH,HOSP EPIDEMIOL SERV,BETHESDA,MD 20892. NIH,IMMUNOL SERV,BETHESDA,MD 20892. NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. NIH,OCCUPAT MED SERV,BETHESDA,MD 20892. NIH,DEPT IONOSPHERE RES,BETHESDA,MD 20892. CTR DIS CONTROL & PREVENT,ATLANTA,GA. NR 27 TC 15 Z9 16 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD JAN PY 1994 VL 15 IS 1 BP 12 EP 17 PG 6 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA MQ231 UT WOS:A1994MQ23100004 PM 8133003 ER PT B AU MILES, FA AF MILES, FA BE DelgadoGarcia, JM Godaux, E Vidal, PP TI STIMULUS SPECIFICITY IN THE PRIMATE OPTOKINETIC SYSTEM SO INFORMATION PROCESSING UNDERLYING GAZE CONTROL SE PERGAMON STUDIES IN NEUROSCIENCE LA English DT Proceedings Paper CT Satellite Workshop on Information Processing Underlying Gaze Control, at the 16th European-Neuroscience-Association Meeting CY SEP 22-24, 1993 CL UNIV SEVILLA, COLEGIO HERNANDO COLON, SEVILLE, SPAIN SP EUROPEAN NEUROSCI ASSOC HO UNIV SEVILLA, COLEGIO HERNANDO COLON C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON PRESS LTD PI OXFORD PA THE BOULEVARD LANGFORD LANE KIDLINGTON, OXFORD, ENGLAND OX5 1GB BN 0-08-042506-2 J9 PERG S NEUR PY 1994 IS 12 BP 251 EP 259 PG 9 WC Neurosciences SC Neurosciences & Neurology GA BC41Z UT WOS:A1994BC41Z00025 ER PT B AU BUSH, GA VANDERSTEEN, J MILES, FA AF BUSH, GA VANDERSTEEN, J MILES, FA BE DelgadoGarcia, JM Godaux, E Vidal, PP TI WHEN THE 2 EYES SEE PATTERNS OF UNEQUAL SIZE THEY PRODUCE SACCADES OF UNEQUAL AMPLITUDE SO INFORMATION PROCESSING UNDERLYING GAZE CONTROL SE PERGAMON STUDIES IN NEUROSCIENCE LA English DT Proceedings Paper CT Satellite Workshop on Information Processing Underlying Gaze Control, at the 16th European-Neuroscience-Association Meeting CY SEP 22-24, 1993 CL UNIV SEVILLA, COLEGIO HERNANDO COLON, SEVILLE, SPAIN SP EUROPEAN NEUROSCI ASSOC HO UNIV SEVILLA, COLEGIO HERNANDO COLON C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. RI van der Steen, Johannes/F-6767-2011 OI van der Steen, Johannes/0000-0002-3989-3075 NR 0 TC 6 Z9 6 U1 0 U2 0 PU PERGAMON PRESS LTD PI OXFORD PA THE BOULEVARD LANGFORD LANE KIDLINGTON, OXFORD, ENGLAND OX5 1GB BN 0-08-042506-2 J9 PERG S NEUR PY 1994 IS 12 BP 261 EP 267 PG 7 WC Neurosciences SC Neurosciences & Neurology GA BC41Z UT WOS:A1994BC41Z00026 ER PT B AU KRAUZLIS, RJ MILES, FA AF KRAUZLIS, RJ MILES, FA BE DelgadoGarcia, JM Godaux, E Vidal, PP TI SIMILAR CHANGES IN THE LATENCY OF PURSUIT AND SACCADIC EYE MOVEMENTS OBSERVED WITH THE GAP PARADIGM SO INFORMATION PROCESSING UNDERLYING GAZE CONTROL SE PERGAMON STUDIES IN NEUROSCIENCE LA English DT Proceedings Paper CT Satellite Workshop on Information Processing Underlying Gaze Control, at the 16th European-Neuroscience-Association Meeting CY SEP 22-24, 1993 CL UNIV SEVILLA, COLEGIO HERNANDO COLON, SEVILLE, SPAIN SP EUROPEAN NEUROSCI ASSOC HO UNIV SEVILLA, COLEGIO HERNANDO COLON C1 NIH,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON PRESS LTD PI OXFORD PA THE BOULEVARD LANGFORD LANE KIDLINGTON, OXFORD, ENGLAND OX5 1GB BN 0-08-042506-2 J9 PERG S NEUR PY 1994 IS 12 BP 269 EP 277 PG 9 WC Neurosciences SC Neurosciences & Neurology GA BC41Z UT WOS:A1994BC41Z00027 ER PT J AU SILLS, RC MORGAN, KT BOORMAN, GA AF SILLS, RC MORGAN, KT BOORMAN, GA TI ACCESSORY NASAL STRUCTURES IN TOXICOLOGY STUDIES SO INHALATION TOXICOLOGY LA English DT Article; Proceedings Paper CT Symposium on Nasal Toxicity and Dosimetry of Inhaled Xenobiotics - Implications for Human Health CY SEP 20-22, 1993 CL DURHAM, NC ID INHALATION EXPOSURE; RAT; TOXICITY; MUCOSA; CAVITY; RELEVANCE; ORGAN; MICE; METABOLISM; INDUCTION AB In addition to air conditioning, the nose has a range of sensory functions that render this organ structurally complex due to the presence of diverse accessory structures, including the vomeronasal and septal olfactory organ, an array of mucoserous glands, and the trigeminal and other sensory nerve endings. The supporting structures of the nasal airways are beautifully ''engineered'' to permit integration of the nose and its accessory organs with adjacent structural components of the head, including the nasolacrimal and incisive ducts, and the bones of the maxilla and anterior cranial vault. A bilaterally symmetric architecture, comprised of muscle, bone, cartilage, nerves, blood vessels, and other connective tissue, is well adapted to the functional integrity of this organ. The purpose of this article is to consider the accessory and supporting nasal structures from the perspective of toxicologic pathology. Brief descriptions of selected spontaneous and treatment-related lesions are presented. C1 CHEM IND INST TOXICOL,RES TRIANGLE PK,NC 27709. RP SILLS, RC (reprint author), NIEHS,ENVIRONM TOXICOL PROGRAM,PATHOL BRANCH,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 47 TC 3 Z9 3 U1 0 U2 0 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0895-8378 J9 INHAL TOXICOL JI Inhal. Toxicol. PY 1994 VL 6 SU S BP 221 EP 248 PG 28 WC Toxicology SC Toxicology GA QD179 UT WOS:A1994QD17900017 ER PT B AU FLANDERS, KC AF FLANDERS, KC BE Burger, HG Findlay, J Robertson, D DeKretser, D Petraglia, F TI EXPRESSION AND FUNCTIONS OF TGF-BETA-S IN THE REPRODUCTIVE-TRACT SO INHIBIN AND INHIBIN-RELATED PROTEINS SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT International Symposium on Inhibin and Inhibin-Related Proteins CY JUN 17-18, 1993 CL SIENA, ITALY SP ARES SERONO SYMPOSIA RP FLANDERS, KC (reprint author), NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-13-9 J9 FRONT ENDOCRINOL PY 1994 VL 3 BP 301 EP 313 PG 13 WC Biochemistry & Molecular Biology; Reproductive Biology SC Biochemistry & Molecular Biology; Reproductive Biology GA BA22Y UT WOS:A1994BA22Y00025 ER PT S AU RAY, JM STETLERSTEVENSON, WG AF RAY, JM STETLERSTEVENSON, WG BE Greenwald, RA Golub, LM TI TIMP-2 EXPRESSION MODULATES HUMAN-MELANOMA CELL-ADHESION AND MOTILITY SO INHIBITION OF MATRIX METALLOPROTEINASES: THERAPEUTIC POTENTIAL SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Inhibition of Matrix Metalloproteinases - Therapeutic Potential CY JAN 19-22, 1994 CL TAMPA, FL SP New York Acad Sci, Long Island Jewish Med Ctr ID HUMAN-TISSUE INHIBITOR; IV COLLAGENASE; METALLOPROTEINASE INHIBITOR; BASEMENT-MEMBRANE; TUMOR-CELLS; MATRIX METALLOPROTEINASES; EXTRACELLULAR-MATRIX; FIBRONECTIN RECEPTOR; SIGNAL TRANSDUCTION; INVASIVE BEHAVIOR RP RAY, JM (reprint author), NCI,EXTRACELLULAR MATRIX PATHOL SECT,PATHOL LAB,BLDG 10,ROOM 2A33,BETHESDA,MD 20892, USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 47 TC 22 Z9 26 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-899-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 732 BP 233 EP 247 DI 10.1111/j.1749-6632.1994.tb24739.x PG 15 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Pharmacology & Pharmacy GA BD10L UT WOS:A1994BD10L00021 PM 7978796 ER PT S AU ZUCKER, S LYSIK, RM ZARRABI, HM MOLL, U TICKLE, SP STETLERSTEVENSON, W BAKER, TS DOCHERTY, AJP AF ZUCKER, S LYSIK, RM ZARRABI, HM MOLL, U TICKLE, SP STETLERSTEVENSON, W BAKER, TS DOCHERTY, AJP BE Greenwald, RA Golub, LM TI PLASMA ASSAY OF MATRIX METALLOPROTEINASES (MMPS) AND MMP-INHIBITOR COMPLEXES IN CANCER - POTENTIAL USE IN PREDICTING METASTASIS AND MONITORING TREATMENT SO INHIBITION OF MATRIX METALLOPROTEINASES: THERAPEUTIC POTENTIAL SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Inhibition of Matrix Metalloproteinases - Therapeutic Potential CY JAN 19-22, 1994 CL TAMPA, FL SP New York Acad Sci, Long Island Jewish Med Ctr ID COLLAGENASE GELATINASE MMP-2; IV COLLAGENASE; TISSUE INHIBITOR; STROMAL CELLS; 72 KILODALTON; COLON CANCER; EXPRESSION; BENIGN; TUMOR; IDENTIFICATION C1 VET AFFAIRS MED CTR, DEPT MED, NORTHPORT, NY 11768 USA. SUNY STONY BROOK, DEPT MED, STONY BROOK, NY 11794 USA. SUNY STONY BROOK, DEPT PATHOL, STONY BROOK, NY 11794 USA. CELLTECH LTD, SLOUGH SL1 4EN, BERKS, ENGLAND. NCI, DEPT PATHOL, BETHESDA, MD 20892 USA. RP ZUCKER, S (reprint author), VET AFFAIRS MED CTR, DEPT RES, MAIL CODE 151, NORTHPORT, NY 11768 USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 42 TC 29 Z9 30 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 0-89766-899-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 732 BP 248 EP 262 DI 10.1111/j.1749-6632.1994.tb24740.x PG 15 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Pharmacology & Pharmacy GA BD10L UT WOS:A1994BD10L00022 PM 7978797 ER PT S AU COSTELLO, PC DELMAESTRO, RF STETLERSTEVENSON, WG AF COSTELLO, PC DELMAESTRO, RF STETLERSTEVENSON, WG BE Greenwald, RA Golub, LM TI GELATINASE-A EXPRESSION IN HUMAN-MALIGNANT GLIOMAS SO INHIBITION OF MATRIX METALLOPROTEINASES: THERAPEUTIC POTENTIAL SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Inhibition of Matrix Metalloproteinases - Therapeutic Potential CY JAN 19-22, 1994 CL TAMPA, FL SP New York Acad Sci, Long Island Jewish Med Ctr ID COLLAGENASE; CELLS C1 UNIV WESTERN ONTARIO,DEPT NEUROSURG,LONDON,ON,CANADA. NIH,DEPT PATHOL,BETHESDA,MD 20902. RP COSTELLO, PC (reprint author), GEORGETOWN UNIV,DEPT NEUROSURG,WASHINGTON,DC 20007, USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 5 TC 9 Z9 10 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-899-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 732 BP 450 EP 452 DI 10.1111/j.1749-6632.1994.tb24782.x PG 3 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Pharmacology & Pharmacy GA BD10L UT WOS:A1994BD10L00064 PM 7978836 ER PT J AU ISSAQ, HJ AF ISSAQ, HJ TI COMPARISON OF CHIRAL SEPARATIONS IN CAPILLARY ZONE ELECTROPHORESIS WITH OTHER METHODS SO INSTRUMENTATION SCIENCE & TECHNOLOGY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; MICELLAR ELECTROKINETIC CHROMATOGRAPHY; SUPERCRITICAL FLUID CHROMATOGRAPHY; HOST-GUEST COMPLEXATION; STATIONARY PHASES; GAS-CHROMATOGRAPHY; BETA-CYCLODEXTRIN; DERIVATIZED CYCLODEXTRINS; OPTICAL RESOLUTION; SILICA CAPILLARIES AB Capillary zone electrophoresis (CZE) is an efficient microseparation technique that can be used for the separation of small as well as large biomolecules. The use of micelles in the buffer makes CZE an acceptable technique for the resolution of charged and neutral molecules. The separation of chiral compounds is an important aspect of the pharmaceutical industry, synthetic organic chemistry and other areas. Optical isomers can be separated from each other using high pressure liquid chromatography (HPLC) and capillary gas chromatography (CGC), however, each of these techniques has its limitations. CGC and HPLC require a chiral column, which is costly, CZE does not. CZE has the highest efficiency and chiral separations are achieved by adding a modifier to the buffer that facilitates the separation of optical isomers. In this review the advantages and disadvantages of HPLC, CGC and CZE for chiral separations will be discussed. RP ISSAQ, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,POB B,FREDERICK,MD 21702, USA. NR 86 TC 14 Z9 14 U1 1 U2 3 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1073-9149 J9 INSTRUM SCI TECHNOL JI Instrum. Sci. Technol. PY 1994 VL 22 IS 2 BP 119 EP 149 DI 10.1080/10739149408001183 PG 31 WC Chemistry, Analytical; Instruments & Instrumentation SC Chemistry; Instruments & Instrumentation GA PA095 UT WOS:A1994PA09500001 ER PT S AU ADAMO, ML KOVAL, A LEROITH, D ROBERTS, CT AF ADAMO, ML KOVAL, A LEROITH, D ROBERTS, CT BE Baxter, RC Gluckman, PD Rosenfeld, RG TI POSTTRANSCRIPTIONAL REGULATION OF IGF-I GENE-EXPRESSION SO INSULIN-LIKE GROWTH FACTORS AND THEIR REGULATORY PROTEINS SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 3rd International Symposium on Insulin-Like Growth Factors CY FEB 06-10, 1994 CL SYDNEY, AUSTRALIA SP PHARMACIA KABI C1 NIH,DIABET BRANCH,BETHESDA,MD 20892. NR 0 TC 6 Z9 6 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 0-444-81756-5 J9 INT CONGR SER PY 1994 VL 1056 BP 23 EP 31 PG 9 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA BB11B UT WOS:A1994BB11B00003 ER PT S AU WERNER, H ROBERTS, CT LEROITH, D AF WERNER, H ROBERTS, CT LEROITH, D BE Baxter, RC Gluckman, PD Rosenfeld, RG TI TRANSCRIPTIONAL REPRESSION OF THE IGF-II AND IGF-I RECEPTOR GENES BY TUMOR SUPPRESSOR-WT1 - IMPLICATIONS FOR NORMAL KIDNEY DEVELOPMENT AND WILMS-TUMOR SO INSULIN-LIKE GROWTH FACTORS AND THEIR REGULATORY PROTEINS SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 3rd International Symposium on Insulin-Like Growth Factors CY FEB 06-10, 1994 CL SYDNEY, AUSTRALIA SP PHARMACIA KABI C1 NIDDK,DIABET BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 0-444-81756-5 J9 INT CONGR SER PY 1994 VL 1056 BP 107 EP 115 PG 9 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA BB11B UT WOS:A1994BB11B00011 ER PT S AU RECHLER, MM SUH, DS BOISCLAIR, YR BROWN, AL OOI, GT AF RECHLER, MM SUH, DS BOISCLAIR, YR BROWN, AL OOI, GT BE Baxter, RC Gluckman, PD Rosenfeld, RG TI TRANSCRIPTIONAL REGULATION OF THE RAT IGFBP-1 AND IGFBP-2 GENES SO INSULIN-LIKE GROWTH FACTORS AND THEIR REGULATORY PROTEINS SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 3rd International Symposium on Insulin-Like Growth Factors CY FEB 06-10, 1994 CL SYDNEY, AUSTRALIA SP PHARMACIA KABI C1 NIDDKD,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 0-444-81756-5 J9 INT CONGR SER PY 1994 VL 1056 BP 163 EP 174 PG 12 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA BB11B UT WOS:A1994BB11B00016 ER PT J AU OCHIAI, K WANG, BH RIEGER, A KILGUS, O MAURER, D FODINGER, D KINET, JP STINGL, G TOMIOKA, H AF OCHIAI, K WANG, BH RIEGER, A KILGUS, O MAURER, D FODINGER, D KINET, JP STINGL, G TOMIOKA, H TI A REVIEW ON FC-EPSILON-RI ON HUMAN EPIDERMAL LANGERHANS CELLS SO INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY LA English DT Article; Proceedings Paper CT Workshop on Eosinophils in Allergy CY JUN 11-12, 1993 CL TOKYO, JAPAN DE LANGERHANS CELL; IGE; FC-EPSILON-RI; MONOCLONAL ANTIBODY ID IGE AB In order to show the surface expression of Fc epsilon RI on human epidermal Langerhans cells (LC), we examined monomeric IgE binding to LC. We demonstrated that the majority of epidermal LC were able to bind monomeric IgE. IgE binding to LC could neither be prevented by preincubation of the tissue with monoclonal antibodies (mAb) against either Fc epsilon RII/CD23 or Fc gamma RII/ CD32, nor by the addition of lactose, but could be entirely abrogated by preincubation with the anti-Fc epsilon RI mAb15-1. These data show that epidermal LC express Fc epsilon RI molecules. C1 UNIV VIENNA,SCH MED,DEPT DERMATOL 1,DIV CUTANEOUS IMMUNOL,A-1010 VIENNA,AUSTRIA. NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD. RP OCHIAI, K (reprint author), TOHO UNIV,SAKURA HOSP,SCH MED,DEPT INTERNAL MED,564-1 SHIMOSHIZU,SAKURA,CHIBA 285,JAPAN. NR 4 TC 7 Z9 7 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-2438 J9 INT ARCH ALLERGY IMM JI Int. Arch. Allergy Immunol. PY 1994 VL 104 SU 1 BP 63 EP 64 PG 2 WC Allergy; Immunology SC Allergy; Immunology GA NK655 UT WOS:A1994NK65500023 PM 8156009 ER PT J AU BARANIUK, JN SILVER, PB KALINER, MA BARNES, PJ AF BARANIUK, JN SILVER, PB KALINER, MA BARNES, PJ TI PERENNIAL RHINITIS SUBJECTS HAVE ALTERED VASCULAR, GLANDULAR, AND NEURAL RESPONSES TO BRADYKININ NASAL PROVOCATION SO INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY LA English DT Article DE ALBUMIN; LYSOZYME; MUCIN; MUCOUS GLYCOCONJUGATES; SEROUS CELLS; MUCOUS CELLS; SECRETION; PARASYMPATHETIC REFLEXES; IPRATROPIUM BROMIDE; VASCULAR PERMEABILITY; HYPERRESPONSIVENESS ID AIRWAY NEUTRAL ENDOPEPTIDASE; SUBSTANCE-P; INDUCED BRONCHOCONSTRICTION; PATHO-PHYSIOLOGY; SENSORY NEURONS; GUINEA-PIG; SECRETIONS; CAPSAICIN; INVIVO; MUCOSA AB Background: Bradykinin (BK) is known to stimulate vascular permeability by direct actions on vascular B2 receptors, and may stimulate nociceptive sensory nerves that recruit parasympathetic reflexes which induces glandular secretion. Differences in these responses may occur in allergic rhinitis. Methods: The effects of bradykinin (BK) on nasal secretion in vivo were studied by unilateral BK nasal challenge in 8 normal subjects and 6 subjects with severe perennial allergic rhinitis. BK (0, 100, 1,000 nmol) were applied to one nostril (ipsilateral, IL) and saline lavage fluids collected separately from the IL and contralateral (CL) nostrils for analysis of total protein, albumin, glycoconjugates, and lysozyme. Results: In both groups, BK induced significant dose-dependent IL total protein and albumin secretion, but significantly more total protein and albumin were stimulated in normal than rhinitis subjects after 1,000 nmol BK. Glycoconjugate and lysozyme secretion was not significantly stimulated on either the IL or CL sides in normal subjects. However, in perennial allergic subjects, BK stimulated significant, dose-dependent glycoconjugate and lysozyme secretion on the IL side. Reflex effects were studied on the CL side. Normal subjects did not have significant CL glandular secretion. In contrast, rhinitis subjects secreted significantly higher amounts of total protein and glycoconjugate on the CL side after 1,000 nmol BK. There was no reflex-mediated albumin exudation in either group. Conclusions: These results indicate that in normal subjects BK stimulates predominantly vascular permeability, and that cholinergic reflexes do not significantly contribute to their BK-induced nasal secretion. In rhinitis subjects, BK again induced albumin exudation, but with less vascular permeability and greater glandular secretion than normal subjects on the challenged side. Only rhinitis subjects demonstrated significant contralateral reflex-mediated glandular secretion, and this response required the highest dose of BK. This suggests that BK is more adept at directly inducing vascular effects than glandular secretion of nociceptive nerve-parasympathetic reflexes. Alterations in BK-induced vascular permeability, glandular secretion, and neural reflexes occur in patients with severe perennial allergic rhinitis, changes suggestive of nasal hyperresponsiveness' to BK. C1 NIAID, CLIN INVEST LAB, ALLERG DIS SECT, BETHESDA, MD 20892 USA. NATL HEART & LUNG INST, LONDON, ENGLAND. RP GEORGETOWN UNIV, DIV RHEUMATOL IMMUNOL & ALLERGY, GL-020 GORMAN BLDG, 3800 RESERVOIR RD, WASHINGTON, DC 20007 USA. NR 36 TC 40 Z9 43 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-2438 EI 1423-0097 J9 INT ARCH ALLERGY IMM JI Int. Arch. Allergy Immunol. PY 1994 VL 103 IS 2 BP 202 EP 208 PG 7 WC Allergy; Immunology SC Allergy; Immunology GA MV212 UT WOS:A1994MV21200013 PM 8292908 ER PT J AU HIRANO, H SCREATON, GR BELL, MV JACKSON, DG BELL, JI HODES, RJ AF HIRANO, H SCREATON, GR BELL, MV JACKSON, DG BELL, JI HODES, RJ TI CD44 ISOFORM EXPRESSION MEDIATED BY ALTERNATIVE SPLICING - TISSUE-SPECIFIC REGULATION IN MICE SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE ALTERNATIVE SPLICING; CD44 ISOFORM ID LYMPHOCYTE HOMING RECEPTOR; T-CELL ACTIVATION; HYALURONIC-ACID; MONOCLONAL-ANTIBODIES; MOLECULAR-CLONING; B-CELLS; ANTIGEN; GLYCOPROTEIN; RECOGNITION; ADHESION AB CD44 is a widely distributed cell surface glycoprotein which shows heterogeneity in molecular expression as a result of post-translational modification as well as alternative splicing of CD44 mRNA. Functional studies have indicated that CD44 plays a role as an adhesion molecule and that different CD44-expressing cells differ in their capacities for CD44-dependent ligand binding. These observations have raised the possibility that structural modifications of CD44, including those resulting from alternatively spliced mRNA isoforms, are involved in the functional heterogeneity of CD44. To assess the expression of CD44 isoforms in the mouse, we examined CD44 cDNA by reverse transcription polymerase chain reaction (RT-PCR). Southern blotting of PCR products with a CD44 cDNA probe or with internal oligonucleotides revealed the expression in mouse tumor cell lines and normal tissues of multiple CD44 mRNA products which are larger than that observed in the absence of variable exon expression. Interestingly, different mouse tissues, including lymphoid cells, showed unique patterns of alternative CD44 mRNA in Southern blotting analysis. The use of exon-specific primers allowed detection of multiple alternatively spliced mRNA species involving expression of at least seven variable exons. Cloning and sequencing of these PCR products revealed sequence identity with recently identified genomic CD44 sequences and confirmed that the PCR products correspond to mature mRNA expressing alternatively spliced CD44 exons. Taken together, these findings demonstrate that the mouse expresses multiple variably spliced CD44 isoforms and that expression is regulated in a tissue- and cell-type specific manner. C1 JOHN RADCLIFFE HOSP,INST MOLEC MED,MOLEC IMMUNOL GRP,OXFORD OX3 9DU,ENGLAND. RP HIRANO, H (reprint author), NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892, USA. NR 47 TC 38 Z9 39 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD JAN PY 1994 VL 6 IS 1 BP 49 EP 59 DI 10.1093/intimm/6.1.49 PG 11 WC Immunology SC Immunology GA MV369 UT WOS:A1994MV36900006 PM 7511928 ER PT J AU LINDBERG, DAB AF LINDBERG, DAB TI GLOBAL INFORMATION INFRASTRUCTURE SO INTERNATIONAL JOURNAL OF BIO-MEDICAL COMPUTING LA English DT Article; Proceedings Paper CT Working Conference on the Health Care Professional Workstation CY JUN 14-16, 1993 CL WASHINGTON, DC SP INT MED INFORMATICS ASSOC DE HIGH-PERFORMANCE-COMPUTING-AND-COMMUNICATIONS-PROGRAM (HPCC); NATIONAL INFORMATION INFRASTRUCTURE; NATIONAL-LIBRARY-OF-MEDICINE (NLM); OUTREACH PROJECTS; FEDERAL INITIATIVES; NATIONAL-INSTITUTES-OF-HEALTH (NIH) AB The High Performance Computing and Communications Program (HPCC) is a multiagency federal initiative under the leadership of the White House office of Science and Technology Policy, established by the High Performance Computing Act of 1991. It has been assigned a critical role in supporting the international collaboration essential to science and to health care. Goals of the HPCC are to extend USA leadership in high performance computing and networking technologies; to improve technology transfer for economic competitiveness, education, and national security; and to provide a key part of the foundation for the National Information Infrastructure. The first component of the National Institutes of Health to participate in the HPCC, the National Library of Medicine (NLM), recently issued a solicitation for proposals to address a range of issues, from privacy to 'testbed' networks, 'virtual reality,' and more. These efforts will build upon the NLM's extensive outreach program and other initiatives, including the Unified Medical Language System (UMLS), MEDLARS, and Grateful Med. New Internet search tools are emerging, such as Gopher and 'Knowbots'. Medicine will succeed in developing future intelligent agents to assist in utilizing computer networks. Our ability to serve patients is so often restricted by lack of information and knowledge at the time and place of medical decision-making. The new technologies, properly employed, will also greatly enhance our ability to serve the patient. RP LINDBERG, DAB (reprint author), NATL LIB MED,8600 ROCKVILLE PIKE,38A-B1N30,BETHESDA,MD 20894, USA. NR 6 TC 19 Z9 21 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0020-7101 J9 INT J BIOMED COMPUT JI Int. J. Bio-Med. Comput. PD JAN PY 1994 VL 34 IS 1-4 BP 13 EP 19 DI 10.1016/0020-7101(94)90006-X PG 7 WC Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Engineering, Biomedical; Medical Informatics SC Computer Science; Engineering; Medical Informatics GA MQ423 UT WOS:A1994MQ42300003 PM 8125625 ER PT J AU ESTERHAY, RJ AF ESTERHAY, RJ TI USER METAPHORS FOR HEALTH-CARE PROFESSIONAL WORKSTATIONS SO INTERNATIONAL JOURNAL OF BIO-MEDICAL COMPUTING LA English DT Article; Proceedings Paper CT Working Conference on the Health Care Professional Workstation CY JUN 14-16, 1993 CL WASHINGTON, DC SP INT MED INFORMATICS ASSOC DE MEDICAL RECORDS; DATABASES; DECISION SUPPORT; INFORMATION SYSTEMS; MODELS; STANDARDS ID 3-DIMENSIONAL CT; INTERFACE AB The problem encountered by health care professionals and software developers has been a lack of demonstrable visions (prototypes) for Computer-based Patient Record (CPR) and Clinical Information System (CIS) applications. This deficiency has resulted in a quest for and consideration of models, metaphors, and mind maps for the Healthcare Professional Workstation (HPW) - the access mechanism for the CPR and the CIS. The familiar physician desktop and traditional paper-based metaphors are not adequate for all aspects of clinical information processes. In the clinical care environment, the flowsheet is a transporting metaphor because many different applications and tasks can be 'transported' into the flowsheet. 3D Rooms, Gopher and Genes are familiar and transporting metaphors to be exploited for HPWs. Using transporting metaphors for HPW software emphasizes commonality and de-emphasizes diversity. Each model and metaphor has an associated mind map. Only the mental model, mental metaphor or mind map for HPW software is important. Metaphors communicate real-world analogies, and communication is at the core of what defines usability. A mind map facilitates communication by building a model in the user's mind. The barriers to HPWs are not technical; they are related to economics, ownership of patient information, liability and information standards. RP ESTERHAY, RJ (reprint author), NCI,CTR INT CANC INFORMAT,COMP COMMUN BRANCH,BETHESDA,MD 20892, USA. NR 19 TC 2 Z9 2 U1 1 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0020-7101 J9 INT J BIOMED COMPUT JI Int. J. Bio-Med. Comput. PD JAN PY 1994 VL 34 IS 1-4 BP 95 EP 113 DI 10.1016/0020-7101(94)90013-2 PG 19 WC Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Engineering, Biomedical; Medical Informatics SC Computer Science; Engineering; Medical Informatics GA MQ423 UT WOS:A1994MQ42300010 PM 8125658 ER PT J AU ORTHNER, HF SCHERRER, JR DAHLEN, R AF ORTHNER, HF SCHERRER, JR DAHLEN, R TI SHARING AND COMMUNICATING HEALTH-CARE INFORMATION - SUMMARY AND RECOMMENDATIONS SO INTERNATIONAL JOURNAL OF BIO-MEDICAL COMPUTING LA English DT Article; Proceedings Paper CT Working Conference on the Health Care Professional Workstation CY JUN 14-16, 1993 CL WASHINGTON, DC SP INT MED INFORMATICS ASSOC DE COMMUNICATIONS; OPEN SYSTEMS; EXCHANGE STANDARDS; VOCABULARIES; CLIENT SERVER ARCHITECTURES; INFORMATION INFRASTRUCTURE AB Sharing and communicating information is a fundamental task in modern medicine. The health care system of the western world is based on teamwork of professionals who participate in the care of patients. Exchange of information (not just data) requires the communicating parties to agree on a communication channel, an exchange protocol, and a common language. The language includes an alphabet, words, phrases, and symbols that express and assign meaning, understood by all. The most common forms of communication are the spoken word and the paper-based patient record. Computers and communication systems improve the sharing of health care information by overcoming the limitations imposed by the dimensions of time and location. However, natural language is still too complex and too ambiguous for current computing devices to handle the complex interactions between health care professional and patients. A simpler 'language' is needed that uses domain specific vocabularies (and/or codes), well-defined exchange protocols for data, information, knowledge, and, in the future, perhaps even wisdom. This simpler 'language' is expected to handle most of the routine information exchange but not eliminate natural language. It is essential that health care information systems preserve and incorporate natural language expressions and integrate them with structured vocabularies. Today, agreeing on standard data exchange protocols and domain specific vocabularies and codes is our greatest challenge. However, standards alone are not sufficient. Acceptance of the standards by the health care professionals, verifications in clinical environments, and implementation agreements by the medical informatics industry are essential. The group on 'Sharing and Communication of Health Care Information' addressed the issues raised above and unanimously recommends a number of steps that will improve the sharing of information. In addition, specific recommendations are offered to governments; health care institutions, and to developers of health care information systems. C1 GENEVA CANTON UNIV HOSP,GENEVA,SWITZERLAND. NIH,NATL LIB MED,DHHS,BETHESDA,MD 20892. RP ORTHNER, HF (reprint author), GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037, USA. NR 33 TC 10 Z9 10 U1 0 U2 8 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0020-7101 J9 INT J BIOMED COMPUT JI Int. J. Bio-Med. Comput. PD JAN PY 1994 VL 34 IS 1-4 BP 303 EP 318 DI 10.1016/0020-7101(94)90030-2 PG 16 WC Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Engineering, Biomedical; Medical Informatics SC Computer Science; Engineering; Medical Informatics GA MQ423 UT WOS:A1994MQ42300027 PM 8125644 ER PT J AU LAWLOR, BA RADCLIFFE, J MOLCHAN, SE MARTINEZ, RA HILL, JL SUNDERLAND, T AF LAWLOR, BA RADCLIFFE, J MOLCHAN, SE MARTINEZ, RA HILL, JL SUNDERLAND, T TI A PILOT PLACEBO-CONTROLLED STUDY OF TRAZODONE AND BUSPIRONE IN ALZHEIMERS-DISEASE SO INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article DE PILOT STUDY; CLINICAL TRIAL; TRAZODONE; BUSPIRONE; ALZHEIMERS DISEASE ID DEMENTIA; AGONIST; SCALE AB The pharmacological management of behavioural symptoms in Alzheimer's disease is limited by the dearth of effective agents in this area. The purpose of this study was to determine whether trazodone or buspirone are helpful in the treatment of behavioural disturbance in AD. Ten patients meeting NINCDS criteria for AD with behavioural complications were administered trazodone (up to 50 mg tid), buspirone (10 mg tid), and placebo in a 12-week double-blind, crossover design. Outcome measures were the Brief Psychiatric Rating Scale (BPRS), the Dementia Mood Assessment Scale (DMAS), and the Buschke Selective Reminding Task. The data were analysed by ANOVA. Compared to placebo, trazodone produced a small but significant reduction in BPRS and DMAS scores (p<0.05), indicating improvement in behaviour but no change in cognitive measures. In contrast, buspirone has no significant effect on either behavioural or cognitive measures compared to placebo. The results of this pilot study suggest a beneficial role for trazodone, but not buspirone, in the treatment of behavioural disturbance in AD. Further studies using a wider range of doses of trazodone in more behaviourally disturbed AD patients should now be initiated in an attempt to replicate and expand on this preliminary finding. C1 NIMH,CLIN SCI LAB,GERIATR PSYCHIAT SECT,BETHESDA,MD 20892. RP LAWLOR, BA (reprint author), ST JAMES HOSP,OLD AGE PSYCHIAT SECT,DUBLIN 8,IRELAND. NR 24 TC 50 Z9 51 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0885-6230 J9 INT J GERIATR PSYCH JI Int. J. Geriatr. Psychiatr. PD JAN PY 1994 VL 9 IS 1 BP 55 EP 59 DI 10.1002/gps.930090112 PG 5 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA MT416 UT WOS:A1994MT41600011 ER PT J AU MUNTANER, C SCHOENBACH, C AF MUNTANER, C SCHOENBACH, C TI PSYCHOSOCIAL WORK-ENVIRONMENT AND HEALTH IN UNITED-STATES METROPOLITAN-AREAS - A TEST OF THE DEMAND-CONTROL AND DEMAND-CONTROL-SUPPORT MODELS SO INTERNATIONAL JOURNAL OF HEALTH SERVICES LA English DT Article ID CORONARY HEART-DISEASE; JOB DECISION LATITUDE; OCCUPATIONAL CHARACTERISTICS; CARDIOVASCULAR-DISEASE; STRAIN; SCHIZOPHRENIA; ORGANIZATION; PERSONALITY; PSYCHOLOGY; REDESIGN AB The authors use confirmatory factor analysis to investigate the psychosocial dimensions of work environments relevant to health outcomes, in a representative sample of five U.S. metropolitan areas. Through an aggregated inference system, scales from Schwartz and associates' job scoring system and from the Dictionary of Occupational Titles (DOT) were employed to examine two alternative models: the demand-control model of Karasek and Theorell and Johnson's demand-control-support model. Confirmatory factor analysis was used to test the two models. The two multidimensional models yielded better fits than an unstructured model. After allowing for the measurement error variance due to the method of assessment (Schwartz and associates' system or DOT), both models yielded acceptable goodness-of-fit indices, but the fit of the demand-control-support model was significantly better. Overall these results indicate that the dimensions of Control (substantive complexity of work, skill discretion, decision authority), Demands (physical exertion, physical demands and hazards), and Social Support (coworker and supervisor social supports) provide an acceptable account of the psychosocial dimensions of work associated with health outcomes. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. RP MUNTANER, C (reprint author), NIH,FED BLDG,ROOM B1A-12,7550 WISCONSIN AVE,BETHESDA,MD 20892, USA. RI Muntaner, C/A-5043-2010 FU NIMH NIH HHS [MH47447] NR 52 TC 17 Z9 18 U1 1 U2 8 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0020-7314 J9 INT J HEALTH SERV JI Int. J. Health Serv. PY 1994 VL 24 IS 2 BP 337 EP 353 DI 10.2190/3LYE-Q9W1-FHWJ-Y757 PG 17 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA NF101 UT WOS:A1994NF10100008 PM 8034396 ER PT J AU SEIDELL, JC ANDRES, R SORKIN, JD MULLER, DC AF SEIDELL, JC ANDRES, R SORKIN, JD MULLER, DC TI THE SAGITTAL WAIST DIAMETER AND MORTALITY IN MEN - THE BALTIMORE-LONGITUDINAL-STUDY-ON-AGING SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE OBESITY; FAT DISTRIBUTION; MORTALITY; CARDIOVASCULAR DISEASE; AGING ID CORONARY HEART-DISEASE; INTRAABDOMINAL FAT ACCUMULATION; CARDIOVASCULAR-DISEASE; COMPUTED-TOMOGRAPHY; ADIPOSE-TISSUE; BODY-FAT; BLOOD-PRESSURE; EUROPEAN MEN; RISK-FACTORS; OBESITY AB The study objective was to determine the relationship between the abdominal sagittal diameter (waist depth) and subsequent mortality. This was a prospective study carried out in 981 male participants of the Baltimore Longitudinal Study on Aging which is a prospective study at the National Institute on Aging in Baltimore. The main outcome measures of the study were total and cause-specific mortality occurring during 17529 person-years. The men were divided by age (cut-off point 55 years) at the start of follow-up. All-cause and coronary heart disease mortality rates (adjusted for age, height and body mass index) increased with increasing sagittal diameter in the younger group but not in the older group. No significant relationship was observed between the sagittal diameter and cancer mortality. Body mass index, skinfolds and waist/hip ratio were not significantly related to any of the endpoints studied. The increased risk of mortality with increasing sagittal diameter was somewhat stronger when the first ten years of follow-up were excluded and was more pronounced at lower levels of risk factors such as serum cholesterol, serum triglycerides, plasma glucose and diastolic blood pressure and in never plus ex-smokers compared to smokers. The study indicates that the abdominal sagittal diameter is a strong predictor of mortality in younger adult men independently of age, height, body mass index and conventional risk factors for mortality such as smoking, serum lipids and blood pressure. Regional adiposity may be a less strong risk factor for mortality in older men. C1 NIA,GERONTOL RES CTR,CLIN PHYSIOL LAB,BALTIMORE,MD 21224. RP SEIDELL, JC (reprint author), NATL INST PUBL HLTH & ENVIRONM PROTECT,DEPT CHRON DIS & ENVIRONM EPIDEMIOL,POB 1,3720 BA BILTHOVEN,NETHERLANDS. RI seidell, jacob/N-7427-2013 NR 35 TC 70 Z9 71 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD JAN PY 1994 VL 18 IS 1 BP 61 EP 67 PG 7 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA MQ400 UT WOS:A1994MQ40000009 PM 8130817 ER PT J AU PRINCIPE, P BROQUET, C PAULL, K GREVER, MR COULOMB, H HUCHET, M MENCIAHUERTA, JM BRAQUET, P AF PRINCIPE, P BROQUET, C PAULL, K GREVER, MR COULOMB, H HUCHET, M MENCIAHUERTA, JM BRAQUET, P TI NEW ANTINEOPLASTIC AZA-PHOSPHOLIPIDS - SYNTHESIS, IN-VITRO CYTOTOXICITY AND DIFFERENTIAL CELLULAR-SENSITIVITY AGAINST 70 HUMAN TUMOR-CELL LINES SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE AZA-PHOSPHOLIPIDS; CYTOTOXICITY; HUMAN TUMOR CELL LINES; CELL DIFFERENTIAL SENSITIVITY ID MEMBRANE CHOLESTEROL CONTENT; ETHER LIPIDS; ALKYL-LYSOPHOSPHOLIPIDS; TETRAZOLIUM ASSAY; NEOPLASTIC-CELLS; DIVERSE PANEL; ANALOGS; FEASIBILITY; DRUGS AB The in vitro cytotoxicity and differential cellular sensitivity of three new synthetic anti-neoplastic aza-phospholipids has been determined in the National Cancer Institute's (NCI) primary antitumor drug screen. Based on a disease-oriented strategy, this screen incorporates seventy human cell lines representing leukemia, ovarian, brain, melanoma, colon, renal, lung, prostate and breast cancers. The analysis of the GI50 values obtained for each aza-derivative has revealed a differential cellular sensitivity among the cell lines examined. The study of the degree of differential growth inhibition has shown a statistically significant differential cell sensitivity for BN 52205 and BN 52211 for colon and melanoma tumor cells. The leukemia cell selectivity for BN 52211 was even more remarkable due to the low molar concentration at which the maximum selective effect occurred. These findings strongly encourage further investigations on the anti-neoplastic activity of aza-phospholipids. C1 NCI, DEPT HLTH & HUMAN SERV, BETHESDA, MD 20892 USA. RP PRINCIPE, P (reprint author), INST HENRI BEAUFOUR, 1 AVE TROP, F-91952 LES ULIS, FRANCE. NR 29 TC 4 Z9 4 U1 0 U2 0 PU SPANDIDOS PUBL LTD PI ATHENS PA POB 18179, ATHENS, 116 10, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1994 VL 4 IS 1 BP 29 EP 36 PG 8 WC Oncology SC Oncology GA MN493 UT WOS:A1994MN49300005 PM 21566885 ER PT J AU OLIVERO, OA BELAND, FA POIRIER, MC AF OLIVERO, OA BELAND, FA POIRIER, MC TI IMMUNOFLUORESCENT LOCALIZATION AND QUANTITATION OF 3'-AZIDO-2',3'-DIDEOXYTHYMIDINE (AZT) INCORPORATED INTO CHROMOSOMAL DNA OF HUMAN, HAMSTER AND MOUSE-CELL LINES SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE 3'-AZIDO-2',3'-DIDEOXYTHYMIDINE; AZT; IMMUNOFLUORESCENCE; RADIOIMMUNOASSAY; CHROMOSOMES ID VIRUS REVERSE-TRANSCRIPTASE; AZIDOTHYMIDINE TRIPHOSPHATE; POLYMERASE-ALPHA; 3'-AZIDO-3'-DEOXYTHYMIDINE; REPLICATION; 5'-TRIPHOSPHATE; PHARMACOLOGY; ZIDOVUDINE; TELOMERASE; ANALOGS AB The incorporation of [H-3] AZT into the DNA of cultured hamster (Chinese hamster ovary, CHO) mouse (NIH 3T3) and human (HL60) cells, was studied by radiolabeling, radioimmunoassay, and localization of the drug in chromosomes by immunohistochemistry. Incorporation of AZT into DNA, in cells exposed to 0.8 mM [H-3] AZT for 24 hours, showed values of 0.82 pmol/mug DNA for HL60, 0.84 pmol/mug DNA for CHO and 4.49 pmol/mug for NIH 3T3 cells. Similar results were obtained by radioimmunoassay with an anti-AZT antibody. Indirect immunofluorescence using the same anti-AZT antiserum demonstrated the chromosomal localization of AZT and showed higher concentrations of AZT in the telomeric regions of CHO cell chromosomes. C1 NATL CTR TOXICOL RES,DIV BIOCHEM TOXICOL,JEFFERSON,AR 72079. RP OLIVERO, OA (reprint author), NCI,CELLULAR CARCINOGENESIS & TUMOR PROMO LAB,BLDG 37,ROOM 3B12,BETHESDA,MD 20892, USA. NR 24 TC 31 Z9 31 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1994 VL 4 IS 1 BP 49 EP 54 PG 6 WC Oncology SC Oncology GA MN493 UT WOS:A1994MN49300008 PM 21566888 ER PT J AU JUN, SH THOMPSON, EW GOTTARDIS, M TORRI, J YAMAMURA, K KIBBEY, MC KIM, WH KLEINMAN, HK AF JUN, SH THOMPSON, EW GOTTARDIS, M TORRI, J YAMAMURA, K KIBBEY, MC KIM, WH KLEINMAN, HK TI LAMININ ADHESION-SELECTED PRIMARY HUMAN COLON-CANCER CELLS ARE MORE TUMORIGENIC THAN THE PARENTERAL AND NONADHERENT CELLS SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE BASEMENT MEMBRANE; LAMININ; COLON CANCER ID HUMAN PROSTATIC-CARCINOMA; TUMOR-GROWTH; BASEMENT-MEMBRANE; EXTRACELLULAR-MATRIX; COLLAGENASE-IV; MESSENGER-RNA; ATHYMIC MICE; METASTASIS; ANGIOGENESIS; INHIBITION AB Laminin has been shown to promote the malignant phenotype and the level of the 32/67 Kd laminin receptor has been found to correlate with Dukes' staging of colon cancer. A biopsy of a Dukes' stage B2 human colon carcinoma formed a tumor in a nude mouse after coinjection with Matrigel. The parental tumor and the murine tumor appeared identical at the histological level. A cell line LCC-C1 was established from the murine tumor. The cell line appeared moderately differentiated although it did not produce mucin in vitro; however, the xenograft in vivo did produce low levels of mucin. Laminin adherent and non-adherent cell lines were selected. The parental and the laminin-selected cell subclones adhered equally well to plastic and to fibronectin and showed similar growth rates on plastic. When injected subcutaneously into nude mice, the laminin-adherent cells formed relatively undifferentiated tumors that were twice as large as the parental cell tumors whereas the laminin non adherent cells formed very small, but highly differentiated tumors. These data demonstrate that subpopulations of tumor cells which differ in their tumorigenic properties can be selected based on their adhesion to laminin and thus provide models for studying the mechanisms of tumor growth. C1 GEORGETOWN UNIV,SCH MED,LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. GEORGETOWN UNIV,SCH MED,DEPT ANAT & CELL BIOL,WASHINGTON,DC 20007. RP JUN, SH (reprint author), NIDR,DEV BIOL LAB,BLDG 30,ROOM 407,BETHESDA,MD 20892, USA. RI Kim, Wooho/G-3703-2011; Thompson, Erik/A-1425-2009 OI Thompson, Erik/0000-0002-9723-4924 NR 26 TC 12 Z9 12 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1994 VL 4 IS 1 BP 55 EP 60 PG 6 WC Oncology SC Oncology GA MN493 UT WOS:A1994MN49300009 PM 21566889 ER PT J AU SHKLAR, G SCHWARTZ, J AF SHKLAR, G SCHWARTZ, J TI A COMMON PATHWAY FOR THE DESTRUCTION OF CANCER-CELLS - EXPERIMENTAL-EVIDENCE AND CLINICAL IMPLICATIONS SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Review DE CHEMOPREVENTATIVES; CAROTENOIDS; RETINOIDS; TOCOPHEROLS ID HAMSTER BUCCAL POUCH; GLUTAMYL-TRANSFERASE TRANSPEPTIDASE; EXPERIMENTAL ORAL CARCINOGENESIS; ACID-RESPONSIVE ELEMENT; BETA-CAROTENE; VITAMIN-E; ALPHA-TOCOPHEROL; RETINOIC ACID; LUNG-CANCER; CHEMICAL CARCINOGENESIS AB Chemopreventatives derived from different classes of chemical inhibit the growth of various cancers. This review concentrates on the chemopreventative activities of carotenoids, retinoids, and tocopherols. In this review we outline a common pathway for the antitumor action of chemopreventative agents. To establish this pathway we reviewed previous in vivo and in vitro studies indicating that the underlying modes of actions for chemopreventative activities were oxidative-reduction changes that developed in the tumor cell. Some of these changes were selective and did not appear in normal cells. The oxidative redox characteristics of the agents interacted with the oxidative redox systems of the tumor cell. Many chemopreventative agents are highly hydrophobic and interact with thiol peptides, and/or metalloproteins, such as glutathione reductase, superoxide dismutases, or flavoproteins. These could then become linked to prenylated membrane associated protein complexes or oxidized proteins. Interactions of the chemopreventative agents with these proteins can result in changes in expression of transcription factors nuclear binding proteins, such as, heat shock proteins (hsps) and p53. Dramatic reductions in mutant p53 and increased expression of wild type (antioncogene) p53 protein product has been associated with some chemopreventative agent inhibition of oral carcinogenesis. Enhanced hsp 70 and 90 expression has also been observed. These changes in protein expression occurred early during the process of oral carcinogenesis. The tumor cells accumulated in GO/G1 of the cell cycle and the induction of some apoptotic like changes (programmed cell death) were noted. Cell to cell communication and differentiation has also been increased with carotenoid, retinoid, and tocopherol treatment of transformed cells. Enhanced cytotoxic responses by macrophages and T lymphocytes at developing tumor sites were found to produce the oxygen reactive cytokine, tumor necrosis factor. The experimental evidence and hypothesized common pathway of antitumor action for chemoprevention may point to possible biomarkers that could be utilized in clinical intervention trials. C1 NIDR, DIV MOLEC EPIDEMIOL, ORAL DIS & PREVENT PROGRAM, BETHESDA, MD 20892 USA. RP SHKLAR, G (reprint author), HARVARD UNIV, SCH DENT MED, DEPT ORAL MED & DIAGNOST SCI, DIV ORAL PATHOL, 188 LONGWOOD AVE, BOSTON, MA 02115 USA. NR 125 TC 15 Z9 15 U1 0 U2 1 PU SPANDIDOS PUBL LTD PI ATHENS PA POB 18179, ATHENS, 116 10, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1994 VL 4 IS 1 BP 215 EP 224 PG 10 WC Oncology SC Oncology GA MN493 UT WOS:A1994MN49300036 PM 21566916 ER PT J AU RUSSELL, KJ CAPLAN, RJ LARAMORE, GE BURNISON, CM MAOR, MH TAYLOR, ME ZINK, S DAVIS, LW GRIFFIN, TW AF RUSSELL, KJ CAPLAN, RJ LARAMORE, GE BURNISON, CM MAOR, MH TAYLOR, ME ZINK, S DAVIS, LW GRIFFIN, TW TI PHOTON VERSUS FAST-NEUTRON EXTERNAL-BEAM RADIOTHERAPY IN THE TREATMENT OF LOCALLY ADVANCED PROSTATE-CANCER - RESULTS OF A RANDOMIZED PROSPECTIVE TRIAL SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE PROSTATE CANCER; NEUTRONS; RADIOTHERAPY ID MEGAVOLTAGE RADIATION-THERAPY; POST-IRRADIATION BIOPSY; METASTATIC DISSEMINATION; CARCINOMA; ADENOCARCINOMA; PROGNOSIS AB Purpose: To evaluate the effectiveness of fast neutron radiation therapy in treatment of locally advanced carcinomas of the prostate. Methods and Materials: From April 1986 to October 1990, 178 patients were entered on a prospective, multi-institutional randomized study of the NCI-sponsored Neutron Therapy Collaborative Working Group. This trial compared external beam photon irradiation (7000-7020 cGy) with external beam neutron irradiation (2040 ncGy) for patients with high-grade T-2 or T-3-4 N-0-1, M(0) adenocarcinomas of the prostate. Eighty-nine patients were randomized to each treatment. Six patients were subsequently judged to be ineligible, leaving 85 photon and 87 neutron randomized patients eligible for analysis. Results: With a follow-up time ranging from 40 to 86 months (68 months median follow-up) the 5-year actuarial clinical local-regional failure rate for patients treated with neutrons was 11%, vs. 32% for photons (p < 0.01). Incorporating the results of routine posttreatment prostate biopsies, the resulting ''histological'' local-regional tumor failure rates were 13% for neutrons vs. 32% for photons (p = 0.01). To date, actuarial survival and cause-specific survival rates are statistically indistinguishable for the two patient cohorts, with 32% of the neutron-treated patient deaths and 41% of the photon-treated patient deaths caused by prostate cancer (p = n.s.). Prostate specific antigen (PSA) values were elevated in 17% of neutron-treated patients and 45% of photon-treated patients at 5 years (p < 0.001). Severe late complications of treatment were higher for the neutron-treated patients (11% vs. 3%), and were inversely correlated with the degree of neutron beam shaping available at the participating institutions. Neutron treatment delivery utilizing a fully rotational gantry and multileaf collimator did not result in an increase in severe late effects when compared to photon treatment. Conclusion: High energy fast neutron radiotherapy is safe and effective when adequate beam delivery systems and collimation are available, and it is significantly superior to external beam photon radiotherapy in the local-regional treatment of large prostate tumors. C1 UNIV WASHINGTON,MED CTR,DEPT RADIAT ONCOL,SEATTLE,WA 98195. RADIAT THERAPY ONCOL GRP,CTR STAT,PHILADELPHIA,PA. UNIV CALIF LOS ANGELES,DEPT RADIAT ONCOL,LOS ANGELES,CA 90024. MD ANDERSON HOSP,DEPT RADIAT ONCOL,HOUSTON,TX. CLEVELAND CLIN,DEPT RADIAT ONCOL,CLEVELAND,OH. NCI,RADIAT RES PROGRAM,BETHESDA,MD. EMORY UNIV,DEPT RADIAT ONCOL,ATLANTA,GA. NR 28 TC 88 Z9 89 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 1 PY 1994 VL 28 IS 1 BP 47 EP 54 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA MP353 UT WOS:A1994MP35300007 PM 8270459 ER PT J AU WALKER, RD HOWARD, MO SUCHINSKY, R KAPLE, J ANDERSON, B AF WALKER, RD HOWARD, MO SUCHINSKY, R KAPLE, J ANDERSON, B TI DRUG-DEPENDENCE TREATMENT WITHIN THE DEPARTMENT-OF-VETERANS-AFFAIRS - EMERGING ISSUES SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Article DE DRUG DEPENDENCE TREATMENT; SUBSTANCE ABUSE TREATMENT; DEPARTMENT-OF-VETERANS-AFFAIRS; VETERANS-ADMINISTRATION ID SUBSTANCE-ABUSE TREATMENT; TREATMENT PROGRAM; OPIOID ADDICTS; MEDICAL-CENTER; ALCOHOL; SERVICES; SEVERITY; COCAINE; CARE; AIDS AB The Department of Veterans Affairs is the largest provider of drug dependence treatment services in the United States. However, a national evaluation of primarily drug-dependent veterans has never been reported. Findings from the Drug Abuse Treatment Services Evaluation Project, a three-year investigation of drug dependence treatment within the Department of Veterans Affairs, are discussed. Demographic and diagnostic data are presented for the population of 46,047 inpatients discharged with drug dependence diagnoses in Fiscal Year 1991. Patient subtypes and clinical issues of growing relevance to the treatment of drug-dependent veterans are discussed. C1 VET AFFAIRS MED CTR,CTR ADDICT TREATMENT,1660 S COLUMBIAN WAY,SEATTLE,WA 98108. UNIV WASHINGTON,DEPT PSYCHIAT & BEHAV SCI,SEATTLE,WA 98195. DEPT VET AFFAIRS,CENT OFF,MENTAL HLTH & BEHAV SCI SERV,WASHINGTON,DC. NIDA,ROCKVILLE,MD. FU ONDIEH CDC HHS [RA-ND-90-37] NR 44 TC 5 Z9 5 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1994 VL 29 IS 1 BP 53 EP 69 PG 17 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA MR833 UT WOS:A1994MR83300004 PM 8144269 ER PT J AU ALLEN, JP FERTIG, JB TOWLE, LH ALTSHULER, VB VRUBLEVSKY, AG VALENTIK, YV ZANIS, DA AF ALLEN, JP FERTIG, JB TOWLE, LH ALTSHULER, VB VRUBLEVSKY, AG VALENTIK, YV ZANIS, DA TI PSYCHOMETRIC ANALYSES OF THE ALCOHOL DEPENDENCE SCALE AMONG UNITED-STATES AND RUSSIAN CLINICAL-SAMPLES SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Article DE ALCOHOL DEPENDENCE SCALE; ALCOHOL DEPENDENCE SYNDROME; ALCOHOLISM; CROSS CULTURAL; FACTOR ANALYSIS; RUSSIAN ID VALIDATION; INSTRUMENT AB This project explores the cross-national construct validity of the Alcohol Dependence Syndrome. The investigation also examines basic psychometric properties of the Alcohol Dependence Scale (ADS), an instrument commonly employed to measure dependence. Subjects consisted of inpatients and outpatients in American and Russian alcoholism treatment programs. Despite some variations, an orthogonal four factor structure of the ADS appears similar across the two cultural samples, thus lending support to the alcohol dependence construct. Analyses of psychometric properties of the Scale generally support its value in future cross-cultural research on alcohol dependence. C1 STATE RES CTR ADDICT,MOSCOW,RUSSIA. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. RP ALLEN, JP (reprint author), NIAAA,TREATMENT RES BRANCH,14C20,5600 FISHERS LANE,ROCKVILLE,MD 20852, USA. NR 20 TC 14 Z9 14 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1994 VL 29 IS 1 BP 71 EP 87 PG 17 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA MR833 UT WOS:A1994MR83300005 PM 8144270 ER PT J AU BROWN, BS NEEDLE, RH AF BROWN, BS NEEDLE, RH TI MODIFYING THE PROCESS OF TREATMENT TO MEET THE THREAT OF AIDS SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Article DE AIDS; OUTREACH; AFTERCARE; DRUG TREATMENT; DRUG POLICY ID HIV AB Treatment for drug users is unlikely to receive sufficient resources to expand to the level of treatment need. Moreover, there is indication that a substantial minority of injection drug users have never initiated needed treatment in spite of long histories of injecting drugs. Given the potential for that population to contract and spread AIDS, it is important that we explore street-based treatment alternatives derived from findings regarding the efficacy of outreach/intervention programs. Those programs were found both to reduce drug-taking behaviors of injecting drug users and to prepare those users for clienthood. Additional strategies that need to be explored include: aftercare, behavioral counseling for sex partners of drug treatment clients, and partial (i.e., survival) treatment services for clients who cannot be accommodated within existing treatment capacity. C1 TEXAS CHRISTIAN UNIV,INST BEHAV RES,FT WORTH,TX. NIDA,LEXINGTON,KY. RP BROWN, BS (reprint author), UNIV N CAROLINA,DEPT PSYCHOL,601 S COLL RD,WILMINGTON,NC 28403, USA. NR 23 TC 22 Z9 22 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1994 VL 29 IS 13 BP 1739 EP 1752 PG 14 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA PU075 UT WOS:A1994PU07500002 PM 7852000 ER PT J AU CARMASSI, F DENEGRI, F MORALE, M PUCCETTI, R CHUNG, SI AF CARMASSI, F DENEGRI, F MORALE, M PUCCETTI, R CHUNG, SI TI ELASTASE-MEDIATED AND PLASMIN-MEDIATED FIBRINOLYSIS IN RHEUMATOID-ARTHRITIS SO INTERNATIONAL JOURNAL OF TISSUE REACTIONS-EXPERIMENTAL AND CLINICAL ASPECTS LA English DT Article ID LATENT COLLAGENASE; SYNOVIAL-CELLS; ACTIVATOR; PROTEASES; INHIBITOR; TISSUE; INVIVO; FLUID AB Selected coagulation and fibrinolytic factors were evaluated in plasma and synovial fluid (SF) of 10 rheumatoid arthritis (RA) patients, increased levels of fibrinogen were observed in plasma (p < 0.01), but only a trace amount of structurally intact fibrinogen was detected in the SF of RA patients, while immunostaining showed deposits of insoluble fibrin in their synovial membranes. Reduced levels of protein C, antithrombin III and coagulation factors II, V, VII, VIII, IX, XII and XIII (p < 0.01), and high levels of thrombin-antithrombin III (TAT) complexes (p < 0.01), were found in SF as compared to their corresponding plasma levels. The increased levels of fibrinogen, TAT complexes, B beta 15-42 peptide and plasminogen activator inhibitor-1 (PAI-1) in plasma (p < 0.01) are consistent with an enhanced fibrin turnover and endothelial perturbation due to a systemic inflammatory state. Plasminogen and alpha(2)-plasmin inhibitor activity in SF were significantly reduced as compared to the plasma levels (p < 0.01), whereas an increase in PAI-1 activity was found in SF as compared to plasma (p < 0.01). The detection of D-dimer and BP 15-42 peptide (p < 0.01) in SF suggests an involvement of plasmin in the degradation of fibrin generated in synovial tissue. The high levels of elastase-alpha(1)-proteinase inhibitor complexes and of thrombin-increasable fibrinopeptide A, as well as the pattern of fibrinogen degradation as identified in SF by double-dimension immunoelectrophoresis, suggest that elastase released from exudated granulocytes may play an important role in fibrino(geno)lysis and tissue damage in RA joints. C1 NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. RP CARMASSI, F (reprint author), UNIV PISA,IST CLIN MED 2,VIA ROMA 67,I-56126 PISA,ITALY. OI Carmassi, Franco/0000-0003-2244-4430 NR 17 TC 8 Z9 8 U1 0 U2 3 PU BIOSCIENCE EDIPRINT INC PI CAROUGE PA RUE ALEXANDRE-GAVARD 16, 1227 CAROUGE, SWITZERLAND SN 0250-0868 J9 INT J TISSUE REACT JI Int. J. Tissue React.-Exp. Clin. Asp. PY 1994 VL 16 IS 2 BP 89 EP 93 PG 5 WC Cell Biology SC Cell Biology GA NW209 UT WOS:A1994NW20900005 PM 7960505 ER PT J AU ELLWEIN, LB FLETCHER, A NEGREL, AD THULASIRAJ, RD AF ELLWEIN, LB FLETCHER, A NEGREL, AD THULASIRAJ, RD TI QUALITY-OF-LIFE ASSESSMENT IN BLINDNESS PREVENTION INTERVENTIONS SO INTERNATIONAL OPHTHALMOLOGY LA English DT Article DE EVALUATION; OUTCOMES; QUALITY OF LIFE; QUESTIONNAIRE; VISUAL FUNCTIONING ID CATARACT-SURGERY; HEALTH-STATUS; OF-LIFE; OUTCOMES; VISION AB This article discusses the importance of self-reported visual function and quality of life (QOL) assessment in evaluating the effectiveness of eye care and prevention of blindness interventions. Traditional clinical measurements do not provide an adequate characterization of the burden of visual disability faced by the patient in day-to-day activities. The validity, reliability and responsiveness of QOL questionnaires should be demonstrated before general use of such instruments is advocated. A visual function questionnaire currently undergoing psychometric evaluation as part of a clinical study of cataract surgery in India is presented. C1 LONDON SCH HYG & TROP MED,DEPT EPIDEMIOL & POPULAT SCI,LONDON WC1,ENGLAND. WHO,PROGRAMME PREVENT BLINDNESS,CH-1211 GENEVA,SWITZERLAND. ARAVIND EYE HOSP,MADURAI,TAMIL NADU,INDIA. RP ELLWEIN, LB (reprint author), NEI,BLDG 31 RM 6A04,BETHESDA,MD 20892, USA. NR 21 TC 14 Z9 14 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0165-5701 J9 INT OPHTHALMOL JI Int. Ophthalmol. PY 1994 VL 18 IS 5 BP 263 EP 268 PG 6 WC Ophthalmology SC Ophthalmology GA QR625 UT WOS:A1994QR62500003 PM 7607806 ER PT B AU BORNSTEIN, MH AF BORNSTEIN, MH BE dYdewalle, G Eelen, P Bertelson, P TI CROSS-CULTURAL PERSPECTIVES ON PARENTING SO INTERNATIONAL PERSPECTIVES ON PSYCHOLOGICAL SCIENCE, VOL 2: THE STATE OF THE ART LA English DT Proceedings Paper CT XXV International Congress of Psychology CY JUL 19-24, 1992 CL BRUSSELS, BELGIUM SP Belgium Psychol Soc, Int Union Psychol Sci, Acad Royal Sci Lett & Beaux Arts Belgique, Koninklijke Acad Wetenschappen Lett Schone Kunsten Belgie C1 NICHHD,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC PUBL PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430 BN 0-86377-300-1 PY 1994 BP 359 EP 369 PG 11 WC Psychology SC Psychology GA BA80R UT WOS:A1994BA80R00017 ER PT B AU RODBELL, M AF RODBELL, M BE Rosselin, G TI G-PROTEINS AND MEMBRANE TRANSDUCTION - A NEW MODEL SO INTERNATIONAL SYMPOSIUM ON VASOACTIVE INTESTINAL PEPTIDE, PITUITARY ADENYLATE CYCLASE ACTIVATING POLYPEPTIDE & RELATED REGULATORY PEPTIDES FROM MOLECULAR BIOLOGY TO CLINICAL APPLICATIONS LA English DT Proceedings Paper CT 6th International Symposium on VIP/3rd PACAP Symposium CY SEP 19-23, 1993 CL BISCHENBERG, FRANCE SP INSERM, COMMISS EUROPEAN COMMUNITIES C1 NIEHS,MOLEC & CELLULAR PHARMACOL LAB,SIGNAL TRANSDUCT SECT,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WORLD SCIENTIFIC PUBL CO PTE LTD PI SINGAPORE PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE BN 981-02-1788-9 PY 1994 BP 101 EP 112 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BB55X UT WOS:A1994BB55X00013 ER PT B AU MOODY, TW ZIA, F BITAR, K COY, DH AF MOODY, TW ZIA, F BITAR, K COY, DH BE Rosselin, G TI PACAP(6-38) IS A PACAP TYPE-I RECEPTOR ANTAGONIST ON SMALL-CELL LUNG-CANCER CELLS SO INTERNATIONAL SYMPOSIUM ON VASOACTIVE INTESTINAL PEPTIDE, PITUITARY ADENYLATE CYCLASE ACTIVATING POLYPEPTIDE & RELATED REGULATORY PEPTIDES FROM MOLECULAR BIOLOGY TO CLINICAL APPLICATIONS LA English DT Proceedings Paper CT 6th International Symposium on VIP/3rd PACAP Symposium CY SEP 19-23, 1993 CL BISCHENBERG, FRANCE SP INSERM, COMMISS EUROPEAN COMMUNITIES C1 NCI,DIV CANC PREVENT & CONTROL,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD 20850. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WORLD SCIENTIFIC PUBL CO PTE LTD PI SINGAPORE PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE BN 981-02-1788-9 PY 1994 BP 537 EP 544 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BB55X UT WOS:A1994BB55X00063 ER PT J AU KIM, WH JUN, SH KIBBEY, MC THOMPSON, EW KLEINMAN, HK AF KIM, WH JUN, SH KIBBEY, MC THOMPSON, EW KLEINMAN, HK TI EXPRESSION OF BETA-1 INTEGRIN IN LAMININ-ADHESION-SELECTED HUMAN COLON-CANCER CELL-LINES OF VARYING TUMORIGENICITY SO INVASION & METASTASIS LA English DT Article DE LAMININ; COLON CANCER; BETA-1 INTEGRIN; MATRIGEL; INVASION ID CARCINOMA-CELLS; TERMINAL DIFFERENTIATION; EXTRACELLULAR-MATRIX; BIOLOGICAL-ACTIVITY; BASEMENT-MEMBRANE; COLORECTAL-CANCER; MELANOMA-CELLS; RECEPTOR; FIBRONECTIN; MOLECULES AB Laminin has been shown to promote the malignant phenotype and the expression of certain laminin receptors has been correlated with the malignant character of the tumors. Here new cell lines were isolated from a human colon cancer cell line (LCC-C1) based on their adhesiveness to laminin. The laminin-adherent subclone formed large tumors in nude mice, whereas the laminin-nonadherent subclone failed to form sizable tumors. Only the laminin-adherent subclone adhered to laminin and invaded through Matrigel-coated filters. The adhesive and invasive ability of the cells was almost completely blocked by low concentrations (1.0 mu g/ml) of anti-beta 1 integrin antibody. The amounts of total cellular beta 1 integrin protein were similar in the two subclones when compared by Western blot, and the mRNA levels also did not differ. The localization of beta 1 integrin laminin receptor varied in the two subclones; the laminin-adherent subclone showed a linear distribution along the cell-cell junctions, while the laminin-nonadherent subclone did not stain between the cells. Using laminin-Sepharose affinity chromatography, more beta 1 integrin was obtained from the laminin-adherent subclone. These findings suggest that alterations in the affinity of beta 1 integrin for laminin and in its membrane distribution might be involved in the increased tumorigenicity observed in colon cancer cells. C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,DEPT CELL BIOL,WASHINGTON,DC. GEORGETOWN UNIV,MED CTR,LOMBARDI CANC RES CTR,WASHINGTON,DC. SEOUL NATL UNIV,COLL MED,DEPT PATHOL,SEOUL,SOUTH KOREA. RI Kim, Wooho/G-3703-2011; Seoul National University, Pathology/B-6702-2012; Thompson, Erik/A-1425-2009 OI Thompson, Erik/0000-0002-9723-4924 NR 29 TC 22 Z9 22 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0251-1789 J9 INVAS METAST JI Invasion Metastasis PD JAN-DEC PY 1994 VL 14 IS 1-6 BP 147 EP 155 PG 9 WC Oncology SC Oncology GA RV538 UT WOS:A1994RV53800015 PM 7544773 ER PT J AU STETLERSTEVENSON, WG AF STETLERSTEVENSON, WG TI PROGELATINASE-A ACTIVATION DURING TUMOR-CELL INVASION SO INVASION & METASTASIS LA English DT Article DE GELATINASE A; TYPE IV COLLAGENASE; ACTIVATION; TISSUE INHIBITOR OF METALLOPROTEINASES; TIMP-2; MEMBRANE-TYPE METALLOPROTEINASE ID HUMAN 72-KDA GELATINASE; TIMP-2 MESSENGER-RNAS; C-TERMINAL DOMAIN; IV COLLAGENASE; TISSUE INHIBITOR; COMPLEX-FORMATION; MR 72,000; METALLOPROTEINASE INHIBITOR; MATRIX METALLOPROTEINASES; INTERSTITIAL COLLAGENASE AB The mechanisms of tumor cell invasion appear to be the same as those of normal cells that invade. Thus malignancy can be defined as a defect in the regulation of a predefined cellular program of invasion. Gelatinase A (MMP-2) has been shown to contribute to the invasive phenotype. Recent work demonstrates that activation of progelatinase A is a key event in the acquisition of malignant potential. This brief report reviews some recent findings on the cellular mechanism of progelatinase A activation and the role of tissue inhibitor of metalloproteinases-2 in this process. RP STETLERSTEVENSON, WG (reprint author), NCI,PATHOL LAB,EXTRACELLULAR MATRIX PATHOL SECT,BLDG 10,ROOM 2A33,BETHESDA,MD 20892, USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 55 TC 66 Z9 67 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0251-1789 J9 INVAS METAST JI Invasion Metastasis PD JAN-DEC PY 1994 VL 14 IS 1-6 BP 259 EP 268 PG 10 WC Oncology SC Oncology GA RV538 UT WOS:A1994RV53800025 PM 7657518 ER PT J AU GREVER, MR BENEDETTI, J BALCERZAK, SP TAYLOR, SA MILLER, TP DAKHIL, SR AF GREVER, MR BENEDETTI, J BALCERZAK, SP TAYLOR, SA MILLER, TP DAKHIL, SR TI A SOUTHWEST-ONCOLOGY-GROUP PHASE-II EVALUATION OF FLUDERABINE MONOPHOSPHATE IN SARCOMA SO INVESTIGATIONAL NEW DRUGS LA English DT Note ID FLUDARABINE PHOSPHATE C1 SW ONCOL GRP,CTR STAT,SEATTLE,WA. NCI,BETHESDA,MD 20892. OHIO STATE UNIV,CTR HLTH,COLUMBUS,OH 43210. UNIV KANSAS,MED CTR,KANSAS CITY,KS 66103. UNIV ARIZONA,CTR CANC,TUCSON,AZ. WICHITA COMMUNITY CLIN ONCOL PROGRAM,WICHITA,KS. FU NCI NIH HHS [CA-12644, CA-38926, CA-04920] NR 6 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1994 VL 12 IS 3 BP 259 EP 261 DI 10.1007/BF00873969 PG 3 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA PX099 UT WOS:A1994PX09900013 PM 7534752 ER PT J AU MARAINI, G ROSMINI, F GRAZIOSI, P TOMBA, MC BONACINI, M COTICHINI, R PASQUINI, P SPERDUTO, RD MILTON, R BATTAINI, C BELPOLITI, M WILLIAMS, SL CORONA, RM CRATERI, RS AF MARAINI, G ROSMINI, F GRAZIOSI, P TOMBA, MC BONACINI, M COTICHINI, R PASQUINI, P SPERDUTO, RD MILTON, R BATTAINI, C BELPOLITI, M WILLIAMS, SL CORONA, RM CRATERI, RS TI INFLUENCE OF TYPE AND SEVERITY OF PURE FORMS OF AGE-RELATED CATARACT ON VISUAL-ACUITY AND CONTRAST SENSITIVITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE VISUAL ACUITY; CONTRAST SENSITIVITY; CORTICAL OPACITIES; NUCLEAR OPACITIES; POSTERIOR SUBCAPSULAR OPACITIES ID II LOCS-II; RELIABILITY AB Purpose. To compare the relationship between logMAR visual acuity (VA) and cataract severity and between contrast sensitivity (CS) and cataract severity in pure types of age-related lens opacities. Methods. Analysis included patients followed in the ongoing Italian-American Study of the Natural History of Age-Related Cataract. Lens opacities were classified and graded according to the Lens Opacities Classification System II (LOCS II). Visual acuity was measured with the Early Treatment Diabetic Retinopathy Study Chart. Contrast sensitivity was measured with the Pelli-Robson chart. Results. Data from 1,076 eyes were used for the analysis (366 clear lenses; 550, 124, and 36 eyes with cortical, nuclear and posterior subcapsular cataract, respectively). In age-adjusted analyses, increasing severity of all three cataract types was associated with progressively higher logMAR VA, which translates into poorer acuity, and lower CS scores. For both VA and CS, the effect of increasing severity was greatest for nuclear and least for cortical opacities. After adjusting for age and VA, CS scores were no longer associated with cataract type and severity, with the exception of advanced cortical opacities. Conclusions. Increased cataract severity, as determined by LOCS II grading, is strongly associated with both VA and CS scores. Contrast sensitivity scores obtained from testing at low spatial frequency do not seem to offer additional information over standard VA testing in early cortical and posterior subcapsular opacities nor in nuclear cataracts. C1 IST SUPER SANITA,ROME,ITALY. NEI,BETHESDA,MD 20892. DATA COLLECT CTR,PARMA,ITALY. COORDINATING CTR,ROME,ITALY. RP MARAINI, G (reprint author), UNIV PARMA,IST OFTALMOL,VIA GRAMSCI 14,I-43100 PARMA,ITALY. FU NEI NIH HHS [EY92108] NR 14 TC 23 Z9 25 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 1994 VL 35 IS 1 BP 262 EP 267 PG 6 WC Ophthalmology SC Ophthalmology GA MU703 UT WOS:A1994MU70300028 PM 8300354 ER PT B AU WALKER, FL THOMA, GR AF WALKER, FL THOMA, GR BE Cibbarelli, PR Nixon, C TI ACCESS TO DOCUMENT IMAGES OVER THE INTERNET SO IOLS'94 - INTEGRATED ONLINE LIBRARY SYSTEMS, PROCEEDINGS - 1994 LA English DT Proceedings Paper CT 9th National Conference on Integrated Online Library Systems (IOLS 94) - Coordinating Access to Multiple Systems CY MAY 11-12, 1994 CL NEW YORK, NY SP LEARNED INFORMAT INC DE ELECTRONIC DOCUMENT DELIVERY; DOCUMENT IMAGING; DOCVIEW C1 NATL LIB MED,BETHESDA,MD 20209. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INFORMATION TODAY INC PI MEDFORD PA 143 OLD MARLTON PIKE, MEDFORD, NJ 08055 BN 0-938734-83-0 PY 1994 BP 185 EP 197 PG 13 WC Information Science & Library Science SC Information Science & Library Science GA BC75D UT WOS:A1994BC75D00024 ER PT J AU STLOUIS, ME PAU, CP NSUAMI, M OU, CY MATELA, B KASHAMUKA, M BROWN, C GEORGE, JR HEYWARD, WL AF STLOUIS, ME PAU, CP NSUAMI, M OU, CY MATELA, B KASHAMUKA, M BROWN, C GEORGE, JR HEYWARD, WL TI LACK OF ASSOCIATION BETWEEN ANTI-V3 LOOP ANTIBODY AND PERINATAL HIV-1 TRANSMISSION IN KINSHASA, ZAIRE, DESPITE USE OF ASSAYS BASED ON LOCAL HIV-1 STRAINS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV-1; V3 LOOP; PRINCIPAL NEUTRALIZING DOMAIN; PERINATAL HIV TRANSMISSION; AFRICA ID HUMAN-IMMUNODEFICIENCY-VIRUS; PRINCIPAL NEUTRALIZING DOMAIN; MATERNAL ANTIBODIES; VERTICAL TRANSMISSION; GLYCOPROTEIN GP120; TYPE-1; INFECTION; AFRICA; SERA; CHIMPANZEES AB Maternal antibodies against the V3 loop principal neutralizing domain (PND) have been reported to protect against perinatal HIV-1 transmission. To study this association in an African city with a long-standing HIV epidemic and no established ''consensus sequence'' for the V3 loop region of gp120, we determined the DNA sequence for the V3 region of HIV-1 from 13 HIV-1-infected residents of Kinshasa, Zaire, and developed peptide enzyme immunoassays (EIAs) reflecting the V3 loop PND for those HIV-1 strains. Using the most broadly reactive locally derived V3 loop peptide in a limited-antigen EIA, there was no significant difference in the perinatal HIV-1 transmission risk between 64 women with anti-V3 loop antibody (transmission risk, 30%) and 104 women without anti-V3 loop antibody (transmission risk, 25%; p = 0.5); this finding was unchanged after we controlled for maternal AIDS and low birth weight. Although we used assays for V3 loop antibody based on local HIV-1 strains and evaluated a large number of mother-child pairs, we found no evidence that maternal anti-V3 loop PND antibody protects against perinatal HIV-1 transmission. C1 NIAID,BETHESDA,MD 20892. PROJET SIDA,KINSHASA,ZAIRE. RP STLOUIS, ME (reprint author), CTR DIS CONTROL,NATL CTR INFECT DIS,DIV HIV AIDS,E-50,1600 CLIFTON RD,ATLANTA,GA 30333, USA. FU PHS HHS [N01-A1-8003] NR 26 TC 18 Z9 18 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN PY 1994 VL 7 IS 1 BP 63 EP 67 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MN428 UT WOS:A1994MN42800010 PM 8263755 ER PT J AU RUFF, AJ COBERLY, J HALSEY, NA BOULOS, R DESORMEAUX, J BURNLEY, A JOSEPH, DJ MCBRIEN, M QUINN, T LOSIKOFF, P OBRIEN, KL LOUIS, MA FARZADEGAN, H AF RUFF, AJ COBERLY, J HALSEY, NA BOULOS, R DESORMEAUX, J BURNLEY, A JOSEPH, DJ MCBRIEN, M QUINN, T LOSIKOFF, P OBRIEN, KL LOUIS, MA FARZADEGAN, H TI PREVALENCE OF HIV-1 DNA AND P24 ANTIGEN IN BREAST-MILK AND CORRELATION WITH MATERNAL FACTORS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE MATERNAL-INFANT HIV-1 TRANSMISSION; BREAST MILK; BREAST- FEEDING; HIV-1 PCR; HIV-1 P24 ANTIGEN ID HUMAN-IMMUNODEFICIENCY-VIRUS; HTLV-I; POSTNATAL TRANSMISSION; HUMAN COLOSTRUM; INFECTION; TYPE-1; AIDS; MOTHERS; INFANT; CELLS AB Breast milk specimens from human immunodeficiency virus type 1 (HIV-1)-seropositive and HIV-1-seronegative women were examined for the presence of HIV-1 p24 antigen by the antigen capture method and for viral DNA using the polymerase chain reaction. HIV-1 DNA was present in 70% of milk specimens collected from 47 HIV-seropositive women 0-4 days after delivery and in similar to 50% of specimens collected 6 and 12 months postpartum. p24 antigen, present in 24% of milk specimens collected from 37 seropositive women within the first 4 days postpartum, was not detected in any of the subsequent specimens. The presence of HIV-1 DNA or p24 antigen in milk was not significantly associated with maternal CD4 lymphocyte count, beta(2)-microglobulin level , or fulfillment of the AIDS clinical case definition. Although the correlation of either HIV-1 proviral DNA or p24 antigen with the presence of infectious virus is not known, these data indicate the need for additional studies examining the role of breastfeeding in maternal-infant transmission of HIV-1. C1 CTR DEV & SANTE,PORT AU PRINCE,HAITI. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,CTR AIDS RES,DEPT EPIDEMIOL,BALTIMORE,MD. JOHNS HOPKINS SCH MED,DEPT MED,BETHESDA,MD. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP RUFF, AJ (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT INT HLTH,615 N WOLFE ST,BALTIMORE,MD 21205, USA. FU NIAID NIH HHS [1RO1 AI26521] NR 34 TC 60 Z9 61 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN PY 1994 VL 7 IS 1 BP 68 EP 73 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MN428 UT WOS:A1994MN42800011 PM 7903381 ER PT J AU SEYDEL, J KRAMER, A ROSENBERG, PS WITTKOWSKI, KM GAIL, MH AF SEYDEL, J KRAMER, A ROSENBERG, PS WITTKOWSKI, KM GAIL, MH TI BACKCALCULATION OF THE NUMBER INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS IN GERMANY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE BACKCALCULATION; BACKPROJECTION; HIV INCIDENCE; EPIDEMIOLOGIC METHODS ID SHORT-TERM PROJECTIONS; INCUBATION PERIOD; CONTROLLED TRIAL; AIDS INCIDENCE; UNITED-STATES; BISEXUAL MEN; EPIDEMIC; HEMOPHILIA; PREVALENCE; COHORT AB The method of backcalculation was used to estimate the cumulative number of human immunodeficiency virus type 1 (HIV-1)-infected adults in Germany from reporting delay-corrected surveillance data on acquired immunodeficiency syndrome (AIDS) in the pretreatment era. Using different backcalculation approaches with various incubation period distributions, a plausible range of 13,100 to 23,900 HIV-1-infected adults as of December 31, 1984, was calculated. Estimates of the number infected at more recent times were subject to much greater uncertainty. On average, the cumulative incidences calculated by the nonparametric backprojection method are about 15% lower than the results from the step function model. Nonparametric backprojection with the Hessol incubation distribution suggests a declining HIV infection rate after 1985, as might be expected from German health policies. This distribution is derived from cohorts of homosexual men, the main fraction of German AIDS cases. C1 UNIV TUBINGEN, INST MED BIOMETRY, DEPT MED BIOMETRY, W-2070 TUBINGEN, GERMANY. UNIV MINNESOTA, SCH PUBL HLTH, DIV EPIDEMIOL, MINNEAPOLIS, MN 55455 USA. NCI, EPIDEMIOL & BIOSTAT PROGRAM, EPIDEMIOL METHODS SECT, ROCKVILLE, MD USA. NR 25 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN PY 1994 VL 7 IS 1 BP 74 EP 78 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MN428 UT WOS:A1994MN42800012 PM 8263756 ER PT J AU THADANI, PV SHARP, C AF THADANI, PV SHARP, C TI DRUGS OF ABUSE AND DYSFUNCTION OF NEUROENDOCRINE AND IMMUNE-SYSTEMS - THE IMPORTANCE OF ANIMAL RESEARCH SO JOURNAL OF ADDICTIVE DISEASES LA English DT Editorial Material ID RAT; ADRENOCORTICOTROPIN; EXPOSURE; SECRETION; RESPONSES; RELEASE; ALPHA RP THADANI, PV (reprint author), NIDA,DIV BASIC RES,PARKLAWN BLDG,ROOM 10A-19,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 26 TC 1 Z9 1 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1994 VL 13 IS 2 BP 1 EP 8 DI 10.1300/J069v13n02_01 PG 8 WC Substance Abuse SC Substance Abuse GA QA187 UT WOS:A1994QA18700001 PM 8204671 ER PT J AU ELMER, GI GEORGE, FR AF ELMER, GI GEORGE, FR TI OPERANT RATE DEPRESSANT EFFECTS OF ETHANOL IN MICE SELECTIVELY BRED FOR DIFFERENTIAL NEUROSENSITIVITY TO ETHANOL SO JOURNAL OF ADDICTIVE DISEASES LA English DT Article ID SHORT-SLEEP MICE; LONG-SLEEP; INBRED MICE; ALKO RATS; TOLERANCE; HYPOTHERMIA; REINFORCER; BEHAVIOR; ALCOHOL AB Few studies have investigated genetic differences in the effects of ethanol on operant schedule-controlled behaviors. The use of genetically defined populations in sensitive measures of complex behavior can help determine genetically covarying responses to ethanol as well as environmental contexts important for demonstrating genetic differences. The purpose of the present study was to investigate the rate depressant effects of ethanol on two lines of mice selectively bred for increased, LS/Ibg (LS), and decreased, SS/Ibg (SS), sensitivity to the acute narcotic effects of ethanol. Ethanol dose-dependently decreased high rates of behavior maintained by fixed ratio responding for water in both the LS and SS mice. Interestingly, the LS and SS mice did not differ in the rate depressant effects of ethanol under these conditions despite the sensitivity of this measure to the CNS effects of drugs and the very large differences between these lines in sensitivity to numerous other ethanol-related effects. While the SS mice were slightly less sensitive, and LS mice tended to show a low dose rate increasing effect, none of the differences were significant as ED50 values for rate depression differed by only 2.5 percent. The results of this experiment demonstrate that sensitivity to the effects of ethanol on fixed ratio responding for water is not genetically related to the acute narcotic effects of ethanol. In addition, the findings show that previously reported differences in operant ethanol self-administration between these two lines of mice are not due to differential sensitivity to the direct effects of ethanol on reinforced behavior. C1 NIDA,ADDICT RES CTR,PRECLIN PHARMACOL BRANCH,BALTIMORE,MD 21224. UNIV NEW MEXICO,CTR ALCOHOLISM SUBSTANCE ABUSE & ADDICT,ALBUQUERQUE,NM 87131. FU NIAAA NIH HHS [AA-07754] NR 28 TC 6 Z9 6 U1 1 U2 4 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1994 VL 13 IS 2 BP 9 EP 19 DI 10.1300/J069v13n02_02 PG 11 WC Substance Abuse SC Substance Abuse GA QA187 UT WOS:A1994QA18700002 PM 8204679 ER PT J AU MONTOYA, ID HAERTZEN, C AF MONTOYA, ID HAERTZEN, C TI REDUCTION OF PSYCHOPATHOLOGY AMONG INDIVIDUALS PARTICIPATING IN NON-TREATMENT DRUG-ABUSE RESIDENTIAL STUDIES SO JOURNAL OF ADDICTIVE DISEASES LA English DT Article ID COCAINE ABUSERS; TREATMENT-SEEKING; ADDICTS; USERS AB The psychological repercussions in drug abusing individuals of their participation in non-treatment residential drug abuse research protocols have been uncertain. To study this, the average raw scores of the Symptom-Check List-90 Revised (SCL-90R) at the time of recruiting and discharge (40.2 +/- 15.6 days later) was studied at the Addiction Research Center of the National Institute on Drug Abuse (NIDA-ARC), in Baltimore, Maryland, in a sample of 233 drug abusers seeking no treatment. There was significant reduction in symptomatology (p < .01) between recruiting and discharge for Obsessive-Compulsive, Interpersonal Sensitivity, Depression, Phobic Anxiety, Paranoid Ideation, Psychoticism, and Total Scores. These findings suggest that participation of drug abusers in non-treatment residential studies is safe and may improve their psychological status, which may be a therapeutic outcome of disengaging individuals from their drug environment and offering a safe and structured milieu. RP MONTOYA, ID (reprint author), NIDA,ARC,POB 5180,BALTIMORE,MD 21224, USA. FU Intramural NIH HHS [Z99 DA999999] NR 13 TC 8 Z9 8 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1994 VL 13 IS 2 BP 89 EP 97 DI 10.1300/J069v13n02_08 PG 9 WC Substance Abuse SC Substance Abuse GA QA187 UT WOS:A1994QA18700008 PM 8204678 ER PT J AU KEENAN, RM JENKINS, AJ CONE, EJ HENNINGFIELD, JE AF KEENAN, RM JENKINS, AJ CONE, EJ HENNINGFIELD, JE TI SMOKED AND IV NICOTINE, COCAINE AND HEROIN HAVE SIMILAR ABUSE LIABILITY SO JOURNAL OF ADDICTIVE DISEASES LA English DT Meeting Abstract C1 NIDA,ADDICT RES CTR,CLIN PHARMACOL BRANCH,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1994 VL 13 IS 4 BP 259 EP 259 PG 1 WC Substance Abuse SC Substance Abuse GA QM231 UT WOS:A1994QM23100032 ER PT J AU FRIEDMAN, BS GERMANO, P MILETTI, J METCALFE, DD AF FRIEDMAN, BS GERMANO, P MILETTI, J METCALFE, DD TI A CLINICOPATHOLOGICAL STUDY OF 10 PATIENTS WITH RECURRENT UNEXPLAINED FLUSHING SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID MAST-CELL DISORDERS; SYSTEMIC MASTOCYTOSIS; CARCINOID-SYNDROME; PLASMA HISTAMINE; PROSTAGLANDIN-D2 AB We describe the clinicopathologic features of 10 patients with recurrent unexplained flushing. These patients were referred to the National Institutes of Health with a diagnosis of mastocytosis or idiopathic anaphylaxis. Both diagnoses were eliminated after evaluation. Patients reported attack of flushing lasting 15 minutes to 2 days and associated with such symptoms as anxiety, chest tightness, paresthesia, slurred speech, weakness, and pruritus. Abdominal pain was a constant feature, often associated with cramping and an increase in stool frequency. Attack witnessed by physicians consisted of an exaggerated blush response of the face and upper part of the chest, and were sometimes associated with tachycardia, mild hypertension, and tachypnea. Hives, angioedema, wheezing, and hypotension were not observed. Routine laboratory studies and 5-hydroxyindoleacetic acid, vanillylmandelic acid, and plasma histamine levels were normal. Plasma histamine levels did not elevate during attacks. When performed, results of bone marrow examinations skin biopsies, and bone scans were normal. Psychiatric examinations frequently revealed somatization disorders. Patients had often been prescribed a wide variety of medications including antihistamines, nonsteroidal anti-inflammatory drugs, and steroids, with little or no benefit Despite the benign nature of the clinical and laboratory findings, patients had undergone repeated, often invasive, examinations for several years. Whether such patients have a prominent flush response exaggerated through a somatization disorder or a relatively benign flushing disorder associated with putative mediator release remains to be determined. Recognition of this category of patients with unexplained flushing will avoid subjecting such patients to unwarranted repeated examinations, procedures, and inappropriate therapy. C1 NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BETHESDA,MD 20892. NR 20 TC 16 Z9 16 U1 0 U2 2 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1994 VL 93 IS 1 BP 53 EP 60 DI 10.1016/0091-6749(94)90232-1 PN 1 PG 8 WC Allergy; Immunology SC Allergy; Immunology GA MT781 UT WOS:A1994MT78100006 PM 8308182 ER PT J AU LENFANT, C AF LENFANT, C TI REPORT OF THE WORKING GROUP ON ASTHMA AND PREGNANCY - EXECUTIVE SUMMARY - MANAGEMENT OF ASTHMA DURING PREGNANCY (REPRINTED FROM NIH PUBLICATION 93-3279A, MARCH 1993) SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Reprint ID CHICK-EMBRYOS; FETAL GROWTH; MALFORMATIONS; AMINOPHYLLINE; RETARDATION; WOMEN; DRUGS RP LENFANT, C (reprint author), NHLBI,BETHESDA,MD 20892, USA. NR 54 TC 0 Z9 0 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1994 VL 93 IS 1 BP 139 EP 162 PN 1 PG 24 WC Allergy; Immunology SC Allergy; Immunology GA MT781 UT WOS:A1994MT78100017 ER PT J AU CHOWDHURY, BA KALINER, MA FRASER, CM AF CHOWDHURY, BA KALINER, MA FRASER, CM TI CLONING OF A GENE ENCODING THE HUMAN H1 HISTAMINE-RECEPTOR SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. INST GENOM RES,GAITHERSBURG,MD. NR 0 TC 4 Z9 4 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1994 VL 93 IS 1 BP 215 EP 215 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA MV317 UT WOS:A1994MV31700313 ER PT J AU BIANCHINE, PJ PAOLINI, R KINET, JP METCALFE, DD AF BIANCHINE, PJ PAOLINI, R KINET, JP METCALFE, DD TI MAST-CELL ADHESION TO VITRONECTIN IS SUFFICIENT TO PHOSPHORYLATE FOCAL ADHESION KINASE SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1994 VL 93 IS 1 BP 226 EP 226 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA MV317 UT WOS:A1994MV31700379 ER PT J AU HERSHKOVIZ, R CAHALON, L SAPIR, T MIRON, S MEKORI, YA AKIYAMA, K YAMADA, KM LIDER, O AF HERSHKOVIZ, R CAHALON, L SAPIR, T MIRON, S MEKORI, YA AKIYAMA, K YAMADA, KM LIDER, O TI IMMOBILIZATION OF TNF-ALPHA ON EXTRACELLULAR-MATRIX GLYCOPROTEINS AMPLIFIES THE CYTOKINES ABILITY TO INDUCE ADHESION OF ACTIVATED CD4+ T-CELLS SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 WEIZMANN INST SCI,DEPT CELL BIOL,IL-76100 REHOVOT,ISRAEL. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1994 VL 93 IS 1 BP 261 EP 261 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA MV317 UT WOS:A1994MV31700590 ER PT J AU GOLDBERGER, BA CONE, EJ GRANT, TM CAPLAN, YH LEVINE, BS SMIALEK, JE AF GOLDBERGER, BA CONE, EJ GRANT, TM CAPLAN, YH LEVINE, BS SMIALEK, JE TI DISPOSITION OF HEROIN AND ITS METABOLITES IN HEROIN-RELATED DEATHS SO JOURNAL OF ANALYTICAL TOXICOLOGY LA English DT Article ID MORPHINE CONCENTRATIONS; AQUEOUS-SOLUTION; BLOOD; BRAIN; 6-ACETYLMORPHINE; CHROMATOGRAPHY; DIAMORPHINE; CODEINE; ABUSE C1 NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. NATL CTR FORENS SCI,BALTIMORE,MD 21227. OFF CHIEF MED EXAMINER,BALTIMORE,MD 21201. NR 23 TC 90 Z9 98 U1 0 U2 6 PU PRESTON PUBLICATIONS INC PI NILES PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648 SN 0146-4760 J9 J ANAL TOXICOL JI J. Anal. Toxicol. PD JAN-FEB PY 1994 VL 18 IS 1 BP 22 EP 28 PG 7 WC Chemistry, Analytical; Toxicology SC Chemistry; Toxicology GA MT227 UT WOS:A1994MT22700005 PM 8127080 ER PT J AU MELNICK, RL MAHLER, J BUCHER, JR THOMPSON, M HEJTMANCIK, M RYAN, MJ MEZZA, LE AF MELNICK, RL MAHLER, J BUCHER, JR THOMPSON, M HEJTMANCIK, M RYAN, MJ MEZZA, LE TI TOXICITY OF DIETHANOLAMINE .1. DRINKING-WATER AND TOPICAL APPLICATION EXPOSURES IN F344 RATS SO JOURNAL OF APPLIED TOXICOLOGY LA English DT Article DE DIETHANOLAMINE; TOPICAL APPLICATION; MICROCYTIC ANEMIA; NEPHROPATHY; DEMYELINATION; SEMINIFEROUS TUBULE; DEGENERATION; ACANTHOSIS; HYPERKERATOSIS ID ZERO DOSE CONTROL AB Toxicology studies of diethanolamine were conducted in male and female F344 rats for 13 weeks' duration to characterize and compare effects of exposure in the drinking water with those caused by topical application. Doses of diethanolamine ranged from 160 to 5000 ppm in the drinking water study (equivalent to daily doses of 25-440 mg kg(-1) in males and 15-240 mg kg(-1) in females) and from 32 to 500 mg kg(-1) in the topical application study. Dose-dependent toxic effects due to exposure to diethanolamine included hematological changes (a poorly regenerative, microcytic anemia), as well as toxic responses in the kidney (increased weight, tubular necrosis, decreased renal function, and/or tubular mineralization), brain and spinal cord (demyelination), testis (degeneration of the seminiferous tubules) and skin (site of application: ulceration, inflammation, hyperkeratosis and acanthosis). A no-observed-adverse-effect level was not achieved for hematological changes, nephropathy or hyperkeratosis of the skin. Differences in dose-response between the drinking water and topical application exposures were attributed largely to the limited dermal absorption of this chemical. C1 BATTELLE MEM INST LABS,COLUMBUS,OH. RP MELNICK, RL (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 24 TC 27 Z9 27 U1 3 U2 6 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0260-437X J9 J APPL TOXICOL JI J. Appl. Toxicol. PD JAN-FEB PY 1994 VL 14 IS 1 BP 1 EP 9 DI 10.1002/jat.2550140103 PG 9 WC Toxicology SC Toxicology GA MV131 UT WOS:A1994MV13100001 PM 8157863 ER PT J AU MELNICK, RL MAHLER, J BUCHER, JR HEJTMANCIK, M SINGER, A PERSING, RL AF MELNICK, RL MAHLER, J BUCHER, JR HEJTMANCIK, M SINGER, A PERSING, RL TI TOXICITY OF DIETHANOLAMINE .2. DRINKING-WATER AND TOPICAL APPLICATION EXPOSURES IN B6C3F(1) MICE SO JOURNAL OF APPLIED TOXICOLOGY LA English DT Article DE DIETHANOLAMINE; TOPICAL APPLICATION; LIVER NECROSIS; MULTINUCLEATED HEPATOCYTES; NEPHROPATHY; HEART, MYOCYTE DEGENERATION; HYPERKERATOSIS; ACANTHOSIS ID ZERO DOSE CONTROL AB Toxicology studies of diethanolamine were conducted in male and female B6C3F(1) mice to characterize and compare effects of exposure in the drinking water with those caused by topical application and to compare responses in mice to those observed in rats. Each study consisted of five dose groups plus controls and the size of each group was 10 animals per sex. Doses of diethanolamine ranged from 630 to 10000 ppm in the drinking water study (approximately equivalent to daily doses of 100-1700 mg kg(-1) in males and 140-1100 mg kg(-1) in females) and from 80 to 1250 mg kg(-1) in the topical application study. Exposure to diethanolamine caused dose-dependent toxic effects in the liver (hepatocellular cytological alterations and necrosis), kidney (nephropathy and tubular epithelial necrosis in males), heart (cardiac myocyte degeneration) and shin (site of application: ulceration, inflammation, hyperkeratosis, and acanthosis). Cytological alterations in the liver consisted of multiple hepatocyte changes, including enlarged cells that were frequently multinucleated, increased nuclear pleomorphism, increased eosinophilia and disruption of hepatic cords. A no-observed-adverse-effect level (NOAEL) was not achieved for hepatocellular cytological alterations or for acanthosis in the skin C1 BATTELLE MEM INST LABS,COLUMBUS,OH. RP MELNICK, RL (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 25 TC 14 Z9 15 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0260-437X J9 J APPL TOXICOL JI J. Appl. Toxicol. PD JAN-FEB PY 1994 VL 14 IS 1 BP 11 EP 19 DI 10.1002/jat.2550140104 PG 9 WC Toxicology SC Toxicology GA MV131 UT WOS:A1994MV13100002 PM 8157864 ER PT J AU ANKENBAUER, RG QUAN, HN AF ANKENBAUER, RG QUAN, HN TI FPTA, THE FE(III)-PYOCHELIN RECEPTOR OF PSEUDOMONAS-AERUGINOSA - A PHENOLATE SIDEROPHORE RECEPTOR HOMOLOGOUS TO HYDROXAMATE SIDEROPHORE RECEPTORS SO JOURNAL OF BACTERIOLOGY LA English DT Article ID OUTER-MEMBRANE RECEPTORS; ESCHERICHIA-COLI; FERRIC-PSEUDOBACTIN; NUCLEOTIDE-SEQUENCE; VIBRIO-ANGUILLARUM; BINDING PROTEIN; IRON TRANSPORT; GENE; PYOCHELIN; TONB AB The Pseudomonas aeruginosa siderophore pyochelin is structurally unique among siderophores and possesses neither hydroxamate- nor catecholate-chelating groups. The structural gene encoding the 75-kDa outer membrane Fe(III)-pyochelin receptor FptA has been isolated by plasmid rescue techniques and sequenced. The N-terminal amino acid sequence of the isolated FptA protein corresponded to that deduced from the nucleotide sequence of the fptA structural gene. The mature FptA protein has 682 amino acids and a molecular mass of 75,993 Da and has considerable overall homology with the hydroxamate siderophore receptors FpvA of P. aeruginosa, PupA and PupB of Pseudomonas putida, and FhuE of Escherichia coli. This observation indicates that homologies between siderophore receptors are an unreliable predictor of siderophore ligand class recognition by a given receptor. The fptA gene was strongly regulated by iron; fptA transcription was totally repressed by 30 muM FeCl3, as determined by Northern (RNA) blotting. The promoter of the fptA gene contained the sequence 5'-ATAATGATAAGCATTATC-3', which matches the consensus E. coli Fur-binding site at 17 of 18 positions. The -10 promoter region and transcriptional start site of the fptA gene reside within this Fur-binding site. RP ANKENBAUER, RG (reprint author), NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,HAMILTON,MT 59840, USA. NR 64 TC 93 Z9 97 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1994 VL 176 IS 2 BP 307 EP 319 PG 13 WC Microbiology SC Microbiology GA MQ782 UT WOS:A1994MQ78200006 PM 8288523 ER PT J AU HENDLER, RW SHRAGER, RI AF HENDLER, RW SHRAGER, RI TI DECONVOLUTIONS BASED ON SINGULAR-VALUE DECOMPOSITION AND THE PSEUDOINVERSE - A GUIDE FOR BEGINNERS SO JOURNAL OF BIOCHEMICAL AND BIOPHYSICAL METHODS LA English DT Review DE CURVE FITTING; SINGULAR VALVE DECOMPOSITION; MATHEMATICAL MODELING; SPECTRAL DECONVOLUTION ID PRINCIPAL COMPONENT ANALYSIS; SPECTRA; RESOLUTION; TRANSITIONS; KINETICS; MIXTURES; PKS AB Singular value decomposition (SVD) is deeply rooted in the theory of linear algebra, and because of this is not readily understood by a large group of researchers who could profit from its application. In this paper, we discuss the subject on a lever that should be understandable to scientists who are not well versed in linear algebra. However, because it is necessary that certain key concepts in linear algebra be appreciated in order to comprehend what is accomplished by SVD, we present the section, 'Bare basics of linear algebra'. This is followed by a discussion of the theory of SVD. Next we present step-by-step examples to illustrate how SVD is applied to deconvolute a titration involving a mixture of three pH indicators. One noiseless case is presented as well as two cases where either a fixed or varying noise level is present. Finally, we discuss additional deconvolutions of mixed spectra based on the use of the pseudoinverse. C1 NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892. RP HENDLER, RW (reprint author), NHLBI,CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 13 TC 143 Z9 143 U1 4 U2 43 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-022X J9 J BIOCHEM BIOPH METH JI J. Biochem. Biophys. Methods PD JAN PY 1994 VL 28 IS 1 BP 1 EP 33 DI 10.1016/0165-022X(94)90061-2 PG 33 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MU501 UT WOS:A1994MU50100001 PM 8151067 ER PT J AU GOTOH, M KOVAC, P AF GOTOH, M KOVAC, P TI SYNTHESIS OF THE METHYL ALPHA-GLYCOSIDE OF THE INTRACATENARY DISACCHARIDE REPEATING UNIT OF THE O-POLYSACCHARIDE OF VIBRIO-CHOLERAE-O-1 - A COMPARISON OF 2 ASSEMBLY STRATEGIES SO JOURNAL OF CARBOHYDRATE CHEMISTRY LA English DT Article ID ANTIGENIC DETERMINANTS; BLOCK SYNTHESIS; PENTASACCHARIDE; THIOGLYCOSIDE AB The two strategies engaged in the construction of the title disaccharide 17 comprise: 1. assembly of a diamino disaccharide and its N-acylation using chiral reagents to introduce the 4-(3-deoxy-L-glycero-tetronyl) group, followed by deprotection, and 2. preparation of a glycosyl acceptor and a glycosyl donor both having the chiral 3-deoxy-L-glycero-tetronamido group already in place, their condensation to give a fully substituted disaccharide, and deprotection. Accordingly, the crystalline diamino disaccharide methyl 2-O-(4-amino-3-O-benzyl-4,6-dideoxy-alpha-D-mannopyranosyl)-4- amino-3-O-benzyl-4,6-dideoxy-(a)lpha-D-mannopyranoside, (14), was prepared from the known [Bundle, D. R. et al., Carbohydr. Res., 174, 239 (1988)] diazido disaccharide 12, and treated with the lactone 30, or its acetylated or benzylated analogs 31 and 32, respectively, as the N-acylating reagents. Subsequent deprotection of the respective products applying standard chemistry gave 17. Alternatively, the methyl alpha-glycoside of the monomeric intracatenary repeating unit of Vibrio cholerae O:1 (2) was converted to the fully benzoylated glycosyl chloride 26, and the latter glycosyl donor was condensed with methyl 3-O-benzyl-4,6-dideoxy-4(2,4-di-O-benzoyl- 3-deoxy-L-glycero-tetronamido)-alpha-D-mannopyranoside (24), to give the corresponding, fully protected derivative 27. Deprotection then readily gave 17. It appears that the title disaccharide can be most efficiently synthesized using synthons 24 and 26. The lactones 30 and 32 appear to be promising acylating reagents for the introduction of the 3-deoxy-L-glycero-tetronamido group when higher oligosaccharides in this series will be synthesized via their (poly)amino precursors. C1 NIDDKD,BETHESDA,MD 20892. NR 14 TC 42 Z9 42 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0732-8303 J9 J CARBOHYD CHEM JI J. Carbohydr. Chem. PY 1994 VL 13 IS 8 BP 1193 EP 1213 DI 10.1080/07328309408011859 PG 21 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA PW292 UT WOS:A1994PW29200011 ER PT J AU VANDERFORD, PA WONG, J CHANG, R KEEFER, LK SOIFER, SJ FINEMAN, JR AF VANDERFORD, PA WONG, J CHANG, R KEEFER, LK SOIFER, SJ FINEMAN, JR TI DIETHYLAMINE NITRIC-OXIDE (NO) ADDUCT, AN NO DONOR, PRODUCES POTENT PULMONARY AND SYSTEMIC VASODILATION IN INTACT NEWBORN LAMBS SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article DE NITROVASODILATORS; NITRIC OXIDE DONORS; NUCLEOPHILE NITRIC OXIDE ADDUCTS; PULMONARY HYPERTENSION ID NITROGLYCERIN-INDUCED TOLERANCE; VASCULAR SMOOTH-MUSCLE; NITRIC-OXIDE; CYCLIC-GMP; MOLECULAR MECHANISMS; SODIUM-NITROPRUSSIDE; NITRATE TOLERANCE; L-ARGININE; RELAXATION; NITROVASODILATOR AB Nitric oxide (NO), a labile humoral factor produced by vascular endothelial cells, is a potent vasodilator and an important mediator of pulmonary vascular tone. Nucleophile/NO adducts are a new class of compounds that spontaneously and predictively release NO. We investigated the hemodynamic effects of intravenous (i.v.) infusions of a recently developed NO-donor drug, the diethylamine-nitric oxide adduct (DEA/NO), in 17 intact newborn lambs. At rest, DEA/NO (1-2 mu g.kg(-1).min(-1)) produced dose-dependent decreases in mean pulmonary (from 10.6 +/- 8.6 to 21.2 +/- 7.9%, p < 0.05) and systemic arterial pressure (from 13.2 +/- 11.7 to 31.0 +/- 15.4%, p < 0.05). Similarly, during pulmonary hypertension induced by infusion of U46619, DEA/NO (0.5-2.0 mu g.kg(-1).min(-1)) produced dose-dependent decreases in mean pulmonary (from 7.3 +/- 5.6 to 24.1 +/- 13.3%, p < 0.05) and systemic arterial pressure (from 2.2 +/- 3.8 to 20.3 +/- 12.9%, p < 0.05). Cardiac output (CO), heart rate (HR), systemic arterial blood gases, and pH were unchanged; atrial pressures decreased at higher doses. Equimolar infusions of S-nitroso-N-acetyl-penicillamine, nitroglycerin (NTG), and sodium nitroprusside (SNP) produced similar decreases in pulmonary and systemic arterial pressure. The nucleophile/NO adducts are potent vasodilators; their predictable and quantitative release of NO make them potentially useful research tools. In addition, because these compounds may decrease the incidence of tolerance and the risk from toxic metabolites associated with use of other nitrovasodilators, they may be clinically useful. C1 UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,SAN FRANCISCO,CA 94143. NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,CHEM SECT,FREDERICK,MD. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 FU NHLBI NIH HHS [HL 35518] NR 33 TC 30 Z9 30 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0160-2446 J9 J CARDIOVASC PHARM JI J. Cardiovasc. Pharmacol. PD JAN PY 1994 VL 23 IS 1 BP 113 EP 119 DI 10.1097/00005344-199401000-00016 PG 7 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA MP895 UT WOS:A1994MP89500018 PM 7511722 ER PT J AU KELLOFF, GJ BOONE, CW STEELE, VE FAY, JR LUBET, RA CROWELL, JA SIGMAN, CC AF KELLOFF, GJ BOONE, CW STEELE, VE FAY, JR LUBET, RA CROWELL, JA SIGMAN, CC TI MECHANISTIC CONSIDERATIONS IN CHEMOPREVENTIVE DRUG DEVELOPMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE CHEMOPREVENTION; DRUG DEVELOPMENT; MECHANISM OF ACTION; CANCER ID ORNITHINE DECARBOXYLASE ACTIVITY; GROWTH-FACTOR-BETA; GAP JUNCTIONAL COMMUNICATION; TUMOR SUPPRESSOR GENES; PROGRAMMED CELL-DEATH; FED METHYL-DEFICIENT; HUMAN-BREAST-CANCER; PROTEIN KINASE-C; PROMOTER 12-O-TETRADECANOYLPHORBOL-13-ACETATE-INDUCED SYNTHESIS; PROSTAGLANDIN SYNTHESIS INHIBITORS AB This overview of the potential mechanisms of chemopreventive activity will provide the conceptual groundwork for chemopreventive drug discovery, leading to structure-activity and mechanistic studies that identify and evaluate new agents. Possible mechanisms of chemopreventive activity with examples of promising agents include carcinogen blocking activities such as inhibition of carcinogen uptake (calcium), inhibition of formation or activation of carcinogen (arylalkyl isothiocyanates, DHEA, NSAIDs, polyphenols), deactivation or detoxification of carcinogen (oltipraz, other GSH-enhancing agents), preventing carcinogen binding to DNA (oltipraz, polyphenols), and enhancing the level or fidelity of DNA repair (NAG, protease inhibitors). Chemopreventive antioxidant activities include scavenging reactive electrophiles (GSH-enhancing agents), scavenging oxygen radicals (polyphenols, vitamin E), and inhibiting arachidonic acid metabolism (glycyrrhetinic acid, NAG, NSAIDs, polyphenols, tamoxifen). Antiproliferation/antiprogression activities include modulation of signal transduction (glycyrrhetinic acid, NSAIDs, polyphenols, retinoids, tamoxifen), modulation of hormonal and growth factor activity (NSAIDs, retinoids, tamoxifen), inhibition of aberrant oncogene activity (genistein, NSAIDs, monoterpenes), inhibition of polyamine metabolism (DFMO, retinoids, tamoxifen), induction of terminal differentiation (calcium, retinoids, vitamin D-3), restoration of immune response (NSAIDs, selenium, vitamin E), enhancing intercellular communication (carotenoids, retinoids), restoration of tumor suppressor function, induction of programmed cell death (apoptosis) (butyric acid, genistein, retinoids, tamoxifen), correction of DNA methylation imbalances (folic acid), inhibition of angiogenesis (genistein, retinoids, tamoxifen), inhibition of basement membrane degradation (protease inhibitors), and activation of antimetastasis genes. A systematic drug development program for chemopreventive agents is only possible with continuing research into mechanisms of action and thoughtful application of the mechanisms to new drug design and discovery. One approach is to construct pharmacological activity profiles for promising agents. These profiles are compared among the promising agents and with untested compounds to identify similarities. Classical structure-activity studies are used to find optimal agents (high efficacy with low toxicity) based on good lead agents. Studies evaluating tissue-specific and pharmacokinetic parameters are very important. A final approach is design of mechanism-based assays and identification of mechanism-based intermediate biomarkers for evaluation of chemopreventive efficacy. (C) 1994 Wiley-Liss, Inc. C1 CCS ASSOCIATES,MT VIEW,CA 94043. RP KELLOFF, GJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT BRANCH,9000 ROCKVILLE PIKE,SUITE 201,BETHESDA,MD 20892, USA. NR 298 TC 31 Z9 32 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. PY 1994 SU 20 BP 1 EP 24 PG 24 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ805 UT WOS:A1994QQ80500002 ER PT J AU KELLOFF, GJ BOONE, CW CROWELL, JA STEELE, VE LUBET, R DOODY, LA AF KELLOFF, GJ BOONE, CW CROWELL, JA STEELE, VE LUBET, R DOODY, LA TI SURROGATE END-POINT BIOMARKERS FOR PHASE-II CANCER CHEMOPREVENTION TRIALS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE CHEMOPREVENTION; COMPUTER-ASSISTED IMAGE ANALYSIS; INTERMEDIATE BIOMARKERS; PHASE II TRIALS AB Three critical aspects govern successful Phase II cancer chemoprevention trials-well-characterized agents, suitable cohorts, and reliable intermediate biomarkers for measuring efficacy. Requirements for the agent are experimental or epidemiological data showing chemopreventive efficacy, safety on chronic administration, and a mechanistic rationale for the chemopreventive activity observed. The cohort should be suitable for measuring the chemopreventive activity of the agent and the intermediate biomarkers chosen. Also, many cohorts proposed for Phase II trials are patients with previous cancers or premalignant lesions. For such patients, the trials should be conducted within the context of standard treatment to avoid unusual risks. The criteria for biomarkers are that they fit expected biological mechanisms (i.e., differential expression in normal and high-risk tissue, on or closely linked to the causal pathway for the cancer, modulated by chemopreventive agents, and short latency compared with cancer), may be assayed reliably and quantitatively, measured easily, and correlate to decreased cancer incidence. They must occur in sufficient incidence to allow their biological and statistical evaluation relevant to cancer. Since carcinogenesis is a multipath process, single biomarkers are difficult to validate as surrogate endpoints, as they may appear on only one or a few of the many possible causal pathways. Panels of biomarkers, particularly those representing the range of carcinogenesis pathways, may prove more useful as surrogate endpoints. It is important to avoid relying solely on biomarkers representing isolated events that may or may not be on the causal pathway or otherwise associated with carcinogenesis. These include markers of normal cellular processes that may be increased or expressed during carcinogenesis, but are nonspecific. Chemoprevention trials should be designed to fully evaluate the two or three biomarkers that appear to be the best models of the cancer. Additional biomarkers should be considered only if they can be analyzed efficiently and the sample size allows the more important biomarkers to be evaluated completely. Two types of biomarkers that stand out in regard to their high correlation to cancer and their ability to be quantified are measures of intraepithelial neoplasia and indicators of cellular proliferation. Measurements made by computer-assisted image analysis that are potentially useful as surrogate endpoint biomarkers include nuclear pleomorphism comprising nuclear size, shape (roundness), and texture (DNA distribution patterns); nucleolar size and number of nucleoli/nucleus; DNA ploidy; and proliferation biomarkers such as S-phase fraction, bromodeoxyuridine uptake, Ki-67, and proliferating cell nuclear antigen. Phase II chemoprevention trials are currently in progress or planned that will evaluate these biomarkers. The cohorts include patients scheduled for surgery for ductal carcinoma in situ in breast or early breast cancer, patients with previously resected colon tumors or adenomas, patients with prostatic intraepithelial neoplasia, and patients scheduled for prostate cancer surgery. (C) 1994 Wiley-Liss, Inc. C1 CCS ASSOCIATES,MENLO PK,CA. RP KELLOFF, GJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT INVEST STUDIES BRANCH,BETHESDA,MD 20892, USA. NR 15 TC 31 Z9 32 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. PY 1994 SU 19 BP 1 EP 9 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PJ098 UT WOS:A1994PJ09800001 ER PT J AU BOONE, CW KELLOFF, GJ AF BOONE, CW KELLOFF, GJ TI DEVELOPMENT OF SURROGATE END-POINT BIOMARKERS FOR CLINICAL-TRIALS OF CANCER CHEMOPREVENTIVE AGENTS - RELATIONSHIPS TO FUNDAMENTAL PROPERTIES OF PREINVASIVE (INTRAEPITHELIAL) NEOPLASIA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE COMPUTER-ASSISTED IMAGE ANALYSIS; INTRAEPITHELIAL NEOPLASIA; SURROGATE END-POINT BIOMARKERS ID STAGE-A2 PROSTATE-CANCER; PRIMARY BREAST-CANCER; NUCLEAR MORPHOMETRY; TUMOR PROGRESSION; INSITU HYBRIDIZATION; GENOMIC INSTABILITY; GENE AMPLIFICATION; ULCERATIVE-COLITIS; ANTIGEN EXPRESSION; MOLECULAR-BIOLOGY AB The tissue changes offering the greatest immediate potential for development as surrogate endpoint biomarkers (SEBs) to be used in Phase Il trials of cancer chemopreventive agents are those derived from the microscopic tissue changes pathologists use to make the diagnosis of preinvasive (intraepithelial) neoplasia. These changes comprise four categories: proliferative index, ploidy, nuclear morphometry (size, shape, texture, and pleomorphism), and nucleolar morphometry (number, size, shape, position, and pleomorphism). Computer-assisted image analysis (CIA) permits dozens of additional morphometric parameters to be developed. Other categories of candidate SEBs are: DNA and chromosomal structural changes associated with genomic instability, activation of oncogenes and inactivation of tumor suppressor genes, structural changes in differentiated molecules, and aberrations of growth factor/receptor structure and function. Self-perpetuating DNA. breakage with secondary mutator mutations in genomic stability genes is a major mechanism by which the genomic instability characteristic of neoplasia occurs, and from which stem other basic neoplastic properties, including clonal evolution, along multiple pathways of genetic variation that are stochastically determined, continuously increasing proliferation, rate and extent of phenotypic heterogeneity. SEBs resulting from genomic instability include homogeneously staining regions, double minute chromosomes, micronuclei, dicentrics, gene amplification, loss of heterozygosity, and alterations in chromosome number. Newly developed assays for detecting genomic instability include comparative genomic hybridization using fluorescence in situ hybridization on >20 micron-thick sections monitored by confocal laser scanning microscopy, assays for microsatellite instability, and restriction landmark genomic scanning. These assays offer promise for detecting the earliest molecular changes of neoplasia in normal-appearing epithelium prior to the onset of the dysplastic phase of intraepithelial neoplasia. (C) 1994 Wiley-Liss, Inc. RP BOONE, CW (reprint author), NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT INVEST STUDIES BRANCH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 90 TC 4 Z9 4 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. PY 1994 SU 19 BP 10 EP 22 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PJ098 UT WOS:A1994PJ09800002 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 GUIDANCE FOR DEVELOPMENT OF CHEMOPREVENTIVE AGENTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article C1 US FDA,CTR DRUG EVALUAT & RES,ROCKVILLE,MD 20852. RP KELLOFF, GJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT BRANCH,9000 ROCKVILLE PIKE,SUITE 201,BETHESDA,MD 20892, USA. NR 1 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. PY 1994 SU 20 BP 25 EP 31 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ805 UT WOS:A1994QQ80500003 ER PT J AU HIRASAWA, N SANTINI, F BEAVEN, MA AF HIRASAWA, N SANTINI, F BEAVEN, MA TI CONVERGENT PATHWAYS FOR THE ACTIVATION OF PHOSPHOLIPASE-A(2) IN A MAST-CELL LINE - STUDIES WITH PERMEABILIZED RBL-2H3 CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,CHEM PHARMACOL 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. PY 1994 SU 18D BP 32 EP 32 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400039 ER PT J AU STEELE, VE MOON, RC LUBET, RA GRUBBS, CJ REDDY, BS WARGOVICH, M MCCORMICK, DL PEREIRA, MA CROWELL, JA BAGHERI, D SIGMAN, CC BOONE, CW KELLOFF, GJ AF STEELE, VE MOON, RC LUBET, RA GRUBBS, CJ REDDY, BS WARGOVICH, M MCCORMICK, DL PEREIRA, MA CROWELL, JA BAGHERI, D SIGMAN, CC BOONE, CW KELLOFF, GJ TI PRECLINICAL EFFICACY EVALUATION OF POTENTIAL CHEMOPREVENTIVE AGENTS IN ANIMAL CARCINOGENESIS MODELS - METHODS AND RESULTS FROM THE NCI CHEMOPREVENTION DRUG DEVELOPMENT PROGRAM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE ANIMAL MODELS; CARCINOGENESIS; CHEMOPREVENTION; DRUG DEVELOPMENT ID INDUCED COLON CARCINOGENESIS; URINARY-BLADDER CARCINOGENESIS; METHYL-N-NITROSOUREA; MALE F344 RATS; NONSTEROIDAL ANTIINFLAMMATORY DRUG; PROSTAGLANDIN SYNTHESIS INHIBITORS; ORNITHINE DECARBOXYLASE INDUCTION; OCCURRING ORGANOSULFUR COMPOUNDS; INDUCED MAMMARY CARCINOGENESIS; GLUTATHIONE S-TRANSFERASE AB In the NCI, Chemoprevention Branch drug development program, potential chemopreventive agents are evaluated for efficacy against chemical carcinogen-induced tumors in animal models. This paper summarizes the results of 144 agents in 352 tests using various animal efficacy models. Of these results, 146 were positive, representing 85 different agents. The target organs selected for the animals model are representative of high-incidence human cancers. The assays include inhibition of tumors induced by MNU in hamster trachea, DEN in hamster lung, AOM in rat colon (including inhibition of AOM-induced aberrant crypts), MAM in mouse colon, DMBA and MNU in rat mammary glands, DMBA promoted by TPA in mouse skin, and OH-BBN in mouse bladder. The agents tested may be classified into various pharmacological and chemical structural categories that are relevant to their chemopreventive potential. These categories include antiestrogens, antiinflammatories (e.g., NSAIDs), antioxidants, arachidonic acid metabolism inhibitors, GST and GSH enhancers, ODC inhibitors, protein kinase C inhibitors, retinoids and carotenoids, organosulfur compounds, calcium compounds, vitamin D-3 and analogs, and phenolic compounds (e.g., flavonoids). The various categories of compounds have different spectra of efficacy in animal models. In hamster lung, GSH-enhancing agents and antioxidants appear to have high potential for inhibiting carcinogenesis. In the colon, NSAIDs and other antiinflammatory agents appear particularly promising. Likewise, NSAIDs are very active in mouse bladder. In rat mammary glands, retinoids and antiestrogens (as would be expected) are efficacious. Several of the chemicals evaluated also appear to be promising chemopreventive agents based on their activity in several of the animal models. Particularly, the ODC inhibitor DFMO was active in the colon, mammary glands, and bladder models, while the dithiolthione, oltipraz, was efficacious in all the models listed above (i.e., lung, colon, mammary glands, skin, and bladder). (C) 1994 Wiley-Liss, Inc. C1 UNIV ILLINOIS,COLL MED,CTR SPECIALIZED CANC,CHICAGO,IL 60612. UNIV ALABAMA,BIRMINGHAM,AL 35294. AMER HLTH FDN,VALHALLA,NY 10595. UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX 77030. IIT,RES INST,CHICAGO,IL 60616. ENVIRONM HLTH RES & TESTING INC,LEXINGTON,KY 40503. CCS ASSOCIATES,MT VIEW,CA 94043. RP STEELE, VE (reprint author), NCI,DIV CANC CHEMOPREVENT & CONTROL,CHEMOPREVENT BRANCH,BETHESDA,MD 20892, USA. NR 181 TC 25 Z9 25 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. PY 1994 SU 20 BP 32 EP 54 PG 23 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ805 UT WOS:A1994QQ80500004 ER PT J AU RODLAND, KD MCNEIL, S KOHN, EC AF RODLAND, KD MCNEIL, S KOHN, EC TI INHIBITION OF PHOSPHOLIPASE-A2 BLOCKS THE ABILITY OF CAI, A NOVEL CHEMOTHERAPEUTIC AGENT, TO INDUCE IMMEDIATE-EARLY GENE-EXPRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,DEPT CELL BIOL & ANAT,PORTLAND,OR 97201. NCI,PATHOL LAB,TIMS,SIGNAL TRANSDUCT & PREVENT 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. PY 1994 SU 18D BP 34 EP 34 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400049 ER PT J AU TRAYNORKAPLAN, A VAJANAPHANICH, M SCHULTZ, C WASSERMAN, M SHEARS, SB TSIEN, RY BARRETT, KE AF TRAYNORKAPLAN, A VAJANAPHANICH, M SCHULTZ, C WASSERMAN, M SHEARS, SB TSIEN, RY BARRETT, KE TI LONG-TERM INHIBITION OF CA2+-DEPENDENT CHLORIDE TRANSPORT BY INS(3,4,5,6)P SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 USCD,DEPT MED & PHARM,LA JOLLA,CA. HOWARD HUGHES MED INST,LA JOLLA,CA. NIEHS,CELLULAR & MOLEC PHARM 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. PY 1994 SU 18D BP 43 EP 43 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400081 ER PT J AU ZIDOVETZKI, R LESTER, DS BORCHARDT, DB GOLDBERG, EM AF ZIDOVETZKI, R LESTER, DS BORCHARDT, DB GOLDBERG, EM TI DEPENDENCE OF PROTEIN-KINASE-C ACTIVATION BY DIACYLGLYCEROLS AND CALCIUM ON LIPID-MEMBRANE STRUCTURE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CALIF RIVERSIDE,DEPT BIOL,RIVERSIDE,CA 92521. UNIV CALIF RIVERSIDE,DEPT CHEM,RIVERSIDE,CA 92521. NIH,NEURAL SYST SECT,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 43 EP 43 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400084 ER PT J AU KELLOFF, GJ CROWELL, JA BOONE, CW STEELE, VE LUBET, RA GREENWALD, P ALBERTS, DS COVEY, JM DOODY, LA KNAPP, GG NAYFIELD, S PARKINSON, DR PRASAD, VK PROROK, PC SAUSVILLE, EA SIGMAN, CC AF KELLOFF, GJ CROWELL, JA BOONE, CW STEELE, VE LUBET, RA GREENWALD, P ALBERTS, DS COVEY, JM DOODY, LA KNAPP, GG NAYFIELD, S PARKINSON, DR PRASAD, VK PROROK, PC SAUSVILLE, EA SIGMAN, CC TI STRATEGY AND PLANNING FOR CHEMOPREVENTIVE DRUG DEVELOPMENT - CLINICAL DEVELOPMENT PLANS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article ID BREAST-CANCER PATIENTS; ANTI-INFLAMMATORY DRUGS; EPITHELIAL-CELL PROLIFERATION; ORNITHINE DECARBOXYLASE ACTIVITY; INDUCED COLON CARCINOGENESIS; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; URINARY-BLADDER CARCINOGENESIS; FAMILIAL ADENOMATOUS POLYPOSIS; SYNTHETIC RETINOID FENRETINIDE; EPIDERMAL GROWTH-FACTOR AB At the National Cancer Institute, Division of Cancer Prevention and Control, the Chemoprevention Branch and Agent Development Committee develop strategies for efficiently identifying procuring, and advancing the most promising drugs into clinical trials. Scientific expertise is applied at each phase of development to critically review the testing methods and results, and to establish and apply criteria for evaluating the agents for further development. The Clinical Development Man, prepared by the Chemoprevention Branch and the Agent Development Committee, is a summary of the status of the agent regarding evidence for safety and chemopreventive efficacy in preclinical and clinical studies. It also contains the strategy for further development of the drug that addresses pharmaco-dynamics, drug effect measurements, intermediate biomarkers for monitoring efficacy, toxicity, supply and formulation, regulatory approval, and proposed clinical trials. Sixteen Clinical Development Plans are presented here: N-acetyl-l-cysteine (NAC), aspirin, calcium, beta-carotene, 2-difluoromethylornithine (DFMO), DHEA analog 8354, 18 beta-glycyrrhetinic acid, N-(4-hydroxyphenyl)retinamide (4-HPR), ibuprofen, oltipraz, piroxicam, Proscar(R), sulindac, tamoxifen, vitamin D-3 and analogs, and vitamin E. The objective of publishing these plans is to stimulate interest and thinking among the scientific community on the prospects for developing chemopreventive drugs. (C) 1994 Wiley-Liss, Inc. C1 UNIV ARIZONA, CTR CANC RES, TUCSON, AZ 85724 USA. NCI, DIV CANC TREATMENT, PHARMACOL BRANCH, BETHESDA, MD 20892 USA. CCS ASSOCIATES, MT VIEW, CA 94043 USA. NCI, DIV CANC PREVENT & CONTROL, EARLY DETECT & COMMUNITY ONCOL PROGRAM, BETHESDA, MD 20892 USA. NCI, DIV CANC TREATMENT, INVEST DRUG BRANCH, BETHESDA, MD 20892 USA. OGDEN BIOSERV CORP, ROCKVILLE, MD 20850 USA. NCI, DIV CANC PREVENT & CONTROL, BIOL CHEM LAB, BETHESDA, MD 20892 USA. RP KELLOFF, GJ (reprint author), NCI, DIV CANC PREVENT & CONTROL, CHEMOPREVENT BRANCH, BETHESDA, MD 20892 USA. NR 1008 TC 12 Z9 12 U1 1 U2 3 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 20 BP 55 EP 303 PG 249 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ805 UT WOS:A1994QQ80500005 ER PT J AU HAWVER, DB CHEN, GA MANJI, HK POTTER, WZ AF HAWVER, DB CHEN, GA MANJI, HK POTTER, WZ TI CHRONIC VALPROATE TREATMENT ALTERS CELL MORPHOLOGY AND PKC LEVELS IN RAT C6 GLIOMA-CELLS AND IN HUMAN SK-N-SH NEUROBLASTOMA-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CLIN PHARMACOL SECT,BETHESDA,MD 20892. NIGMS,PRAT,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. PY 1994 SU 18D BP 57 EP 57 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400139 ER PT J AU CHEN, G MANJI, HK HAWVER, DB WRIGHT, CB POTTER, WZ AF CHEN, G MANJI, HK HAWVER, DB WRIGHT, CB POTTER, WZ TI PROTEIN-KINASE-C - A MOLECULAR TARGET FOR LONG-TERM PSYCHOTROPIC-DRUG ACTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIMH,EXPTL THERAPEUT BRANCH,CLIN PHARMACOL 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. PY 1994 SU 18D BP 74 EP 74 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400186 ER PT J AU MISCHAK, H PIERCE, JH GOODNIGHT, JA KAZANIETZ, MG BLUMBERG, PM MUSHINSKI, JF AF MISCHAK, H PIERCE, JH GOODNIGHT, JA KAZANIETZ, MG BLUMBERG, PM MUSHINSKI, JF TI PHORBOL ESTER-INDUCED MYELOID DIFFERENTIATION IS MEDIATED ONLY BY PROTEIN KINASE-C-ALPHA AND C-DELTA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,GENET LAB,BETHESDA,MD 20892. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. RI Mischak, Harald/E-8685-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 77 EP 77 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400198 ER PT J AU SZALLASI, Z SMITH, CB DENNING, MF DLUGOSZ, AA YUSPA, SH PETTIT, GR BLUMBERG, PM AF SZALLASI, Z SMITH, CB DENNING, MF DLUGOSZ, AA YUSPA, SH PETTIT, GR BLUMBERG, PM TI INHIBITION OF DOWN-REGULATION OF PROTEIN KINASE-C-DELTA BY BRYOSTATIN-1 CORRELATES WITH INHIBITION OF PHORBOL 12-MYRISTATE 13-ACETATE (PMA) INDUCED-DIFFERENTIATION IN MOUSE KERATINOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. ARIZONA STATE UNIV,CANC RES INST,TEMPE,AZ 85287. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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. PY 1994 SU 18D BP 79 EP 79 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400209 ER PT J AU LEHEL, C OLAH, Z JAKAB, G SZALLASI, Z BLUMBERG, PM ANDERSON, WB AF LEHEL, C OLAH, Z JAKAB, G SZALLASI, Z BLUMBERG, PM ANDERSON, WB TI INTRACELLULAR-LOCALIZATION AND BIOLOGICAL EFFECTS OF DIFFERENT DOMAIN FRAGMENTS OF PROTEIN KINASE-C-EPSILON OVEREXPRESSED IN NIH 3T3 CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NINCDS,CLIN NEUROSCI 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. PY 1994 SU 18D BP 85 EP 85 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400230 ER PT J AU KAZANIETZ, MG BRUNS, JD AXEEN, M ARECES, LB BLUMBERG, PM AF KAZANIETZ, MG BRUNS, JD AXEEN, M ARECES, LB BLUMBERG, PM TI CYSTEINE-RICH REGIONS AND PHORBOL ESTER BINDING - HIGH-AFFINITY INTERACTIONS IN PKC ISOZYMES, N-CHIMERIN AND UNC-13 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NR 1 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. PY 1994 SU 18D BP 90 EP 90 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400252 ER PT J AU WALDMANN, TA AF WALDMANN, TA TI THE INTERLEUKIN-2 RECEPTOR - A TARGET FOR IMMUNOTHERAPY OF LEUKEMIA-LYMPHOMA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 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. PY 1994 SU 18D BP 100 EP 100 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400278 ER PT J AU MAJUMDAR, A KERBY, S STENBERG, P MULLIKIN, B ARTHUR, P LEELIN, SQ COONEY, DA SEIDMAN, M AF MAJUMDAR, A KERBY, S STENBERG, P MULLIKIN, B ARTHUR, P LEELIN, SQ COONEY, DA SEIDMAN, M TI INDUCTION OF TERMINAL DIFFERENTIATION OF A MEGAKARYOCYTIC LEUKEMIA-CELL LINE WITH IL-3 AND RIBAVIRIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 OTSUKA AMER PHARMACEUT INC,ROCKVILLE,MD. OREGON HLTH SCI UNIV,DEPT PATHOL,PORTLAND,OR 97201. NCI,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 102 EP 102 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400286 ER PT J AU BARNEI, M MAGRATH, IT SAMID, D AF BARNEI, M MAGRATH, IT SAMID, D TI PHENYLACETATE AND PHENYLBUTYRATE MODULATE THE EXPRESSION OF CELLULAR AND VIRAL GENES IN BURKITT-LYMPHOMA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,PEDIAT ONCOL BRANCH,BETHESDA,MD 20892. NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 109 EP 109 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400314 ER PT J AU WOSIKOWSKI, K SACEDA, M MARTIN, MB BATES, SE AF WOSIKOWSKI, K SACEDA, M MARTIN, MB BATES, SE TI INVOLVEMENT OF GROWTH-FACTOR SIGNALING PATHWAY IN MULTIDRUG-RESISTANCE IN HUMAN BREAST-CANCER CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MED BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. RI Saceda, Miguel/A-1581-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 109 EP 109 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400313 ER PT J AU BARRETT, J GUIMARAES, A AF BARRETT, J GUIMARAES, A TI ALLO-T-CELL AND AUTO-T-CELL RECOGNITION OF CML CELLS DOES NOT INVOLVE BCR/ABL FUSION PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,MARROW TRANSPLANT 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. PY 1994 SU 18D BP 110 EP 110 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400315 ER PT J AU HERMOUET, S AZNAVOORIAN, S STEEG, PS SPIEGEL, AM AF HERMOUET, S AZNAVOORIAN, S STEEG, PS SPIEGEL, AM TI ROLE OF G(I)(2) PROTEINS IN TUMOR AND METASTASIS FORMATION IN MURINE MELANOMA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIADDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 110 EP 110 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400316 ER PT J AU KUAN, CT WANG, QC PASTAN, I AF KUAN, CT WANG, QC PASTAN, I TI PRE-INVESTIGATION ON PEGYLATION OF B3(FV)PE38 FUSION TOXIN BY CYSTEINE MUTAGENESIS OF PSEUDOMONAS EXOTOXIN A SURFACE-EXPOSED RESIDUES MODIFIED WITH PEG IN A SITE-SPECIFIC MANNER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,DCBDC,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. PY 1994 SU 18D BP 111 EP 111 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400319 ER PT J AU SLOANE, BF SAMENI, M BERQUIN, IM ROZHIN, J ZIEGLER, G BUCK, MR REMPEL, S ROSENBLUM, ML SINHA, A VISSCHER, D AF SLOANE, BF SAMENI, M BERQUIN, IM ROZHIN, J ZIEGLER, G BUCK, MR REMPEL, S ROSENBLUM, ML SINHA, A VISSCHER, D TI CATHEPSIN-B AND PROGRESSION OF HUMAN TUMORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 WAYNE STATE UNIV,DETROIT,MI 48201. NCI,BETHESDA,MD 20892. HENRY FORD MED CTR,DETROIT,MI. VET ADM MED CTR,MINNEAPOLIS,MN. RI Sloane, Bonnie/A-1050-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 121 EP 121 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400351 ER PT J AU KEMPF, DJ FLENTGE, C MARSH, KC MCDONALD, E ROBINS, T VASAVANONDA, S CHEN, CM WIDEBURG, NE PARK, C KONG, XP DENISSEN, J HO, DD MARKOWITZ, M TOYOSHIMA, T SINGH, MK ERICKSON, J SHAM, HL STEWART, K GREEN, BE TURON, M SALDIVAR, A NORBECK, DW AF KEMPF, DJ FLENTGE, C MARSH, KC MCDONALD, E ROBINS, T VASAVANONDA, S CHEN, CM WIDEBURG, NE PARK, C KONG, XP DENISSEN, J HO, DD MARKOWITZ, M TOYOSHIMA, T SINGH, MK ERICKSON, J SHAM, HL STEWART, K GREEN, BE TURON, M SALDIVAR, A NORBECK, DW TI SYMMETRY-BASED INHIBITORS OF HIV PROTEASE - ORAL BIOAVAILABILITY AND RESISTANCE EMERGENCE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ABBOTT LABS,DIV PHARMACEUT PROD,ABBOTT PK,IL. AARON DIAMOND AIDS RES CTR,NEW YORK,NY. NCI,FREDERICK BIOMED SUPERCOMP CTR,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21701. 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. PY 1994 SU 18D BP 130 EP 130 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400378 ER PT J AU BRISTOL, LA BACHOVCHIN, W GYURIS, T PETERFY, M GIUNTA, M TAKACS, L AF BRISTOL, LA BACHOVCHIN, W GYURIS, T PETERFY, M GIUNTA, M TAKACS, L TI THE ROLE OF DIPEPTIDYL DIPEPTIDASE-IV (DPP-IV, E.C.N.3.4.14.5) CD 26 ENZYMATIC-ACTIVITY IN REGULATION OF HEMATOPOIETIC AND EARLY T-CELL PROLIFERATION IN-VITRO AND IN-VIVO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 AMGEN INC,THOUSAND OAKS,CA. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. TUFTS UNIV,SCH MED,DEPT BIOCHEM,BOSTON,MA 02111. 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. PY 1994 SU 18D BP 142 EP 142 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400423 ER PT J AU GULNIK, SV MAJER, P COLLINS, JR YU, BR RANDAD, RS BEYER, B DUNN, BM ERICKSON, JW AF GULNIK, SV MAJER, P COLLINS, JR YU, BR RANDAD, RS BEYER, B DUNN, BM ERICKSON, JW TI DESIGN AND ACTIVITY OF LINEAR AND CYCLIC STATINE - BASED INHIBITORS OF CATHEPSIN-D SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 PRI DYNCORP,NCI,FCRDC,STRUCT BIOCHEM,FREDERICK,MD 21702. UNIV FLORIDA,DEPT BIOCHEM & MOLEC BIOL,GAINESVILLE,FL 32610. NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 143 EP 143 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400428 ER PT J AU BECERRA, SP TWINING, SS CHADER, GJ AF BECERRA, SP TWINING, SS CHADER, GJ TI PIGMENT EPITHELIUM-DERIVED FACTOR - A SERPIN WITH NEUROTROPHIC ACTIVITY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. MED COLL WISCONSIN,DEPT BIOCHEM,MILWAUKEE,WI 53226. 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. PY 1994 SU 18D BP 150 EP 150 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400458 ER PT J AU CHEN, CM SALDIVAR, A TURON, M WIDEBURG, NE ROBINS, T VASAVANONDA, S STEWART, K PARK, C KONG, XP KEMPF, DJ HO, D ERICKSON, J NORBECK, DW AF CHEN, CM SALDIVAR, A TURON, M WIDEBURG, NE ROBINS, T VASAVANONDA, S STEWART, K PARK, C KONG, XP KEMPF, DJ HO, D ERICKSON, J NORBECK, DW TI BIOCHEMICAL-CHARACTERIZATION OF HIV-1 PROTEASE MUTANTS RESISTANT TO A-77003, A-80987 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ABBOTT LABS,DIV PHARMACEUT PROD,ABBOTT PK,IL 60064. AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10016. NCI,FREDERICK BIOMED SUPERCOMP CTR,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702. 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. PY 1994 SU 18D BP 166 EP 166 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400519 ER PT J AU THANKI, N HUMBLET, CC LUNNEY, EA WLODAWER, A AF THANKI, N HUMBLET, CC LUNNEY, EA WLODAWER, A TI CRYSTAL-STRUCTURES OF 2 RATIONALLY SELECTED, STRUCTURALLY NOVEL HIV-1 PROTEASE INHIBITORS - COMPARISONS WITH MODELING SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. PARKE DAVIS CO,DEPT CHEM,DIV PHARMACEUT,ANN ARBOR,MI 48105. 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. PY 1994 SU 18D BP 175 EP 175 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400555 ER PT J AU MARK, GE PADLAN, EA AF MARK, GE PADLAN, EA TI CDR-GRAFTING AND VENEERING APPROACHES TO MAB HUMANIZATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MERCK SHARP & DOHME LTD,RAHWAY,NJ 07065. NIDDK,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. PY 1994 SU 18D BP 180 EP 180 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400568 ER PT J AU PINCUS, SH AF PINCUS, SH TI ANTI-HIV IMMUNOTOXINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 181 EP 181 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400570 ER PT J AU SEGAL, DM JOST, CR GEORGE, AJT KURUCZ, I TITUS, JA AF SEGAL, DM JOST, CR GEORGE, AJT KURUCZ, I TITUS, JA TI EXPRESSION OF SINGLE-CHAIN FV MOLECULES IN BACTERIAL AND MAMMALIAN SYSTEMS AND THEIR USE AS CYTOTOXIC TARGETING AGENTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 181 EP 181 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400571 ER PT J AU BURTON, DR BARBAS, CF BINLEY, JM DITZEL, H HENDRY, M LANE, HC WALKER, R MOORE, JP NARA, PM NORRBY, E THALI, M SODROSKI, J AF BURTON, DR BARBAS, CF BINLEY, JM DITZEL, H HENDRY, M LANE, HC WALKER, R MOORE, JP NARA, PM NORRBY, E THALI, M SODROSKI, J TI RECOMBINANT NEUTRALIZING HUMAN-ANTIBODIES TO HIV-1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 SCRIPPS RES INST, LA JOLLA, CA USA. CALIF INST PUBL HLTH, BERKELEY, CA USA. NIAID, BETHESDA, MD 20892 USA. NCI, FREDERICK, MD 21701 USA. AARON DIAMOND AIDS RES CTR, NEW YORK, NY USA. KAROLINSKA INST, S-10401 STOCKHOLM, SWEDEN. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 185 EP 185 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400581 ER PT J AU COUTO, JR PADLAN, EA BLANK, EW PETERSON, JA CERIANI, RL AF COUTO, JR PADLAN, EA BLANK, EW PETERSON, JA CERIANI, RL TI HUMANIZATION OF KC4G3, AN ANTI-HUMAN BREAST EPITHELIAL MUCIN ANTIBODY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 CANC RES FUND CONTRA COSTA,WALNUT CREEK,CA 94596. NIH,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 190 EP 190 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400597 ER PT J AU CHAUDHARY, VK ABROL, S PASTAN, I AF CHAUDHARY, VK ABROL, S PASTAN, I TI CELL AFFINITY ENRICHMENT OF PHAGES DISPLAYING SINGLE-CHAIN ANTIBODIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV DELHI S CAMPUS,DEPT BIOCHEM,NEW DELHI 110021,INDIA. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 198 EP 198 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400628 ER PT J AU JUNG, SH PASTAN, I LEE, BK AF JUNG, SH PASTAN, I LEE, BK TI DESIGN OF INTERCHAIN DISULFIDE BONDS IN THE FRAMEWORK OF FV FRAGMENTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,MOLEC BIOL LAB,BETHESDA,MD 20892. RI Lee, Byungkook/E-4564-2011 OI Lee, Byungkook/0000-0002-3339-4582 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. PY 1994 SU 18D BP 207 EP 207 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400663 ER PT J AU SLAVINCHIORINI, DC HAND, PH KASHMIRI, SVS CALVO, B SCHOTT, ME MILENIC, DE SCHLOM, J AF SLAVINCHIORINI, DC HAND, PH KASHMIRI, SVS CALVO, B SCHOTT, ME MILENIC, DE SCHLOM, J TI BIOLOGIC PROPERTIES OF AN ANTI-CARCINOMA CH2 DOMAIN-DELETED RECOMBINANT IMMUNOGLOBULIN 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. PY 1994 SU 18D BP 208 EP 208 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400668 ER PT J AU BRINKMANN, U REITER, Y JUNG, SH WEBBER, K LEE, BK PASTAN, I AF BRINKMANN, U REITER, Y JUNG, SH WEBBER, K LEE, BK PASTAN, I TI DISULFIDE STABILIZED FV FRAGMENTS (DSFV) AND DSFV-IMMUNOTOXINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. RI Lee, Byungkook/E-4564-2011 OI Lee, Byungkook/0000-0002-3339-4582 NR 6 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. PY 1994 SU 18D BP 210 EP 210 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400675 ER PT J AU DICKSON, RB AMUNDADOTTIR, LT MARTINEZLACACI, I JOHNSON, MD PLOWMAN, G SACEDA, M NORMANNO, N SMITH, G SALOMON, DS MERLINO, GT AF DICKSON, RB AMUNDADOTTIR, LT MARTINEZLACACI, I JOHNSON, MD PLOWMAN, G SACEDA, M NORMANNO, N SMITH, G SALOMON, DS MERLINO, GT TI GROWTH FACTOR-SEX STEROID INTERACTIONS IN BREAST TUMORIGENESIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,LOMBARDI CANC RES CTR,WASHINGTON,DC 20057. BRISTOL MYERS SQUIBB,SEATTLE,WA. NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. RI Saceda, Miguel/A-1581-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 220 EP 220 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400707 ER PT J AU SALOMON, DS BRANDT, R CIARDIELLO, F NORMANNO, N AF SALOMON, DS BRANDT, R CIARDIELLO, F NORMANNO, N TI EPIDERMAL GROWTH FACTOR-RELATED PEPTIDES IN BREAST-CANCER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR IMMUNOL & BIOL LAB,TUMOR GROWTH FACTOR SECT,BETHESDA,MD 20892. UNIV NAPLES,FAC MED & CHIRURG,CATTEDRA ONCOL MED,I-80131 NAPLES,ITALY. UNIV NAPLES,FDN PASCALE,INST NAZL STUDIO CURA TUMORI,I-80131 NAPLES,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. PY 1994 SU 18D BP 220 EP 220 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400706 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,LOMBARDI CANC CTR,WASHINGTON,DC 20007. NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 228 EP 228 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400727 ER PT J AU GRIZZLE, WE MYERS, RB OELSCHLAGER, D SRIVASTAVA, S AF GRIZZLE, WE MYERS, RB OELSCHLAGER, D SRIVASTAVA, S TI TGF-ALPHA EXPRESSION IS A RELATIVELY LATE EVENT IN THE PROGRESSION OF PROSTATIC ADENOCARCINOMA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV ALABAMA,DEPT PATHOL,BIRMINGHAM,AL 35294. 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. PY 1994 SU 18D BP 230 EP 230 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400735 ER PT J AU GROSSE, R YAN, YM SPITZER, E ZSCHIESCHE, W SMITH, GH SALOMON, D AF GROSSE, R YAN, YM SPITZER, E ZSCHIESCHE, W SMITH, GH SALOMON, D TI MAMMARY-DERIVED GROWTH INHIBITOR (MDGI) IS A NEW DIFFERENTIATION FACTOR FOR THE MAMMARY-GLAND SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MAX DELBRUCK CTR MOLEC MED,D-13122 BERLIN,GERMANY. NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. UNIV BERGEN,HAUKELAND HOSP,INST GADE,N-5021 BERGEN,NORWAY. 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. PY 1994 SU 18D BP 230 EP 230 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400737 ER PT J AU JAHNKE, GD TREMPUS, CS KARI, F DIAUGUSTINE, RP AF JAHNKE, GD TREMPUS, CS KARI, F DIAUGUSTINE, RP TI DETECTION OF A PROLACTIN-LIKE FACTOR IN NEOPLASTIC MOUSE MAMMARY EPITHELIAL-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,HORMONES & CANC WORKGROUP,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. PY 1994 SU 18D BP 231 EP 231 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400740 ER PT J AU RAE, JM GOTTARDIS, MM SIEGALL, CB PASTAN, I LIPPMAN, ME AF RAE, JM GOTTARDIS, MM SIEGALL, CB PASTAN, I LIPPMAN, ME TI PENTOSAN POLYSULFATE PRODUCES A SYNERGISTIC INCREASE IN THE CYTOTOXIC EFFECTS OF ACIDIC FIBROBLAST GROWTH FACTOR-PSEUDOMONAS EXOTOXIN FUSION PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 LOMBARDI CANC CTR,WASHINGTON,DC 20007. BRISTOL MYERS SQUIBB,SEATTLE,WA 98121. NCI,BETHESDA,MD 20205. 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. PY 1994 SU 18D BP 233 EP 233 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400750 ER PT J AU MAROULAKOU, I GARRETT, I ANVER, M PAPAS, I GREEN, J AF MAROULAKOU, I GARRETT, I ANVER, M PAPAS, I GREEN, J TI PROSTATE AND BREAST ADENOCARCINOMA DEVELOPMENT IN TRANSGENIC MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,LMO,FREDERICK,MD 21701. PRI,DYNCORP,FREDERICK,MD. HCC,CMSB,CHARLESTON,SC. 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. PY 1994 SU 18D BP 243 EP 243 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400785 ER PT J AU RINKENSCHAEFFER, CW DONG, JT LAMB, P BARRETT, JC ISAACS, JT AF RINKENSCHAEFFER, CW DONG, JT LAMB, P BARRETT, JC ISAACS, JT TI CHARACTERIZATION OF THE METASTASIS SUPPRESSOR ACTIVITY ON HUMAN-CHROMOSOME 11P11.2-13 - IDENTIFICATION OF A PUTATIVE METASTASIS SUPPRESSOR GENE FOR PROSTATIC-CANCER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. 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. PY 1994 SU 18D BP 244 EP 244 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400791 ER PT J AU SLAWIN, K KADMON, D PARK, SH SCARDINO, PT ANZANO, M SPORN, MB THOMPSON, TC AF SLAWIN, K KADMON, D PARK, SH SCARDINO, PT ANZANO, M SPORN, MB THOMPSON, TC TI FENRETINIDE SELECTS FOR ALTERNATIVE PATHWAYS OF CARCINOGENESIS IN THE MOUSE PROSTATE RECONSTITUTION (MPR) MODEL SYSTEM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 BAYLOR COLL MED,SCOTT DEPT UROL,HOUSTON,TX 77030. 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. PY 1994 SU 18D BP 245 EP 245 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400795 ER PT J AU BERGAN, RC KYLE, E NECKERS, L AF BERGAN, RC KYLE, E NECKERS, L TI GENISTEIN - A PROTEIN-TYROSINE KINASE INHIBITOR INHIBITS THE GROWTH OF PROSTATE-CANCER CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 251 EP 251 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400816 ER PT J AU HORAK, E HARTMANN, F GARMESTANI, K WU, CC GANSOW, OA LANDOLFI, NF WALDMANN, TA AF HORAK, E HARTMANN, F GARMESTANI, K WU, CC GANSOW, OA LANDOLFI, NF WALDMANN, TA TI RADIOIMMUNOTHERAPY OF NUDE-MICE BEARING A HUMAN HER2/NEU POSITIVE TUMOR UTILIZING THE ALPHA-EMITTING RADIONUCLIDE-CONJUGATED MONOCLONAL-ANTIBODY PB-212-DOTA-AE1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,METAB BRANCH,BETHESDA,MD 20892. NCI,RADIAT ONCOL BRANCH,MT VIEW,CA 94043. PROT DESIGN LABS,MT VIEW,CA 94043. 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. PY 1994 SU 18D BP 252 EP 252 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400823 ER PT J AU KARR, JF KANTOR, J HAND, PH PARANAVITANA, C SCHLOM, J AF KARR, JF KANTOR, J HAND, PH PARANAVITANA, C SCHLOM, J TI EXPRESSION OF HUMAN PROSTATE-SPECIFIC ANTIGEN IN A TRANSFECTED MURINE ADENOCARCINOMA CELL-LINE - DEVELOPMENT OF A MURINE TUMOR-MODEL FOR IMMUNOTHERAPY OF PROSTATE-CANCER 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. PY 1994 SU 18D BP 253 EP 253 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400826 ER PT J AU BARRETT, JC DONG, JT LAMB, PW RINKERSCHAEFFER, CW ISAACS, JT AF BARRETT, JC DONG, JT LAMB, PW RINKERSCHAEFFER, CW ISAACS, JT TI CLONING AND CHARACTERIZATION OF A PUTATIVE METASTASIS SUPPRESSOR GENE ON HUMAN CHROMOSOME-11P11.2-13 FOR PROSTATIC-CANCER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. JOHNS HOPKINS UNIV,CTR ONCOL,BALTIMORE,MD 21231. 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. PY 1994 SU 18D BP 254 EP 254 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400828 ER PT J AU WEINSTATSASLOW, DL ZABRENETZKY, VS ROBERTS, DD STEEG, PS AF WEINSTATSASLOW, DL ZABRENETZKY, VS ROBERTS, DD STEEG, PS TI THROMBOSPONDIN OVEREXPRESSION IN THE HUMAN MDA-MB-435 BREAST-CARCINOMA CELL-LINE SUPPRESSES TUMOR-GROWTH AND METASTATIC POTENTIAL SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,PATHOL 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. PY 1994 SU 18D BP 254 EP 254 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400829 ER PT J AU GRIZZLE, WE MYERS, RB ARNOLD, MM SRIVASTAVA, S AF GRIZZLE, WE MYERS, RB ARNOLD, MM SRIVASTAVA, S TI EVALUATION OF BIOMARKERS IN BREAST AND PROSTATE-CANCER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE BIOMARKERS; BREAST; ERBB-2 FIXATION; P53; PROSTATE; TISSUE PROCESSING ID P53 PROTEIN; EXPRESSION; ACCUMULATION; PROGNOSIS; CARCINOMA; MUTATION AB p53, p185(erbB-2), and epidermal growth factor (EGF) receptor are well-characterized biomarkers in invasive adenocarcinoma of the breast and in ductal carcinoma in situ. erbB-2 Protein (p185(erbB-2)) must be identified clearly on cytoplasmic membranes while cytoplasmic expression is ignored for breast cancers to be classified as overexpressing p185(erbB-2). For p53, nuclear staining and the percent positive cells are considered, but rules for ''cut-offs'' are not defined. Evaluation criteria for biomarkers in prostate cancer are preliminary and the ''rules'' may not be the same as for breast cancer. Because the initial methods of fixation and tissue processing can change both the pattern and intensity of immunohistochemical identification of specific antigens and localization of receptors may change after the receptor-ligand interactions, we evaluated the effects of fixation both on the immunolocalization and intensity of expression of p53, p185(erbB-2), and EGF receptor. We also studied the patterns of p185(erbB-2), and p53 expression in a series of breast cancers evaluated concomitantly with a group of prostate cancers. Our results confirm that p53 mutations are common in breast cancer and that there is strong expression of p185(erbB-2) on the membranes of a subset of breast cancers. The patterns of staining for both p53 and p185(erbB-2), different in prostate and breast cancers. A much lower proportion of prostate tumors than breast tumors have more than 10% of tumor cells with detectable nuclear p53 protein, but this proportion increases markedly in metastatic tumors or in primary stage D prostate cancer. In addition, a higher concentration of primary antibody is necessary to demonstrate nuclei showing p53 accumulation in prostate cancers than in breast cancers. The expression of p185(erbB-2) in prostate cancer is much coarser and more punctate than that observed in breast cancer; extensive cytoplasmic staining usually is detected in most prostatic adenocarcinomas. Concentrations of primary antibody to p185(erbB-2) that will stain membranes of breast cancers will not stain prostate cancer cells as strongly. However, the expression of p53 and/or p185(erbB-2) should not be ignored in prostate cancer since the rules for correlation of these biomarkers with the clinical outcome, or for use as surrogate endpoint biomarkers, have not been developed. Neutral buffered formalin is a poor initial fixative compared with other fixatives for demonstrating p53 accumulation or p185(erbB-2) expression. The effect of formalin fixation can be reversed with antigen retrieval methods, increasing detection markedly in cells with p53 accumulation. (C) 1994 Wiley-Liss, Inc. C1 NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. RP GRIZZLE, WE (reprint author), UNIV ALABAMA,DEPT PATHOL,UNIV STN,BIRMINGHAM,AL 35294, USA. NR 14 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 19 BP 259 EP 266 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PJ098 UT WOS:A1994PJ09800038 ER PT J AU ROBERTS, DD GUO, NH VOGEL, T ZABRENETZKY, VS BLAKE, DA INMAN, JK KRUTZSCH, HC AF ROBERTS, DD GUO, NH VOGEL, T ZABRENETZKY, VS BLAKE, DA INMAN, JK KRUTZSCH, HC TI THROMBOSPONDIN INTERACTIONS WITH SULFATED GLYCOCONJUGATES REGULATE TUMOR-CELL ADHESION, MOTILITY, AND PROLIFERATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. TULANE UNIV,SCH MED,DEPT OPHTHALMOL,NEW ORLEANS,LA 70112. 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. PY 1994 SU 18D BP 261 EP 261 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400846 ER PT J AU BALAJI, PV QASBA, PK RAO, VSR AF BALAJI, PV QASBA, PK RAO, VSR TI MOLECULAR-DYNAMICS SIMULATIONS OF HIGH-MANNOSE OLIGOSACCHARIDES - POSSIBLE PATHWAYS FOR PROCESSING OF MAN(9)GLCNAC(2) TO MAN(5)GLCNAC(2) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,LMMB,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. PY 1994 SU 18D BP 269 EP 269 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400871 ER PT J AU BARTOSZEWICZ, ZP QUARLES, RH AF BARTOSZEWICZ, ZP QUARLES, RH TI ABNORMAL GLYCOSYLATION OF MAG IN THE DYSMYELINATING, QUAKING MUTANT 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. PY 1994 SU 18D BP 276 EP 276 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400899 ER PT J AU DULLFORCE, P MATZINGER, P GRAY, D AF DULLFORCE, P MATZINGER, P GRAY, D TI CELL-INTERACTIONS NECESSARY FOR THE MAINTENANCE OF MEMORY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. ROYAL POSTGRAD MED SCH,DEPT IMMUNOL,LONDON W12 0HS,ENGLAND. 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. PY 1994 SU 18D BP 286 EP 286 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400929 ER PT J AU GERMAIN, RN CASTELLINO, F RINKER, AG SADEGHNASSERI, S ROMAGNOLI, P AF GERMAIN, RN CASTELLINO, F RINKER, AG SADEGHNASSERI, S ROMAGNOLI, P TI THE BIOCHEMISTRY AND CELL BIOLOGY OF MHC CLASS-II ANTIGEN PRESENTATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BETHESDA,MD 20892. RI Romagnoli, Paola/K-2237-2014 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. PY 1994 SU 18D BP 286 EP 286 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400928 ER PT J AU YE, C SIDNEY, J SOUTHWOOD, S BENJAMIN, D COX, AL SAKAGUCHI, K HENDERSON, RA APPELLA, E HUNT, DF SETTE, A ENGELHARD, VH AF YE, C SIDNEY, J SOUTHWOOD, S BENJAMIN, D COX, AL SAKAGUCHI, K HENDERSON, RA APPELLA, E HUNT, DF SETTE, A ENGELHARD, VH TI NATURALLY PROCESSED PEPTIDES LONGER THAN 9 AMINO-ACID-RESIDUES BIND TO THE CLASS-I MHC MOLECULE HLA-A2.1 WITH HIGH-AFFINITY AND IN DIFFERENT CONFORMATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV VIRGINIA,DEPT MICROBIOL,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,DEPT MED,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,BEIRNE CARTER CTR IMMUNOL RES,CHARLOTTESVILLE,VA 22908. NCI,BETHESDA,MD 20892. RI Hunt, Donald/I-6936-2012 OI Hunt, Donald/0000-0003-2815-6368 NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 289 EP 289 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400937 ER PT J AU LOFTUS, DJ SAKAGUCHI, K YE, C SAKAMOTO, H SETTE, A ENGELHARD, VH APPELLA, E AF LOFTUS, DJ SAKAGUCHI, K YE, C SAKAMOTO, H SETTE, A ENGELHARD, VH APPELLA, E TI ANALYSIS OF TCR RECOGNITION OF A CLASS-1 PEPTIDE EPITOPE AIDED BY THE USE OF A SYNTHETIC, COMBINATORIAL PEPTIDE LIBRARY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CYTEL,SAN DIEGO,CA 92121. UNIV VIRGINIA,BEIRNE CARTER CTR IMMUNOL RES,CHARLOTTESVILLE,VA 22908. NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 291 EP 291 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400948 ER PT J AU PARKER, KC DIBRINO, M BIDDISON, WE COLIGAN, JE AF PARKER, KC DIBRINO, M BIDDISON, WE COLIGAN, JE TI BINDING MOTIFS AND ANTIGENIC PEPTIDES IN HUMAN MHC CLASS-I MOLECULES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BIOL RESOURCES BRANCH,BETHESDA,CA. NINCDS,NEUROIMMUNOL 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. PY 1994 SU 18D BP 292 EP 292 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400951 ER PT J AU CHANG, AC WADSWORTH, S HONG, MJP COLIGAN, JE AF CHANG, AC WADSWORTH, S HONG, MJP COLIGAN, JE TI THE AVIDITY BETWEEN VLAS AND THEIR LIGANDS IS DEPENDENT ON THE STAGE OF T-CELL MATURATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 296 EP 296 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400965 ER PT J AU COLIGAN, JE CHANG, A HONG, MJP WADSWORTH, S AF COLIGAN, JE CHANG, A HONG, MJP WADSWORTH, S TI BETA(1)-INTEGRIN CHAIN CONFORMATION AND ANTI-BETA(1)-ANTIBODY MEDIATED ENHANCEMENT OF FIBRONECTIN-BINDING ARE DEPENDENT ON THE STAGE OF T-CELL MATURATION AND ACTIVATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 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. PY 1994 SU 18D BP 296 EP 296 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400967 ER PT J AU THEVENIN, C SHIRAKATA, Y COLIGAN, J KEHRL, JH AF THEVENIN, C SHIRAKATA, Y COLIGAN, J KEHRL, JH TI DETECTION OF IN-VIVO DNA-PROTEIN INTERACTIONS AT THE PROMOTER OF THE CD20 GENE IN B-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 302 EP 302 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400990 ER PT J AU CASSELL, DJ SCHWARTZ, RH AF CASSELL, DJ SCHWARTZ, RH TI STIMULATION OF NAIVE CD4 T-LYMPHOCYTES BY ACTIVATED B-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,CELLULAR & MOLEC IMMUNOL,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. PY 1994 SU 18D BP 307 EP 307 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400994 ER PT J AU KELSALL, BL EHRHARDT, RO STROBER, W AF KELSALL, BL EHRHARDT, RO STROBER, W TI PEYERS PATCH DENDRITIC CELLS - PHENOTYPIC CHARACTERIZATION BY FACS ANALYSIS AND IN-VITRO PRIMARY AND SECONDARY T-CELL RESPONSES USING A TCR-TRANSGENIC MOUSE MODEL 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. PY 1994 SU 18D BP 310 EP 310 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401006 ER PT J AU DAVIDSON, WF GIESE, T AF DAVIDSON, WF GIESE, T TI ANTI-CD8 MAB THERAPY PREVENTS THE ACCUMULATION OF B220+ DN T-CELLS BUT NOT AUTOANTIBODY PRODUCTION IN C3H-LPR/LPR AND C3H-GLD/GLD MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,GENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 315 EP 315 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401024 ER PT J AU PELFREY, C TROTTER, J TRANQUILL, L MCFARLAND, H AF PELFREY, C TROTTER, J TRANQUILL, L MCFARLAND, H TI MYELIN PROTEOLIPID PROTEIN (PLP) REACTIVITY IN MULTIPLE-SCLEROSIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. 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. PY 1994 SU 18D BP 319 EP 319 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401043 ER PT J AU RACKE, MK MCFARLIN, DE SCOTT, DE AF RACKE, MK MCFARLIN, DE SCOTT, DE TI MODIFICATION OF CYTOKINE PRODUCTION BY T-CELLS ACTIVATED IN THE PRESENCE OF RETINOIC ACID SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. US FDA,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. PY 1994 SU 18D BP 320 EP 320 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401044 ER PT J AU LINK, H BENNINK, J YEWDELL, J AF LINK, H BENNINK, J YEWDELL, J TI PROTEOLYTIC PROCESSING OF ANTIGENIC PEPTIDES IN THE ENDOPLASMIC-RETICULUM 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. PY 1994 SU 18D BP 335 EP 335 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401103 ER PT J AU PINET, VM MALNATI, MS LONG, EO AF PINET, VM MALNATI, MS LONG, EO TI 2 PROCESSING PATHWAYS FOR THE CLASS-II MHC-RESTRICTED PRESENTATION OF EXOGENOUS ANTIGENS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 336 EP 336 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401108 ER PT J AU ROCHE, PA WARMERDAM, PAM LONG, EO AF ROCHE, PA WARMERDAM, PAM LONG, EO TI TARGETING OF MHC CLASS-II ALPHA-BETA-II COMPLEXES TO ENDOSOMES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 336 EP 336 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401110 ER PT J AU WARMERDAM, PAM ROCHE, PA LONG, EO AF WARMERDAM, PAM ROCHE, PA LONG, EO TI BIOSYNTHETIC RATE AND TRANSPORT OF MHC CLASS-II MOLECULES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 338 EP 338 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401117 ER PT J AU WHITE, KL LINK, HT KRZYCH, U AF WHITE, KL LINK, HT KRZYCH, U TI REQUIREMENT FOR T-CELL ACTIVATION BY INTACT PLASMODIUM-BERGHEI SPOROZOITES VERSUS CIRCUMSPOROZOITE PROTEIN-PEPTIDES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,DEPT VIRAL DIS,BETHESDA,MD 20892. CATHOLIC UNIV AMER,DEPT BIOL,WASHINGTON,DC 20064. WALTER REED ARMY INST RES,WASHINGTON,DC 20307. 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. PY 1994 SU 18D BP 338 EP 338 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401116 ER PT J AU NAKAYAMA, T WIEST, DL ABRAHAM, KM MUNITZ, TI PERLMUTTER, RM SINGER, A AF NAKAYAMA, T WIEST, DL ABRAHAM, KM MUNITZ, TI PERLMUTTER, RM SINGER, A TI DECREASED SIGNALING COMPETENCE AS A RESULT OF RECEPTOR OVEREXPRESSION - OVEREXPRESSION OF CD4 REDUCES ITS ABILITY TO ACTIVATE P56ICK AND TO REGULATE TCR EXPRESSION IN IMMATURE CD4+CD8+ THYMOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV TOKYO,FAC MED,DEPT IMMUNOL,TOKYO 113,JAPAN. NCI,E1B,BETHESDA,MD 20892. UNIV WASHINGTON,SEATTLE,WA 98195. RI Nakayama, Toshinori/E-1067-2017 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 344 EP 344 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401139 ER PT J AU SHIRAI, M VACCHIO, MS HODES, RJ BERZOFSKY, JA AF SHIRAI, M VACCHIO, MS HODES, RJ BERZOFSKY, JA TI STRONG PREDOMINANCE OF V-BETA-8 OR 14 TCR USAGE BY CYTOTOXIC T-CELLS CROSS-REACTIVE TO 2 HIV-1 EPITOPES AND DEGENERATE IN PRESENTATION TO CLASS-I MHC MOLECULES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC IMMUNOGENET & VACCINE RES SECT,METAB BRANCH,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 346 EP 346 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401150 ER PT J AU JACOBSON, S ELOVAARA, I BOHEME, S AF JACOBSON, S ELOVAARA, I BOHEME, S TI INHIBITION OF IMMUNOPATHOGENIC HTLV-I SPECIFIC CD8+ CYTOTOXIC T-CELL RESPONSES IN PATIENTS WITH HTLV-I-ASSOCIATED NEUROLOGIC DISEASE 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. PY 1994 SU 18D BP 356 EP 356 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401189 ER PT J AU MORAWETZ, R GIESE, N DOHERTY, M MULLER, W KUHN, R RAJEWSKY, K COFFMANN, RL MORSE, HC AF MORAWETZ, R GIESE, N DOHERTY, M MULLER, W KUHN, R RAJEWSKY, K COFFMANN, RL MORSE, HC TI CYTOKINE EXPRESSION AND CONTROL OF RETROVIRUS-INDUCED IMMUNODEFICIENCY IN THE MOUSE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV COLOGNE,INST GENET,W-5000 COLOGNE 41,GERMANY. NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. DNAX RES INST MOLEC & CELLULAR BIOL INC,RES INST,PALO ALTO,CA 94304. 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. PY 1994 SU 18D BP 359 EP 359 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401199 ER PT J AU GIESE, N MCCARTY, TJ DERIVERA, C GIESE, T MORSE, HC AF GIESE, N MCCARTY, TJ DERIVERA, C GIESE, T MORSE, HC TI MHC CLASS II-POSITIVE CELLS ARE REQUIRED FOR DEVELOPMENT OF MAIDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,GENET LAB,BETHESDA,MD 20892. NIAID,IMMUNOPATHOL 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. PY 1994 SU 18D BP 365 EP 365 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401221 ER PT J AU PUCILLO, C CAPEDA, R HODES, RJ AF PUCILLO, C CAPEDA, R HODES, RJ TI EXPRESSION OF A MHC CLASS-II TRANSGENE DETERMINES BOTH SUPERANTIGENICITY AND SUSCEPTIBILITY TO MAMMARY-TUMOR VIRUS-INFECTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NIA,BETHESDA,MD 20892. RI Pucillo, Carlo/A-5515-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 368 EP 368 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401233 ER PT J AU BECKWITH, M OCONNELL, C TUCKER, PW HILL, S BAGINSKI, L LONGO, DL KENNY, JJ AF BECKWITH, M OCONNELL, C TUCKER, PW HILL, S BAGINSKI, L LONGO, DL KENNY, JJ TI ARRESTED B-CELL DEVELOPMENT IN TRANSGENIC MICE EXPRESSING A CHIMERIC IGM-KAPPA-IA-ALPHA-TRANSMEMBRANE MOLECULE AS THEIR ANTIGEN-SPECIFIC RECEPTOR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. UNIV TEXAS,DALLAS,TX 75235. DYNCORP,PROGRAM RESOURCES INC,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. PY 1994 SU 18D BP 372 EP 372 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401248 ER PT J AU GERETY, SJ KLUG, CA CHEN, YY RICE, NR ROSENBERG, N SINGH, H AF GERETY, SJ KLUG, CA CHEN, YY RICE, NR ROSENBERG, N SINGH, H TI THE V-ABL TYROSINE KINASE NEGATIVELY REGULATES NF-KAPPA-B AND BLOCKS KAPPA GENE-TRANSCRIPTION IN PRE-B-LYMPHOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CHICAGO,HOWARD HUGHES MED INST,CHICAGO,IL 60637. TUFTS UNIV,SCH MED,BOSTON,MA 02111. NCI,CTR RES & DEV,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. PY 1994 SU 18D BP 373 EP 373 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401254 ER PT J AU NEURATH, MF STROBER, W WAKATSUKI, Y AF NEURATH, MF STROBER, W WAKATSUKI, Y TI THE MURINE IMMUNOGLOBULIN HEAVY-CHAIN 3'ALPHA ENHANCER IS A TARGET SITE WITH REPRESSOR FUNCTION FOR THE B-CELL LINEAGE-SPECIFIC TRANSCRIPTION FACTOR BSAP (NF-HB, S-ALPHA-BP) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,MUCOSAL IMMUN SECT,BETHESDA,MD 20895. 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. PY 1994 SU 18D BP 377 EP 377 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401269 ER PT J AU KENNY, JJ FISCHER, RT REED, JC LONGO, DL AF KENNY, JJ FISCHER, RT REED, JC LONGO, DL TI BCL-2 PREVENTS THE CLONAL DELETION OF PHOSPHOCHOLINE-SPECIFIC B-CELLS IN MU-KAPPA M167 TRANSGENIC XID MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702. NCI,FCRDC,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 386 EP 386 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401305 ER PT J AU MALNATI, MS LONG, EO AF MALNATI, MS LONG, EO TI PROTECTIVE ROLE OF MHC CLASS-I ALLELES ON TARGET-CELL RECOGNITION BY NK CLONES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 392 EP 392 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401327 ER PT J AU TING, CC HARGROVE, ME WANG, J AF TING, CC HARGROVE, ME WANG, J TI DIFFERENTIAL REQUIREMENT OF PROTEIN-KINASE-C AND PROTEIN-TYROSINE KINASE IN THE ACTIVATION OF IL-2-INDUCED AND ALPHA-CD3-INDUCED ACTIVATED KILLER-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 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. PY 1994 SU 18D BP 393 EP 393 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401330 ER PT J AU FRANCO, JL WILTROUT, RH MOMOZAKI, N OSHEA, JJ LONGO, DL KOMSCHLIES, KL AF FRANCO, JL WILTROUT, RH MOMOZAKI, N OSHEA, JJ LONGO, DL KOMSCHLIES, KL TI ADMINISTRATION OF BIOLOGICAL RESPONSE MODIFIERS (BRM) INDUCES TRANSIENT T-CELL SIGNAL-TRANSDUCTION MOLECULE ALTERATIONS IN NORMAL MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 PRJ,DYNCORP,EXPT IMMUNOL LAB,FREDERICK,MD 21702. PRI,DYNCORP,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. PRI,DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. ONCOTHERAPEUT,CRANBURY,NJ 08512. 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. PY 1994 SU 18D BP 399 EP 399 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401355 ER PT J AU GHOSH, P SICA, A YOUNG, HA YE, JP FRANCO, JL WILTROUT, RH LONGO, DL RICE, NR KOMSCHLIES, KL AF GHOSH, P SICA, A YOUNG, HA YE, JP FRANCO, JL WILTROUT, RH LONGO, DL RICE, NR KOMSCHLIES, KL TI ALTERATIONS IN NF-KAPPA-B/REL FAMILY PROTEINS IN SPLENIC T-CELLS FROM TUMOR-BEARING MICE AND REVERSAL FOLLOWING THERAPY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI,DYNCORP,APPL BIOSCI LABS,FREDERICK,MD 21702. NCI,FCRDC,PRI,DYNCORP,BCOP,FREDERICK,MD 21702. RP GHOSH, P (reprint author), NCI,FCRDC,PRI,DYNCORP,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 400 EP 400 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401358 ER PT J AU HARADA, N SANTOSARGUMEDO, L LEONARD, WJ IZUHARA, K AF HARADA, N SANTOSARGUMEDO, L LEONARD, WJ IZUHARA, K TI STIMULATION OF THE B-CELL RECEPTOR INDUCES TYROSINE PHOSPHORYLATION OF A 75 KDA PROTEIN WHICH ASSOCIATES WITH THE INTERLEUKIN-4 RECEPTOR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DNAX INC,RES INST,PALO ALTO,CA 94304. NHLBI,PULM & MOLEC IMMUNOL 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. PY 1994 SU 18D BP 401 EP 401 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401363 ER PT J AU KIRKEN, RA RUI, H FARRAR, WL AF KIRKEN, RA RUI, H FARRAR, WL TI ACTIVATION OF DISTINCT RECEPTOR-ASSOCIATED TYROSINE KINASES BY INTERLEUKIN-2 AND PROLACTIN IN T-LYMPHOCYTES - ROLE OF JAK FAMILY KINASES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI, FCRDC, BRMP, LMI, CYTOKINE MOLEC MECHANISMS SECT, FREDERICK, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 403 EP 403 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401369 ER PT J AU MCVICAR, DW MUSSO, T LAL, BK LLOYD, A KAWAMURA, M CHEN, YQ ZHANG, XY STAPLES, JE ORTALDO, JR OSHEA, JJ AF MCVICAR, DW MUSSO, T LAL, BK LLOYD, A KAWAMURA, M CHEN, YQ ZHANG, XY STAPLES, JE ORTALDO, JR OSHEA, JJ TI STRUCTURE AND EXPRESSION OF THE NOVEL CSK-LIKE TISSUE-SPECIFIC TYROSINE KINASE, ISK SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI,DYNCORP,BRMP,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. NCI,FCRDC,PRI,DYNCORP,BCDP,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. PY 1994 SU 18D BP 406 EP 406 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401382 ER PT J AU DEJONG, R VANLIER, RAW RUSCETTI, FW SCHMITT, C DEBRE, P MOSSALAYI, MD AF DEJONG, R VANLIER, RAW RUSCETTI, FW SCHMITT, C DEBRE, P MOSSALAYI, MD TI DIFFERENTIAL EFFECT OF TRANSFORMING GROWTH-FACTOR-BETA-1 ON ACTIVATION OF HUMAN NAIVE AND MEMORY CD4+ T-LYMPHOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV AMSTERDAM,EXP & CLIN IMMUN LAB,AMSTERDAM,NETHERLANDS. UNIV AMSTERDAM,NETHERLANDS RED CROSS,BLOOD TRANSFUS SERV,CENT LAB,AMSTERDAM,NETHERLANDS. CHU PITIE SALPETRIERE,IMMUNOL CELL & TISS,F-75634 PARIS 13,FRANCE. NCI,LEUCOCYTE BIOL LAB,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 414 EP 414 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401413 ER PT J AU WILSON, CB PENIX, LA WEAVER, WM OSBORN, J YOUNG, HA AF WILSON, CB PENIX, LA WEAVER, WM OSBORN, J YOUNG, HA TI DETERMINANTS OF SELECTIVE INTERFERON-GAMMA EXPRESSION IN T-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV WASHINGTON,DEPT PEDIAT,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT IMMUNOL,SEATTLE,WA 98195. NCI,FCRDC,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 418 EP 418 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401431 ER PT J AU VACCHIO, MS ASHWELL, JD AF VACCHIO, MS ASHWELL, JD TI STEROID-PRODUCTION IN THE THYMUS - IMPLICATIONS FOR THYMOCYTE DEVELOPMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,IMMUNE 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. PY 1994 SU 18D BP 425 EP 425 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401456 ER PT J AU HATHCOCK, KS LASZLO, G DICKLER, HB BRADSHAW, J LINSLEY, P HODES, RJ AF HATHCOCK, KS LASZLO, G DICKLER, HB BRADSHAW, J LINSLEY, P HODES, RJ TI IDENTIFICATION OF AN ALTERNATIVE CTLA4 LIGAND THAT IS COSTIMULATORY FOR MURINE T-CELL ACTIVATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NIA,BETHESDA,MD 20892. BRISTOL MEYERS SQUIBB PRI,SEATTLE,WA 98121. 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. PY 1994 SU 18D BP 428 EP 428 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401467 ER PT J AU LENSCHOW, DJ FREEMAN, G HODES, R COOKE, M ZENG, Y HATHCOCK, K GRAY, G THISTLETHWAITE, JR GOODNOW, C NADLER, LM BLUESTONE, JA AF LENSCHOW, DJ FREEMAN, G HODES, R COOKE, M ZENG, Y HATHCOCK, K GRAY, G THISTLETHWAITE, JR GOODNOW, C NADLER, LM BLUESTONE, JA TI B7-2, AND NOT B7-1(B7), IS THE PRIMARY COSTIMULATORY MOLECULE FOR T-CELL ACTIVATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CHICAGO,COMM IMMUNOL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT SURG,CHICAGO,IL 60637. NIA,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. STANFORD UNIV,HOWARD HUGHES MED INST,STANFORD,CA 94305. REPLIGEN CORP,CAMBRIDGE,MA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 431 EP 431 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401479 ER PT J AU TAN, TH RICE, N BRYAN, R RICH, R LI, YQ HORVATH, G LAI, JH AF TAN, TH RICE, N BRYAN, R RICH, R LI, YQ HORVATH, G LAI, JH TI FUNCTIONAL INVOLVEMENT OF C-REL IN THE ACTIVATION OF THE IL-2 PROMOTER BY CD28 COSTIMULATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 BAYLOR COLL MED,DEPT MICROBIOL & IMMUNOL,HOUSTON,TX 77030. NCI,FCRDC,FREDERICK,MD 21701. NR 3 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 434 EP 434 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401494 ER PT J AU UMLAUF, SW BEVERLY, B SCHWARTZ, RH AF UMLAUF, SW BEVERLY, B SCHWARTZ, RH TI MESSENGER-RNA STABILIZATION IS THE MAJOR MOLECULAR MECHANISM OF CD28 COSTIMULATION OF IL-2 PRODUCTION IN MOUSE T-CELL CLONES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ANERGEN INC,REDWOOD CITY,CA 94063. NIH,CELLULAR & MOLEC 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. PY 1994 SU 18D BP 435 EP 435 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401497 ER PT J AU KIM, WK TANG, Y HUGIN, A HOLMES, K MORSE, HC AF KIM, WK TANG, Y HUGIN, A HOLMES, K MORSE, HC TI ANALYSES OF THE CONTRIBUTIONS OF B-CELLS TO ABNORMALITIES IN MAIDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOPATHOL 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. PY 1994 SU 18D BP 438 EP 438 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401507 ER PT J AU LAI, JC VISTICA, BP MATURI, RK SHIRKEY, BL SASAMOTO, Y WHITCUP, SM GERY, I AF LAI, JC VISTICA, BP MATURI, RK SHIRKEY, BL SASAMOTO, Y WHITCUP, SM GERY, I TI IN-VITRO INDUCTION OF ANERGY IN RAT LYMPHOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NEI,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. PY 1994 SU 18D BP 446 EP 446 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401539 ER PT J AU LOVE, PE SHORES, EW LEE, EJ GRINBERG, A MUNITZ, TI WESTPHAL, H SINGER, A AF LOVE, PE SHORES, EW LEE, EJ GRINBERG, A MUNITZ, TI WESTPHAL, H SINGER, A TI ZETA-OVEREXPRESSION IN EARLY THYMOCYTES ACTIVATES A TCR-INDEPENDENT SIGNALING RESPONSE THAT REGULATES RAG-1 AND RAG-2 EXPRESSION AND ALPHA-BETA-T-CELL DEVELOPMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MAMMALIAN GENES & DEV LAB,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 456 EP 456 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401580 ER PT J AU TAKAHAMA, Y SHEARD, M SUZUKI, H SINGER, A AF TAKAHAMA, Y SHEARD, M SUZUKI, H SINGER, A TI TCR SIGNALS INDUCE UP-REGULATION OF CD5 EXPRESSION ON DEVELOPING THYMOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. SYNTEX INST IMMUNOL,NIIHARI 30041,JAPAN. 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. PY 1994 SU 18D BP 459 EP 459 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401590 ER PT J AU PATERSON, BM SHRAKATA, M WEI, Q KARSCHMIZRACHI, I ZHANG, JM AF PATERSON, BM SHRAKATA, M WEI, Q KARSCHMIZRACHI, I ZHANG, JM TI STUDIES ON THE DIMERIZATION OF THE MYOGENIC HELIX-LOOP-HELIX DNA-BINDING FACTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 469 EP 469 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401619 ER PT J AU SUTRAVE, P LANA, DP LEFEROVICH, J FEDERSPIEL, MJ ENGERT, JC SHELTON, L ROSENTHAL, N KELLY, A HUGHES, SH AF SUTRAVE, P LANA, DP LEFEROVICH, J FEDERSPIEL, MJ ENGERT, JC SHELTON, L ROSENTHAL, N KELLY, A HUGHES, SH TI SKI AND FIBER-TYPE HYPERTROPHY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. UNIV PENN,SCH VET MED,DEPT PATHOBIOL,PHILADELPHIA,PA 19104. HARVARD UNIV,MASSACHUSETTS GEN HOSP E,SCH MED,BOSTON,MA. RI Rosenthal, Nadia/O-7009-2015 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. PY 1994 SU 18D BP 471 EP 471 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401625 ER PT J AU MAHON, KA AMESSE, LS VENKATESAN, A GLEIZER, L AF MAHON, KA AMESSE, LS VENKATESAN, A GLEIZER, L TI NKX-3.1 - A NOVEL HOMEOBOX GENE EXPRESSED IN DEVELOPING SOMITES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MAMMALIAN GENES & DEV LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 479 EP 479 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401653 ER PT J AU BHATIADEY, N DIRKSEN, ML ADELSTEIN, RS JAMRICH, M AF BHATIADEY, N DIRKSEN, ML ADELSTEIN, RS JAMRICH, M TI FORKHEAD DOMAIN-CONTAINING TRANSCRIPTION FACTOR EXPRESSED IN PRESOMITIC MESODERM OF XENOPUS-EMBRYOS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. US FDA,DEV BIOL LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 487 EP 487 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401682 ER PT J AU BRADHAM, DM WIESCHE, BID PRECHT, P BALAKIR, R HORTON, W AF BRADHAM, DM WIESCHE, BID PRECHT, P BALAKIR, R HORTON, W TI TRANSREPRESSION OF TYPE-II COLLAGEN BY TGF-BETA AND FGF IS PROTEIN-KINASE-C DEPENDENT AND IS MEDIATED THROUGH REGULATORY SEQUENCES IN THE PROMOTER AND 1ST INTRON SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID GROWTH FACTOR-BETA; DIFFERENTIATED CHONDROCYTES; SIGNAL TRANSDUCTION; COLONY FORMATION; HEPARIN-BINDING; NUCLEAR FACTOR; 3T3 CELLS; SOFT AGAR; FACTOR-A; PHOSPHORYLATION AB Transforming growth factor beta and basic fibroblast growth factor are multipotential factors found in bone and cartilage that may be involved in both the proliferation and differentiation of chondrocytes. It was previously reported that TGF-beta plus FGF caused a modulation of chondrocyte phenotype that included the down-regulation of steady-state level of the collagen II transcript. In this report, the results of nuclear run-off data indicate that repression of transcript initiation from the collagen II gene is the primary mechanism involved in the growth factor induced inhibition. Transient transfection assays with CAT expression vectors containing portions of the collagen II gene show that the TGF-beta/FGF induced transrepression requires a region in the first intron previously reported to have transcriptional enhancer activity and to bind chondrocyte nuclear proteins. In addition, silencer elements in the promoter also appear to play a role. Protein data as well as transient transfection experiments indicate that the activation of protein kinase C is necessary for the growth factor-induced down-regulation of collagen II expression. These studies suggest that a cascade initiating with PKC activation is responsible for modifying transcription factors that interact with regulatory sequences in the collagen II gene. A detailed understanding of the factors involved in cartilage-specific gene regulation in chondrocytes would facilitate development of therapeutic protocols for the repair of degenerated cartilage in diseases such as osteoarthritis. (C) 1994 Wiley-Liss, Inc.* C1 NIA,GERONTOL RES INST,BALTIMORE,MD 21224. NR 45 TC 34 Z9 34 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD JAN PY 1994 VL 158 IS 1 BP 61 EP 68 DI 10.1002/jcp.1041580109 PG 8 WC Cell Biology; Physiology SC Cell Biology; Physiology GA MM962 UT WOS:A1994MM96200008 PM 8263029 ER PT J AU CHEN, JC SHAO, ZM SHEIKH, MS HUSSAIN, A LEROITH, D ROBERTS, CT FONTANA, JA AF CHEN, JC SHAO, ZM SHEIKH, MS HUSSAIN, A LEROITH, D ROBERTS, CT FONTANA, JA TI INSULIN-LIKE GROWTH FACTOR-BINDING PROTEIN ENHANCEMENT OF INSULIN-LIKE GROWTH FACTOR-I (IGF-I)-MEDIATED DNA-SYNTHESIS AND IGF-I BINDING IN A HUMAN BREAST-CARCINOMA CELL-LINE SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID ESTROGEN-RECEPTOR STATUS; GENE-EXPRESSION; MOLECULAR-CLONING; CANCER-CELLS; BIOLOGICAL-ACTIVITIES; HUMAN FIBROBLAST; FACTOR-BETA; 2 FORMS; IGFBP-3; MODULATION AB The insulin-like growth factors (IGFs) are potent milogens for malignant cell proliferation. The majority of secreted IGFs are bound to specific IGF-binding proteins (IGFBPs) that are secreted by a large number of cells. These proteins may either inhibit or enhance IGF actions. Breast carcinoma cells secrete a variety of IGFBPs. We have previously demonstrated that retinoic acid (RA) inhibition of IGF-1-stimulated MCF-7 cell proliferation is associated with increased IGFBP-3 levels in the conditioned media. We therefore investigated the effect of recombinant IGFBP-3 as well as IGFBP-2, -4 and -5 on IGF-I stimulation of DNA synthesis and IGF-I binding in the MCF-7 human breast carcinoma cell line. IGFBP-2 and -3 enhanced IGF-I stimulation of DNA synthesis in MCF-7 cells while IGFBP-4 and -5 had no effect. Transfection of MCF-7 cells with an IGFBP-3 expression vector resulted in the enhanced secretion of IGFBP-3 with an accompanying increase in IGF-I binding as well as increased cell proliferation upon treatment of the cells with IGF-I. IGF-I preincubation of MCF-7 cells transfected with control pSVneo plasmids results in cells refractory to further IGF-I stimulation of thymidine incorporation while IGF-I continues to stimulate [H-3]-thymidine incorporation in IGFBP-3-transfected MCF-7 cells, suggesting that IGFBP-3 protects the cells from IGF-1-mediated down regulation of its receptor. Therefore, IGFBP-3 secreted by MCF-7 cells can enhance IGF-I stimulation of DNA synthesis, increase IGF-I binding to these cells, and prevent IGF-I-induced desensitization of its own receptor, suggesting that IGFBP-3 plays a significant role in IGF-I-mediated breast carcinoma proliferation. (C) 1994 Wiley-Liss, Inc. C1 UNIV MARYLAND,SCH MED,CTR CANC,DEPT MED,DIV ONCOL,BALTIMORE,MD 21201. DEPT VET AFFAIRS MED CTR,BALTIMORE,MD 21201. NIDDKD,DIABET BRANCH,BETHESDA,MD 20982. OI Fontana, Joseph/0000-0003-3829-3358; Roberts, Charles/0000-0003-1756-5772 NR 51 TC 143 Z9 144 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 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD JAN PY 1994 VL 158 IS 1 BP 69 EP 78 DI 10.1002/jcp.1041580110 PG 10 WC Cell Biology; Physiology SC Cell Biology; Physiology GA MM962 UT WOS:A1994MM96200009 PM 7505280 ER PT J AU NAVERI, L STROMBERG, C SAAVEDRA, JM AF NAVERI, L STROMBERG, C SAAVEDRA, JM TI ANGIOTENSIN-II AT(2) RECEPTOR STIMULATION EXTENDS THE UPPER LIMIT OF CEREBRAL BLOOD-FLOW AUTOREGULATION - AGONIST EFFECTS OF CGP-42112 AND PD-123319 SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE CEREBRAL CIRCULATION; AUTOREGULATION; CGP 42112; PD 123319; LOSARTAN; SAR(1),ILE(8)-ANGIOTENSIN II ID CONVERTING ENZYME-INHIBITION; MICROVASCULAR PRESSURE; BINDING-SITES; ARTERIES; ANTAGONISTS; RELAXATION; LOSARTAN; SUBTYPES; DUP-753; PEPTIDE AB The effects of the angiotensin II AT(2) receptor ligands CGP 42112 and PD 123319, the AT(1) antagonist losartan, and the nonselective angiotensin II antagonist Sar(1),Ile(8)-angiotensin II on the upper limit of CBF autoregulation were studied in pentobarbital-anesthetized rats. Blood pressure was increased by intravenous phenylephrine infusion, while CBF was measured continuously from the parietal cortex by laser-Doppler flowmetry. Intravenous infusions of CGP 42112 (0.1 and 1 mg kg(-1) min(-1)) and PD 123319 (0.36 and 1 mg kg(-1) min(-1)) shifted the upper limit of CBF autoregulation toward higher blood pressures without affecting baseline CBF. Sar(1),Ile(8)-angiotensin II (4 mu g kg(-1) min(-1)) had no effect on baseline CBF or CBF autoregulation but antagonized the effect of CGP 42112 and PD 123319. Losartan (10 mg/kg i.v. bolus) reduced baseline blood pressure and CBF and shifted the autoregulation curve toward higher blood pressures. Sar(1),Ile(8)-angiotensin II blocked the effect of losartan on baseline CBF but not on CBF autoregulation. These results suggest that both CGP 42112 and PD 123319 exert their effects on CBF autoregulation through stimulation of angiotensin II AT(2) receptors. The mechanism by which losartan affects CBF remains unclear. RP NAVERI, L (reprint author), NIMH,CLIN SCI LAB,PHARMACOL SECT,BLDG 10,ROOM 2D-45,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 31 TC 33 Z9 33 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1994 VL 14 IS 1 BP 38 EP 44 PG 7 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA MW236 UT WOS:A1994MW23600006 PM 8263056 ER PT J AU CRUZ, NF DIENEL, GA AF CRUZ, NF DIENEL, GA TI BRAIN GLUCOSE-LEVELS IN PORTACAVAL-SHUNTED RATS WITH CHRONIC, MODERATE HYPERAMMONEMIA - IMPLICATIONS FOR DETERMINATION OF LOCAL CEREBRAL GLUCOSE-UTILIZATION SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE GLUCOSE METABOLISM; DEOXYGLUCOSE; LUMPED CONSTANT; AMMONIA; PORTACAVAL SHUNT ID PORTAL-SYSTEMIC ENCEPHALOPATHY; AMINO-ACIDS; AUTORADIOGRAPHIC DETERMINATION; CAVAL ANASTOMOSIS; BLOOD-FLOW; IN-VIVO; METABOLISM; AMMONIA; BARRIER; TRANSPORT AB Rates of glucose utilization (lCMR(glc)) in many structures of the brain of fed, portacaval-shunted rats, when assayed with the [C-14]deoxyglucose (DG) method in our laboratory, were previously found to be unchanged (30 of 36 structures) or depressed (6 structures) during the first 4 weeks after shunting, but to rise progressively to higher than normal values in 25 of 36 structures from 4-12 weeks. In contrast, lCMR(glc), when assayed with the [C-14]glucose method in another laboratory, was depressed in most structures of brains of 4-8-week shunted rats that had relatively high brain ammonia levels. There was a possibility that the increases in lCMR(glc) obtained with the [C-14]DG method may have been artifactual, due, in part, to a change in brain glucose content which could alter the value of the lumped constant of the DG method. Brain glucose levels of shunted rats were, therefore, assayed by both direct chemical measurement in freeze-blown samples and by determination of steady-state brain:plasma distribution ratios for [C-14]methylglucose; the methylglucose distribution ratio varies as a function of plasma and tissue glucose contents. Within a week after shunting, ammonia levels in blood and brain rose to 0.25-0.30 mM and 0.35-0.70 mu mol/g, respectively, and mean plasma glucose levels fell from 9-10 mM to 7.4-8.5 mM, and then remained nearly constant. Brains of fed-shunted rats had normal glycogen levels and stable but moderately reduced glucose contents between 1 and 12 weeks (i.e., 1.9-2.2 mu mol/g), [C-14]Methylglucose distribution ratios were essentially the same as those in controls in 22 brain structures at 2 and 8 weeks after shunting. Because brain glucose levels remained stable from 1 to 12 weeks after shunting, there is no evidence to support the hypothesis that the value of the lumped constant would have changed and caused an artifactual rise in lCMR(glc). C1 NIMH, CEREBRAL METAB LAB, BETHESDA, MD 20892 USA. FU NIDDK NIH HHS [DK16739] NR 67 TC 7 Z9 7 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1994 VL 14 IS 1 BP 113 EP 124 PG 12 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA MW236 UT WOS:A1994MW23600016 PM 8263046 ER PT J AU KLEIN, HG AF KLEIN, HG TI TREATMENT METHODS FOR LDL APHERESIS - REPLY SO JOURNAL OF CLINICAL APHERESIS LA English DT Letter RP KLEIN, HG (reprint author), NIH,DEPT TRANSFUS MED,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0733-2459 J9 J CLIN APHERESIS JI J. Clin. Apheresis PY 1994 VL 9 IS 4 BP 241 EP 241 PG 1 WC Hematology SC Hematology GA QH757 UT WOS:A1994QH75700009 ER PT J AU MAGIAKOU, MA MASTORAKOS, G GOMEZ, MT ROSE, SR CHROUSOS, GP AF MAGIAKOU, MA MASTORAKOS, G GOMEZ, MT ROSE, SR CHROUSOS, GP TI SUPPRESSED SPONTANEOUS AND STIMULATED GROWTH-HORMONE SECRETION IN PATIENTS WITH CUSHINGS-DISEASE BEFORE AND AFTER SURGICAL CURE SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID BINDING PROTEIN; RELEASE; OBESITY; RADIOIMMUNOASSAY; RESPONSIVENESS; CHILDREN; PLASMA AB Growth retardation to complete growth arrest is the hallmark of Cushing's syndrome in children. The major mechanism for this has been considered the glucocorticoid-induced resistance of target tissues to insulin-like growth factor-I (IGF-I) and other growth factors. The purpose of this study was to examine the GH secretory dynamics of patients with Cushing's disease before and up to 12 months after their cure by transsphenoidal adenomectomy. In 14 patients, blood sampling every 20 min over 24 h for determination of plasma GH was performed before and 10-11 days and 3, 6, and 12 months after therapy. These patients also underwent arginine infusion and L-dopa stimulation tests and had measurements of morning baseline GH-binding protein (GHBP), IGF-I, and IGF-binding protein-3 (IGFBP-3) plasma concentrations. Fourteen sex- and pubertal stage-matched normal volunteers were used as controls. Before therapy, the patient group had an increased body mass index (31.5 +/- 5 kg/m(2)) and markedly decreased plasma mean 24-h GH concentration, mean peak height, and peak area values, with pulse frequency (mean number of peaks) similar to that in the controls. GH Values after arginine and L-dopa stimulation were also subnormal in many of these patients, with 2 of 8 and 8 of 10 failing to show GH responses greater than 7 ng/mL in the respective test. In spite of these findings, plasma concentrations of IGF-I, IGFBP-3, and GHBP were within the normal range in these patients. Surprisingly, a pattern of GH suppression similar to that observed in patients with active disease was also seen in patients who were studied 10-11 days and 3, 6, and 12 months after their cure, when their body mass indexes were progressively normalizing, being relatively stable at 10 days, 26.9 +/- 3.8 kg/m(2) at 3 months, and 24.8 +/- 3.3 kg/m(2) at 12 months. In these patients, plasma IGF-I and GHBP remained normal, whereas IGFBP-3 decreased significantly, albeit within the normal range. The growth rate of 4 patients who were Tanner stage III or below and had not completed their growth at the time of the study increased the year after surgical cure. These findings suggest that patients with Cushing's disease have marked GH suppression during their illness, which, however, does not appear to be a major contributor to the growth suppression observed in this condition. GH hyposecretion continues for at least a year during convalescence, in spite of significant increases in the growth rate in all growing patients. The latter could be explained by the increase in unbound IGF-I levels (normal total plasma IGF-I concentrations with decreased IGFBP-3 plasma levels) in addition to the correction of the glucocorticoid-induced target tissue resistance to IGF-I and other growth factors. C1 UNIV TENNESSEE, DEPT PEDIAT, MEMPHIS, TN 38103 USA. RP MAGIAKOU, MA (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10N 262, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 38 TC 126 Z9 127 U1 0 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1994 VL 78 IS 1 BP 131 EP 137 DI 10.1210/jc.78.1.131 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MR054 UT WOS:A1994MR05400027 PM 7507118 ER PT J AU CHIN, E MICHELS, K BONDY, CA AF CHIN, E MICHELS, K BONDY, CA TI PARTITION OF INSULIN-LIKE GROWTH-FACTOR (IGF)-BINDING SITES BETWEEN THE IGF-I AND IGF-II RECEPTORS AND IGF-BINDING PROTEINS IN THE HUMAN KIDNEY SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID MESSENGER RIBONUCLEIC-ACID; GENE-EXPRESSION; HUMAN-FETUS; TISSUE DISTRIBUTION; RENAL HYPERTROPHY; DIABETIC RATS; FETAL KIDNEY; PI TRANSPORT; WILMS TUMOR; RNA AB Quantitative ligand binding autoradiography and in situ hybridization were employed to analyze [I-125]insulin-like growth factor-I ([I-125] IGF-I) and [I-125] IGF-II-binding sites in human kidney sections. Binding sites for both ligands were concentrated in the inner medulla and glomeruli, with low levels present in the tubulo-interstitial cortex. Competition with cold IGF-I, IGF-II, and insulin was used to determine nonspecific binding and differentiate binding of ligands to the IGF-I and IGF-II receptors and IGF-binding proteins (IGFBPs). Nonspecific binding was less than 20% of the total for both ligands. Insulin (10(-5) mol/L), which binds to the IGF-I receptor, but not to the IGF-II receptor or IGFBPs, displaced 39 +/- 8% of [I-125]IGF-I binding in glomeruli, 60 +/- 7% in the tubulo-interstitial cortex, and 32 +/- 7% in the medulla. Insulin produced no detectable decrease in [I-125]IGF-II binding in any region. IGF-I (10(-8) mol/L), which binds strongly to IGFBPs, but not appreciably to the IGF-II receptor, produced reductions of 46 +/- 9%, 35 +/- 8%, and 39 +/- 12% in [I-125]IGF-II binding in glomeruli, tubulo-interstitial cortex, and medulla, respectively. In situ hybridization showed that IGFBP-1-5 mRNAs were all expressed in glomeruli. IGFBP-2 mRNA was abundant in medullary collecting duct epithelium, whereas IGFBP-3, -4, and -5 mRNAs were localized in interstitial and vascular cells throughout the kidney. IGF-I and -II receptor mRNAs were widely distributed in renal epithelium. The abundance of local IGFBP gene expression was positively correlated with insulin-nondisplaceable IGF binding in specific kidney regions. In summary, [I-125]IGF-I binding appears to be partitioned largely to IGFBPs in glomeruli and largely to the IGF-I receptor in the tubulointerstitial cortex, with binding in the medulla more evenly divided. The proportion and regional distribution of [I-125]IGF-II binding to IGFBPs are similar, but the balance appears to be primarily associated with the IGF-II, rather than the IGF-I, receptor. Finally, this study shows that [I-125]IGF binding autoradiography combined with in situ hybridization can be used to localize and potentially quantitate expression of IGFBPs in tissue sections. C1 NIMH, PHARMACOL SECT, BETHESDA, MD 20892 USA. RP CHIN, E (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10N262, BETHESDA, MD 20892 USA. NR 50 TC 38 Z9 38 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1994 VL 78 IS 1 BP 156 EP 164 DI 10.1210/jc.78.1.156 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MR054 UT WOS:A1994MR05400032 PM 7507121 ER PT J AU MEIER, CA BRAVERMAN, LE EBNER, SA VERONIKIS, I DANIELS, GH ROSS, DS DERASKA, DJ DAVIES, TF VALENTINE, M DEGROOT, LJ CURRAN, P MCELLIN, K REYNOLDS, J ROBBINS, J WEINTRAUB, BD AF MEIER, CA BRAVERMAN, LE EBNER, SA VERONIKIS, I DANIELS, GH ROSS, DS DERASKA, DJ DAVIES, TF VALENTINE, M DEGROOT, LJ CURRAN, P MCELLIN, K REYNOLDS, J ROBBINS, J WEINTRAUB, BD TI DIAGNOSTIC USE OF RECOMBINANT HUMAN THYROTROPIN IN PATIENTS WITH THYROID-CARCINOMA (PHASE I/II STUDY) SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID TRIIODOTHYRONINE WITHDRAWAL; SERUM THYROGLOBULIN; CANCER; CELLS AB Current diagnostic studies [radioiodine uptake and serum thyroglobulin (Tg) levels] for residual or metastatic thyroid tissue in patients with differentiated thyroid carcinoma require a hypothyroid status necessary for adequate endogenous TSH stimulation. However, almost all patients have symptoms of clinical hypothyroidism during this period. As shown in the present study, recombinant human TSH (rhTSH) allows stimulation of I-131 uptake and Tg release from residual thyroid tissue in euthyroid patients. To assess safety, dosage, and preliminary efficacy, comparison was made of the stimulation of I-131 uptake and Tg release after rhTSH administration and after T-3 Withdrawal in 19 patients after a recent thyroidectomy for differentiated thyroid carcinoma. Various doses (10-40 U) of rhTSH were injected im for 1-3 days in patients receiving suppressive doses of T-3. Twenty-four hours after the last dose of rhTSH, 1-2 mCi I-131 were administered, followed by a neck and whole body scan 48 h later. After discontinuing T-3 for a median period of 19 days (range, 15-28), endogenous serum TSH levels were markedly elevated, and the patients were given a second dose of I-131 and rescanned 48 h later. The injections of rhTSH were tolerated well. No major adverse effects were reported; nausea was reported in 3 (16%) and vomiting in 1 of the patients treated with high doses. The quality of life, as measured by two psychometric scales, was far better during rhTSH treatment than after T-3 withdrawal. The peak levels of serum TSH (mean +/- so) after a single dose of 10, 20, or 30 U were 127 +/- 19, 309 +/- 156, and 510 +/- 156 mU/L, respectively, and occurred 2-8 h after injection. Twenty-four hours after the injection, TSH levels decreased to 83 +/- 31, 173 +/- 73, and 463 +/- 148 mU/L in these treatment groups, respectively. The quality of the thyroid scans and the number of sites of abnormal I-131 uptake were similar after rhTSH treatment and in the hypothyroid scans in 12 (63%) patients. Two additional sites of uptake in the chest and one in the thyroid bed, not visible on the hypothyroid scans, were identified in 3 (16%) patients after rhTSH. In 1 patient a focus of uptake was better visualized after rhTSH than after withdrawal. In 3 (16%) other patients, 1 lesion in the chest and 2 in the neck were seen only after T-3 withdrawal. The amount of radioiodine uptake in the thyroid bed was lower after rhTSH in 68% of patients; however, the uptake was similar to that measured after T-3 withdrawal when corrected for the increased whole body retention of I-131 during hypothyroidism. Serum Tg levels increased more than 2-fold in response to rhTSH in 73% (11 of 15) of the patients who also had a greater than 2-fold elevation of Tg after T-3 withdrawal. However, the increase was quantitatively lower after rhTSH in 93% (14 of 15) of the patients. In conclusion, rhTSH shows promise in humans as a safe and effective method to stimulate I-131 uptake and Tg secretion without the disadvantages of induced hypothyroidism. A phase III trial is required to definitely demonstrate efficacy. C1 NIDDKD, BETHESDA, MD USA. NIH, DEPT NUCL MED, BETHESDA, MD 20892 USA. UNIV MASSACHUSETTS, MED CTR, DIV ENDOCRINOL & METAB, WORCESTER, MA 01655 USA. MASSACHUSETTS GEN HOSP, THYROID UNIT, BOSTON, MA 02114 USA. MT SINAI SCH MED, DIV ENDOCRINOL & METAB, NEW YORK, NY 10029 USA. UNIV CHICAGO, MED CTR, THYROID STUDY UNIT, CHICAGO, IL 60637 USA. GENZYME CORP, CAMBRIDGE, MA 01239 USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X FU NIDDK NIH HHS [NIDDK DK-18919] NR 41 TC 199 Z9 203 U1 1 U2 3 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1994 VL 78 IS 1 BP 188 EP 196 DI 10.1210/jc.78.1.188 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MR054 UT WOS:A1994MR05400037 PM 8288703 ER PT J AU CASTILLO, C BOGARDUS, C BERGMAN, R THUILLEZ, P LILLIOJA, S AF CASTILLO, C BOGARDUS, C BERGMAN, R THUILLEZ, P LILLIOJA, S TI INTERSTITIAL INSULIN CONCENTRATIONS DETERMINE GLUCOSE-UPTAKE RATES BUT NOT INSULIN-RESISTANCE IN LEAN AND OBESE MEN SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE LYMPH; LYMPHATIC CANNULATION; EUGLYCEMIC CLAMP; SKELETAL MUSCLE; ARTERIOVENOUS DIFFERENCE ID SKELETAL-MUSCLE; DIABETES-MELLITUS; FIBER TYPE; INVIVO; KINETICS; TRANSPORT; PULSATILE; DISPOSAL; PERMEABILITY; SECRETION AB Insulin action and obesity are both correlated with the density of muscle capillary supply in humans. Since the altered muscle anatomy in the obese might affect interstitial insulin concentrations and reduce insulin action, we have cannulated peripheral lymphatic vessels in lean and obese males, and compared peripheral lymph insulin concentrations with whole body glucose uptake during a euglycemic, hyperinsulinemic clamp. Lymph insulin concentrations in the lower limb averaged only 34% of arterial insulin concentrations during 150 min of insulin infusion. Obese subjects had the highest arterial (P less than or equal to 0.0001) and lymph insulin (P < 0.005) concentrations, but the lowest glucose uptake rates (P < 0.002). In contrast to the initial steep rise then plateau of arterial insulins, both lymph insulin and whole body glucose uptake rates rose slowly and did not consistently reach a plateau. In each individual, the glucose uptake closely correlated with peripheral lymphatic insulin concentrations (mean r(2) = 0.95). The coupling between glucose uptake and lymph insulin (glucose uptake/pmol insulin) was much steeper in lean subjects than in the obese(P less than or equal to 0.0001). These results indicate that even if insulin diffusion into tissues is rate limiting for insulin action, a tissue defect rather than an insulin diffusion defect causes insulin resistance in obese subjects. C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. UNIV SO CALIF,DEPT PHYSIOL,LOS ANGELES,CA 90033. RI Lillioja, Stephen/A-8185-2012; OI Lillioja, Stephen/0000-0001-5333-5240 NR 59 TC 104 Z9 106 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1994 VL 93 IS 1 BP 10 EP 16 DI 10.1172/JCI116932 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MY159 UT WOS:A1994MY15900004 PM 8282776 ER PT J AU CID, MC KLEINMAN, HK GRANT, DS SCHNAPER, HW FAUCI, AS HOFFMAN, GS AF CID, MC KLEINMAN, HK GRANT, DS SCHNAPER, HW FAUCI, AS HOFFMAN, GS TI ESTRADIOL ENHANCES LEUKOCYTE BINDING TO TUMOR-NECROSIS-FACTOR (TNF)-STIMULATED ENDOTHELIAL-CELLS VIA AN INCREASE IN TNF-INDUCED ADHESION MOLECULES E-SELECTIN, INTERCELLULAR-ADHESION MOLECULE TYPE-1, AND VASCULAR CELL-ADHESION MOLECULE TYPE-1 SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ESTROGEN; CYTOKINES; ENDOTHELIAL CELL; INFLAMMATION; VASCULITIS ID DIRECT EXPRESSION CLONING; T-CELLS; BASEMENT-MEMBRANE; INTERFERON-GAMMA; ACTIVATION; ESTROGEN; NEUTROPHILS; MECHANISMS; LYMPHOCYTES; RECEPTORS AB Adhesion of leukocytes to endothelial cells is a critical step in the development of acute and chronic inflammatory lesions. We report here that estradiol treatment of cultured human umbilical vein endothelial cells stimulated up to a twofold increase in TNP-induced adhesion of both polymorphonuclear leukocytes and PMA-activated peripheral blood mononuclear cells. This effect was more evident (threefold increase) when endothelial cells were cultured on the basement membrane glycoprotein laminin. Progesterone, but not testosterone, had a similar stimulatory effect. Estradiol also promoted a slight increase in interferon gamma-stimulated endothelial cell adherence for peripheral blood mononuclear cells, but no effect of estradiol was observed when adhesion of leukocytes to endothelial cells was stimulated with IL-1 or IL-4. The estradiol-induced increase in leukocyte binding to human umbilical vein endothelial cells was partially blocked by antibodies to the adhesion molecules E-selectin, intercellular adhesion molecule type 1 (ICAM-1), and vascular cell adhesion molecule type 1 (VCAM-1). Indirect immunofluorescence techniques showed that estradiol produces an increase in TNF-induced cell surface expression of these molecules. Northern blot analysis demonstrated a transient increase in TNF-induced expression of mRNA for E-selectin, ICAM-1, and VCAM-1 in endothelial cells treated with estradiol. Our data demonstrate that estradiol has important regulatory functions in promoting leukocyte-endothelial cell interactions that might contribute to the observed predominance in females of some autoimmune inflammatory diseases. C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. HOSP CLIN BARCELONA,DEPT INTERNAL MED,E-08036 BARCELONA,SPAIN. OI Cid Xutgla, Maria Cinta/0000-0002-4730-0938 FU NHLBI NIH HHS [R01 HL053918]; NIDDK NIH HHS [DK-08712] NR 59 TC 192 Z9 194 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1994 VL 93 IS 1 BP 17 EP 25 DI 10.1172/JCI116941 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MY159 UT WOS:A1994MY15900005 PM 7506711 ER PT J AU PINCUS, SH MESSER, KG HU, SL AF PINCUS, SH MESSER, KG HU, SL TI EFFECT OF NONPROTECTIVE VACCINATION ON ANTIBODY-RESPONSE TO SUBSEQUENT HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE HIV; AIDS; VACCINE; VACCINIA ID RECOMBINANT VACCINIA VIRUS; ENVELOPE GLYCOPROTEIN; NEUTRALIZING ANTIBODIES; MONOCLONAL-ANTIBODIES; CONFERS PROTECTION; SYNTHETIC PEPTIDE; HIV-1; TYPE-1; CHIMPANZEES; GP160 AB We have investigated the systemic anti-HIV antibody response in chimpanzees who were immunized,vith live vaccinia containing either the HIV envelope glycoprotein (gp160(IIIB)) or a control antigen (herpes simplex virus glycoprotein D) and then challenged with either a high dose (300,000 TCID50) or low dose(100 TCID50) of HIVIIIB. HIV was subsequently isolated from all animals, indicating failure of the vaccination to protect against HIV infection. Serum antibody responses were evaluated before immunization, at the time of challenge with HIV, and at multiple time points in the 9 mo after challenge. Immunization resulted in a more rapid rise of antibody to gp160 in both high and low dose animals. Antibodies to the V3 loop induced upon infection were unaffected by immunization. In low dose animals, neutralizing antibody rose more rapidly and to higher levels in the immunized animals as compared with the control. There was no difference in neutralizing antibodies between immunized and control chimpanzees in the high dose group. Epitope mapping of the anti-gp160 response indicated that immunization with gp160 vaccinia induced a postinfection antibody response to a region of gp41 (amino acids 718-743) that was not immunogenic in control-vaccinated animals. These data indicate that failed vaccination with the HIV envelope can alter both the timing and epitope specificity of the subsequent anti-HIV antibody response. These studies also define the evolution and fine specificity of the antibody response during the critical period immediately postinfection. C1 BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA 98121. RP PINCUS, SH (reprint author), NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,HAMILTON,MT 59840, USA. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 NR 31 TC 18 Z9 18 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1994 VL 93 IS 1 BP 140 EP 146 DI 10.1172/JCI116937 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MY159 UT WOS:A1994MY15900020 PM 8282780 ER PT J AU YOO, JH ERZURUM, SC HAY, JG LEMARCHAND, P CRYSTAL, RG AF YOO, JH ERZURUM, SC HAY, JG LEMARCHAND, P CRYSTAL, RG TI VULNERABILITY OF THE HUMAN AIRWAY EPITHELIUM TO HYPEROXIA - CONSTITUTIVE EXPRESSION OF THE CATALASE GENE IN HUMAN BRONCHIAL EPITHELIAL-CELLS DESPITE OXIDANT STRESS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CATALASE; GENE EXPRESSION; HYPEROXIA; ADENOVIRUS; GENE TRANSFER ID ADENOVIRUS-MEDIATED TRANSFER; RESPONSIVE ELEMENT; LUNG; SEQUENCES; VIRUS; PROMOTER; ENHANCER; ASSAYS; INVIVO; CDNA AB Although catalase is a major intracellular antioxidant, the expression of the human catalase gene appears to be limited in the airway epithelium, making these cells vulnerable to oxidant stress. The basis for this limited gene expression was examined by evaluation of the expression of the endogenous gene in human bronchial epithelial cells in response to hyperoxia. Hyperoxia failed to upregulate endogenous catalase gene expression, in contrast to a marked increase in expression of the heat shock protein gene. Sequence analysis of 1.7 kb of the flanking region of the human catalase gene showed features of a ''housekeeping'' gene (no TATA box, high GC content, multiple CCAAT boxes, and transcription start sites). Transfection of human bronchial epithelial cells with fusion genes composed of various lengths of the catalase 5'-flanking region and luciferase as a reporter gene showed low level constitutive promoter activity that did not change after exposure to hyperoxia. Importantly, using a replication-deficient recombinant adenoviral vector containing the human catalase cDNA, levels of catalase were significantly increased in human airway epithelial cells and this was associated with increased survival of the cells when exposed to hyperoxia. These observations provide a basis for understanding the sensitivity of the human airway epithelium to oxidant stress and a strategy for protecting the epithelium from such injury. C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. RI lemarchand, patricia/C-3247-2011 NR 41 TC 43 Z9 45 U1 0 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1994 VL 93 IS 1 BP 297 EP 302 DI 10.1172/JCI116959 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MY159 UT WOS:A1994MY15900039 PM 8282800 ER PT J AU RADER, DJ IKEWAKI, K DUVERGER, N SCHMIDT, H PRITCHARD, H FROHLICH, J CLERC, M DUMON, MF FAIRWELL, T ZECH, L SANTAMARINAFOJO, S BREWER, HB AF RADER, DJ IKEWAKI, K DUVERGER, N SCHMIDT, H PRITCHARD, H FROHLICH, J CLERC, M DUMON, MF FAIRWELL, T ZECH, L SANTAMARINAFOJO, S BREWER, HB TI MARKEDLY ACCELERATED CATABOLISM OF APOLIPOPROTEIN A-II (APOA-II) AND HIGH-DENSITY-LIPOPROTEINS CONTAINING APOA-II IN CLASSIC LECITHIN - CHOLESTEROL ACYLTRANSFERASE DEFICIENCY AND FISH-EYE DISEASE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE APOLIPOPROTEIN A-I; ATHEROSCLEROSIS; CHOLESTEROL; KINETICS; STABLE ISOTOPES ID MASSIVE CORNEAL OPACITIES; CORONARY-ARTERY DISEASE; AMINO-ACID EXCHANGE; FAMILIAL LECITHIN; PLASMA-LIPOPROTEINS; INVIVO METABOLISM; MOLECULAR DEFECT; HEART-DISEASE; ALPHA-LCAT; RAT-LIVER AB Classic (complete) lecithin:cholesterol acyltransferase (LCAT) deficiency and Fish-eye disease (partial LCAT deficiency) are genetic syndromes associated with markedly decreased plasma levels of high density lipoprotein (HDL) cholesterol but not with an increased risk of atherosclerotic cardiovascular disease. We investigated the metabolism of the HDL apolipoproteins (ape) apoA-I and apoA-II in a total of five patients with LCAT deficiency, one with classic LCAT deficiency and four with Fish-eye disease. Plasma levels of apoA-II were decreased to a proportionately greater extent (23% of normal) than apoA-I (30% of normal). In addition, plasma concentrations of HDL particles containing both apoA-I and apoA-II (LpA-I:A-II) were much lower (18% of normal) than those of particles containing only apoA-I (LpA-I) (51% of normal). The metabolic basis for the low levels of apoA-II and LpA-I:A-II was investigated in all five patients using both exogenous radiotracer and endogenous stable isotope labeling techniques. The mean plasma residence time of apoA-I was decreased at 2.08 +/- 0.27 d (controls 4.74 +/- 0.65 days); however, the residence time of apoA-II was even shorter at 1.66 +/- 0.24 d (controls 5.25 +/- 0.61 d). In addition, the catabolism of apoA-I in LpA-I:A-II was substantially faster than that of apoA-I in LpA-I. In summary, genetic syndromes of either complete or partial LCAT deficiency result in low levels of HDL through preferential hypercatabolism of apoA-II and HDL particles containing apoA-II. Because LpA-I has been proposed to be more protective than LpA-I:A-II against atherosclerosis, this selective effect on the metabolism of LpA-I:A-II may provide a potential explanation why patients with classic LCAT deficiency and Fish-eye disease are not at increased risk for premature atherosclerosis despite markedly decreased levels of HDL cholesterol and apoA-I. C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. UNIV BRITISH COLUMBIA,LIPOPROT RES GRP,VANCOUVER V5Z 4H4,BC,CANADA. HOP ST ANDRE,LAB CENT BIOCHIM,F-33075 BORDEAUX,FRANCE. NR 84 TC 101 Z9 102 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1994 VL 93 IS 1 BP 321 EP 330 DI 10.1172/JCI116962 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MY159 UT WOS:A1994MY15900042 PM 8282802 ER PT J AU STRONG, TV BOEHM, K COLLINS, FS AF STRONG, TV BOEHM, K COLLINS, FS TI LOCALIZATION OF CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR MESSENGER-RNA IN THE HUMAN GASTROINTESTINAL-TRACT BY IN-SITU HYBRIDIZATION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CYSTIC FIBROSIS; EXPRESSION; INTESTINE; CHLORIDE SECRETION; EPITHELIA ID POTENTIAL DIFFERENCE; ENDOCRINE-CELLS; DOWN-REGULATION; MESSENGER-RNA; GENE; CHLORIDE; CFTR; TRANSPORT; SECRETION; IDENTIFICATION AB We have used in situ hybridization to localize expression of the cystic fibrosis transmembrane conductance regulator (CFTR) gene in the human gastrointestinal tract and associated organs. The stomach exhibits a low level of CFTR expression throughout gastric mucosa. In the small intestine, expression is relatively high in the mucosal epithelium, with a decreasing gradient of expression along the crypt to tip axis. The cells of the Brunner's glands express high levels of CFTR mRNA. In addition, there is a small subpopulation of highly positive cells scattered along the epithelium in the duodenum and jejunum, but not in the ileum. These cells do not represent endocrine cells, as determined by lack of colocalization with an endocrine-specific marker. The distribution of CFTR mRNA in the colon is similar to the small intestine, with highest level of expression in the epithelial cells at the base of the crypts. In the pancreas, CFTR is expressed at high levels in the small, intercalated ducts and at lower levels in the interlobular ducts. CFTR transcripts are expressed at uniformly high levels in the epithelium of the gallbladder. Throughout the gastrointestinal tract, CFTR expression is increased in mucosal epithelial cells that are near lymph nodules. C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. UNIV MICHIGAN,MED CTR,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,ANN ARBOR,MI 48109. FU NIDDK NIH HHS [DK-39690, DK-42718] NR 49 TC 178 Z9 178 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1994 VL 93 IS 1 BP 347 EP 354 DI 10.1172/JCI116966 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MY159 UT WOS:A1994MY15900045 PM 7506713 ER PT J AU MOSS, RB KALINER, MA AF MOSS, RB KALINER, MA TI PRIMED IN-SITU DNA AMPLIFICATION (PIDA) SO JOURNAL OF CLINICAL LABORATORY ANALYSIS LA English DT Note DE PIDA; PCR IN SITU; HIV-1 ID POLYMERASE CHAIN-REACTION; INSITU; PROVIRUS AB A novel PCR in situ protocol is described which can be implemented in one day. An initial amplification step with a single primer pair is followed by an amplification with an internal oligonucleotide probe with labeled nucleotides (dig-dUTP). Detection is then accomplished with an antidigoxigenin antibody and substrate solution. This rapid and sensitive method may be useful in diagnosing low copy DNA in tissue specimens and cells. (C) 1994 Wiley-Liss, Inc. C1 NIAID,CLIN INVEST LAB,ALLERG DIS SECT,BETHESDA,MD 20892. NR 6 TC 3 Z9 3 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-8013 J9 J CLIN LAB ANAL JI J. Clin. Lab. Anal. PY 1994 VL 8 IS 2 BP 120 EP 122 DI 10.1002/jcla.1860080211 PG 3 WC Medical Laboratory Technology SC Medical Laboratory Technology GA MY115 UT WOS:A1994MY11500010 PM 8189322 ER PT J AU SANDERS, JW HOOK, EW WELSH, LE SHEPHERD, ME QUINN, TC AF SANDERS, JW HOOK, EW WELSH, LE SHEPHERD, ME QUINN, TC TI EVALUATION OF AN ENZYME-IMMUNOASSAY FOR DETECTION OF CHLAMYDIA-TRACHOMATIS IN URINE OF ASYMPTOMATIC MEN SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID NONGONOCOCCAL URETHRITIS; NEISSERIA-GONORRHOEAE; INFECTIONS; DIAGNOSIS; SAMPLE; MALES; SWABS AB In a study of 1,486 men attending two sexually transmitted disease clinics, of whom 891 had no symptoms of urethritis, we compared an enzyme immunoassay (EIA) (Baxter-Bartels, formerly Northumbria AntigEnz) of urine sediment to urethral culture for the detection of Chlamydia trachomatis. C. trachomatis prevalence by culture alone was 7.7% in asymptomatic men and 10.9% in symptomatic men. Discrepant results between EIA of urine and urethral culture were evaluated by direct fluorescent-antibody staining (DFA) for elementary bodies in urine sediment or in culture transport media. When chlamydial infection was defined as either a positive urethral culture or positive EIA confirmed by DFA, chlamydia prevalence increased to 8.9% in asymptomatic men and 11.6% in symptomatic men. The urine EIA sensitivity, specificity, and positive and negative predictive values for chlamydia detection in asymptomatic men were 84.8, 99.3, 91.8, and 98.5%, respectively, with nearly identical results for symptomatic men. The sensitivities of urethral culture alone compared with the combination of urethral culture and urine EIA (with DFA confirmation) were 87.3 and 94.3% for asymptomatic and symptomatic men, respectively. The present EIA of urine sediment is both highly sensitive and specific for the detection of C. trachomatis in asymptomatic men, thus providing a noninvasive screening method for chlamydia infection in asymptomatic men attending sexually transmitted disease clinics. C1 BALTIMORE CITY DEPT HLTH,BALTIMORE,MD 21205. NIAID,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,BALTIMORE,MD 21205. NR 23 TC 23 Z9 23 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1994 VL 32 IS 1 BP 24 EP 27 PG 4 WC Microbiology SC Microbiology GA MP316 UT WOS:A1994MP31600005 PM 8126190 ER PT J AU SWITCHENKO, AC MIYADA, CG GOODMAN, TC WALSH, TJ WONG, B BECKER, MJ ULLMAN, EF AF SWITCHENKO, AC MIYADA, CG GOODMAN, TC WALSH, TJ WONG, B BECKER, MJ ULLMAN, EF TI AN AUTOMATED ENZYMATIC METHOD FOR MEASUREMENT OF D-ARABINITOL, A METABOLITE OF PATHOGENIC CANDIDA SPECIES SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID INVASIVE CANDIDIASIS; ENANTIOSELECTIVE MEASUREMENT; GAS-CHROMATOGRAPHY; HUMAN-SERUM; QUANTIFICATION; DIAGNOSIS; FUNGEMIA; CANCER AB An automated enzymatic method wa developed for the measurement Of D-arabinitol in human serum. The assay is based on a novel, highly specific D-arabinitol dehydrogenase from Candida tropicalis. This enzyme catalyzes the oxidation of D-arabinitol to D-ribulose and the concomitant reduction of NAD+ to NADH. The NADH produced is used in a second reaction to reduce p-iodonitrotetrazolium violet (INT) to INT-formazan, which is measured spectrophotometrically. The entire reaction sequence can be performed automatically on a COBAS MIRA-S clinical chemistry analyzer (Roche Diagnostic Systems, Inc., Montclair, N.J.). Replicate analyses of human sera supplemented With D-arabinitol over a concentration range of 0 to 40 muM demonstrated that the pentitol could be measured with an accuracy of +/-7% and a precision (standard deviation) of +/-0.4 muM. SeruM D-arabinitol measurements correlated with those determined by gas chromatography (r = 0.94). The enzymatic method is unaffected by L-arabinitol, D-mannitol, or other polyols commonly found in human serum. Any of 17 therapeutic drugs potentially present in serum did not significantly influence assay performance. Data illustrating the application of the assay in patients for possible diagnosis of invasive candidiasis and the monitoring of therapeutic intervention are presented. The automated assay described here was developed to facilitate the investigation of D-arabinitol as a serum marker for invasive Candida infections. C1 NCI,INFECT DIS SECT,PEDIAT BRANCH,BETHESDA,MD 20892. UNIV CINCINNATI,COLL MED,DEPT INTERNAL MED,CINCINNATI,OH 45221. RP SWITCHENKO, AC (reprint author), SYVA CO,RES DEPT,ROOM S2-218,900 ARASTRADERO RD,PALO ALTO,CA 94304, USA. FU NIAID NIH HHS [AI28392] NR 25 TC 30 Z9 30 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1994 VL 32 IS 1 BP 92 EP 97 PG 6 WC Microbiology SC Microbiology GA MP316 UT WOS:A1994MP31600018 PM 8126210 ER PT J AU YORK, DM BARTOLOTTI, LJ DARDEN, TA PEDERSEN, LG ANDERSON, MW AF YORK, DM BARTOLOTTI, LJ DARDEN, TA PEDERSEN, LG ANDERSON, MW TI SIMULATIONS OF THE SOLUTION STRUCTURE OF HIV-1 PROTEASE IN THE PRESENCE AND ABSENCE OF BOUND ZINC SO JOURNAL OF COMPUTATIONAL CHEMISTRY LA English DT Article ID IMMUNODEFICIENCY VIRUS-1 PROTEASE; ASPARTIC PROTEASE; MOLECULAR-DYNAMICS; CRYSTAL-STRUCTURE; NUCLEIC-ACIDS; FORCE-FIELD; METAL-IONS; PROTEINS; RESOLUTION; MECHANISM AB Zinc ions have been shown to inhibit human immunodeficiency virus type 1 (HIV-1) protease in vitro at neutral pH [Zhang et al. Biochemistry, 36, 8717 (1991)]. Kinetic data from this study support a reversible binding mechanism of zinc in the active;site. Preliminary calculations of the ion-protein potential energy based on the geometry of the crystallographic structure [Wlodawer et al. Science, 245, 616 (1989)] are consistent with this proposed mechanism. To examine the structure of HIV-1 protease with zinc bound in the active site, molecular dynamics simulations in the presence and absence of zinc at this site have been carried out to 200 ps. These simulations suggest zinc remains stably bound to the catalytic aspartate residues without disruption of the dimer or significant alteration of the active site structure. These data are consistent with those observed by Zhang et al. (1991), and together give strong evidence that this is the binding site that leads to inactivation. A proposed model of zinc binding at the active site based on quantum mechanical calculations indicates Zn+2 coordination is monodentate with each catalytic aspartate, leaving at least two ligand positions potentially free (occupied by water molecules in the calculations). (C) 1994 by John Wiley and Sons, Inc. C1 UNIV N CAROLINA,DEPT CHEM,CHAPEL HILL,NC 27599. N CAROLINA SUPERCOMP CTR,RES TRIANGLE PK,NC 27709. RP YORK, DM (reprint author), NIEHS,MOLEC TOXICOL LAB,RES TRIANGLE PK,NC 27709, USA. RI Pedersen, Lee/E-3405-2013 OI Pedersen, Lee/0000-0003-1262-9861 NR 37 TC 4 Z9 4 U1 0 U2 3 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0192-8651 J9 J COMPUT CHEM JI J. Comput. Chem. PD JAN PY 1994 VL 15 IS 1 BP 61 EP 71 DI 10.1002/jcc.540150108 PG 11 WC Chemistry, Multidisciplinary SC Chemistry GA MP334 UT WOS:A1994MP33400007 ER PT J AU GREIG, NH BROSSI, A SONCRANT, TT HOLLOWAY, HW PEI, XF RAPOPORT, SI INGRAM, DK AF GREIG, NH BROSSI, A SONCRANT, TT HOLLOWAY, HW PEI, XF RAPOPORT, SI INGRAM, DK TI NOVEL, LONG-ACTING AND SELECTIVE PHYSOSTIGMINE ANALOGS AS POTENTIAL THERAPEUTICS FOR ALZHEIMERS-DISEASE SO JOURNAL OF CONTROLLED RELEASE LA English DT Article; Proceedings Paper CT 6th International Symposium on Recent Advances in Drug Delivery Systems CY FEB 21-24, 1993 CL SALT LAKE CITY, UT SP 3M PHARM, BAXTER HEALTHCARE COMP, CIBA GEIGY PHARM DIV, DUPONT MERCK PHARM CO, HOFFMANN LA ROCHE INC, LOHMANN THERAPIE SYST GMBH & CO, PHARMA DELIVERY SYST INC, SAM YANG CO LTD, SHISEIDO RES CTR, SMITHKLINE BEECHAM PHARM, TEKEDA CHEM IND LTD, THERATECH INC, UPJOHN CO, YAMANOUCHI PHARM CO LTD C1 NIA,CELLULAR & MOLEC BIOL LAB,WASHINGTON,DC. GEORGE WASHINGTON UNIV,DEPT CHEM,WASHINGTON,DC 20052. RP GREIG, NH (reprint author), NIA,NEUROSCI LAB,WASHINGTON,DC, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-3659 J9 J CONTROL RELEASE JI J. Control. Release PD JAN PY 1994 VL 28 IS 1-3 BP 313 EP 313 DI 10.1016/0168-3659(94)90193-7 PG 1 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Chemistry; Pharmacology & Pharmacy GA NA912 UT WOS:A1994NA91200046 ER PT J AU CHOW, LC TAKAGI, S SHERN, RJ CHOW, TH TAKAGI, KK SIECK, BA AF CHOW, LC TAKAGI, S SHERN, RJ CHOW, TH TAKAGI, KK SIECK, BA TI EFFECTS ON WHOLE SALIVA OF CHEWING GUMS CONTAINING CALCIUM PHOSPHATES SO JOURNAL OF DENTAL RESEARCH LA English DT Article DE SALIVA; MINERALS; SALIVATION; STIMULATION; CALCIUM PHOSPHATES ID FLOW-RATE; FLUORIDE; ENAMEL; PH AB To evaluate chewing gums as a vehicle to increase salivary mineral saturation levels and enhance salivation, monocalcium phosphate monohydrate (MCPM) and an equimolar mixture of tetracalcium phosphate (TTCP) with dicalcium phosphate anhydrous (DCPA) were chosen as experimental chewing gum additives. Each of eight subjects chewed a commercial sugarless bubble gum (control) for 16 min or the same gum to which 5 wt% of MCPM or the TTCP-DCPA mixture had been added. The saliva samples collected every 2 min were analyzed for weight, pH, and total calcium (Ca) and phosphate (P) concentrations. Both experimental gums were found to increase significantly the Ca and P concentrations of saliva during the 16-minute period even more than with a previously evaluated gum that contained dicalcium phosphate dihydrate. The degree of saturation of tooth mineral was significantly increased by both experimental gums, with the greater increase being produced by the TTCP-DCPA gum. The MCPM gum produced a significantly greater saliva flow and a lower salivary pH than did the control and TTCP-DCPA gums. The results suggest that the experimental gums may be useful for promoting remineralization in general and for inducing salivation in xerostomic patients. C1 NIDR,BETHESDA,MD. RP CHOW, LC (reprint author), NATL INST STAND & TECHNOL,PAFFENBARGER RES CTR,AMER DENT ASSOC HLTH FDN,GAITHERSBURG,MD 20899, USA. FU NIDCR NIH HHS [DE05354] NR 23 TC 23 Z9 23 U1 0 U2 3 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD JAN PY 1994 VL 73 IS 1 BP 26 EP 32 DI 10.1177/00220345940730010401 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MU736 UT WOS:A1994MU73600005 PM 8294615 ER PT J AU MARCUS, SE KASTE, LM BROWN, LJ AF MARCUS, SE KASTE, LM BROWN, LJ TI PREVALENCE AND SOCIAL CORRELATES OF TOOTH LOSS AMONG THE ELDERLY IN THE UNITED-STATES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 142 EP 142 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500328 ER PT J AU CRALL, J BEAZOGLOU, T NAINAR, H BROWN, LJ AF CRALL, J BEAZOGLOU, T NAINAR, H BROWN, LJ TI PREVALENCE AND DISTRIBUTION OF EXTENSIVE ROOT CARIES IN EXTRACTED TEETH SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV CONNECTICUT,SCH DENT MED,FARMINGTON,CT 06032. NIDR,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 145 EP 145 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500351 ER PT J AU MATSUKI, Y AMIZUKA, N WARSHAWSKY, H GOLTZMAN, D NAKASHIMA, M YAMADA, KM YAMADA, Y AF MATSUKI, Y AMIZUKA, N WARSHAWSKY, H GOLTZMAN, D NAKASHIMA, M YAMADA, KM YAMADA, Y TI IDENTIFICATION OF GENES EXPRESSED IN RAT INCISOR SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. ROYAL VICTORIA HOSP,CALCIUM RES LAB,MONTREAL H3A 1A1,QUEBEC,CANADA. MCGILL UNIV,MONTREAL H3A 2T5,QUEBEC,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 146 EP 146 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500354 ER PT J AU YAMADA, S BROWN, KE AMAGASA, T YAMADA, KM AF YAMADA, S BROWN, KE AMAGASA, T YAMADA, KM TI INTEGRIN REGULATORY SWITCHING IN TOOTH DEVELOPMENT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. TOKYO MED & DENT UNIV,DEPT ORAL MAXILLOFACIAL SURG 1,TOKYO 113,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 175 EP 175 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500592 ER PT J AU CHAI, Y ROBBINS, K SLAVKIN, HC AF CHAI, Y ROBBINS, K SLAVKIN, HC TI SUGGESTED FUNCTION OF PDGF-A AND COGNATE RECEPTOR IN REGULATING TOOTH FORMATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV SO CALIF,SCH DENT,CTR CRANIOFACIA MOLEC BIOL,LOS ANGELES,CA 90089. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 179 EP 179 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500622 ER PT J AU HO, D KULKARNI, AB LITZ, M DSOUZA, RN AF HO, D KULKARNI, AB LITZ, M DSOUZA, RN TI TOOTH DEVELOPMENT IN KNOCKOUT MICE BEARING A TGF-BETA-1 NULL MUTATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DENT BRANCH,HOUSTON,TX 77225. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 179 EP 179 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500618 ER PT J AU WRIGHT, JT MAHLER, J SPALDING, J SZCZESNIAK, C HANSEN, L AF WRIGHT, JT MAHLER, J SPALDING, J SZCZESNIAK, C HANSEN, L TI ODONTOGENIC-TUMORS IN THE V-HA-RAS (TG AC) TRANSGENIC MOUSE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV N CAROLINA,DEPT PEDIAT DENT,CHAPEL HILL,NC 27514. NIEHS,LECM,RES TRIANGLE PK,NC 27709. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 179 EP 179 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500617 ER PT J AU TOMAR, SL SWANGO, PA KLEINMAN, DV BURT, BA AF TOMAR, SL SWANGO, PA KLEINMAN, DV BURT, BA TI PERIODONTAL ATTACHMENT LOSS IN HIV-SEROPOSITIVE MILITARY PERSONNEL SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV MICHIGAN,SCH PUBL HLTH,ANN ARBOR,MI 48109. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 187 EP 187 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500688 ER PT J AU DIEHL, S WANG, S LOPEZ, N LAKE, K WALCZAK, C SUN, C LANDA, B AF DIEHL, S WANG, S LOPEZ, N LAKE, K WALCZAK, C SUN, C LANDA, B TI HLA REGION EXCLUDED BY LINKAGE ANALYSES OF EARLY-ONSET PERIODONTITIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. UNIV CHILE,SANTIAGO,CHILE. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 188 EP 188 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500693 ER PT J AU NOWJACKRAYMER, RE GIFT, HC AF NOWJACKRAYMER, RE GIFT, HC TI USE OF MOUTHGUARDS AND HEADGEAR BY CHILDREN DURING SPORTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 194 EP 194 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500737 ER PT J AU BERTHOLD, CW DIONNE, RA AF BERTHOLD, CW DIONNE, RA TI COMPARISON OF SUBLINGUALLY AND ORALLY-ADMINISTERED TRIAZOLAM FOR PREMEDICATION PRIOR TO ORAL-SURGERY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NAB,CLIN PHARMACOL UNIT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 210 EP 210 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500872 ER PT J AU HANEY, S EICHMILLER, F MEIERS, J AF HANEY, S EICHMILLER, F MEIERS, J TI IN-VITRO STUDY OF INTRAORAL WELDING PROCEDURES FOR PURE TITANIUM SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NDS,BETHESDA,MD 20892. NIST,GAITHERSBURG,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 212 EP 212 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500887 ER PT J AU NAGLER, R BAUM, BJ FOX, PC AF NAGLER, R BAUM, BJ FOX, PC TI LONG-TERM EFFECTS OF X-IRRADIATION ON RAT SALIVARY-GLANDS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 213 EP 213 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500896 ER PT J AU CODE, JE ANTONUCCI, JM BENNETT, PS AF CODE, JE ANTONUCCI, JM BENNETT, PS TI PHOTOACTIVATED DENTIN BONDING WITH N-PHENYLIMINODIACETIC ACID SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIH,CODC,BETHESDA,MD 20892. NIST,GAITHERSBURG,MD. ADAHF,GAITHERSBURG,MD. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 223 EP 223 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500972 ER PT J AU SKRTIC, D EANES, ED ANTONUCCI, JM AF SKRTIC, D EANES, ED ANTONUCCI, JM TI DISSOLUTION BEHAVIOR OF AMORPHOUS CALCIUM-PHOSPHATE METHACRYLATE COMPOSITES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDA,LEXINGTON,KY 40583. NIST,GAITHERSBURG,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 229 EP 229 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501017 ER PT J AU WHITE, BA MCKENNA, G KASTE, LM AF WHITE, BA MCKENNA, G KASTE, LM TI TYPES OF DENTAL SERVICES PROVIDED IN THE UNITED-STATES IN 1987 SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UNIV CONNECTICUT,FARMINGTON,CT 06032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 236 EP 236 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501074 ER PT J AU MERTZ, PM WAHL, LM AF MERTZ, PM WAHL, LM TI IL-10 SUPPRESSION OF MONOCYTE PROSTAGLANDIN-H SYNTHASE-2, PROSTAGLANDINS AND MATRIX METALLOPROTEINASE PRODUCTION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,LI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 252 EP 252 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501207 ER PT J AU RUHL, S SANDBERG, AL CISAR, JO AF RUHL, S SANDBERG, AL CISAR, JO TI LEUKOSIALIN (CD43), A GRANULOCYTE RECEPTOR FOR STREPTOCOCCAL AND ACTINOMYCES LECTINS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 252 EP 252 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501206 ER PT J AU SCHWARTZ, JL SHKLAR, D AF SCHWARTZ, JL SHKLAR, D TI SUPPRESSION OF ORAL-CANCER, CELL-GROWTH AND MUTANT P53 BY VITAMIN-E SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 264 EP 264 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501296 ER PT J AU TRICKLER, D WEST, K SHKLAR, G SCHWARTZ, J AF TRICKLER, D WEST, K SHKLAR, G SCHWARTZ, J TI MUTANT P53 DECREASE DURING GLUTATHIONE INHIBITION OF ORAL CARCINOGENESIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,CAMBRIDGE,MA 02138. NIDR,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 264 EP 264 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501298 ER PT J AU WEST, K SCHWARTZ, J SHKLAR, G SANTOS, H AF WEST, K SCHWARTZ, J SHKLAR, G SANTOS, H TI P53, PCNA IN DYSPLASTIC AND NON-DYSPLASTIC LICHEN-PLANUS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. HARVARD UNIV,SCH DENT,CAMBRIDGE,MA 02138. TUFTS UNIV,SCH DENT MED,MEDFORD,MA 02155. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 264 EP 264 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501301 ER PT J AU BOYD, RL KORN, EL MAXWELL, R BAUMRIND, S AF BOYD, RL KORN, EL MAXWELL, R BAUMRIND, S TI CLINICIAN REASONS FOR EXTRACTING IN ORTHODONTIC TREATMENT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. NCI,BIOMETR RES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 273 EP 273 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501370 ER PT J AU MAXWELL, R KORN, EL BOYD, RL BAUMRIND, S AF MAXWELL, R KORN, EL BOYD, RL BAUMRIND, S TI THE DECISION TO EXTRACT IN ORTHODONTIC TREATMENT - AGREEMENT AMONG CLINICIAN SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. NCI,BIOMETR RES BRANCH,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 273 EP 273 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501366 ER PT J AU ANTONUCCI, JM BENNETT, PS CODE, JE AF ANTONUCCI, JM BENNETT, PS CODE, JE TI EFFECT OF REDOX METALS ON DENTIN BONDING WITH PMDM-N-PHENYL-IMINODIACETIC ACID SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIST,GAITHERSBURG,MD. ADAHF,GAITHERSBURG,MD. NIH,CODC,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 277 EP 277 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501403 ER PT J AU SCHUMACHER, GE ANTONUCCI, JM BENNETT, PS AF SCHUMACHER, GE ANTONUCCI, JM BENNETT, PS TI N-PHENYLIMINODIACETIC ACID AS AN ETCHANT PRIMER FOR DENTIN BONDING SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIH,CODC,BETHESDA,MD 20892. NIST,GAITHERSBURG,MD. ADAHF,GAITHERSBURG,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 277 EP 277 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501399 ER PT J AU INOUE, K KARASAWA, N ISOMURA, G NAGATSU, I CREVELING, CR AF INOUE, K KARASAWA, N ISOMURA, G NAGATSU, I CREVELING, CR TI CATECHOLAMINES AND ITS RELATED ENZYMES IN THE RAT DENTAL-PULP SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 MATSUMOTO DENT COLL,MATSUMOTO,JAPAN. FUJITA HLTH UNIV,FUJITA,JAPAN. NIH,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 288 EP 288 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501487 ER PT J AU HONG, IK LOCKWICH, TP HIRAMATSU, Y AMBUDKAR, LS AF HONG, IK LOCKWICH, TP HIRAMATSU, Y AMBUDKAR, LS TI RESOLUTION OF CA2+ INFLUX COMPONENTS IN THE RAT PAROTID BASOLATERAL MEMBRANE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 289 EP 289 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501499 ER PT J AU ANDERSEN, RN GANESHKUMAR, N KOLENBRANDER, PE AF ANDERSEN, RN GANESHKUMAR, N KOLENBRANDER, PE TI NUCLEOTIDE-SEQUENCE OF COAGGREGATION ADHESIN GENE, SCAA, FROM STREPTOCOCCUS-GORDONII PK488 SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 301 EP 301 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501592 ER PT J AU CLEMANS, DL KOLENBRANDER, PE AF CLEMANS, DL KOLENBRANDER, PE TI CLONING AND CHARACTERIZATION OF COAGGREGATION-RELEVANT GENES OF STREPTOCOCCUS-GORDONII DL1 SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 301 EP 301 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501588 ER PT J AU KINGMAN, A BROWN, LJ ALBERTINI, T AF KINGMAN, A BROWN, LJ ALBERTINI, T TI CORRELATIONS BETWEEN URINARY MERCURY CONCENTRATIONS AND AMALGAM EXPOSURE AMONG NIDR AMALGAM STUDY PARTICIPANTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 307 EP 307 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501642 ER PT J AU ANN, DK TU, ZJ LAZOWSKI, KW WU, G KOUSVELARI, E LIN, HH AF ANN, DK TU, ZJ LAZOWSKI, KW WU, G KOUSVELARI, E LIN, HH TI MULTIFACTORIAL REGULATION OF SALIVARY PRP EXPRESSION IN TRANSGENIC MICE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV MINNESOTA,SCH MED,DEPT PHARMACOL,MINNEAPOLIS,MN 55455. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 310 EP 310 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501661 ER PT J AU OCONNELL, BC MASTRANGELI, A OPPENHEIM, FG CRYSTAL, RG BAUM, BJ AF OCONNELL, BC MASTRANGELI, A OPPENHEIM, FG CRYSTAL, RG BAUM, BJ TI ADENOVIRUS-MEDIATED TRANSFER OF HISTATIN-3 TO RAT SALIVARY-GLANDS IN-VIVO SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. CORNELL UNIV,MED CTR,NEW YORK,NY 10021. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 310 EP 310 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501662 ER PT J AU GIFT, HC OLDAKOWSKI, RJ AF GIFT, HC OLDAKOWSKI, RJ TI REPORTED DENTAL CONDITIONS AND BEHAVIORS AMONG DIABETICS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 333 EP 333 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501850 ER PT J AU STRECKFUS, C AF STRECKFUS, C TI PAROTID-GLAND FLOW-RATES IN CAUCASIAN AND AFRICAN-AMERICAN ELDERLY INDIVIDUALS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,EODPP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 335 EP 335 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501865 ER PT J AU BRUNELLE, JA HEIFETZ, SB SLOTS, J AF BRUNELLE, JA HEIFETZ, SB SLOTS, J TI A SALIVARY RINSE FOR SAMPLING MICROORGANISMS ASSOCIATED WITH DECIDUOUS CARIES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. USC,LOS ANGELES,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 337 EP 337 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501880 ER PT J AU ADESANYA, MR OCONNELL, BC OPPENHEIM, FG BAUM, BJ AF ADESANYA, MR OCONNELL, BC OPPENHEIM, FG BAUM, BJ TI CLONING A RECOMBINANT HUMAN SALIVARY HISTATIN FRAGMENT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. BOSTON UNIV,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 343 EP 343 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501930 ER PT J AU KOUSVELARI, E BRADO, C KITAMUA, C AF KOUSVELARI, E BRADO, C KITAMUA, C TI TYROSINE PHOSPHORYLATION CHANGES IN A5 CELLS CULTURED ON LAMININ AND COLLAGEN IV SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LI,NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 343 EP 343 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501928 ER PT J AU WEISS, EI DOTAN, M METZGER, Z KOLENBRANDER, PE GANESHKUMAR, N AF WEISS, EI DOTAN, M METZGER, Z KOLENBRANDER, PE GANESHKUMAR, N TI ADHERENCE OF F-NUCLEATUM TO MAMMALIAN-CELLS AND TO PERIOPATHOGENIC BACTERIA INVOLVE SIMILAR MECHANISMS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TEL AVIV UNIV,IL-69978 TEL AVIV,ISRAEL. NIDR,BETHESDA,MD 20892. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 347 EP 347 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501961 ER PT J AU TAKAHASHI, Y CISAR, JO SANDBERG, AL AF TAKAHASHI, Y CISAR, JO SANDBERG, AL TI MULTIPLE LECTIN ACTIVITIES OF STREPTOCOCCUS-GORDONII SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 350 EP 350 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501986 ER PT J AU SWANGO, PA KLEINMAN, DV KONZELMAN, J NOWJACKRAYMER, RE RAMS, TE AF SWANGO, PA KLEINMAN, DV KONZELMAN, J NOWJACKRAYMER, RE RAMS, TE TI INTERDENTAL PAPILLARY DESTRUCTION IN HIV-INFECTION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 352 EP 352 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502001 ER PT J AU SHKLAR, G WEST, K SCHWARTZ, J AF SHKLAR, G WEST, K SCHWARTZ, J TI ALTERED CYTOKERATIN EXPRESSION IN ORAL CARCINOGENESIS INHIBITION BY ANTIOXIDANT NUTRIENTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,CAMBRIDGE,MA 02138. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 359 EP 359 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502058 ER PT J AU BRAVEMAN, N AF BRAVEMAN, N TI SYMPOSIUM - GRANTSMANSHIP - SUBMITTING AND GETTING AN NIH GRANT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 366 EP 366 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502109 ER PT J AU FELDMAN, RS BRUNELLE, JA LEVY, RM AF FELDMAN, RS BRUNELLE, JA LEVY, RM TI TOOTH LOSS AND PERIODONTAL THERAPY - CASE MANAGER EFFECT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV PENN,VET ADM MED CTR,SCH DENT MED,PHILADELPHIA,PA 19104. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 366 EP 366 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502114 ER PT J AU SHIP, J BALAKIR, L PEARSON, J AF SHIP, J BALAKIR, L PEARSON, J TI 3 YEAR LONGITUDINAL-STUDY ON SMELL IDENTIFICATION IN HEALTHY-ADULTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV MICHIGAN,SCH DENT,ANN ARBOR,MI 48109. NIA,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 372 EP 372 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502159 ER PT J AU WINN, DM MARCUS, SE BROWN, LJ AF WINN, DM MARCUS, SE BROWN, LJ TI ORAL HEALTH-PROBLEMS IN REMAINING DENTITION OF OLDER PERSONS IN THE UNITED-STATES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 372 EP 372 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502158 ER PT J AU TOWNSLEY, JD KINGMAN, A AF TOWNSLEY, JD KINGMAN, A TI SYMPOSIUM - FUNDAMENTALS OF THE DESIGN AND CONDUCT OF DENTAL AND CRANIOFACIAL CLINICAL-TRIALS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 383 EP 383 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502248 ER PT J AU WHITE, BA MCKENNA, G KASTE, LM AF WHITE, BA MCKENNA, G KASTE, LM TI INDIVIDUALS PATTERNS OF DENTAL-CARE DURING 1987 SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UNIV CONNECTICUT,FARMINGTON,CT 06032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 383 EP 383 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502250 ER PT J AU ALBERTINI, T KINGMAN, A BROWN, LJ AF ALBERTINI, T KINGMAN, A BROWN, LJ TI DISTRIBUTION OF AMALGAM RESTORATIVE MATERIAL IN THE NIDR AMALGAM STUDY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 384 EP 384 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502256 ER PT J AU REDFORD, M WEBBER, RL HORTON, RA TELL, G AF REDFORD, M WEBBER, RL HORTON, RA TELL, G TI FRACTAL DIMENSION AS A MEASURE OF CLINICAL CHANGES IN ALVEOLAR BONE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. BGSM,WINSTOM SALEM,GA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 390 EP 390 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502301 ER PT J AU GUCKES, AD BRAHIM, JS MCCARTHY, GR SIEBRING, N MCCULLAGH, LA AF GUCKES, AD BRAHIM, JS MCCARTHY, GR SIEBRING, N MCCULLAGH, LA TI USE OF TITANIUM SCREW IMPLANTS IN ADOLESCENTS WITH ECTODERMAL DYSPLASIA SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 399 EP 399 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502376 ER PT J AU HAGHIGHAT, N ALHASHIMI, I FOX, PC AF HAGHIGHAT, N ALHASHIMI, I FOX, PC TI ELECTROPHORETIC PROFILE OF SALIVARY PROTEINS IN SJOGRENS-SYNDROME SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 BAYLOR COLL DENT,DEPT PERIODONT,DALLAS,TX. NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 420 EP 420 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502544 ER PT J AU WU, AJ FOX, PC KURRASCH, RHM BAUM, BJ ATKINSON, JC AF WU, AJ FOX, PC KURRASCH, RHM BAUM, BJ ATKINSON, JC TI THE EFFECT OF INTERFERON-GAMMA AND TNF-ALPHA ON THE GROWTH OF A SALIVARY CELL-LINE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 420 EP 420 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502545 ER PT J AU MANCHCITRON, JN LONDON, J AF MANCHCITRON, JN LONDON, J TI RIBOSOMAL HOPPING AND FRAMESHIFTING IN THE PREVOTELLA-IOESCHEII ADHESIN GENE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UMKE,SCH DENT,DEPT ORAL BIOL,KANSAS CITY,MO. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 431 EP 431 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502626 ER PT J AU GORDON, SM TAHARA, MA ROWAN, JS DIONNE, RA DUBNER, R AF GORDON, SM TAHARA, MA ROWAN, JS DIONNE, RA DUBNER, R TI COMPARATIVE ANALGESIC EFFICACY OF PERIPHERALLY VERSUS ORALLY-ADMINISTERED KETOPROFEN GEL SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NAB,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 438 EP 438 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502686 ER PT J AU SEDER, RA GERMAIN, RN LINSLEY, PS PAUL, WE AF SEDER, RA GERMAIN, RN LINSLEY, PS PAUL, WE TI CD28-MEDIATED COSTIMULATION OF INTERLEUKIN-2 (IL-2) PRODUCTION PLAYS A CRITICAL ROLE IN T-CELL PRIMING FOR IL-4 AND INTERFERON-GAMMA PRODUCTION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID MONOCLONAL-ANTIBODY; ACTIVATION PATHWAY; CD28; RECEPTOR; MOLECULE; INVITRO; GENE AB Naive T cells require interleukin 4 (IL-4) to develop into IL-4-producing T cells and IL-4 blocks development of such cells into interferon gamma (IFN-gamma) producers. Prior studies in accessory cell-independent priming systems using antireceptor antibodies as agonists have demonstrated that IL-2 is also necessary for the development of IL-4-producing cells under these culture conditions. Here we have examined the role of IL-2 and the CD28 costimulation pathway in priming for IL-4 and IFN-gamma production using a more physiologic model. This involved antigen presentation by accessory cells to naive CD4(+) T cells from transgenic mice whose cells express a T cell receptor (TCR) specific for a cytochrome c peptide in association with I-E(k). With splenic antigen-presenting cells (APCs), inhibition of CD28 costimulation by the fusion protein CTLA4- immunoglobulin (Ig) blocked effective priming. Similarly, transfected fibroblasts expressing both MHC class II and the CD28 ligand B7 could prime for IL-4 production and such priming also was blocked by CTLA4-Ig. However, APCs deficient in CD28 ligands also could prime TCR transgenic T cells to become IL-4 producers if an exogenous source of IL-2, as well as IL-4, was provided, and the inhibition of priming seen with splenic or transfected fibroblast APCs in the presence of CTLA4-Ig could be reversed by addition of IL-2. Likewise, priming for IFN-gamma production could be blocked by CTLA4-lg and reversed by IL-2. Thus, we conclude that IL-2 plays a critical role in priming naive CD4(+) T cells to become IL-4 or IFN-gamma producers. Engagement of the CD28 pathway, although normally important in such priming, is unnecessary in the presence of exogenous IL-2. C1 BRISTOL MYERS SQUIBB,SEATTLE,WA 98121. RP SEDER, RA (reprint author), NIAID,CLIN INVEST LAB,BLDG 10,ROOM 11C215,BETHESDA,MD 20892, USA. NR 30 TC 192 Z9 193 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1994 VL 179 IS 1 BP 299 EP 304 DI 10.1084/jem.179.1.299 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA MP517 UT WOS:A1994MP51700029 PM 8270872 ER PT J AU LONDON, AS MORGAN, SP AF LONDON, AS MORGAN, SP TI RACIAL-DIFFERENCES IN 1ST NAMES IN 1910 SO JOURNAL OF FAMILY HISTORY LA English DT Article; Proceedings Paper CT Annual Meeting of the Population-Association-of-America CY MAY 02, 1992 CL DENVER, CO SP POPULAT ASSOC AMER ID FAMILY-STRUCTURE; SEGREGATION; KINSHIP; SOUTH AB This research examines concentration and similarity in the first name distributions of African Americans and whites resident in Mississippi in 1910. Data are drawn from the Public Use Sample of the 1910 Census, with names added from microfilm copies of original Census manuscripts. We find little difference in the degree of concentration of the name distributions and only modest dissimilarity in name choice. Multivariate analysis using age as a proxy for period of name assignment (birth cohort) indicates that racial differentiation in name choice increased over the period 1870 to 1910 primarily as a result of changes in the name choices of whites. We discuss these results in conjunction with the recent work of Lieberson and Bell (1992) on contemporary racial differences in naming patterns. Lieberson and Bell (1992) argue that African Americans in the contemporary period emphasize group differences by choosing ''African'' or ''African sounding'' names. In Mississippi in the period between the abolition of slavery and 1910, we argue that whites distanced themselves from African Americans by choosing increasingly the ''whitest'' names (e.g., those disproportionately chosen by whites). Changing naming patterns are not orchestrated group responses. Instead, they reflect emergent cultural responses to fundamental social change. C1 UNIV PENN,CHAIR SOCIOL,PHILADELPHIA,PA 19104. RP LONDON, AS (reprint author), UNIV CALIF LOS ANGELES,DEPT SOCIOL,NIMH,TRAINING PROGRAM PSYCHOSOCIAL ISSUES & MENTAL HLTH SERV,LOS ANGELES,CA 90024, USA. NR 50 TC 7 Z9 7 U1 1 U2 2 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0363-1990 J9 J FAM HIST JI J. Fam. Hist. PY 1994 VL 19 IS 3 BP 261 EP 284 PG 24 WC Anthropology; Family Studies; History; History Of Social Sciences SC Anthropology; Family Studies; History; Social Sciences - Other Topics GA PK454 UT WOS:A1994PK45400004 ER PT J AU SMIALEK, JE LEVINE, B CHIN, L WU, SC JENKINS, AJ AF SMIALEK, JE LEVINE, B CHIN, L WU, SC JENKINS, AJ TI A FENTANYL EPIDEMIC IN MARYLAND 1992 SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE TOXICOLOGY; FENTANYL; EPIDEMIC; CHROMATOGRAPHIC ANALYSIS; CHEMICAL ANALYSIS ID DEATH AB In early 1992, the Office of the Chief Medical Examiner, State of Maryland, encountered 30 cases where fentanyl was identified in the postmortem specimens. Twenty-five of the decedents were found in Baltimore City and five were found in the surrounding counties. Four of the decedents were female and eight of the victims were white. The blood fentanyl concentrations ranged from 2.2 to 100 mu g/L. Ethanol and other abused drugs were detected in 28 of these cases. The cause of death in all cases was ethanol-, drug intoxication, or both. C1 OFF CHIEF MED EXAMINER,BALTIMORE,MD. NIDA,DIV EPIDEMIOL & PREVENT RES,ROCKVILLE,MD. NR 13 TC 24 Z9 24 U1 5 U2 5 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD JAN PY 1994 VL 39 IS 1 BP 159 EP 164 PG 6 WC Medicine, Legal SC Legal Medicine GA MT466 UT WOS:A1994MT46600017 PM 8113698 ER PT J AU COSTA, PT METTER, EJ MCCRAE, RR AF COSTA, PT METTER, EJ MCCRAE, RR TI PERSONALITY STABILITY AND ITS CONTRIBUTION TO SUCCESSFUL AGING SO JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium of the Boston-Society-for-Gerontological-Psychiatry: the Psychology of Successful Aging CY NOV 06-07, 1993 CL BOSTON, MA SP BOSTON SOC GERONTOL PSYCHIAT ID 5-FACTOR MODEL; FOLLOW-UP; ADULTHOOD; RATINGS; COLLEGE; WOMEN C1 NIA,LONGITUDINAL STUDIES BRANCH,BALTIMORE,MD 21224. NIA,PERSONAL STRESS & COPING SECT,BALTIMORE,MD 21224. RP COSTA, PT (reprint author), NIA,GERONTOL RES CTR,PERSONAL & COGNIT LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. OI Costa, Paul/0000-0003-4375-1712 NR 41 TC 31 Z9 31 U1 1 U2 4 PU INT UNIV PRESS INC PI MADISON PA 59 BOSTON POST RD PO BOX 1524, MADISON, CT 06443-1524 SN 0022-1414 J9 J GERIATR PSYCHIAT JI J. Geriatr. Psychiatry PY 1994 VL 27 IS 1 BP 41 EP 59 PG 19 WC Geriatrics & Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA ND146 UT WOS:A1994ND14600006 ER PT J AU BERGASA, NV ALLING, DW VERGALLA, J JONES, EA AF BERGASA, NV ALLING, DW VERGALLA, J JONES, EA TI CHOLESTASIS IN THE MALE-RAT IS ASSOCIATED WITH NALOXONE-REVERSIBLE ANTINOCICEPTION SO JOURNAL OF HEPATOLOGY LA English DT Article DE ANTINOCICEPTION; CHOLESTASIS; OPIOIDS; RATS; TAIL- FLICK ASSAY ID PLASMA METHIONINE ENKEPHALIN; PRIMARY BILIARY-CIRRHOSIS; OPIOID-PEPTIDES; LIVER-DISEASE; MORPHINE; ANALGESIA; PRURITUS; MODEL; BILE AB Clinical observations have suggested that cholestasis is associated with increased neurotransmission mediated by the opioid system in the central nervous system. As opiate agonists (e.g. morphine) mediate analgesia, increased opioidergic tone in cholestasis should be associated with a decreased response to pain. To test this hypothesis, the response of rats with acute cholestasis to a nociceptive stimulus was measured by the use of the tail-flick test, an extensively validated assay for measuring opiate-induced antinociception. Five and 7 days after bile-duct resection, the mean tail-flick latency was longer than before surgery (p<0.05), whereas the corresponding means for unoperated and sham-resected controls were not significantly different from their respective baseline values. The increase in the mean tail-hick latency in the bile-duct resection group was reversed by (-)-naloxone (1 mg/kg subcutaneously), but not by its enantiomer (+)-naloxone (10 mg/kg subcutaneously) (p<0.001). The stereoselective reversal of antinociception in cholestasis by naloxone indicates that this phenomenon is opioid-receptor mediated. In contrast, prolongation of the mean TFL found in the rat model of thioacetamide-induced acute hepatocellular necrosis was not reversed by (-)-naloxone, indicating that antinociception in this model is not opioid mediated. These findings provide support for the hypothesis that cholestasis is associated with increased opioidergic tone. (C) Journal of Hepatology. C1 NIDDKD,DIGEST DIS BRANCH,LIVER DIS SECT,BETHESDA,MD. NIAID,DIV INTRAMURAL RES,BETHESDA,MD. NR 30 TC 93 Z9 94 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0168-8278 J9 J HEPATOL JI J. Hepatol. PD JAN PY 1994 VL 20 IS 1 BP 85 EP 90 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MT027 UT WOS:A1994MT02700013 PM 8201227 ER PT J AU STEINBERG, SA KLEIN, E KILLENS, RL UHDE, TW AF STEINBERG, SA KLEIN, E KILLENS, RL UHDE, TW TI INHERITED DEAFNESS AMONG NERVOUS POINTER DOGS SO JOURNAL OF HEREDITY LA English DT Note ID AUDITORY-EVOKED RESPONSE; DALMATIAN DOGS AB A high incidence of deafness, confirmed by brainstem auditory evoked response testing, was found in a colony of pointer dogs selectively bred for excessive nervous behavior. The results of outcross and F-1 backcross breedings were consistent with an autosomal recessive mode of inheritance of deafness in this family of dogs. C1 TECHNION ISRAEL INST TECHNOL,FAC MED,RAMBAM MED CTR,DEPT PSYCHIAT,HAIFA,ISRAEL. ANIM CTR SECT,CARNIVORE UNIT,POOLESVILLE,MD. NIMH,ANXIETY & AFFECT DISORDERS SECT,POOLESVILLE,MD. RP STEINBERG, SA (reprint author), UNIV PENN,SCH VET,DEPT CLIN STUDIES PHILADELPHIA,NEUROL OPHTHALMOL SECT,PHILADELPHIA,PA 19104, USA. FU NCRR NIH HHS [RR02512] NR 11 TC 13 Z9 13 U1 0 U2 7 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0022-1503 J9 J HERED JI J. Hered. PD JAN-FEB PY 1994 VL 85 IS 1 BP 56 EP 59 PG 4 WC Evolutionary Biology; Genetics & Heredity SC Evolutionary Biology; Genetics & Heredity GA MV870 UT WOS:A1994MV87000014 PM 8120360 ER PT J AU BRISCOE, D STEPHENS, JC OBRIEN, SJ AF BRISCOE, D STEPHENS, JC OBRIEN, SJ TI LINKAGE DISEQUILIBRIUM IN ADMIXED POPULATIONS - APPLICATIONS IN GENE-MAPPING SO JOURNAL OF HEREDITY LA English DT Note ID DROSOPHILA-MELANOGASTER; NATURAL-POPULATIONS AB A method to detect linkage of genetic traits to polymorphic DNA markers in outbred populations when pedigree analysis is not feasible is presented. The procedure takes advantage of increased linkage disequilibrium that occurs when isolated races or subspecies mate and interbreed. By selecting restriction fragment length polymorphism (RFLP) or microsatellite marker loci that have different allele frequencies in admired populations, genetic associations produced de novo by hybridization will persist as a function of theta (map distance) for 10-20 generations after initial interbreeding. By careful selection of loci and study populations, the procedure detects linkage of traits otherwise refractory to linkage analysis. RP BRISCOE, D (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702, USA. NR 33 TC 83 Z9 88 U1 0 U2 9 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0022-1503 J9 J HERED JI J. Hered. PD JAN-FEB PY 1994 VL 85 IS 1 BP 59 EP 63 PG 5 WC Evolutionary Biology; Genetics & Heredity SC Evolutionary Biology; Genetics & Heredity GA MV870 UT WOS:A1994MV87000015 PM 8120361 ER PT J AU DICESARE, JC BURGESS, JP MASCARELLA, SW CARROLL, FI ROTHMAN, RB AF DICESARE, JC BURGESS, JP MASCARELLA, SW CARROLL, FI ROTHMAN, RB TI SYNTHESIS AND STRUCTURAL DETERMINATION OF 5H-BENZOCYCLOHEPTEN-5,8-IMINES SO JOURNAL OF HETEROCYCLIC CHEMISTRY LA English DT Article ID NMR AB Treatment of 4-hydroxy-N-methylisoquinolinium iodide with triethylamine in tetrahydrofuran or acetonitrile forms 2-methyl-4-oxidoisoquinolinium (2) in situ. Once formed, 2 can be trapped with dipolarophiles possessing varying degrees of activation to form the 5H-benzocyclohepten-5,8-imine ring system. Various 2-D nmr experiments were used in the identification of the stereochemical and regiochemical assignments for the ring system. C1 NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,BALTIMORE,MD 21224. RP DICESARE, JC (reprint author), RES TRIANGLE INST,CHEM & LIFE SCI UNIT,RES TRIANGLE PK,NC 27709, USA. NR 9 TC 14 Z9 14 U1 0 U2 0 PU HETERO CORPORATION PI TAMPA PA BOX 20285, TAMPA, FL 33622-0285 SN 0022-152X J9 J HETEROCYCLIC CHEM JI J. Heterocycl. Chem. PD JAN-FEB PY 1994 VL 31 IS 1 BP 187 EP 192 PG 6 WC Chemistry, Organic SC Chemistry GA MZ758 UT WOS:A1994MZ75800031 ER PT J AU WATSON, EL OLIVER, C DSILVA, N BELTON, CM AF WATSON, EL OLIVER, C DSILVA, N BELTON, CM TI LOCALIZATION OF THE G-PROTEIN G(0) IN EXOCRINE GLANDS SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article DE GTP-BINDING PROTEIN; G(0); G(0) ANTISERA; SALIVARY GLANDS; MOUSE; RAT; HSG-PA CELLS; IMMUNOHISTOCHEMISTRY IMMUNOCYTOCHEMISTRY ID NUCLEOTIDE-BINDING PROTEIN; SECRETORY GRANULE MEMBRANES; NEOPLASTIC EPITHELIAL DUCT; HUMAN SALIVARY-GLAND; RAT PAROTID-GLAND; MUSCARINIC RECEPTORS; REGULATORY PROTEINS; ALPHA-SUBUNIT; CELL-LINE; BRAIN AB The GTP-binding protein G(o) was localized immunohistochemically in the rat parotid gland and in other exocrine glands with specific G(o) antibodies. Immunohistochemical studies revealed that affinity-purified G(o alpha) polyclonal antibody (GO/85) immunoreacted primarily with duct cells of the rat parotid gland; immunoreactivity was also noted in duct cells of the rat submandibular, mouse parotid, and mouse submandibular glands. Light labeling of rat parotid and submandibular gland acinar cells was also noted. G(o alpha) antiserum (9072) differing in specificity for epitopes within G(o alpha) produced similar results. This antiserum also immunoreacted with rat submandibular duct cell secretory granule membranes. In contrast, in rat and mouse pancreas G(o alpha) antibodies immunoreacted primarily with islet cells. Duct cells were negative but there was light labeling of rat pancreatic acinar cells. The apparent duct specificity of G(o alpha) staining was further verified by demonstrating that G(o alpha) antibodies immunoreacted with HSG-PA cells, a human transformed salivary duct cell line. Specificity in immunohistochemical labeling of HSG-PA cells was confirmed by Western blot analysis. The results demonstrate that G(o) appears to be selectively expressed in the duct cells of rat parotid gland and other salivary glands. The selective enrichment of G(o) in duct cells suggests that this G-protein plays an important role in duct cell physiology. C1 UNIV WASHINGTON,DEPT PHARMACOL,SEATTLE,WA 98195. NIDR,IMMUNOL LAB,BETHESDA,MD 20892. RP WATSON, EL (reprint author), UNIV WASHINGTON,DEPT ORAL BIOL,SB-22,SEATTLE,WA 98195, USA. FU NIDCR NIH HHS [DE 05249] NR 29 TC 8 Z9 8 U1 0 U2 0 PU HISTOCHEMICAL SOC INC PI NEW YORK PA MT SINAI MEDICAL CENTER 19 EAST 98TH ST SUTIE 9G, NEW YORK, NY 10029 SN 0022-1554 J9 J HISTOCHEM CYTOCHEM JI J. Histochem. Cytochem. PD JAN PY 1994 VL 42 IS 1 BP 41 EP 47 PG 7 WC Cell Biology SC Cell Biology GA MM570 UT WOS:A1994MM57000005 PM 7505300 ER PT J AU SACKS, FM HEBERT, P APPEL, LJ BORHANI, NO APPLEGATE, WB COHEN, JD CUTLER, JA KIRCHNER, KA KULLER, LH ROTH, KJ TAYLOR, JO HENNEKENS, CH AF SACKS, FM HEBERT, P APPEL, LJ BORHANI, NO APPLEGATE, WB COHEN, JD CUTLER, JA KIRCHNER, KA KULLER, LH ROTH, KJ TAYLOR, JO HENNEKENS, CH TI THE EFFECT OF FISH-OIL ON BLOOD-PRESSURE AND HIGH-DENSITY LIPOPROTEIN-CHOLESTEROL LEVELS IN PHASE-I OF THE TRIALS OF HYPERTENSION PREVENTION SO JOURNAL OF HYPERTENSION LA English DT Article DE DIETARY FATS; POLYUNSATURATED FATTY ACIDS; FISH OILS; BLOOD PRESSURE; LIPOPROTEINS; CLINICAL TRIAL; HYPERTENSION ID N-3 FATTY-ACIDS; INSULIN-DEPENDENT DIABETICS; SERUM-LIPIDS; DIETARY FISH; CARDIOVASCULAR-DISEASE; CLINICAL-CHEMISTRY; PLATELET-FUNCTION; HEART-DISEASE; BLEEDING-TIME; HEALTHY-MEN AB Objective: To study the effects of moderate doses of fish oil on blood pressure and high-density lipoprotein (HDL)-cholesterol. Methods The participants were 350 normotensive men and women aged 30-54 years who were enrolled from seven academic medical centers in phase I of the Trials of Hypertension Prevention. They were randomly assigned to receive placebo or 6 g purified fish oil once a day, which supplied 3 g n-3 polyunsaturated fatty acids for 6 months. Results: Baseline blood pressure was (mean+/-SD) 123 +/- 9/81 +/- 5 mmHg. The mean differences in the blood pressure changes between the fish oil and placebo groups were not statistically significant. There was no tendency for fish oil to reduce blood pressure more in subjects with baseline blood pressures in the upper versus the lower quartile (132/87 versus 114/75 mmHg), low habitual fish consumption (0.4 versus 2.9 times a week) or low baseline plasma levels of n-3 fatty acids. Fish oil increased HDL(2)-cholesterol significantly compared with the placebo group. Subgroup analysis showed this effect to be significant in the women but not in the men. Increases in serum phospholipid n-3 fatty acids were significantly correlated with increases in HDL(2)-cholesterol and decreases in systolic blood pressure. Conclusion: Moderate amounts of fish oil (6 g/day) are unlikely to lower blood pressure in normotensive persons, but may increase HDL(2)-cholesterol, particularly in women. C1 BRIGHAM & WOMENS HOSP,CHANNING LAB,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV PREVENT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD. UNIV CALIF DAVIS,DAVIS,CA 95616. UNIV TENNESSEE,MEMPHIS,TN. ST LOUIS UNIV,ST LOUIS,MO 63103. NHLBI,BETHESDA,MD 20892. UNIV MISSISSIPPI,JACKSON,MS 39216. UNIV PITTSBURGH,SCH PUBL HLTH,PITTSBURGH,PA 15260. E BOSTON NEIGHBORHOOD HLTH CTR,BOSTON,MA. NR 59 TC 13 Z9 13 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0263-6352 J9 J HYPERTENS JI J. Hypertens. PY 1994 VL 12 SU 7 BP S23 EP S31 PG 9 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA QQ806 UT WOS:A1994QQ80600003 PM 7769501 ER PT J AU HAKIM, FT PAYNE, S SHEARER, GM AF HAKIM, FT PAYNE, S SHEARER, GM TI RECOVERY OF T-CELL POPULATIONS AFTER ACUTE GRAFT-VS-HOST REACTION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; COLONY-STIMULATING FACTORS; CLONAL DELETION; LYMPHOCYTES-T; ENTEROTOXIN-B; BONE-MARROW; INCOMPATIBLE STRUCTURES; PARENTAL LYMPHOCYTES; SELF-TOLERANCE; CYCLOSPORINE-A AB We previously have observed that T dependent immune functions were deficient for several months after induction of acute suppressive graft-vs-host-reaction (GVHR) by injection of parental C57BL/10 donor spleen cells into unirradiated (B10 x B10.BR) F, hosts. We therefore investigated whether new T cells matured after acute GVHR, and whether these were tolerant of host Ag. By 8 to 17 mo after GVHR, the frequencies of splenic CD4 and CD8 T cells were found to be comparable to age-matched untreated hosts, although the lymphoid organ size and hence the total number of T cells was significantly reduced. When GVHR was induced with a combination of C57BL/6 (Thy-1.2) mature lymphocytes and B6.PL (Thy-1.1) bone marrow stem cells, the mature donor Thy-1.2 T cells initially predominated during the acute GVHR. After several months, however, 75% of the CD4 and 50% of the CD8 T cell population was derived from donor Thy-1.1+ pre-T cells that had matured in the host. Long term GVHR spleen cells were unresponsive to host Ag in CTL assays, but did not suppress anti-host CTL responses. Finally, host-reactive Vbeta11 TCR expressing cells were found to be clonally deleted from splenic CD4 and CD8 populations, consistent with intrathymic negative selection. This evidence suggests that the post-GVHR thymus has the capacity to produce and negatively select phenotypically mature CD4 and CD8 T cells and that a failure to clonally delete self-reactive populations is not a contributing factor to the development of chronic GVHR in this system. C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 44 TC 10 Z9 10 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1994 VL 152 IS 1 BP 58 EP 64 PG 7 WC Immunology SC Immunology GA MN408 UT WOS:A1994MN40800008 PM 8254206 ER PT J AU PARKER, KC BEDNAREK, MA COLIGAN, JE AF PARKER, KC BEDNAREK, MA COLIGAN, JE TI SCHEME FOR RANKING POTENTIAL HLA-A2 BINDING PEPTIDES BASED ON INDEPENDENT BINDING OF INDIVIDUAL PEPTIDE SIDE-CHAINS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CYTOTOXIC LYMPHOCYTES-T; VIRUS MATRIX PROTEIN; CLASS-I MOLECULES; ANTIGENIC PEPTIDES; VIRAL PEPTIDES; MHC; MOTIFS; SELF; IDENTIFICATION AB A method to predict the relative binding strengths of all possible nonapeptides to the MHC class I molecule HLA-A2 has been developed based on experimental peptide binding data. These data indicate that, for most peptides, each side-chain of the peptide contributes a certain amount to the stability of the HLA-A2 complex that is independent of the sequence of the peptide. To quantify these contributions, the binding data from a set of 154 peptides were combined together to generate a table containing 180 coefficients (20 amino acids X 9 positions), each of which represents the contribution of one particular amino acid residue at a specified position within the peptide to binding to HLA-A2. Eighty peptides formed stable HLA-A2 complexes, as assessed by measuring the rate of dissociation of beta2m. The remaining 74 peptides formed complexes that had a half-life of beta2m dissociation of less than 5 min at 37-degrees-C, or did not bind to HLA-A2, and were included because they could be used to constrain the values of some of the coefficients. The ''theoretical'' binding stability (calculated by multiplying together the corresponding coefficients) matched the experimental binding stability to within a factor of 5. The coefficients were then used to calculate the theoretical binding stability for all the previously identified self or antigenic nonamer peptides known to bind to HLA-A2. The binding stability for all other nonamer peptides that could be generated from the proteins from which these peptides were derived was also predicted. In every case, the previously described HLA-A2 binding peptides were ranked in the top 2% of all possible nonamers for each source protein. Therefore, most biologically relevant nonamer peptides should be identifiable using the table of coefficients. We conclude that the side-chains of most nonamer peptides to the first approximation bind independently of one another to the HLA-A2 molecule. C1 MERCK SHARP & DOHME LTD,RAHWAY,NJ 07065. RP PARKER, KC (reprint author), NIAID,BIOL RESOURCES BRANCH,BLDG 4,ROOM 413,BETHESDA,MD 20892, USA. OI Parker, Kenneth/0000-0002-6282-2478 NR 34 TC 1060 Z9 1105 U1 0 U2 6 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1994 VL 152 IS 1 BP 163 EP 175 PG 13 WC Immunology SC Immunology GA MN408 UT WOS:A1994MN40800020 PM 8254189 ER PT J AU DASTYCH, J METCALFE, DD AF DASTYCH, J METCALFE, DD TI STEM-CELL FACTOR INDUCES MAST-CELL ADHESION TO FIBRONECTIN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID C-KIT RECEPTOR; GROWTH-FACTOR; DIFFERENTIAL EXPRESSION; TYROSINE KINASE; SI-LOCUS; LIGAND; MOUSE; IDENTIFICATION; FIBROBLASTS; ATTACHMENT AB Stem cell factor (SCF) or c-kit ligand is a growth factor cytokine produced by stromal cells that is known to influence mast cell proliferation and differentiation. We hypothesized that SCF may also influence the adhesion of mast cells to connective tissue matrix. To examine this hypothesis, we stimulated MCP5/L mast cells or murine bone marrow-derived cultured mast cells (BMCMC) with either SCF or PMA and observed adhesion to fibronectin (FN). As expected, 80 to 90% of PMA-activated MCP5/L cells or BMCMC adhered to FN. In addition, SCF promoted MCP5/L cell or BMCMC adhesion to FN in a dose-response fashion with 50 to 60% of BMCMC adhering to FN at a concentration 10 ng/ml of SCF. BMCMC adhesion was observed with as little as 200 pg/ml of SCF. Adhesion of SCF stimulated BMCMC to FN did not require IL-3, but was dependent on the concentration of FN used to coat the assay surface. Mast cell adhesion in the presence of SCF appeared to occur through an integrin receptor as adhesion was calcium dependent and could be blocked by an RGD (Ang,Gly,Asp)-containing peptide. SCF did not directly mediate adhesion through interaction with c-kit, as FN-coated surfaces exposed to SCF before initiation of the adhesion assay did not promote adhesion in the absence of soluble SCF. Rather, SCF appeared to stimulate adhesion to FN by activating mast cells through its interaction with c-kit. Thus, antibody to SCF blocked adhesion, and rat and murine SCF stimulated BMCMC adhesion to FN, but human SCF, which does not bind to murine c-kit, did not stimulate adhesion. Genistein, which inhibits tyrosine kinase activity, partially inhibited SCF-induced adhesion. SCF thus stimulates mast cell adhesion and, because SCF is produced normally in tissues, it may be a major factor responsible for the adhesion of mast cells to connective tissue matrix under physiologic conditions. RP DASTYCH, J (reprint author), NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BLDG 10,ROOM 11CZ06,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 35 TC 177 Z9 178 U1 1 U2 7 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1994 VL 152 IS 1 BP 213 EP 219 PG 7 WC Immunology SC Immunology GA MN408 UT WOS:A1994MN40800025 PM 7504710 ER PT J AU POCKAJ, BA YANG, JC LOTZE, MT LANGE, JR SPENCER, WF STEINBERG, SM TOPALIAN, SL SCHWARTZENTRUBER, DJ WHITE, DE ROSENBERG, SA AF POCKAJ, BA YANG, JC LOTZE, MT LANGE, JR SPENCER, WF STEINBERG, SM TOPALIAN, SL SCHWARTZENTRUBER, DJ WHITE, DE ROSENBERG, SA TI A PROSPECTIVE RANDOMIZED TRIAL EVALUATING COLLOID VERSUS CRYSTALLOID RESUSCITATION IN THE TREATMENT OF THE VASCULAR LEAK SYNDROME-ASSOCIATED INTERLEUKIN-2 THERAPY SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE INTERLEUKIN-2; VASCULAR LEAK SYNDROME; COLLOID; CRYSTALLOID; SHOCK ID HIGH-DOSE INTERLEUKIN-2; ADVANCED CANCER; IMMUNOTHERAPY; TOXICITY; SHOCK AB Interleukin-2 (IL-2)-based therapy induces a vascular leak syndrome (VLS), manifested by hypotension, tachycardia, and oliguria, as is also seen with septic shock. The optimal method for treating such VLS is not known. A prospective randomized trial was undertaken to compare crystalloid and colloid fluid resuscitation for patients receiving bolus IL-2-based therapy for metastatic cancer. Ah patients received maintenance crystalloid fluid administration and were randomized to receive crystalloid (0.9% normal saline) or colloid (5% human serum albumin) fluid boluses to maintain acceptable vital signs and urine output. Patients refractory to fluid boluses were given dopamine for oliguria and/or phenylephrine for hypotension. Of 107 patients who completed one cycle of therapy on study, 76 completed a full treatment course (two cycles) on study. The total number of saline and albumin fluid boluses given were 9.5+/-0.9 versus 7.7+/-0.7 (p = 0.36, n = 107) for the first cycle and 19.2+/-1.8 versus 16.1+/-1.6 (p = 0.33, n = 76) for a complete course, respectively. Although patients receiving saline boluses had significantly more oliguria during a course of therapy, weight gain, number of IL-2 doses, tachycardia, hypotension, vasopressor use, hospital stay, and clinical response rates did not significantly differ between arms. Changes in hematocrit, hemoglobin, protein, albumin, blood urea nitrogen (BUN), and creatinine were analyzed, and patients receiving crystalloid showed greater decreases in albumin (p < 0.0001) and total protein (p < 0.05) as expected. A 40-fold greater cost associated with albumin suggested that crystalloid resuscitation be used to treat the VLS associated with IL-2 therapy. C1 NCI,DIV CANC TREATMENT,SURG BRANCH,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NR 18 TC 44 Z9 45 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1994 VL 15 IS 1 BP 22 EP 28 DI 10.1097/00002371-199401000-00003 PG 7 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA MN046 UT WOS:A1994MN04600003 PM 8110727 ER PT J AU HAWKINS, MJ ATKINS, MB DUTCHER, JP FISHER, RI WEISS, GR MARGOLIN, KA RAYNER, AA SZNOL, M PARKINSON, DR PAIETTA, E GAYNOR, ER BOLDT, DH DOROSHOW, JH ARONSON, FR AF HAWKINS, MJ ATKINS, MB DUTCHER, JP FISHER, RI WEISS, GR MARGOLIN, KA RAYNER, AA SZNOL, M PARKINSON, DR PAIETTA, E GAYNOR, ER BOLDT, DH DOROSHOW, JH ARONSON, FR TI A PHASE-II CLINICAL-TRIAL OF INTERLEUKIN-2 AND LYMPHOKINE-ACTIVATED KILLER-CELLS IN ADVANCED COLORECTAL-CARCINOMA SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE INTERLEUKIN-2; LYMPHOKINE-ACTIVATED KILLER CELLS; COLORECTAL CARCINOMA ID RECOMBINANT INTERLEUKIN-2; CANCER; THERAPY; IMMUNOTHERAPY; TOXICITY AB Patients (n = 22) with metastatic or unresectable colorectal carcinoma were treated with interleukin (IL)-2 and lymphokine-activated killer (LAK) cells in a phase II study conducted by the IL-2/LAK Working Group (ILWG). Eligibility criteria for the study included bidimensionally measurable disease, performance status 0 or 1, and normal function of all vital organs. The median age of patients was 49 (range, 28-61) years. Eight (36%) patients had never received prior treatment other than their initial surgery; eight (36%) had received prior radiotherapy, and 12 (55%) chemotherapy. No patients had received prior immunotherapy. Treatment consisted of IL-2, 600,000 IU/kg administered by 15-min intravenous infusion every 8 h on days 1-5 and 12-16. Patients underwent 4-h leukapheresis on days 8-12, and cells were placed in in vitro culture with IL-2 for 3-4 days and the activated LAK cells were infused over 1 h on days 12, 13, and 15. All doses of IL-2 and LAK cells were administered to patients in intensive care unit (ICU) settings. The mean +/- SD number of IL-2 doses administered during days 1-5 was 13.4 +/- 1.2, the mean number of LAK cells reinfused was 6.8 +/- 2.2 x 10(10), and the mean number of IL-2 doses administered during the last phase was 9.8 +/- 2.5. Nineteen patients completed the IL-2 priming phase and received at least one LAK cell infusion. One patient achieved a complete response and was progression free for 8 months from the beginning of treatment, for an overall objective response rate of 5% (95% confidence interval: 0-13%). Hypotension, weight gain, anemia, and elevations of serum creatinine and liver enzymes were common, but there were no treatment-related deaths. Treatment delivered and toxicity were comparable to those reported in studies conducted concurrently for other malignancies. We conclude that high-dose IL-2 has minimal activity in metastatic colorectal cancer; however, the low level of activity should not preclude future studies combining IL-2 with other immunotherapeutic approaches. C1 NCI, DIV CANC TREATMENT, CANC THERAPY EVALUAT PROGRAM, INVEST DRUG BRANCH, BETHESDA, MD 20892 USA. TUFTS UNIV NEW ENGLAND MED CTR, BOSTON, MA 02111 USA. ALBERT EINSTEIN CANC CTR, NEW YORK, NY USA. LOYOLA UNIV, MED CTR, MAYWOOD, IL 60153 USA. UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. CITY HOPE CANC RES CTR, DUARTE, CA USA. UNIV CALIF SAN FRANCISCO, SAN FRANCISCO, CA USA. FU NCI NIH HHS [N01-CM73704, N01-CM73703, N01-CM73702] NR 12 TC 26 Z9 26 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 1524-9557 EI 1537-4513 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1994 VL 15 IS 1 BP 74 EP 78 DI 10.1097/00002371-199401000-00010 PG 5 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA MN046 UT WOS:A1994MN04600010 PM 8110733 ER PT J AU HORSKY, J PITHA, J AF HORSKY, J PITHA, J TI INCLUSION COMPLEXES OF PROTEINS - INTERACTION OF CYCLODEXTRINS WITH PEPTIDES CONTAINING AROMATIC-AMINO-ACIDS STUDIED BY COMPETITIVE SPECTROPHOTOMETRY SO JOURNAL OF INCLUSION PHENOMENA AND MOLECULAR RECOGNITION IN CHEMISTRY LA English DT Article DE ALPHA-CYCLODEXTRIN; BETA-CYCLODEXTRIN; BETA-CYCLODEXTRIN DERIVATIVES; AROMATIC AMINO ACIDS; PEPTIDES; P-NITROPHENOL; INCLUSION COMPLEXES; STABILITY CONSTANTS; COMPETITIVE SPECTROPHOTOMETRY ID HYDROXYPROPYL-BETA-CYCLODEXTRIN; ALPHA-CYCLODEXTRIN; L-PHENYLALANINE; NASAL ABSORPTION; INSULIN; CONSTANTS; FORMULATIONS; DERIVATIVES; AGGREGATION; DELIVERY AB The stability constants were measured of inclusion complexes formed from aromatic amino acids and their oligopeptides with alpha- and beta-cyclodextrin, hydroxypropyl beta-cyclodextrin, and partially methylated beta-cyclodextrin. The method of competitive spectrophotometry with p-nitrophenol as a competing reagent was used, and measurements were made at pH 7.4. beta-Cyclodextrin formed complexes of higher stability than the other hosts. The stability of complexes of oligopeptides containing L-phenylalanine was invariably higher than that of L-phenylalanine itself. A model for interaction of proteins with cyclodextrins is proposed, in which the most stable complexes are formed when the native functional form of proteins is unfolded and the nonpolar residues that are buried inside the structure are exposed to water. The complexation of the unfolded structure favors its formation; thus thermal denaturation of proteins is easier in the presence of cyclodextrins. On the other hand, this complexation prevents the intermolecular association of unfolded structures by noncovalent hydrophobic bonding between the exposed nonpolar residues; furthermore, the unfolded complexed forms may revert to the native functional form. This prevention of intermolecular association may explain the stabilizing effect of cyclodextrins on solutions of proteins: a return to the native form is achieved more easily from the complexed, unfolded form than from the unfolded, aggregated forms. RP HORSKY, J (reprint author), NIA,GRC,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. RI Horsky, Jiri/G-3442-2014 NR 31 TC 48 Z9 48 U1 0 U2 10 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-0750 J9 J INCLUS PHENOM MOL JI J. Incl. Phenom. Mol. Recogn. Chem. PY 1994 VL 18 IS 3 BP 291 EP 300 DI 10.1007/BF00708735 PG 10 WC Chemistry, Multidisciplinary; Crystallography SC Chemistry; Crystallography GA QB677 UT WOS:A1994QB67700009 ER PT J AU YARCHOAN, R LIETZAU, JA NGUYEN, BY BRAWLEY, OW PLUDA, JM SAVILLE, MW WYVILL, KM STEINBERG, SM AGBARIA, R MITSUYA, H BRODER, S AF YARCHOAN, R LIETZAU, JA NGUYEN, BY BRAWLEY, OW PLUDA, JM SAVILLE, MW WYVILL, KM STEINBERG, SM AGBARIA, R MITSUYA, H BRODER, S TI A RANDOMIZED PILOT-STUDY OF ALTERNATING OR SIMULTANEOUS ZIDOVUDINE AND DIDANOSINE THERAPY IN PATIENTS WITH SYMPTOMATIC HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; HIV-1 REVERSE-TRANSCRIPTASE; HIGH-LEVEL RESISTANCE; PHASE-I; DOUBLE-BLIND; 2',3'-DIDEOXYINOSINE DDI; AZIDOTHYMIDINE AZT; HTLV-III/LAV; SINGLE AGENT AB A randomized pilot study comparing alternating and simultaneous regimens of zidovudine and didanosine (ddl) was conducted in 41 patients with AIDS or symptomatic human immunodeficiency virus (HIV) infection. Patients on each regimen received the same overall amounts of zidovudine and didanosine over time. CD4 cell counts in patients on the simultaneous regimen reached a maximum (mean +/- SE) of 108 +/- 16/mm3 above baseline (two-tailed P less-than-or-equal-to .0001) and were significantly higher than in patients on the alternating regimen at all time points during weeks 6-45. At 54 weeks, the CD4 cell counts in the patients on the simultaneous regimen were still 40 +/- 19/mm3 above baseline. Patients on the simultaneous regimen also had significantly greater weight gain. While toxicities were generally mild and comparable between the regimens, 1 patient on the simultaneous regimen died of pancreatitis and lactic acidosis. Thus, simultaneous therapy provided more sustained elevations in CD4 cells than alternating therapy over 1 year and may be worth exploring in larger controlled trials. C1 NCI,OFF DIRECTOR,BETHESDA,MD 20892. RP YARCHOAN, R (reprint author), NCI,MED CHEM LAB,BIOSTAT & DATA MANAGEMENT SECT,MED BRANCH,BLDG 10,ROOM 12N226,BETHESDA,MD 20892, USA. NR 47 TC 91 Z9 92 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1994 VL 169 IS 1 BP 9 EP 17 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MP527 UT WOS:A1994MP52700002 PM 7903976 ER PT J AU HUGHES, MD STEIN, DS GUNDACKER, HM VALENTINE, FT PHAIR, JP VOLBERDING, PA AF HUGHES, MD STEIN, DS GUNDACKER, HM VALENTINE, FT PHAIR, JP VOLBERDING, PA TI WITHIN-SUBJECT VARIATION IN CD4 LYMPHOCYTE COUNT IN ASYMPTOMATIC HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION - IMPLICATIONS FOR PATIENT MONITORING SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HIV-1 INFECTION; QUALITY-CONTROL; T SUBSETS; AIDS; COHORT; TYPE-1; PATTERNS; DISEASE AB Changes in CD4 lymphocyte counts are widely used in monitoring human immunodeficiency virus (HIV)-infected patients for disease progression. However, random fluctuations may obscure clinically significant changes. CD4 cell counts from 1020 untreated subjects with asymptomatic HIV infection monitored by standardized methods for up to 2 years were assessed. The within-subject coefficient of variation averaged 25% but was higher in subjects with lower counts; in 6% of subjects the count was half or double the one obtained 8 weeks before. Proportionate rates of decline, which had negligible correlation with the baseline count, averaged 14.3%/year but varied considerably between subjects: An estimated 29% had increasing trends. Declines were greater in HIV p24-positive subjects and those with higher lymphocyte percentages or lower platelet counts or hemoglobin levels. With such high variation, changes between single counts should be interpreted cautiously. Using multiple counts and other markers may provide more precise assessment of immune status. C1 NIAID,DIV AIDS,BETHESDA,MD 20892. NYU,SCH MED,NEW YORK,NY 10003. NORTHWESTERN UNIV,SCH MED,DEPT MED,CHICAGO,IL 60611. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. RP HUGHES, MD (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,667 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-95030] NR 29 TC 106 Z9 107 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1994 VL 169 IS 1 BP 28 EP 36 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MP527 UT WOS:A1994MP52700004 PM 7903975 ER PT J AU RUSSO, TA LIANG, Y CROSS, AS AF RUSSO, TA LIANG, Y CROSS, AS TI THE PRESENCE OF K54 CAPSULAR POLYSACCHARIDE INCREASES THE PATHOGENICITY OF ESCHERICHIA-COLI IN-VIVO SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID CARDIOVASCULAR DYSFUNCTION; SEPTIC SHOCK; VIRULENCE; BACTEREMIA; K1; PATHOGENESIS; MENINGITIS; MODEL; HOST; MICE AB Proven isogenic capsule-negative derivatives (CP9.29, CP9.108, CP9.137, CP9.171, CP9.443, and CP9.C56), generated from an O4/K54/H5 blood isolate (CP9) of Escherichia coli by IS50L=phoA (TnphoA)-mediated transposon mutagenesis, were used to assess the function of a non-K1 capsule in three animal models. Intraperitoneal injection of CP9 (K54+) into mice resulted in an LD50 at 24 h of 5.5 X 10(6) cfu compared with LD50s of 2.6 x 10(7) cfu and 3.8 x 10(7) cfu for CP9.108 (K54-) and CP9.C56 (K54-) (P < .001). CP9 was cleared less rapidly from the bloodstream, after intravascular injection, than was CP9.108 (P < .01). In the rat granuloma pouch model, CP9 could proliferate from starting inocula as low as 1.0 x 10(3) cfu/mL. In contrast, capsule-deficient derivatives underwent transient log kills with starting inocula as high as 1.0 x 10(6) cfu/mL. Because proven isogenic strains were evaluated, a clear contribution of the K54 capsular polysaccharide to virulence in vivo is demonstrated. C1 WALTER REED ARMY INST RES,DEPT BACTERIAL DIS,WASHINGTON,DC 20307. RP RUSSO, TA (reprint author), NIAID,CLIN INVEST LAB,BACTERIAL PATHOGENESIS UNIT,BETHESDA,MD 20892, USA. NR 33 TC 43 Z9 43 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1994 VL 169 IS 1 BP 112 EP 118 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MP527 UT WOS:A1994MP52700016 PM 8277173 ER PT J AU WILBUR, WJ AF WILBUR, WJ TI NONPARAMETRIC SIGNIFICANCE TESTS OF RETRIEVAL PERFORMANCE COMPARISONS SO JOURNAL OF INFORMATION SCIENCE LA English DT Article ID INFORMATION AB It has been observed that statistical tests are infrequently applied in analysing differences in the performance of different retrieval methods. We believe this is explained on the one hand by the complexity of the subject, and on the other hand by the desire to avoid misleading conclusions. Because practical retrieval methods cannot be explained by simple models, parametric statistical tests are generally not suitable. Some non-parametric tests require a symmetry in the null hypothesis that seems inappropriate to the required task. A second class of non-parametric tests comprise the bootstrap methods. Here, the null hypothesis seems appropriate to practical testing, but the bootstrap assumption (that the sample may adequately represent the whole population) may be in question. If the bootstrap assumption is false, one may be led to erroneous conclusions (type I or type II errors). Here, by use of a mathematical model [11] which approximates the behaviour of practical retrieval systems, we show that bootstrap methods perform well in performance comparisons based on actual test sets used in practice. Type I error is appropriately predictable and the power loss of the tests, when compared with the theoretically most powerful test in the most realistic setting, may not exceed ten percentage points. We conclude that the bootstrap methods provide a practical approach to statistical testing in the field of retrieval performance analysis. RP WILBUR, WJ (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BLDG 38A,ROOM 8S806,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 25 TC 17 Z9 17 U1 0 U2 2 PU BOWKER-SAUR LTD PI E GRINSTEAD PA MAYPOLE HOUSE, MAYPOLE RD, E GRINSTEAD, W SUSSEX, ENGLAND RH19 1HH SN 0165-5515 J9 J INFORM SCI JI J. Inf. Sci. PY 1994 VL 20 IS 4 BP 270 EP 284 DI 10.1177/016555159402000405 PG 15 WC Computer Science, Information Systems; Information Science & Library Science SC Computer Science; Information Science & Library Science GA PA330 UT WOS:A1994PA33000005 ER PT J AU MATALON, R MICHALS, K AZEN, C FRIEDMAN, E KOCH, R ROUSE, B HANLEY, WB DELACRUZ, F AF MATALON, R MICHALS, K AZEN, C FRIEDMAN, E KOCH, R ROUSE, B HANLEY, WB DELACRUZ, F TI MATERNAL PKU COLLABORATIVE STUDY - PREGNANCY OUTCOME AND POSTNATAL HEAD GROWTH SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article; Proceedings Paper CT Symposium: From Genotype to Phenotype, at the 31st Annual Meeting of the Society-for-the-Study-of-Inborn-Errors-of-Metabolism CY SEP 07-10, 1993 CL MANCHESTER, ENGLAND SP SOC STUDY INBORN ERRORS METAB ID PHENYLKETONURIA C1 UNIV ILLINOIS,CHICAGO,IL. CHILDRENS HOSP LOS ANGELES,LOS ANGELES,CA 90027. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77550. HOSP SICK CHILDREN,TORONTO M5G 1X8,ON,CANADA. NIH,BETHESDA,MD 20892. RP MATALON, R (reprint author), MIAMI CHILDRENS HOSP,RES INST,MIAMI,FL 33155, USA. FU NICHD NIH HHS [1-HD-4-3807] NR 6 TC 5 Z9 5 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1994 VL 17 IS 3 BP 353 EP 355 DI 10.1007/BF00711828 PG 3 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA PB070 UT WOS:A1994PB07000027 PM 7807951 ER PT J AU GOLDIN, E IMAI, Y KANESKI, CR PENTCHEV, PG BRADY, RO HASCALL, VC AF GOLDIN, E IMAI, Y KANESKI, CR PENTCHEV, PG BRADY, RO HASCALL, VC TI MUCOLIPIDOSIS-IV FIBROBLASTS SYNTHESIZE NORMAL AMOUNTS OF HYALURONIC-ACID SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article ID PROTEOGLYCANS; ACCUMULATION AB Mucolipidosis IV (ML IV) (McKusick 252650) is an autosomal recessive metabolic disorder that displays signs of both lipid and mucopolysaccharide (glycosaminoglycan) storage. It has been reported that fibroblasts from ML IV patients exhibit abnormally high synthesis of hyaluronic acid in culture. In our search for a biochemical marker that will enable positive identification of ML IV, we studied glycosaminoglycan synthesis in fibroblast cultures from patients with this disease. ML IV and normal control fibroblasts were incubated with [H-3]glucosamine and [S-35]sulphate. Labelled glycosaminoglycans were extracted from the cell layer and medium. Chondroitin sulphate and hyaluronic acid were determined by analysis of disaccharides after digestion with chondroitinase ABC. Synthesis of neither of these two glycosaminoglycans differed significantly between control and ML IV fibroblasts. Synthesis of hyaluronic acid was nearly linear for 24 h, with mean calculated values of 11.7 +/- 1.4 and 14.4 +/- 1.6 pg/cell per 24 h in control and ML IV cultures respectively. The variability within the two groups is attributed primarily to population variability and possibly to culture density. These experiments exclude the possibility that a general metabolic defect in hyaluronic acid synthesis is responsible for the ML IV phenotype, nor can such a defect be used as a diagnostic tool for the disease. C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. RP GOLDIN, E (reprint author), NINCDS,DEV & METAB NEUROL BRANCH,BETHESDA,MD 20892, USA. OI Kaneski, Christine/0000-0003-1453-2502 NR 15 TC 3 Z9 3 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1994 VL 17 IS 5 BP 545 EP 553 DI 10.1007/BF00711589 PG 9 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA PK186 UT WOS:A1994PK18600005 PM 7837760 ER PT J AU YANG, JM CHIPEV, CC DIGIOVANNA, JJ BALE, SJ MAREKOV, LN STEINERT, PM COMPTON, JG AF YANG, JM CHIPEV, CC DIGIOVANNA, JJ BALE, SJ MAREKOV, LN STEINERT, PM COMPTON, JG TI MUTATIONS IN THE H1 AND 1A DOMAINS IN THE KERATIN-1 GENE IN EPIDERMOLYTIC HYPERKERATOSIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE GENODERMATOSES; INTERMEDIATE FILAMENTS; EPIDERMOLYSES BULLOSA SIMPLEX; EPIDERMIS ID CLUSTER; SUBDOMAIN; SEQUENCES; LINKAGE; REGION AB In the autosomal dominant disorder epidermolytic hyperkeratosis, the structural integrity of the keratin intermediate filaments is altered in the suprabasal layers of the epidermis. We and others have used genetic linkage studies and mutation analysis to establish that single amino acid substitutions in either the keratin 1 or keratin 10 chains can cause epidermolytic hyperkeratosis. However, a larger database of mutations is required to better understand the relationship between specific mutations in these keratin chains and their effect on keratin filament structure. A larger database will also provide a catalog that may be useful for genetic counseling purposes. In this paper, we report the identification of three new mutations of the keratin 1 chain of epidermolytic hyperkeratosis probands in highly conserved residues in the H1 or beginning of the 1A rod domain segments. These correspond to regions involved in molecular overlaps between neighboring molecules in keratin filaments. Using an in vitro assay, synthetic peptides bearing these substitutions show diminished capacity to disassemble preformed filaments in vitro in comparison to the wild type peptides. Moreover, analyses of all mutations in epidermolytic hyperkeratosis known to date demonstrate remarkable clustering in the molecular overlap region. We conclude that non-conservative substitutions in the overlap region are likely to interfere with normal keratin filament structure and function, leading to pathology. C1 NIAMSD,SKIN BIOL BRANCH,BETHESDA,MD 20892. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 32 TC 62 Z9 63 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JAN PY 1994 VL 102 IS 1 BP 17 EP 23 PG 7 WC Dermatology SC Dermatology GA MR507 UT WOS:A1994MR50700005 PM 7507151 ER PT J AU FALANGA, V GRINNELL, F GILCHREST, B MADDOX, YT MOSHELL, A AF FALANGA, V GRINNELL, F GILCHREST, B MADDOX, YT MOSHELL, A TI WORKSHOP ON THE PATHOGENESIS OF CHRONIC WOUNDS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Editorial Material ID SKIN ULCERS; METALLOPROTEINASES; EXPRESSION; GROWTH; FIBRIN; ALPHA; FLUID C1 UNIV MIAMI,DEPT DERMATOL,MIAMI,FL. UNIV TEXAS,SW MED SCH,DALLAS,TX. BOSTON UNIV,DEPT CELL BIOL & NEUROSCI,BOSTON,MA. BOSTON UNIV,DEPT DERMATOL,BOSTON,MA. NIGMS,BETHESDA,MD. NIAMS,BETHESDA,MD. NR 16 TC 45 Z9 45 U1 0 U2 3 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JAN PY 1994 VL 102 IS 1 BP 125 EP 127 DI 10.1111/1523-1747.ep12371745 PG 3 WC Dermatology SC Dermatology GA MR507 UT WOS:A1994MR50700024 PM 8288905 ER PT J AU HE, XS MATECKA, D LEE, KS GU, ZQ RICE, KC WONG, G SKOLNICK, P DECOSTA, BR AF HE, XS MATECKA, D LEE, KS GU, ZQ RICE, KC WONG, G SKOLNICK, P DECOSTA, BR TI SYNTHESIS OF [I-123] TERT-BUTYL-8-IODO-5,6-DIHYDRO-5-METHYL-6-OXO-4H-IMIDAZO[1,5-A][1,4]BENZO DIAZEPINE 3-CARBOXYLATE, A POTENTIAL SPECT IMAGING AGENT FOR DIAZEPAM-INSENSITIVE (DI) BENZODIAZEPINE RECEPTORS SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE [I-123]TERT-BUTYL 8-IODO-5,6-DIHYDRO-5-METHYL-6-OXO-4H-IMIDAZO[1,5-A][1,4]BENZODIAZEPINE 3-CARBOXYLATE ([I-123]3]; HIGH AFFINITY; SELECTIVE; DIAZEPAM-INSENSITIVE; SPECT; IMAGING AGENT; IODODESTANNYLATION ID ALCOHOL ANTAGONIST; BINDING; RO-15-4513; INVITRO AB [I-123]tert-Butyl 8-iodo-5,6-dihydro-5-methyl-6-oxo-4H-imidazo [1,5-a][1,4]benzodiazepine 3-carboxylate ([I-123]3], a high affinity and selective radioligand for the diazepam insensitive (DI) benzodiazepine receptor was synthesized in 2 steps from tert-butyl 8-bromo-5,6-dihydro-5-methyl-6-oxo-4H-imidazo[1,5-a][1,4]benzodiazepine 3-carboxylate (4). A key step in the synthesis of this potential SPECT imaging agent utilized (Ph3P)3Pd mediated stannylation of 4 with (Bu3Sn)2 to the corresponding 8-tributyltin derivative 5. Iododestannylation of 5 with no carrier added (I-123]NaI in aqueous ethanolic CH3CO3H furnished [I-123]3 (85%) in greater than 98% radiochemical purity following TLC purification. C1 NIDDKD,MED CHEM LAB,BETHESDA,MD 20892. NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892. NIMH,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. NR 22 TC 7 Z9 7 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0362-4803 J9 J LABELLED COMPD RAD JI J. Label. Compd. Radiopharm. PD JAN PY 1994 VL 34 IS 1 BP 27 EP 32 DI 10.1002/jlcr.2580340105 PG 6 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA MQ325 UT WOS:A1994MQ32500004 ER PT J AU NELSON, BJ DANIELPOUR, D ROSSIO, JL TURPIN, J NACY, CA AF NELSON, BJ DANIELPOUR, D ROSSIO, JL TURPIN, J NACY, CA TI INTERLEUKIN-2 SUPPRESSES ACTIVATED MACROPHAGE INTRACELLULAR KILLING ACTIVITY BY INDUCING MACROPHAGES TO SECRETE TGF-BETA SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE MACROPHAGES; LEISHMANIA; INTERLEUKIN-2; INTERFERON-GAMMA; TRANSFORMING GROWTH FACTOR BETA; INTRACELLULAR KILLING; SUPPRESSION ID TRANSFORMING GROWTH-FACTOR; NECROSIS-FACTOR-ALPHA; T-CELL GROWTH; HUMAN B-CELLS; RECOMBINANT INTERFERON-GAMMA; PERIPHERAL-BLOOD MONOCYTES; IL-2 RECEPTOR; IFN-GAMMA; ANTIMICROBIAL ACTIVITIES; GRANULOCYTE-MACROPHAGE AB Phorbol myristate acetate (PMA) treatment of an EL-4 thymoma cell line (EL-4(FARRAR)) induced secretion of a factor that inhibited intracellular killing of Leishmania major amastigotes by activated macrophages. Analysis of the cytokines produced by EL-4 cells after PMA stimulation identified interleukin-2 (IL-2, 2500 U/mI), IL-4 (1280 U/ml), interferon-gamma (IFN-gamma; 100 U/ml), and granulocyte-macrophage colony-stimulating factor (GM-CSF; 50 U/ml). Neither tumor necrosis factor nor transforming growth factor beta (TGF-beta) was detected. Each of the cytokines present in EL-4 fluids was assessed for capacity to activate macrophages for destruction of parasites or to suppress intracellular killing. IFN-gamma and GM-CSF both activated macrophages to kill Leishmania; IL-2 and lL-4 had no activity for induction of this antimicrobial effector function. IL-2 and IL-4 were tested for their capacity to inhibit lymphokine- or IFN-gamma-induced destruction of L. major by macrophages: lL-4 was ineffective, but IL-2 markedly suppressed the activation of macrophages for intracellular killing. Addition of greater than or equal to 10 U/ml of IL-2 at the time of infection, or up to 4 h before, blocked up to 100% of the capacity of activated macrophages to kill intracellular amastigotes. Immunoaffinity treatment of EL-4 fluids with anti-IL-2 antibody resulted in >80% reduction in suppression of intracelluIar killing. The suppressive effects of IL-2 were not direct, but mediated by TGF-beta. IL-2 induced resident peritoneal macrophages to secrete >5000 pg/ml TGF-beta 1, a quantity that is >500-fold higher than constitutive background levels (20-40 pg/ml) and is sufficient to block intracellular killing activities. This increase in secretion of TGF-beta was not dependent increases in TGF-beta 1 mRNA. Treatment of cultures with EL-4 fluids or recombinant IL-2 in the presence of antibody to TGF-beta 1 blocked the suppressive activity of both. Thus, IL-2 was the major suppressor factor in EL-4 fluids, and it acted indirectly through the induction and autocrine action of TGF-beta. C1 WALTER REED ARMY INST RES,DEPT CELLULAR IMMUNOL,WASHINGTON,DC. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NCI,DYN CORP,PROGRAM RESOURCES INC,FREDERICK,MD. NR 64 TC 14 Z9 14 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD JAN PY 1994 VL 55 IS 1 BP 81 EP 90 PG 10 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA MT016 UT WOS:A1994MT01600012 PM 8283143 ER PT J AU ROBINS, ED NELSON, LM HOEG, JM AF ROBINS, ED NELSON, LM HOEG, JM TI ABERRANT HYPOTHALAMIC-PITUITARY-OVARIAN AXIS IN THE WATANABE HERITABLE HYPERLIPIDEMIC RABBIT SO JOURNAL OF LIPID RESEARCH LA English DT Article DE FAMILIAL HYPERCHOLESTEROLEMIA; PROGESTERONE; ESTROGEN; OOCYTE; GONADOTROPIN; HMG-COA REDUCTASE INHIBITOR ID DENSITY LIPOPROTEIN RECEPTOR; COENZYME-A REDUCTASE; WHHL RABBITS; FAMILIAL HYPERCHOLESTEROLEMIA; PRAVASTATIN SODIUM; PREGNANT RABBIT; ANIMAL-MODEL; CHOLESTEROL; ATHEROSCLEROSIS; PROGESTERONE AB The WHHL rabbit has a defective low density lipoprotein receptor and is a model for familial hypercholesterolemia. WHHL rabbits are less fecund than NZW rabbits, the strain into which the defect has been inbred. This lower fecundity could be related to impaired ovarian steroidogenesis due to reduced intracellular availability of cholesterol. Here we compare the WHHL and NZW rabbits with regard to oocyte morphology and fertilization rates after stimulation with equine chorionic gonadotropin. We also compare hypothalamic-pituitary-ovarian axis function by measuring baseline and gonadotropin releasing hormone-stimulated plasma estradiol, progesterone, and gonadotropin levels, both before and after simvastatin inhibition of de novo cholesterol synthesis. WHHL rabbit oocytes remained encased in cumulus and had a lowered fertilization rate (9/50 vs. 83/87, P < 0.05). WHHL rabbits had lower baseline estradiol levels (7.1 +/- 0.72 vs. 10.2 +/- 0.94, P < 0.05) and had higher baseline follicle stimulating hormone (P < 0.05) and luteinizing hormone (P < 0.05) levels. Simvastatin lowered luteal progesterone concentrations only in WHHL rabbits (P < 0.05). We conclude that the hypothalamic-pituitary-ovarian axis in WHHL rabbits is abnormal. The reduced availability of intracellular cholesterol for progesterone synthesis by inhibition of de novo cholesterol biosynthesis leads to a significant reduction in plasma progesterone concentrations in the WHHL. These findings have implications for women with familial hypercholesterolemia, particularly regarding treatment with inhibitors of de novo cholesterol synthesis. C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20852. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20852. NR 31 TC 11 Z9 11 U1 0 U2 1 PU LIPID RESEARCH INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD JAN PY 1994 VL 35 IS 1 BP 52 EP 59 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MQ387 UT WOS:A1994MQ38700007 PM 8138722 ER PT J AU CHAO, FF BLANCHETTEMACKIE, EJ DICKENS, BF GAMBLE, W KRUTH, HS AF CHAO, FF BLANCHETTEMACKIE, EJ DICKENS, BF GAMBLE, W KRUTH, HS TI DEVELOPMENT OF UNESTERIFIED CHOLESTEROL-RICH LIPID PARTICLES IN ATHEROSCLEROTIC LESIONS OF WHHL AND CHOLESTEROL-FED NZW RABBITS SO JOURNAL OF LIPID RESEARCH LA English DT Article DE LIPOPROTEINS; PHOSPHOLIPIDS; LIPOSOMES; SPHINGOMYELIN; CARDIOVASCULAR DISEASE ID L-ALPHA-DIMYRISTOYLPHOSPHATIDYLCHOLINE; HIGH-DENSITY LIPOPROTEIN; HYPERLIPIDEMIC RABBIT; DIFFERENT MECHANISMS; CA++ ANTAGONISTS; A-I; APOLIPOPROTEIN; LIPOSOMES; EFFLUX; CELLS AB Previously, we isolated and characterized unesterified cholesterol-rich lipid particles (UCLP) that accumulate in extracellular spaces of atherosclerotic lesions of humans and cholesterol-fed rabbits. In the present study, we examined early developing atherosclerotic lesions to determine when UCLP appear and when they become enriched in cholesterol and sphingomyelin. Cholesterol-fed NZW rabbits, which rapidly develop atherosclerotic lesions, and genetically hyperlipidemic WHHL rabbits, which develop lesions over a longer period of time, were studied. UCLP of peak density 1.04 g/ml appear as early as 4 weeks after the onset of cholesterol feeding and progressively accumulate during atherosclerotic lesion development. Beginning with their appearance and afterwards, UCLP contain a saturating level (2:1 molar ratio) of cholesterol relative to phospholipid. Whereas, early UCLP are enriched in phosphatidylcholine, with time UCLP become enriched with sphingoymelin. Another UCLP population having a peak density of 1.09 g/ml was present in control aortas and increased in amount more slowly than the d 1.04 g/ml UCLP during cholesterol feeding. The d 1.09 g/ml particles were predominantly unilamellar vesicles, the majority between 100 and 200 nm in diameter. They contained > 90% of their cholesterol in unesterified form and their ratio of unesterified cholesterol to phospholipid progressively increased from 0.6 to 1.7 during cholesterol feeding. Liposome resistance to solubilization by high density lipoproteins is known to be increased by enrichment with unesterified cholesterol and sphingomyelin. Sphingomyelin enrichment of unesterified cholesterol-rich lipid particles (UCLP) could stabilize cholesterol in a form that does not readily crystallize. However, at the same time, the early and progressive accumulation of UCLP in developing atherosclerotic lesions may limit reverse cholesterol transport and accelerate disease progression. C1 NHLBI,EXPTL ATHEROSCLEROSIS SECT,BETHESDA,MD 20892. NIADDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,DEPT MED,WASHINGTON,DC. OREGON STATE UNIV,DEPT BIOCHEM & BIOPHYS,CORVALLIS,OR 97331. NR 50 TC 27 Z9 27 U1 0 U2 1 PU LIPID RESEARCH INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD JAN PY 1994 VL 35 IS 1 BP 71 EP 83 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MQ387 UT WOS:A1994MQ38700009 PM 8138724 ER PT J AU THIBAULT, A FIGG, WD MCCALL, N SAMID, D MYERS, CE COOPER, MR AF THIBAULT, A FIGG, WD MCCALL, N SAMID, D MYERS, CE COOPER, MR TI A SIMULTANEOUS ASSAY OF THE DIFFERENTIATING AGENTS, PHENYLACETIC ACID AND PHENYLBUTYRIC ACID, AND ONE OF THEIR METABOLITES, PHENYLACETYL-GLUTAMINE, BY REVERSED-PHASE, HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID WASTE NITROGEN-EXCRETION; FETAL HEMOGLOBIN; HYPERAMMONEMIA; UREA AB This paper describes a reversed-phase, high performance liquid chromatographic (HPLC) method for the isolation, detection and quantification of phenylacetic acid, phenylbutyric acid and one of their metabolites, phenylacetylglutamine, from serum. The compounds are initially extracted from serum after protein precipitation with perchloric acid. The solution is neutralized with potassium bicarbonate and injected onto a C-18 column. The compounds are then differentially eluted using an increasing gradient of acetonitrile. Ionization of the two acids is suppressed by adding phosphoric acid to the mobile phase. The compounds are detected by UV absorbance at 208 nm. The assay yields a lower limit of detection of 2 mu g/ml and is linear to concentrations as high as 2,000 mu g/ml. Between 20 and 1,000 mu g/ml the interassay percent coefficient of variation is less than 10%. RP THIBAULT, A (reprint author), NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,CLIN PHARMACOL BRANCH,CLIN PHARMACOKINET SECT,BETHESDA,MD 20892, USA. RI Figg Sr, William/M-2411-2016 NR 13 TC 6 Z9 6 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1994 VL 17 IS 13 BP 2895 EP 2900 DI 10.1080/10826079408013507 PG 6 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA PD500 UT WOS:A1994PD50000010 ER PT J AU MA, Y ITO, Y TOROK, DS ZIFFER, H AF MA, Y ITO, Y TOROK, DS ZIFFER, H TI SEPARATION OF THE 2-NITRO-3-ACETAMIDO-4-CHLOROBENZOIC AND 6-NITRO-3-ACETAMIDO-4-CHLOROBENZOIC ACID PRECURSORS OF A POTENT HYDROXY-ANTHRANILIC ACID OXYGENASE INHIBITOR BY PH-ZONE-REFINING-COUNTERCURRENT CHROMATOGRAPHY SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article AB Multigram quantities of 2- and 6-nitro-3-acetamido-4-chlorobenzoic acids were separated by pH-zone-refining CCC. A two-phase solvent system composed of methyl tertiary-butyl ether, acetonitrile and water was employed using trifluoroacetic acid as a displacer acid in the organic mobile phase and ammonia as a retainer base in the aqueous stationary phase. C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. RP MA, Y (reprint author), NHLBI,BIOPHYS CHEM LAB,BLDG 10,BETHESDA,MD 20892, USA. NR 10 TC 17 Z9 17 U1 1 U2 6 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1994 VL 17 IS 16 BP 3507 EP 3517 DI 10.1080/10826079408013527 PG 11 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA PL381 UT WOS:A1994PL38100013 ER PT J AU WALSH, TJ DEPAUW, B ANAISSIE, E MARTINO, P AF WALSH, TJ DEPAUW, B ANAISSIE, E MARTINO, P TI RECENT ADVANCES IN THE EPIDEMIOLOGY, PREVENTION AND TREATMENT OF INVASIVE FUNGAL-INFECTIONS IN NEUTROPENIC PATIENTS SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article; Proceedings Paper CT XII Congress of the International-Society-for-Human-and-Animal-Mycology (ISHAM) CY MAR 13-18, 1994 CL ADELAIDE, AUSTRALIA ID BONE-MARROW TRANSPLANTATION; COLONY-STIMULATING FACTOR; LIPOSOMAL-AMPHOTERICIN-B; GRANULOCYTOPENIC CANCER-PATIENTS; CENTRAL NERVOUS-SYSTEM; ACUTE-LEUKEMIA; IMMUNOCOMPROMISED PATIENTS; RISK-FACTORS; PULMONARY ASPERGILLOSIS; EMPIRIC THERAPY C1 ST RADBSUD HOSP, DEPT INTERNAL MED, DIV HAEMATOL, NIJMEGEN, NETHERLANDS. UNIV TEXAS, MD ANDERSON CANC CTR, HOUSTON, TX USA. UNIV ROMA LA SAPIENZA, SEZ ENATOL, ROME, ITALY. RP WALSH, TJ (reprint author), NCI, INFECT DIS SECT, BETHESDA, MD 20892 USA. NR 113 TC 26 Z9 27 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 SU 1 BP 33 EP 51 PG 19 WC Mycology SC Mycology GA QB967 UT WOS:A1994QB96700005 PM 7722797 ER PT J AU HOSTETLER, JS CATANZARO, A STEVENS, DA GRAYBILL, JR SHARKEY, PK LARSEN, RA TUCKER, RM ALHAIDARY, AD RINALDI, MG CLOUD, GA GALGIANI, JN AF HOSTETLER, JS CATANZARO, A STEVENS, DA GRAYBILL, JR SHARKEY, PK LARSEN, RA TUCKER, RM ALHAIDARY, AD RINALDI, MG CLOUD, GA GALGIANI, JN TI TREATMENT OF COCCIDIOIDOMYCOSIS WITH SCH-39304 SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article ID AMBULATORY PERITONEAL-DIALYSIS; FLUCONAZOLE; SCH-39304; THERAPY AB A new oral triazole antifungal, SCH 39304, was administered to 54 patients with progressive infections due to Coccidioides immitis from six collaborating centers. Patients were grouped according to site of infection including chronic pulmonary (25), bone/joint (17) and skin/soft tissue (12). The median age was 40 years; 83% were male, 52% white, 13% HIV-infected and 35% had failed previous therapy. The majority of patients were treated with either 100 mg or 200 mg day(-1). One patient on renal dialysis received 300 mg day(-1). Baseline abnormalities were reassessed for evidence of efficacy every 4 months and expressed in a standardized scoring system. Cumulative overall response rates at 4, 8 and 12 months were 7%, 36% and 66% respectively. Twelve month response rates by disease were 77% (pulmonary), 62% (skin/soft tissue) and 31% (bone/joint). Fifteen patients failed therapy although seven of these were still on treatment when the study was discontinued. Two failed due to toxicity. Possible symptoms or signs of toxicity occurred in 24 (44%) patients and were generally mild. SCH 39304 is an effective and well tolerated therapy for progressive forms of coccidioidomycosis. C1 SANTA CLARA VALLEY MED CTR,DEPT MED,DIV INFECT DIS,SAN JOSE,CA 95128. STANFORD UNIV,SCH MED,DEPT MED,DIV INFECT DIS & GEOG MED,STANFORD,CA 94305. CALIF INST MED RES,SAN JOSE,CA 95128. NIAID,MYCOSES STUDY GRP,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DIV PULM MED,SAN DIEGO,CA 92103. AUDIE L MURPHY MEM VET ADM MED CTR,MED LAB,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. UNIV SO CALIF,LOS ANGELES CTY MED CTR,LOS ANGELES,CA 90033. WENATCHEE VALLEY CLIN,DIV CLIN RES,WENATCHEE,WA. VET AFFAIRS MED CTR,MED SERV,TUCSON,AZ. UNIV ARIZONA,DEPT MED,TUCSON,AZ. UNIV ALABAMA,CTR COMPREHENS CANC,BIOSTAT UNIT,BIRMINGHAM,AL 35294. FU NIAID NIH HHS [N01-AI-15082] NR 14 TC 9 Z9 9 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 IS 2 BP 105 EP 114 PG 10 WC Mycology SC Mycology GA NH896 UT WOS:A1994NH89600003 PM 8064541 ER PT J AU DEHOOG, GS SIGLER, L UNTEREINER, WA KWONCHUNG, KJ GUEHO, E UIJTHOF, JMJ AF DEHOOG, GS SIGLER, L UNTEREINER, WA KWONCHUNG, KJ GUEHO, E UIJTHOF, JMJ TI CHANGING TAXONOMIC CONCEPTS AND THEIR IMPACT ON NOMENCLATURAL STABILITY SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article; Proceedings Paper CT XII Congress of the International-Society-for-Human-and-Animal-Mycology (ISHAM) CY MAR 13-18, 1994 CL ADELAIDE, AUSTRALIA ID FUNGI C1 UNIV ALBERTA,MICROFUNGUS COLLECT,EDMONTON,AB,CANADA. UNIV TORONTO,DEPT BOT,TORONTO,ON,CANADA. NIH,CLIN MYCOL SECT,BETHESDA,MD 20892. INST PASTEUR,UNITE MYCOL,PARIS,FRANCE. RP DEHOOG, GS (reprint author), CENT BUR SCHIMMELCULTURES,POB 273,3740 AG BAARN,NETHERLANDS. NR 23 TC 9 Z9 9 U1 0 U2 2 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 SU 1 BP 113 EP 122 PG 10 WC Mycology SC Mycology GA QB967 UT WOS:A1994QB96700011 PM 7722780 ER PT J AU WALSH, TJ KELLY, P PEEBLES, R LEE, J LECCIONES, J PIZZO, PA AF WALSH, TJ KELLY, P PEEBLES, R LEE, J LECCIONES, J PIZZO, PA TI BIOCHEMICAL AND PHARMACOLOGICAL FACTORS CAUSING INDUCTION AND SUPPRESSION OF GERMINATION OF TRICHOSPORON BEIGELII SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article ID GERM TUBE FORMATION; CANDIDA-ALBICANS; INFECTION; POLYSACCHARIDE; PATHOGENESIS; PROLINE; GROWTH AB Trichosporon beigelii is an emerging fungal pathogen, which is morphologically characterized by blastoconidia, arthroconidia and hyphae. The non-hyphal forms of T. beigelii germinate to form hyphae in plasma in vitro and in tissues in vivo, suggesting possible pathophysiological significance of this process. Little is known, however, about the mechanisms of germination of T. beigelii. We therefore studied relevant biochemical and pharmacological factors that may regulate germination of T. beigelii. Germination was significantly enhanced by temperature at 37 degrees C, chemically defined cell culture media such as RPMI-1640, plasma, physiological pH, N-acetylglucosamine and proline. N-acetylglucosamine was equivalent to proline in inducing germination. Germination was suppressed by high concentrations of glucose, increasing inocula, low pH, and amphotericin B at achievable serum concentrations. Thus, many of the factors regulating germination of T. beigelii appear to be similar to those for Candida albicans. RP WALSH, TJ (reprint author), NCI,PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, USA. NR 25 TC 1 Z9 1 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 IS 2 BP 123 EP 132 PG 10 WC Mycology SC Mycology GA NH896 UT WOS:A1994NH89600005 PM 8064543 ER PT J AU WALSH, TJ LEE, JW SIEN, T SCHAUFELE, R BACHER, J SWITCHENKO, AC GOODMAN, TC PIZZO, PA AF WALSH, TJ LEE, JW SIEN, T SCHAUFELE, R BACHER, J SWITCHENKO, AC GOODMAN, TC PIZZO, PA TI SERUM D-ARABINITOL MEASURED BY AUTOMATED QUANTITATIVE ENZYMATIC ASSAY FOR DETECTION AND THERAPEUTIC MONITORING OF EXPERIMENTAL DISSEMINATED CANDIDIASIS - CORRELATION WITH TISSUE CONCENTRATIONS OF CANDIDA-ALBICANS SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article ID INVASIVE CANDIDIASIS; ENANTIOSELECTIVE MEASUREMENT; GAS-CHROMATOGRAPHY; CANCER; QUANTIFICATION; METABOLITE; DIAGNOSIS; FUNGEMIA AB In order to further understand serum D-arabinitol (DA) as a marker for the diagnosis of disseminated candidiasis and for monitoring response to antifungal therapy, we studied the serum levels of this Candida carbohydrate metabolite by rapid automated enzymatic assay in rabbits with experimental disseminated candidiasis. The enzymatic reaction steps were performed on a standard automated clinical chemistry analyser. As a correction for renal impairment, data were expressed as serum D-arabinitol/creatinine ratio (DA/Cr). Serum creatinine concentrations were determined from the same sample with the same instrument, thereby allowing rapid determination of the DA/Cr within one laboratory. The DA/Cr was determined in 321 samples from 132 rabbits. The mean serum DA/Cr in 31 normal non-infected rabbits was 1.51+/-0.2 mu M mg(-1) dl(-1). Among 84 rabbits with disseminated candidiasis and pre-terminal samples, there was a direct correlation between DA/Cr and tissue concentration of Candida albicans (r=0.80; P<0.001). A threshold of elevated DA/Cr (greater than or equal to 3.0 mu M mg(-1) dl(-1)) was evident in rabbits with a tissue concentration of C. albicans greater than or equal to 3 x 10(4) colony forming units (CFU) g(-1). Elevated DA/Cr was detected in 48 (89%) of 54 rabbits at a C. albicans tissue concentration of greater than or equal to 3 x 10(4) CFU g(-1) vs, one (3%) of 30 rabbits with <3 x 10(4) CFU g(-1) (P<0.0001). Among all 101 rabbits with disseminated candidiasis, an elevated DA/Cr was detected at any point during infection in 60 (92%) of 65 rabbits having a C. albicans tissue concentration greater than or equal to 3 x 10(4) CFU g(-1) vs. 13 (36%) of 36 rabbits with <3 x 10(4) CFU g(-1) (P<0.0001). The relationship between the tissue response to antifungal therapy and change in DA/Cr was then further analysed. Ten (91%) of 11 rabbits with a tissue-proven response to antifungal therapy (defined as greater than or equal to 10(2)-fold reduction of CFU g(-1) in comparison to untreated controls) had a >50% reduction in elevated DA/Cr levels. By comparison, 10 (83%) of 12 treated rabbits with no response to therapy had persistently elevated DA/Cr levels (P<0.001). These findings provide an experimental basis for understanding the patterns of expression of serum DA in disseminated candidiasis and further indicate that serial DA/Cr measurements may be useful for diagnosis and therapeutic monitoring of disseminated candidiasis. C1 NIH,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,SURG BRANCH,BETHESDA,MD 20892. SYVA CO,PALO ALTO,CA. RP WALSH, TJ (reprint author), NCI,INFECT DIS SECT,BLDG 10,RM 13N-240,BETHESDA,MD 20892, USA. NR 24 TC 18 Z9 18 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 IS 3 BP 205 EP 215 PG 11 WC Mycology SC Mycology GA NU156 UT WOS:A1994NU15600006 PM 7965491 ER PT J AU MARESCA, B BENNETT, J FONZI, W HITCHCOCK, CA LODGE, JK WILLIAMSON, PR AF MARESCA, B BENNETT, J FONZI, W HITCHCOCK, CA LODGE, JK WILLIAMSON, PR TI MOLECULAR APPROACHES TO IDENTIFY NOVEL TARGETS FOR FUTURE-DEVELOPMENT OF ANTIFUNGAL AGENTS SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article; Proceedings Paper CT XII Congress of the International-Society-for-Human-and-Animal-Mycology (ISHAM) CY MAR 13-18, 1994 CL ADELAIDE, AUSTRALIA ID ADP-RIBOSYLATION FACTOR; PROTEIN N-MYRISTOYLTRANSFERASE; MYRISTIC ACID AUXOTROPHY; SACCHAROMYCES-CEREVISIAE; CRYPTOCOCCUS-NEOFORMANS; CANDIDA-ALBICANS; DIFFERENTIAL DISPLAY; MESSENGER-RNA; FACTOR ARF; GENE C1 NIH,CTR CLIN,BETHESDA,MD 20892. PFIZER LTD,CENT RES,DEPT DISCOVERY BIOL,SANDWICH CT13 9NJ,KENT,ENGLAND. WASHINGTON UNIV,SCH MED,DEPT BIOL CHEM,ST LOUIS,MO 63110. RP MARESCA, B (reprint author), INT INST GENET & BIOPHYS,I-80125 NAPLES,ITALY. NR 47 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 SU 1 BP 287 EP 298 PG 12 WC Mycology SC Mycology GA QB967 UT WOS:A1994QB96700025 PM 7722794 ER PT J AU MATSUMOTO, T AJELLO, L MATSUDA, T SZANISZLO, PJ WALSH, TJ AF MATSUMOTO, T AJELLO, L MATSUDA, T SZANISZLO, PJ WALSH, TJ TI DEVELOPMENTS IN HYALOHYPHOMYCOSIS AND PHEOHYPHOMYCOSIS SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article; Proceedings Paper CT XII Congress of the International-Society-for-Human-and-Animal-Mycology (ISHAM) CY MAR 13-18, 1994 CL ADELAIDE, AUSTRALIA ID CENTRAL-NERVOUS-SYSTEM; FUNGUS WANGIELLA-DERMATITIDIS; PSEUDALLESCHERIA-BOYDII INFECTION; SCEDOSPORIUM-INFLATUM INFECTION; BONE-MARROW TRANSPLANTATION; BIPOLARIS-HAWAIIENSIS; PETRIELLIDIUM-BOYDII; DEMATIACEOUS FUNGUS; BRAIN-ABSCESS; CLADOSPORIUM-TRICHOIDES C1 EMORY UNIV,SCH MED,ATLANTA,GA. UNIV TEXAS,AUSTIN,TX 78712. KYUSHU UNIV,FAC MED,FUKUOKA 812,JAPAN. NCI,BETHESDA,MD 20892. RP MATSUMOTO, T (reprint author), TOSHIBA HOSP,DEPT DERMATOL,SHINAGAWA KU,6-3-22 HIGASHI OI,TOKYO 140,JAPAN. FU NEI NIH HHS [P30 EY06360] NR 101 TC 92 Z9 93 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 SU 1 BP 329 EP 349 PG 21 WC Mycology SC Mycology GA QB967 UT WOS:A1994QB96700029 PM 7722796 ER PT J AU GUEHO, E FAERGEMANN, J LYMAN, C ANAISSIE, EJ AF GUEHO, E FAERGEMANN, J LYMAN, C ANAISSIE, EJ TI MALASSEZIA AND TRICHOSPORON - 2 EMERGING PATHOGENIC BASIDIOMYCETOUS YEAST-LIKE FUNGI SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article; Proceedings Paper CT XII Congress of the International-Society-for-Human-and-Animal-Mycology (ISHAM) CY MAR 13-18, 1994 CL ADELAIDE, AUSTRALIA ID LATEX AGGLUTINATION-TEST; BEIGELII INFECTION; SEBORRHEIC DERMATITIS; BLASTOSCHIZOMYCES-CAPITATUS; CRYPTOCOCCAL ANTIGEN; GENUS TRICHOSPORON; AMPHOTERICIN-B; THERAPY; POLYSACCHARIDE; SEROVARS C1 GOTHENBURG UNIV,GOTHENBURG,SWEDEN. NCI,BETHESDA,MD 20892. UNIV TEXAS,MD ANDERSON CANCER CTR,HOUSTON,TX 77030. RP GUEHO, E (reprint author), INST PASTEUR,UNITE MYCOL,25 RUE DR ROUX,F-75724 PARIS 15,FRANCE. NR 48 TC 20 Z9 22 U1 1 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 SU 1 BP 367 EP 378 PG 12 WC Mycology SC Mycology GA QB967 UT WOS:A1994QB96700031 PM 7722799 ER PT J AU KWONCHUNG, KJ PFEIFFER, T CHANG, YC WICKES, BL MITCHELL, D STERN, JJ AF KWONCHUNG, KJ PFEIFFER, T CHANG, YC WICKES, BL MITCHELL, D STERN, JJ TI MOLECULAR-BIOLOGY OF CRYPTOCOCCUS-NEOFORMANS AND THERAPY OF CRYPTOCOCCOSIS SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article; Proceedings Paper CT XII Congress of the International-Society-for-Human-and-Animal-Mycology (ISHAM) CY MAR 13-18, 1994 CL ADELAIDE, AUSTRALIA ID UPSTREAM ACTIVATING SEQUENCES; AMPHOTERICIN-B; MENINGITIS; PROTEIN; URA5; GENE; TRANSFORMATION; POLYSACCHARIDE; FLUCYTOSINE; FLUCONAZOLE C1 UNIV SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94117. WESTMEAD HOSP,CTR INFECT DIS & MICROBIOL,SYDNEY,NSW,AUSTRALIA. UNIV PENN,SCH MED,DIV INFECT DIS,PHILADELPHIA,PA 19104. RP KWONCHUNG, KJ (reprint author), NIAID,CLIN INVEST LAB,BLDG 10,BETHESDA,MD 20892, USA. NR 27 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 SU 1 BP 407 EP 415 PG 9 WC Mycology SC Mycology GA QB967 UT WOS:A1994QB96700033 PM 7722801 ER PT J AU SORLIE, PD ADAM, E MELNICK, SL FOLSOM, A SKELTON, T CHAMBLESS, LE BARNES, R MELNICK, JL AF SORLIE, PD ADAM, E MELNICK, SL FOLSOM, A SKELTON, T CHAMBLESS, LE BARNES, R MELNICK, JL TI CYTOMEGALOVIRUS HERPESVIRUS AND CAROTID ATHEROSCLEROSIS - THE ARIC STUDY SO JOURNAL OF MEDICAL VIROLOGY LA English DT Article DE ULTRASONOGRAPHY; VIRUSES; CORONARY HEART DISEASE ID SMOOTH-MUSCLE CELLS; CYTOMEGALO-VIRUS; INFECTION; ATHEROGENESIS; CHOLESTEROL; ASSOCIATION; TISSUE AB Ubiquitous viruses such as members of the human herpes virus group, particularly cytomegalovirus (CMV), have been proposed to be clinically important agents in the initiation and progression of atherosclerosis. Antibodies to CMV and herpes simplex virus type 1 (HSV1) and type 2 (HSV2) were determined in 340 matched case-control pairs from the Atherosclerosis Risk in Communities (ARIC) Study. Cases were defined by B-mode ultrasonography as persons with thickened carotid artery walls consistent with early atherosclerosis but without a history of cardiovascular disease. Controls were defined as persons without thickened walls or history of cardiovascular disease. The case-control odds ratio for CMV antibodies was 1.55 (P=.03), for HSV 1.41 (P=.07), and for HSV2 0.91 (P=.63). When adjustment was made for potential confounders, the odds ratios were 1.36 for CMV (P=.24), 1.21 for HSV1 (P=.45), and 0.61 (P=.05) for HSV2. These results suggest a modest association between CMV and asymptomatic carotid wall thickening consistent with early atherosclerosis. C1 BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. NIAID,BETHESDA,MD 20892. UNIV MINNESOTA,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. UNIV N CAROLINA,CTR COLLABORAT STUDIES COORDINATING,CHAPEL HILL,NC. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC. RP SORLIE, PD (reprint author), NHLBI,FED BLDG,ROOM 3A10,BETHESDA,MD 20892, USA. FU NHLBI NIH HHS [N01-HC-55018, N01-HC-55015, N01-HC-55016] NR 20 TC 100 Z9 103 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 0146-6615 J9 J MED VIROL JI J. Med. Virol. PD JAN PY 1994 VL 42 IS 1 BP 33 EP 37 DI 10.1002/jmv.1890420107 PG 5 WC Virology SC Virology GA MN700 UT WOS:A1994MN70000006 PM 8308517 ER PT J AU NATELSON, BH YE, N MOUL, DE JENKINS, FJ OREN, DA TAPP, WN CHENG, YC AF NATELSON, BH YE, N MOUL, DE JENKINS, FJ OREN, DA TAPP, WN CHENG, YC TI HIGH TITERS OF ANTI-EPSTEIN-BARR VIRUS-DNA POLYMERASE ARE FOUND IN PATIENTS WITH SEVERE FATIGUING ILLNESS SO JOURNAL OF MEDICAL VIROLOGY LA English DT Article DE HHV-6; SEROLOGY; CHRONIC FATIGUE SYNDROME; SEASONAL AFFECTIVE DISORDER; VIRAL REPLICATING ENZYMES ID NASOPHARYNGEAL CARCINOMA; INFECTION; ANTIBODIES; PERSISTENT; FREQUENCY; MONONUCLEOSIS; DISORDERS AB Forty-one patients with chronic fatigue syndrome (CFS), 76 healthy controls matched with the patient group for age range, sex, race, and socioeconomic class, and 22 symptomatic patients with seasonal affective disorder (SAD) had serum sampled for antibodies against 2 Epstein-Barr virus (EBV) replicating enzymes. Abnormal titers of antibodies were found twice as often in CFS patients as controls (34.1% vs. 17.1%), with SAD patients having an intermediate frequency (27.3%). Stratifying for disease severity sharpened the differences considerably, with the sicker CFS and SAD patients having 52% and 50% abnormal tests, respectively; more mildly afflicted CFS and SAD patients had a frequency of abnormal tests in the normal range. Antibodies to EBV DNA polymerase (DNAP) were the more sensitive of the two tests in that they were positive in all cases but one. These findings suggest that antibodies against EBV DNAP may be a useful marker in delineating a subset of patients with severe fatiguing illness for appropriate treatment trials and for monitoring their outcomes, C1 UMDNJ,NEW JERSEY MED SCH,CTR CHRON FATIGUE SYNDROME,NEWARK,NJ. UMDNJ,NEW JERSEY MED SCH,DEPT NEUROSCI,NEWARK,NJ. VET AFFAIRS MED CTR,E ORANGE,NJ. NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT MICROBIOL,BETHESDA,MD 20814. YALE UNIV,SCH MED,DEPT PHARMACOL,NEW HAVEN,CT 06510. RI Jenkins, Frank/A-8529-2009 FU NCI NIH HHS [CA-44358]; NIAID NIH HHS [AI-32247] NR 25 TC 25 Z9 26 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 0146-6615 J9 J MED VIROL JI J. Med. Virol. PD JAN PY 1994 VL 42 IS 1 BP 42 EP 46 DI 10.1002/jmv.1890420109 PG 5 WC Virology SC Virology GA MN700 UT WOS:A1994MN70000008 PM 8308519 ER PT J AU FLORES, J WHITE, L BLANCO, M PEREZSCHAEL, I AF FLORES, J WHITE, L BLANCO, M PEREZSCHAEL, I TI SEROLOGICAL RESPONSE TO ROTAVIRUS INFECTION IN NEWBORN-INFANTS SO JOURNAL OF MEDICAL VIROLOGY LA English DT Article DE VP7 SEROTYPE 4; M37 ROTAVIRUS; VP4 TYPING; NEONATAL ROTAVIRUS INFECTION ID MONOCLONAL-ANTIBODIES; VACCINE MMU-18006; YOUNG-CHILDREN; ANTIGENICITY; GASTROENTERITIS; REACTOGENICITY; CONSERVATION; SEROTYPES; ASSAY AB We report the identification of rotavirus in stools of newborn infants at the ''Hospital Materno Infantil de Caricuao'' (HMIC) as well as the infants' serological responses to various rotavirus strains. The serological responses of another group of rotavirus-positive neonates studied previously at the ''Maternidad Concepcion Palacios'' (MCP) hospital was also evaluated. Fifty-four of 266 (20%) newborns examined at HMIC shed rotavirus. The infection rate was higher among infants admitted to the nursery (75%) than in those ''rooming in'' with their mothers (7%) (P<.01). Eleven of the 54 neonates (20%) had diarrhea; seven of them experienced mild, short-lived episodes, whereas five had frequent diarrhea bouts or diarrhea lasting for over 3 days; the remaining 43 infants were asymptomatic. Twenty-seven of 28 rotavirus specimens tested at HMIC had VP7 serotype 4 specificity and one belonged to VP7 serotype 1; VP4 typing performed on 24 of the viruses by RNA hybridization showed these viruses to be similar to the M37 strain, a rotavirus previously associated with asymptomatic infections in newborns at MCP. IgA seroresponses were detected in eight of 11 infants born at HMIC (73%), but most failed to developed neutralization responses to homologous or heterologous strains. Newborn infants who had shed the M37 rotavirus strain at MCP reacted similarly: 16 of 24 (67%) developed a rotavirus IgA rise, but only 29% developed a neutralization response, C1 MINIST SANIDAD & ASISTENCIA SOCIAL,INST BIOMED,CARACAS,VENEZUELA. RP FLORES, J (reprint author), NIAID,INFECT DIS LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 24 TC 4 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 0146-6615 J9 J MED VIROL JI J. Med. Virol. PD JAN PY 1994 VL 42 IS 1 BP 97 EP 102 DI 10.1002/jmv.1890420118 PG 6 WC Virology SC Virology GA MN700 UT WOS:A1994MN70000017 PM 8308526 ER PT J AU CHANTURIYA, AN NIKOLOSHINA, HV AF CHANTURIYA, AN NIKOLOSHINA, HV TI CORRELATIONS BETWEEN CHANGES IN MEMBRANE CAPACITANCE INDUCED BY CHANGES IN IONIC ENVIRONMENT AND THE CONDUCTANCE OF CHANNELS INCORPORATED INTO BILAYER-LIPID MEMBRANES SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE BLM; LATROTOXIN; LANTHANUM; CADMIUM; IONIC CHANNELS; MEMBRANE CAPACITANCE ID PHOSPHOLIPID-MEMBRANES; FUSION; CALCIUM; CATIONS; PHOSPHATIDYLCHOLINE; DIVALENT; PH; PHOSPHATIDYLSERINE; GRAMICIDIN; VESICLES AB The action of metal polycations and pH on ionic channels produced in bilayer lipid membranes (BLM) by three different toxins was studied by measuring membrane capacitance and channel conductance. Here, we show that critical concentrations of Cd2+, La3+ or Tb3+ induce complex changes in membrane capacitance. The time course of capacitance changes is similar to the time course of channel blocking by these ions at low concentration. No changes in BLM capacitance or conductance were observed in the range of pH 5.8-9.0. A pH shift from 7.4 to 3-4 or 11-12 induced large changes in BLM capacitance and channel conductance. For all studied channel-forming proteins, the initial capacitance increase preceded the conductance decrease caused by addition of polycations or by a change in pH. A close relationship between membrane lipid packing and ion channel protein is suggested. C1 AV PALLADIN BIOCHEM INST,DEPT NEUROCHEM,KIEV 252030,UKRAINE. NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. NR 36 TC 15 Z9 16 U1 3 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD JAN PY 1994 VL 137 IS 1 BP 71 EP 77 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA MU177 UT WOS:A1994MU17700007 PM 7516435 ER PT J AU FARINA, M KACHAR, B LINS, U BRODERICK, R DEBARROS, HL AF FARINA, M KACHAR, B LINS, U BRODERICK, R DEBARROS, HL TI THE OBSERVATION OF LARGE MAGNETITE (FE3O4) CRYSTALS FROM MAGNETOTACTIC BACTERIA BY ELECTRON AND ATOMIC-FORCE MICROSCOPY SO JOURNAL OF MICROSCOPY-OXFORD LA English DT Article DE MAGNETOTACTIC BACTERIA; ATOMIC FORCE MICROSCOPY; ELECTRON MICROSCOPY; CRYSTALLINE HABITS; MAGNETIC SINGLE DOMAINS; BIOMINERALIZATION ID DEEP-SEA SEDIMENTS; GREIGITE FE3S4; BIOGENIC MAGNETITE; PROBE MICROSCOPES; BIOMINERALIZATION; ULTRASTRUCTURE; MICROORGANISM; MORPHOLOGY; SPIRILLUM; PARTICLES AB Magnetite crystals inside coccoid magnetotactic bacteria found in lagoons near Rio deJaneiro city were examined by electron microscopy (EM) and atomic force microscopy (AFM). For AFM, ultrathin sections of bacteria embedded in Epon resin were etched with an ethanolic NaOH solution and observed both in the height and in the force modes. Comparative electron microscope images were useful for identifying crystalline reliefs in the etched sections. Different situations representing particular arrangements of crystal chains were observed by AFM. The majority of the bacteria examined presented unusually large magnetite crystals which remained strongly attached in linear chains even after the laboratory procedures for their isolation. This behaviour is different from all other biogenic magnetite crystals isolated so far. It is suggested that this attachment is due to the strong field between individual crystals as well as to the contact areas, which are the largest observed until now. The correct identification of a particular topography by AFM as a crystal relief may be critical when crystals are not aligned in chains; in these cases the linear dimensions and the presence of well-defined edges and faces are important features to be taken into account. Characterization of the crystal faces is important for the study of magnetotactic micro-organisms since the crystalline habits seem to be species-specific. Observation of etched sections proved to be a helpful approach for crystal relief observation, especially when small amounts of bacteria were available. C1 NIDOCD,CELLULAR BIOL LAB,BETHESDA,MD. UNIV MARYLAND,SCH MED,DEPT PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21201. MUSEU ASTRON & CIENCIAS AFINS,RIO JANEIRO,RJ,BRAZIL. RP FARINA, M (reprint author), UNIV FED RIO DE JANEIRO,INST BIOFIS CARLOS CHAGAS FILHO,CCS,BLOCO G,BR-21949900 RIO JANEIRO,RJ,BRAZIL. RI Farina, Marcos/I-3744-2014; Lins, Ulysses/N-7282-2015 OI Lins, Ulysses/0000-0002-1786-1144 NR 46 TC 29 Z9 29 U1 0 U2 5 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0022-2720 J9 J MICROSC-OXFORD JI J. Microsc.-Oxf. PD JAN PY 1994 VL 173 BP 1 EP 8 PN 1 PG 8 WC Microscopy SC Microscopy GA MT638 UT WOS:A1994MT63800001 ER PT J AU FURANO, AV HAYWARD, BE CHEVRET, P CATZEFLIS, F USDIN, K AF FURANO, AV HAYWARD, BE CHEVRET, P CATZEFLIS, F USDIN, K TI AMPLIFICATION OF THE ANCIENT MURINE LX FAMILY OF LONG INTERSPERSED REPEATED DNA OCCURRED DURING THE MURINE RADIATION SO JOURNAL OF MOLECULAR EVOLUTION LA English DT Article DE L1 FAMILY; LINE FAMILY; MOLECULAR SYNAPOMORPHY; ANCIENT L1 FAMILY; RODENT SYSTEMATICS ID RAT L1 L1RN; TRANSPOSABLE ELEMENTS; SEQUENCES; EVOLUTION; END; REASSOCIATION; RETROPOSONS; PROMOTER; PROTEIN; TIME AB We identified and characterized the relies of an ancient rodent L1 family, referred to as Lx, which was extensively amplified at the time of the murine radiation about 12 million years ago, and which we showed was ancestral to the modern L1 families in rat and mouse. Here we have extended our analysis of the Lx amplification by examining more murine and nonmurine species for Lx sequences using both blot hybridization and the polymerase chain reaction for a total of 36 species. In addition we have determined the relative copy number and sequence divergence, or age, of Lx elements in representative murine genera. Our results show that while Lx sequences are confined to murine genera, the extent of the amplification was different in the different murine lineages, indicating that the amplification of Lx did not precede, but was coincident with, the murine radiation. The implications of our findings for the evolutionary dynamics of L1 families and the utility of ancestral amplification events for systematics are discussed. C1 UNIV MONTPELLIER 2,INST SCI EVOLUT,CNRS,UA 327,F-34095 MONTPELLIER,FRANCE. RP FURANO, AV (reprint author), NIDDKD,GEN STRUCT & FUNCT SECT,BIOCHEM PHARMACOL LAB,BLDG 8,ROOM 203,BETHESDA,MD 20892, USA. RI Chevret, Pascale/B-7299-2009 NR 47 TC 44 Z9 44 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2844 J9 J MOL EVOL JI J. Mol. Evol. PD JAN PY 1994 VL 38 IS 1 BP 18 EP 27 PG 10 WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity GA MN382 UT WOS:A1994MN38200002 PM 8151711 ER PT J AU LILLING, G WOLLMAN, Y GOLDSTEIN, MN RUBINRAUT, S FRIDKIN, M BRENNEMAN, DE GOZES, I AF LILLING, G WOLLMAN, Y GOLDSTEIN, MN RUBINRAUT, S FRIDKIN, M BRENNEMAN, DE GOZES, I TI INHIBITION OF HUMAN NEUROBLASTOMA GROWTH BY A SPECIFIC VIP ANTAGONIST SO JOURNAL OF MOLECULAR NEUROSCIENCE LA English DT Article DE VASOACTIVE INTESTINAL PEPTIDE; NEUROBLASTOMA; AUTOCRINE GROWTH FACTOR; MITOGENIC FACTOR; VIP HYBRID ANTAGONIST; NEUROTENSIN(6-11)-VIP7-28 ID VASOACTIVE-INTESTINAL-PEPTIDE; LUNG-CANCER GROWTH; CELL-LINES; DIFFERENTIATION; RECEPTORS; EMBRYOS; GENE AB The 28-amino-acid neuropeptide, vasoactive intestinal peptide (VIP), is a potent mitogen during embryonic development and plays a vital role in brain growth. VIP is also mitogenic for tumor cells, including the human neuroblastoma (NMB). Northern blot analysis has revealed VIP mRNA transcripts in NMB. We now report VIP-like immunoreactivity within these neuroblastoma cells that increased during logarithmic growth and decreased after attaining confluency. About 10(6) seeded cells secreted 5-40 pg of VIP-like immunoreactivity into the medium. These results suggest an autocrine role for VIP in the regulation of neuroblastoma growth. A VIP hybrid antagonist (neurotensin(6-11)VIP(7-28)) that has been shown to inhibit lung cancer proliferation was now tested for inhibition of neuroblastoma growth. Receptor binding studies indicated that the hybrid antagonist displaced [I-125]-VIP binding in the neuroblastoma cells (EC(50) = 5 x 10(-6)M). Furthermore, as measured by thymidine incorporation and by cell counts, the potent VIP hybrid antagonist inhibited neuroblastoma multiplication in a dose-dependent manner. In conclusion, VIP may be an important regulator of growth of nerve cell progenitors and of tumors derived from neuronal origin and intervening with VIP function may lead to improved treatment of cancer. C1 TEL AVIV UNIV,SACKLER SCH MED,DEPT CLIN BIOCHEM,IL-69978 TEL AVIV,ISRAEL. TEL AVIV MED CTR & SCH MED,DEPT NEPHROL,TEL AVIV,ISRAEL. WASHINGTON UNIV,BARNES SCH MED,DEPT ANAT & NEUROBIOL,ST LOUIS,MO. WEIZMANN INST SCI,DEPT ORGAN CHEM,IL-76100 REHOVOT,ISRAEL. NICHHD,DEV NEUROBIOL LAB,DEV & MOLEC PHARMACOL SECT,BETHESDA,MD. NR 30 TC 15 Z9 15 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07012 SN 0895-8696 J9 J MOL NEUROSCI JI J. Mol. Neurosci. PY 1994 VL 5 IS 4 BP 231 EP 239 DI 10.1007/BF02736724 PG 9 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RL465 UT WOS:A1994RL46500003 PM 7577366 ER PT J AU PETTIT, GR XU, JP WILLIAMS, MD CHRISTIE, ND DOUBEK, DL SCHMIDT, JM BOYD, MR AF PETTIT, GR XU, JP WILLIAMS, MD CHRISTIE, ND DOUBEK, DL SCHMIDT, JM BOYD, MR TI ISOLATION AND STRUCTURE OF CEPHALOSTATIN-10 AND CEPHALOSTATIN-11 SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID TUMOR-CELL-LINES; ANTINEOPLASTIC AGENTS; SPONGE; STEROIDS AB Further investigation of antineoplastic constituents from the marine worm Cephalodiscus gilchristi, employing a 450 kg re-collection from the Indian Ocean (Southeast Africa), has led to isolation and structural determination of two previously undetected members of the cephalostatin series, designated cephalostatins 10 [4] and 11 [5]. Structural analyses were conducted primarily employing high field 2D nmr and high resolution mass spectral techniques. All the stereochemical assignments were deduced using the original X-ray crystal structure of cephalostatin 1 and ROESY 2D nmr methods. Both cephalostatins 10 and 11 strongly inhibited growth of a series of important human cancer cell lines. C1 ARIZONA STATE UNIV,DEPT CHEM,TEMPE,AZ 85287. NCI,FCRDC,DCT,DTP,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. RP PETTIT, GR (reprint author), ARIZONA STATE UNIV,CANC RES INST,TEMPE,AZ 85287, USA. FU NCI NIH HHS [CA-16049-09-12, CA 44344-01A1-04-05] NR 22 TC 42 Z9 45 U1 0 U2 4 PU AMER SOC PHARMACOGNOSY PI CINCINNATI PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202 SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD JAN PY 1994 VL 57 IS 1 BP 52 EP 63 DI 10.1021/np50103a007 PG 12 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA MW760 UT WOS:A1994MW76000007 PM 8158165 ER PT J AU LESCH, KP BALLING, U GROSS, J STRAUSS, K WOLOZIN, BL MURPHY, DL RIEDERER, P AF LESCH, KP BALLING, U GROSS, J STRAUSS, K WOLOZIN, BL MURPHY, DL RIEDERER, P TI ORGANIZATION OF THE HUMAN SEROTONIN TRANSPORTER GENE SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Note DE HUMAN; SEROTONIN TRANSPORTER; GENE ORGANIZATION; VNTR ID IMIPRAMINE BINDING-SITES; TRITIATED IMIPRAMINE; DEPRESSED-PATIENTS; PLATELETS; CLONING; FAMILY AB The gene encoding the human serotonin transporter (5-HTT) has been isolated and characterized. The human 5-HTT gene is composed of 14 exons spanning similar to 31 kb. The sequence of all exons including adjacent intronic sequences and a tandem repeat DNA polymorphism (VNTR) has been determined and deposited in the EMBL/GenBank data base with the accession numbers X76753 to X76762. The characterization of 5-HTT gene will aid to advance molecular pharmacologic studies of 5-HT uptake regulation and facilitate investigations of its role in psychiatric disorders. C1 NIMH,LCS,CTR CLIN,BETHESDA,MD 20892. RP LESCH, KP (reprint author), UNIV WURZBURG,DEPT PSYCHIAT,FUCHSLEINSTR 15,D-97080 WURZBURG,GERMANY. RI Lesch, Klaus-Peter/J-4906-2013 OI Lesch, Klaus-Peter/0000-0001-8348-153X NR 21 TC 475 Z9 492 U1 1 U2 20 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1994 VL 95 IS 2 BP 157 EP 162 DI 10.1007/BF01276434 PG 6 WC Neurosciences SC Neurosciences & Neurology GA MY599 UT WOS:A1994MY59900008 PM 7865169 ER PT J AU ALAFUZOFF, I ALMQVIST, E ADOLFSSON, R LAKE, S WALLACE, W GREENBERG, DA WINBLAD, B AF ALAFUZOFF, I ALMQVIST, E ADOLFSSON, R LAKE, S WALLACE, W GREENBERG, DA WINBLAD, B TI A COMPARISON OF MULTIPLEX AND SIMPLEX FAMILIES WITH ALZHEIMERS-DISEASE SENILE DEMENTIA OF ALZHEIMER-TYPE WITHIN A WELL-DEFINED POPULATION SO JOURNAL OF NEURAL TRANSMISSION-PARKINSONS DISEASE AND DEMENTIA SECTION LA English DT Article DE FAMILIAL ALZHEIMERS DISEASE; EPIDEMIOLOGY; DURATION OF DISEASE; AGE OF ONSET; HISTOPATHOLOGY ID EARLY-ONSET; RISK; HETEROGENEITY; DISORDERS; RELATIVES; PREVALENCE; DIAGNOSIS; KINDREDS; HISTORY; AGE AB A study was made on 150 clinically demented patients presenting at autopsy at Umea University Hospital in Sweden. In 90 of the cases dementia was considered to be primary in nature and of these forty six per cent (41 cases), fulfilled both the clinical and histopathological criteria for the diagnosis of Alzheimer's disease/Senile dementia of Alzheimer type (AD/SDAT). The families of these 41 AD/SDAT cases were then studied, and a family history obtained through interviews with multiple family informants and from civil and medical records. Additional diseased family members suffering from progressive dementia (multiplex families) were observed in 12 probands out of 41 (29%). Multiplex families exhibited similar clinical and histopathological characteristics as simplex families containing a single affected individual. The secondary cases in the multiplex families exhibited similar demographic and clinical characteristics as the probands. 39% of the multiplex and 14% of the simplex cases had an early age of onset of the disease, that was under 65 years. The overall prevalence of progressive dementia disorders in the 41 families was 5.9%. The prevalence of a progressive dementia disorder was 11% in the multiplex families (14% for the early onset cases) and 3.5% in the simplex families (2% for the early onset cases). The prevalence of progressive dementia disorder for family members who had passed the mean age of the onset of the disease for their family, was 45% for multiplex and 18% for simplex families. Furthermore the incidence rate for dementia was significantly higher (p < 0.005) in multiplex families (5.5 per 1,000 personyears) when compared to simplex families (2.5 per 1,000 personyears). No differences could be seen in parental age at birth of the diseased when comparing the two sets of families. However in multiplex families the duration of the disease was significantly (p < 0.025) shorter, in subjects with parental age at birth over 35 years compared to those with a parental age under 35 years. The multiplex families contained significantly (p < 0.025) larger sibships; and showed a significantly lower age of onset for the disease (p < 0.001), and a significantly longer duration of disease (p < 0.05) compared to the simplex families. A significant intra familial correlation of age at disease onset was observed in both sets of the families. C1 KAROLINSKA INST,ALZHEIMERS DIS RES CTR,DEPT GERIATR MED,S-14186 HUDDINGE,SWEDEN. UMEA UNIV HOSP,DEPT PSYCHIAT,S-90185 UMEA,SWEDEN. ST ELIZABETH HOSP,NIMH,WASHINGTON,DC 20032. CUNY MT SINAI SCH MED,DEPT PSYCHIAT,MACK LAB,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,CTR NEUROBIOL,NEW YORK,NY 10029. RP ALAFUZOFF, I (reprint author), KAROLINSKA INST,HUDDINGE UNIV HOSP,DEPT PATHOL,S-14186 HUDDINGE,SWEDEN. FU NIDDK NIH HHS [DK31775]; NINDS NIH HHS [NS27941] NR 32 TC 1 Z9 2 U1 0 U2 1 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0936-3076 J9 J NEURAL TRANSM-PARK JI J. Neural Transm.-Park. Dis. Dement. Sect. PY 1994 VL 7 IS 1 BP 61 EP 72 DI 10.1007/BF02252663 PG 12 WC Clinical Neurology SC Neurosciences & Neurology GA ND021 UT WOS:A1994ND02100006 PM 8579770 ER PT J AU CHIUEH, CC HUANG, SJ MURPHY, DL AF CHIUEH, CC HUANG, SJ MURPHY, DL TI SUPPRESSION OF HYDROXYL RADICAL FORMATION BY MAO INHIBITORS - A NOVEL POSSIBLE NEUROPROTECTIVE MECHANISM IN DOPAMINERGIC NEUROTOXICITY SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Article; Proceedings Paper CT 5th International Amine Oxidase Workshop - Amine Oxidases: Function and Dysfunction CY AUG 22-25, 1992 CL GALWAY, IRELAND ID PARKINSONS-DISEASE; SUBSTANTIA NIGRA; INTRACRANIAL MICRODIALYSIS; MANGANESE NEUROTOXICITY; LIPID-PEROXIDATION; TRANSITION-METALS; PRIMATE MODEL; L-DEPRENYL; MPTP; NEURONS AB Prior studies concluded that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, a toxin causing parkinsonism) and its analogues are bioactivated by monoamine oxidase (MAO) to toxic pyridinium metabolites. Recently, a dissociation between the neuroprotective effects of deprenyl and its MAO inhibiting effects has been proposed. Furthermore, we have demonstrated that pyridinium metabolites of MPTP stimulate dopamine efflux and the formation of cytotoxic hydroxyl free radicals (.OH) in the striatum. Therefore, we investigated possible neuroprotective mechanisms of propargyl MAO inhibitors by studying their effects on the formation of oxygen free radicals produced by dopamine autoxidation. Our recent in vivo results indicate that deprenyl and clorgyline given systemically suppressed the generation of .OH that followed administration of 2'-methyl-MPTP. Combined deprenyl and clorgyline pretreatment are needed to block dopamine neurotoxicity elicited by 2'-methyl-MPTP. The present in vitro studies reveal that propargyl MAO inhibitors suppress non-enzymatic dopamine autoxidation and associated free radical production. Thus, .OH generation evoked by MPTP analogues may be due mainly to a burst increase in iron-catalyzed autoxidation of released dopamine in the basal ganglia where high levels of iron and oxygen are present. Our present in vitro and prior in vivo results suggest that a novel antioxidant property of propargyl MAO inhibitors may contribute to protection against nigral lesions elicited by dopamine autoxidation following the administration of MPTP analogues. RP CHIUEH, CC (reprint author), NIMH,CLIN SCI LAB,CLIN CTR BLDG 10,RM 3D-41,BETHESDA,MD 20892, USA. NR 38 TC 42 Z9 42 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0303-6995 J9 J NEURAL TRANSM-SUPP JI J. Neural Transm.-Suppl. PY 1994 IS 41 BP 189 EP 196 PG 8 WC Neurosciences SC Neurosciences & Neurology GA PW142 UT WOS:A1994PW14200027 ER PT J AU MALKIN, MG GREEN, SB BYAR, DP STRIKE, TA BURGER, PC VOGEL, FS PISTENMAA, DA MAHALEY, MS RANSOHOFF, J SHAPIRO, WR MEALEY, J ROBERTSON, JT SELKER, RG VANGILDER, JC AF MALKIN, MG GREEN, SB BYAR, DP STRIKE, TA BURGER, PC VOGEL, FS PISTENMAA, DA MAHALEY, MS RANSOHOFF, J SHAPIRO, WR MEALEY, J ROBERTSON, JT SELKER, RG VANGILDER, JC TI SUPERIORITY OF PCNU OVER AZQ IN THE TREATMENT OF PRIMARY BRAIN-TUMORS - RESULTS OF A PROSPECTIVE RANDOMIZED TRIAL-(81-20) BY THE BRAIN-TUMOR STUDY-GROUP SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE BRAIN TUMORS; RADIATION THERAPY; PCNU; AZQ ID MALIGNANT GLIOMAS; PHASE-II; AZIRIDINYLBENZOQUINONE AZQ; INTRAVENOUS BCNU; ONCOLOGY-GROUP; RECURRENT; DIAZIQUONE; RADIOTHERAPY; NITROSOUREAS; RADIATION AB Purpose. A two-arm randomized clinical trial was performed to determine the efficacy of PCNU and AZQ in the treatment of de novo or recurrent primary brain tumors. An additional objective was to gather information on the administration and toxicity of these compounds, supplementing that obtained previously in phase I/II studies. Methods. During 1982 and 1983 the Brain Tumor Study Group randomized 152 adult patients with primary brain tumors to receive PCNU 75-100 mg/m(2) intravenously (IV) every 8 weeks or AZQ 15 mg/m(2) IV once a week for 4 weeks, every 6-8 weeks. All patients who had not received 'full dose' radiotherapy before randomization received it concurrently with the first course of protocol chemotherapy. The data were analyzed for the total randomized population (RP), and for 130 patients in the valid study group (VSG) formed by excluding 22 patients for whom the histologic diagnosis was not documented by central review. Results. Median survival times were 11.0 months for the PCNU group and 8.4 months for the AZQ group. The difference in survival curves was statistically significant for the RP (p = 0.01) and the VSG (p = 0.02). Life-table analysis of the VSG showed estimated 2-year survivals of 34% for PCNU and 11% for AZQ. The advantage of PCNU remained significant (p = 0.006) after adjustment for histopathologic category, age, initial performance status, and interval from initial reported surgery. Myelosuppression was the principal toxicity in both groups. Conclusion. PCNU conferred a significant survival advantage to patients with newly diagnosed or recurrent primary brain tumors compared to AZQ. C1 NCI,BETHESDA,MD. DUKE UNIV,MED CTR,DURHAM,NC. UNIV N CAROLINA,CHAPEL HILL,NC. NYU,MED CTR,NEW YORK,NY. INDIANA UNIV,SCH MED,INDIANAPOLIS,IN. UNIV TENNESSEE,MEMPHIS,TN. UNIV IOWA HOSP & CLIN,IOWA CITY,IA. WESTERN PENN CANC INST,CTR NEUROONCOL,PITTSBURGH,PA. RP MALKIN, MG (reprint author), MEM SLOAN KETTERING CANC CTR,DEPT NEUROL,1275 YORK AVE,NEW YORK,NY 10021, USA. FU NCI NIH HHS [CA 36046, CA 36005, CA 36047] NR 40 TC 8 Z9 8 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1994 VL 22 IS 1 BP 55 EP 65 DI 10.1007/BF01058355 PG 11 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA QD494 UT WOS:A1994QD49400007 PM 7714551 ER PT J AU KAPLITT, MG TJUVAJEV, JG LEIB, DA BERK, J PETTIGREW, KD POSNER, JB PFAFF, DW RABKIN, SD BLASBERG, RG AF KAPLITT, MG TJUVAJEV, JG LEIB, DA BERK, J PETTIGREW, KD POSNER, JB PFAFF, DW RABKIN, SD BLASBERG, RG TI MUTANT HERPES-SIMPLEX VIRUS-INDUCED REGRESSION OF TUMORS GROWING IN IMMUNOCOMPETENT RATS SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE HSV; THYMIDINE KINASE; RIBONUCLEOTIDE REDUCTASE; VIRAL VECTOR; ANTITUMOR EFFECT ID RIBONUCLEOTIDE REDUCTASE; PROGNOSTIC IMPLICATIONS; CELL-KINETICS; HUMAN GLIOMAS; GENE-TRANSFER; BRAIN-TUMORS; THYMIDINE; GROWTH; INVIVO; REPLICATION AB Herpes simplex virus (HSV) mutants kill dividing tumor cells but spare non-proliferating, healthy brain tissue and may be useful in developing new treatment strategies for malignant brain tumors. Two HSV mutants, a thymidine kinase deficient virus (TK-) and a ribonucleotide reductase mutant (RR-), killed 7/7 human tumor cell lines in tissue culture. The TK- HSV killed Rat RG2 glioma and W256 carcinoma lines but not the rat C6 glioma in culture. TK- HSV replication (12 pfu/cell) was similar to wild-type HSV (10 pfu/cell) in rapidly dividing W256 cells in tissue culture, but was minimal (< 1 pfu/cell) in serum-starved cells, suggesting that the proliferative activity of tumor cells at the site and time of TK- HSV injection may influence efficacy in vivo. Subcutaneous W256 tumors in male Sprague-Dawley rats were injected with TK- HSV or virus free inoculum. A significant effect of TK- HSV therapy on W256 tumor growth was demonstrated compared to controls (p = 0.002). Complete regression was observed in 4/9 experimental tumors, with no recurrence over 6 months. Tumor growth in the remaining 5/9 animals was attenuated during the first 3 to 5 days after treatment, but not beyond 5 days compared to 9 matched control animals; no tumor regression was observed in any of the control animals. These results suggest that HSV mutants are potentially useful as novel therapeutic agents in the treatment of tumors in immunocompetent subjects. C1 ROCKEFELLER UNIV,NEUROBIOL & BEHAV LAB,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,DEPT NEUROL,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,PROGRAM MOLEC BIOL,NEW YORK,NY 10021. WASHINGTON UNIV,SCH MED,DEPT OPHTHALMOL & VISUAL SCI,ST LOUIS,MO 63110. NIMH,DIV APPL & SERV RES,BETHESDA,MD 20892. RI rabkin, samuel/C-2443-2012 OI rabkin, samuel/0000-0003-2344-2795 FU NEI NIH HHS [R01 EY009083] NR 44 TC 52 Z9 53 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1994 VL 19 IS 2 BP 137 EP 147 DI 10.1007/BF01306455 PG 11 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA PB982 UT WOS:A1994PB98200006 PM 7964989 ER PT J AU THORGEIRSSON, UP LINDSAY, CK COTTAM, DW GOMEZ, DE AF THORGEIRSSON, UP LINDSAY, CK COTTAM, DW GOMEZ, DE TI TUMOR INVASION, PROTEOLYSIS, AND ANGIOGENESIS SO JOURNAL OF NEURO-ONCOLOGY LA English DT Review DE TUMOR INVASION; PROTEINASES; PROTEINASE INHIBITORS; CYTOKINES; GROWTH FACTORS; ANGIOGENESIS ID ENDOTHELIAL GROWTH-FACTOR; ERYTHROID-POTENTIATING ACTIVITY; PLASMINOGEN-ACTIVATOR INHIBITORS; CENTRAL-NERVOUS-SYSTEM; HUMAN BRAIN-TUMORS; NEURITE-PROMOTING FACTOR; HUMAN-TISSUE INHIBITOR; HUMAN GLIOMAS INVIVO; FACTOR RECEPTOR GENE; EXTRACELLULAR-MATRIX AB In this review, some of the current literature on the regulation of proteolysis and angiogenesis during tumor invasion is discussed. Due to the critical location of brain tumors, an understanding of tumor cell interactions with the local environment is particularly relevant. Tissue breakdown during tumor invasion is associated with proteolytic activity, mediated by tumor cells, and surrounding host cells. This review covers two classes of proteinases and inhibitors that have commonly been associated with tumor invasion i.e., plasminogen activator (PA)/plasmin and matrix metalloproteinases (MMP) with special emphasis on the MMP inhibitors, TIMP-1 and TIMP-2. At different steps of the metastatic process, tumor cells interact with endothelial cells. Tumor cells also stimulate the formation of new vessels through the expression of specific angiogenic molecules. At least eight angiogenic molecules have been purified, sequenced and cloned, four of which are discussed here. Regulation of angiogenic activity has been the focus of intense studies recently, and a wide range of synthetic and natural angiogenesis inhibitors have been discovered. Targeting of angiogenic molecules and tumor vasculature may prove useful in future cancer therapeutic strategies. RP THORGEIRSSON, UP (reprint author), NCI, OFF DIRECTOR, BLDG 37, ROOM 2D02, BETHESDA, MD 20892 USA. NR 171 TC 50 Z9 50 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1994 VL 18 IS 2 BP 89 EP 103 DI 10.1007/BF01050415 PG 15 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA NT097 UT WOS:A1994NT09700002 PM 7525888 ER PT J AU RAO, JS STECK, PA TOFILON, P BOYD, D ALIOSMAN, F STETLERSTEVENSON, WG LIOTTA, LA SAWAYA, R AF RAO, JS STECK, PA TOFILON, P BOYD, D ALIOSMAN, F STETLERSTEVENSON, WG LIOTTA, LA SAWAYA, R TI ROLE OF PLASMINOGEN-ACTIVATOR AND OF 92-KDA TYPE-IV COLLAGENASE IN GLIOBLASTOMA INVASION USING AN IN-VITRO MATRIGEL MODEL SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE GLIOBLASTOMA INVASION; MATRIGEL; SERINE PROTEASES; METALLOPROTEASES; SERPINS; TISSUE INHIBITORS OF METALLOPROTEASES ID TUMOR-CELL INVASION; BASEMENT-MEMBRANE COLLAGEN; BRAIN-TISSUE INVITRO; PROTEASE NEXIN-I; EXTRACELLULAR-MATRIX; UROKINASE-TYPE; RAT-BRAIN; MELANOMA-CELLS; HUMAN GLIOMAS; CATHEPSIN-B AB The invasive nature of human gliomas represents a major factor in preventing their total resection. The exact nature of the underlying mechanisms of tumor cell invasion are still unclear. In this study, we have quantitatively assayed a glioblastoma cell line for its ability to migrate through a polycarbonate filter coated with matrigel which contains a complex of multiple basement membrane components. At 48 h the glioblastoma cell line (U251) showed a rate of invasiveness of 42% and also dependent on the concentration of matrigel. The U251 cell, line produced a urokinase type plasminogen activator and a 92-KDa type IV collagenase. Both enzymes were inhibited by the addition of uPA and 92-KDa type IV collagenase antibodies. Those same antibodies reduced the invasion rate of U251 cells from 42% to 12 and 21%, respectively. Similarly, the addition of epsilon-aminocaproic acid (a plasmin inhibitor) or tissue inhibitor of metalloprotease (TIMP(2), a collagenase inhibitor) reduced the invasiveness of U251 cells from 42% to 14% and 10%, respectively. Additionally, the other two glioblastoma cell lines (LG11, UWR1) and astrocytes showed a rate of invasiveness at 41%, 61% and 12%, respectively. Finally the addition of hyaluronic acid to the matrigel, a constituent of brain extracellular matrix, enhanced the rate of invasion. These findings provide evidence for the role of serine proteases and metalloproteases in facilitating the invasion of extracellular matrix components by glioblastoma cell line and suggest a therapeutic role for protease inhibitors in attempting to minimize the invasive propensity of gliomas. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT NEUROONCOL,HOUSTON,TX 77030. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT EXPTL RADIOTHERAPY,HOUSTON,TX 77030. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT TUMOR BIOL,HOUSTON,TX 77030. UNIV TEXAS,MD ANDERSON CANCER CTR,DEPT EXPTL PEDIAT,HOUSTON,TX 77030. NCI,PATHOL LAB,BETHESDA,MD 20892. RP RAO, JS (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,DEPT NEUROSURG,BOX 064,1515 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 FU NCI NIH HHS [CA567902-01A2] NR 68 TC 64 Z9 67 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1994 VL 18 IS 2 BP 129 EP 138 DI 10.1007/BF01050419 PG 10 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA NT097 UT WOS:A1994NT09700006 PM 7964975 ER PT J AU ERICKSON, JD VAROQUI, H SCHAFER, MKH MODI, W DIEBLER, MF WEIHE, E RAND, J EIDEN, LE BONNER, TI USDIN, TB AF ERICKSON, JD VAROQUI, H SCHAFER, MKH MODI, W DIEBLER, MF WEIHE, E RAND, J EIDEN, LE BONNER, TI USDIN, TB TI IDENTIFICATION OF ME MAMMALIAN VESICULAR ACETYLCHOLINE TRANSPORTER AND TTS EXPRESSION FROM A CHOLINERGIC GENE LOCUS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. CNRS,DEPT NEUROCHIM,NEUROBIOL CELLULAIRE LAB,F-75700 PARIS,FRANCE. UNIV MAINZ,DEPT ANAT,W-6500 MAINZ,GERMANY. NCI,FREDERICK CANC RES FACIL,FREDERICK,MD 20797. OKLAHOMA MED RES FDN,PROGRAM MOLEC & CELL BIOL,OKLAHOMA CITY,OK 73104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S13 EP S13 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800052 ER PT J AU GOZES, I LILLING, G GLAZER, R TICHER, A ASHKENAZI, IE DAVIDSON, A RUBINRAUT, S FRIDKIN, M BRENNEMAN, DE AF GOZES, I LILLING, G GLAZER, R TICHER, A ASHKENAZI, IE DAVIDSON, A RUBINRAUT, S FRIDKIN, M BRENNEMAN, DE TI PHARMACOLOGICAL DISCRIMINATION OF MULTIPLE VIP RECEPTORS WITH SUPERACTIVE LIPOPHILIC PEPTIDES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 TEL AVIV UNIV,IL-69978 TEL AVIV,ISRAEL. WEIZMANN INST SCI,REHOVOT,ISRAEL. NICHHD,BETHESDA,MD. NR 5 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S10 EP S10 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800039 ER PT J AU GRESSENS, P HILL, JM GOZES, I FRIDKIN, M BRENNEMAN, DE AF GRESSENS, P HILL, JM GOZES, I FRIDKIN, M BRENNEMAN, DE TI PRENATAL ADMINISTRATION OF VIP ANTAGONIST PRODUCES SEVERE MICROCEPHALY SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD. TEL AVIV UNIV,IL-69978 TEL AVIV,ISRAEL. UNIV LOUVAIN,BRUSSELS,BELGIUM. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S10 EP S10 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800037 ER PT J AU KRIZBAI, I SZABO, G DELI, M MADERSPACH, K OLAH, Z LEHEL, C JOO, F AF KRIZBAI, I SZABO, G DELI, M MADERSPACH, K OLAH, Z LEHEL, C JOO, F TI PKC ISOFORMS IN CEREBRAL ENDOTHELIAL-CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 HUNGARIAN ACAD SCI,BIOL RES CTR,INST BIOPHYS,H-6701 SZEGED,HUNGARY. HUNGARIAN ACAD SCI,BIOL RES CTR,INST BIOCHEM,H-6701 SZEGED,HUNGARY. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S76 EP S76 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800302 ER PT J AU MAGER, S MIN, C HENRY, DJ CHAVKIN, C HOFFMAN, BJ DAVIDSON, N LESTER, H AF MAGER, S MIN, C HENRY, DJ CHAVKIN, C HOFFMAN, BJ DAVIDSON, N LESTER, H TI CONDUCTING STATES TRANSPORTER SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 CALTECH,DIV BIOL 15629,PASADENA,CA 91125. CALTECH,DIV ENGN & APPL SCI,PASADENA,CA 91125. UNIV WASHINGTON,DEPT PHARMACOL SJ30,SEATTLE,WA 98125. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S13 EP S13 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800049 ER PT J AU MANJI, HK CHEN, G SHIMON, H HSIAO, JK POTTER, WZ BELMAKER, RH AF MANJI, HK CHEN, G SHIMON, H HSIAO, JK POTTER, WZ BELMAKER, RH TI G-PROTEINS IN BIPOLAR AFFECTIVE-DISORDER - THE EFFECTS OF LONG-TERM LITHIUM TREATMENT SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD. BEN GURION UNIV NEGEV,BEER SHEVA,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S61 EP S61 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800242 ER PT J AU MINCGOLOMB, D YADID, G TSARFATY, I SCHWARTZ, JP AF MINCGOLOMB, D YADID, G TSARFATY, I SCHWARTZ, JP TI EXPRESSION OF INDUCIBLE NITRIC-OXIDE SYNTHASE IN CEREBELLAR NEURONS BOTH IN-VITRO AND IN-VIVO SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,CNB,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S34 EP S34 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800134 ER PT J AU PARADA, LF AF PARADA, LF TI TRK RECEPTORS AND NEUROTROPHINS IN-VIVO MODELS AND FUNCTIONAL ASSAYS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MOLEC EMBRYOL SECT,FREDERICK,MD 21702. RI Parada, luis/B-9400-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S16 EP S16 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800061 ER PT J AU REINER, O ALBRECHT, U CARROZZO, R WONG, C LEDBETTER, DH EICHELE, G BUCHBERG, AM CASKEY, CT AF REINER, O ALBRECHT, U CARROZZO, R WONG, C LEDBETTER, DH EICHELE, G BUCHBERG, AM CASKEY, CT TI LIS1, A GENE DELETED IN LISSENCEPHALY, A HUMAN NEURONAL MIGRATION DISORDER - GENE ISOLATION AND EXPRESSION SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 WEIZMANN INST SCI,DEPT MOLEC GENET & VIROL,IL-76100 REHOVOT,ISRAEL. BAYLOR COLL MED,HOUSTON,TX 77030. NIH,BETHESDA,MD 20892. THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,PHILADELPHIA,PA 19107. NR 0 TC 0 Z9 0 U1 2 U2 7 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S3 EP S3 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800012 ER PT J AU SHAPIRA, H WAY, J LIPINSKY, D ORON, Y BATTEY, JF AF SHAPIRA, H WAY, J LIPINSKY, D ORON, Y BATTEY, JF TI G(ALPHA-Q) DISCRIMINATES BETWEEN 2 BOMBESIN RECEPTOR SUBTYPES EXPRESSED IN XENOPUS-OOCYTES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 TEL AVIV UNIV,SACKLER FAC MED,DEPT PHYSIOL & PHARMACOL,IL-69978 TEL AVIV,ISRAEL. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BIOL CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S25 EP S25 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800097 ER PT J AU VAROQUI, H DIEBLER, MF MEUNIER, FM RAND, JB USDIN, TB BONNER, TI EIDEN, LE ERICKSON, JD AF VAROQUI, H DIEBLER, MF MEUNIER, FM RAND, JB USDIN, TB BONNER, TI EIDEN, LE ERICKSON, JD TI A TORPEDO ELECTRIC LOBE CDNA ENCODES A VESAMICOL BINDING-PROTEIN WHICH IS HOMOLOGOUS TO THE VESICULAR MONOAMINE TRANSPORTER SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 CNRS,DEPT NEUROCHIM,NEUROBIOL CELLULAIRE LAB,F-91190 GIF SUR YVETTE,FRANCE. OKLAHOMA MED RES FDN,PROGRAM MOLEC & CELL BIOL,OKLAHOMA CITY,OK 73104. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S12 EP S12 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800047 ER PT J AU VONAGOSTON, D SANTHA, E BRENNEMAN, DE MATSUMOTO, K DOBI, AL AF VONAGOSTON, D SANTHA, E BRENNEMAN, DE MATSUMOTO, K DOBI, AL TI GENE STRUCTURE AND THE MOLECULAR ESTABLISHMENT OF THE NEURONAL PHENOTYPE SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,LDN,BETHESDA,MD. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 63 SU 1 BP S18 EP S18 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NX468 UT WOS:A1994NX46800069 ER PT J AU FUHRMAN, S PALKOVITS, M CASSIDY, M NEALE, JH AF FUHRMAN, S PALKOVITS, M CASSIDY, M NEALE, JH TI THE REGIONAL DISTRIBUTION OF N-ACETYLASPARTYLGLUTAMATE (NAAG) AND PEPTIDASE ACTIVITY AGAINST NAAG IN THE RAT NERVOUS-SYSTEM SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE NEUROPEPTIDE; N-ACETYLASPARTYLGLUTAMATE; EXTRACELLULAR PEPTIDASE; MICROPUNCH TISSUE SAMPLES; RADIOIMMUNOASSAY; GLUTAMATE; N-ACETYLASPARTATE ID ASPARTYL-L-GLUTAMATE; ACIDIC DIPEPTIDASE ACTIVITY; RETINAL NEURONS; NMDA RECEPTORS; SPINAL-CORD; BRAIN; RELEASE; INVIVO; IMMUNOREACTIVITY; LOCALIZATION AB N-Acetylaspartylglutamate (NAAG), a prevalent peptide in the vertebrate nervous system, may be hydrolyzed by extracellular peptidase activity to produce glutamate and N-acetylaspartate. Hydrolysis can be viewed as both inactivating the peptide after synaptic release and increasing synaptic levels of ambient glutamate. To test the hypothesis that NAAG and the peptidase activity that hydrolyzes it coexist as a unique, two-stage system of chemical neurotransmission, 50 discrete regions of the rat CNS were microdissected for assay. In each microregion, the concentration of NAAG was determined by radioimmunoassay and the peptidase activity was assayed using tritiated peptide as substrate. The NAAG concentration ranged from 2.4 nmol/mg of soluble protein in median eminence to 64 in thoracic spinal cord. Peptidase activity against NAAG ranged from 54 pmol of glutamate produced per milligram of membrane protein per minute in median eminence to 148 in superior colliculus. A linear relationship was observed between NAAG peptidase and NAAG concentration in 46 of the 50 areas, with a slope of 2.26 and a correlation coefficient of 0.45. These data support the hypothesis that hydrolysis of NAAG to glutamate and N-acetylaspartate is a consistent aspect of the physiology and metabolism of this peptide after synaptic release. The ratio of peptide concentration to peptidase activity was >0.3 in the following four areas: ventrolateral medulla and reticular formation where the peptide is concentrated in axons of passage, thoracic spinal cord, where NAAG is concentrated in ascending sensory tracts as well as motoneuron cell bodies, and ventroposterior thalamic nucleus. C1 GEORGETOWN UNIV,DEPT BIOL,WASHINGTON,DC 20057. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RI Palkovits, Miklos/F-2707-2013; OI Palkovits, Miklos/0000-0003-0578-0387 FU NIDA NIH HHS [NIDA DA 02297] NR 41 TC 66 Z9 66 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1994 VL 62 IS 1 BP 275 EP 281 PG 7 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MM536 UT WOS:A1994MM53600032 PM 8263527 ER PT J AU DHARIWAL, KR SHIRVAN, MH LEVINE, M AF DHARIWAL, KR SHIRVAN, MH LEVINE, M TI ROLE OF MG-ATP IN NOREPINEPHRINE BIOSYNTHESIS IN INTACT CHROMAFFIN GRANULES SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE NOREPINEPHRINE; CHROMAFFIN GRANULES; DOPAMINE BETA-MONOOXYGENASE; MG-ATP ID DOPAMINE BETA-MONOOXYGENASE; CELL-VOLUME REGULATION; ASCORBIC-ACID; ELECTRON-TRANSFER; ADRENAL-MEDULLA; ADENOSINE-TRIPHOSPHATASE; MYCOPLASMA-GALLISEPTICUM; N-ETHYLMALEIMIDE; INSITU KINETICS; MEMBRANE AB Dopamine beta-monooxygenase converts dopamine to norepinephrine in intact chromaffin granules using intragranular ascorbic acid as a cosubstrate. Mg-ATP with external ascorbic acid is required for maximal norepinephrine biosynthesis. Mechanisms to explain these requirements were investigated specifically using intact granules. The effect of Mg-ATP was independent of membrane potential (Delta Psi) because norepinephrine biosynthesis was unchanged whether Delta Psi was positive or collapsed. Furthermore, the effect of Mg-ATP was independent of absolute intragranular and extragranular pH as well as the pH difference across the chromaffin granule membrane (Delta pH). Nevertheless, norepinephrine biosynthesis was inhibited by N-ethylmaleimide, 4-chloro-7-nitrobenzofurazane, and N,N-dicyclohexylcarbodiimide, specific inhibitors of the secretory vesicle ATPase that may directly affect proton pumping. Biosynthesis occurred normally with other ATPase inhibitors that do not inhibit the ATPase in secretory vesicles. The data indicate that the effect of Mg-ATP with ascorbic acid is mediated by the granule membrane ATPase but independent of maintaining Delta Psi and Delta pH. An explanation of these findings is that Mg-ATP, via the granule ATPase, may change the rate at which protons or dopamine are made available to dopamine beta-monooxygenase. C1 NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892. NR 35 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1994 VL 62 IS 1 BP 355 EP 360 PG 6 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MM536 UT WOS:A1994MM53600043 PM 8263536 ER PT J AU CADET, JL SHENG, PL ALI, S ROTHMAN, R CARLSON, E EPSTEIN, C AF CADET, JL SHENG, PL ALI, S ROTHMAN, R CARLSON, E EPSTEIN, C TI ATTENUATION OF METHAMPHETAMINE-INDUCED NEUROTOXICITY IN COPPER/ZINC SUPEROXIDE-DISMUTASE TRANSGENIC MICE SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE TRANSGENIC MICE; SUPEROXIDE DISMUTASE; METHAMPHETAMINE; NEUROTOXICITY; FREE RADICALS; FRONTAL CORTEX; STRIATUM; DOPAMINE; SEROTONIN ID TYROSINE-HYDROXYLASE ACTIVITY; RAT-BRAIN; DOPAMINE; 6-HYDROXYDOPAMINE; TOXICITY AB Administration of methamphetamine (METH) to rats and nonhuman primates causes loss of terminals in the nigrostriatal dopaminergic system. The mechanism by which METH causes its neurotoxicity is not known. To evaluate further the role of oxyradicals in METH-induced neurotoxicity, we have tested its effects in CuZn superoxide dismutase (SOD) transgenic (Tg) mice, which express the human CuZnSOD gene. In non-Tg mice, acute METH administration causes significant decreases in levels of dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the striata and cortices of non-Tg mice. In contrast, there were no significant decreases in cortical or striatal DA in the SOD-Tg mice. The effects of METH on DOPAC were also attenuated in both structures of these SOD-Tg mice. Chronic METH administration caused decreases in levels of striatal DA and DOPAC in the non-Tg mice, whereas the SOD-Tg mice were not affected. These results suggest that METH-induced dopaminergic toxicity in mice may be secondary to increased production of reactive oxygen species such as the superoxide radical. C1 NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,BALTIMORE,MD 21224. NATL CTR TOXICOL RES,DIV NEUROTOXICOL,JEFFERSON,AR 72079. UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. RP CADET, JL (reprint author), NIDA,ADDICT RES CTR,MOLEC NEUROPSYCHIAT SECT,POB 5180,BALTIMORE,MD 21224, USA. FU NIA NIH HHS [AG-09838] NR 24 TC 223 Z9 224 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1994 VL 62 IS 1 BP 380 EP 383 PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MM536 UT WOS:A1994MM53600048 PM 7505315 ER PT J AU ADACHI, K CRUZ, NF SOKOLOFF, L DIENEL, GA AF ADACHI, K CRUZ, NF SOKOLOFF, L DIENEL, GA TI LOSS OF LABELED METABOLITES OF [6-C-14]GLUCOSE FROM BRAIN DURING SPREADING CORTICAL DEPRESSION SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract ID GLUCOSE C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S99 EP S99 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900392 ER PT J AU CHANG, MCJ GRANGE, E BELL, JM ALLEN, DD RAPOPORT, SI AF CHANG, MCJ GRANGE, E BELL, JM ALLEN, DD RAPOPORT, SI TI EFFECT OF CHRONIC LITHIUM TREATMENT OF INCORPORATION OF FATTY-ACIDS INTO BRAIN SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S74 EP S74 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900293 ER PT J AU DACUNHA, A NESKOVIC, N PINE, PS VITKOVIC, L AF DACUNHA, A NESKOVIC, N PINE, PS VITKOVIC, L TI POTENTIAL ROLE OF GAP-43 IN MEMBRANE SYNTHESIS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 CTR NEUROCHIM,F-67084 STRASBOURG,FRANCE. US FDA,WASHINGTON,DC 20204. NIMH,DIV NEUROSCI & BEHAV SCI,ROCKVILLE,MD 20857. RP DACUNHA, A (reprint author), NIMH,CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S66 EP S66 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900260 ER PT J AU DIENEL, GA TOFELGREHL, B CRUZ, CC LULUDIS, K PETTIGREW, K SOKOLOFF, L GIBSON, GE AF DIENEL, GA TOFELGREHL, B CRUZ, CC LULUDIS, K PETTIGREW, K SOKOLOFF, L GIBSON, GE TI ASSAY OF LOCAL-RATES OF CA-45 INFLUX INTO BRAIN BY QUANTITATIVE AUTORADIOGRAPHY - INFLUENCE OF AGING SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NIMH,DESR,BETHESDA,MD 20892. CORNELL UNIV,COLL MED,BURKE MED RES INST,WHITE PLAINS,NY 10605. RI Cruz, Celia/K-3977-2013 OI Cruz, Celia/0000-0001-8922-5713 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S102 EP S102 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900405 ER PT J AU DRISCOLL, BF DEIBLER, GE LAW, MJ AF DRISCOLL, BF DEIBLER, GE LAW, MJ TI POTASSIUM, CELL-DAMAGE AND GLUTAMATE PRODUCTION SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S48 EP S48 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900189 ER PT J AU GRANGE, E PURDON, D RAPOPORT, SI AF GRANGE, E PURDON, D RAPOPORT, SI TI INCORPORATION OF PLASMA [3H]PALMITATE INTO BRAIN ACYL-COA SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S75 EP S75 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900298 ER PT J AU HITRI, A CASANOVA, MF DEUTSCH, SI WYATT, RJ GABAY, S AF HITRI, A CASANOVA, MF DEUTSCH, SI WYATT, RJ GABAY, S TI EFFECTS OF MATURATION OF THE DOPAMINE TRANSPORTER SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 DVAMC,WASHINGTON,DC 20422. NIMH,NPB,BETHESDA,MD 20892. NIDA,WASHINGTON,DC 20422. NIMH,CBDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S16 EP S16 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900061 ER PT J AU JONES, CR ARAI, T BELL, J RAPOPORT, SI DEGEORGE, JJ AF JONES, CR ARAI, T BELL, J RAPOPORT, SI DEGEORGE, JJ TI ARECOLINE STIMULATED INCORPORATION OF INTRAVENOUSLY ADMINISTERED H-3 ARACHIDONIC-ACID INTO RAT-BRAIN SUBCELLULAR-FRACTIONS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S74 EP S74 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900295 ER PT J AU LACORAZZA, HD JENDOUBI, M AF LACORAZZA, HD JENDOUBI, M TI BETA-HEXOSAMINIDASE ALPHA-SUBUNIT GENE-TRANSFER INTO MULTIPOTENT NEURAL CELL-LINES - SUCCESSFUL ENGRAFTING INTO RAT-BRAIN SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S51 EP S51 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900202 ER PT J AU MESSING, A KIM, SJ GALBREATH, EJ BRENNER, M AF MESSING, A KIM, SJ GALBREATH, EJ BRENNER, M TI GFAP-TGF-BETA-1 TRANSGENIC MICE DEVELOP HYDROCEPHALUS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI 53706. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S11 EP S11 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900042 ER PT J AU MOLLER, JR SASAKI, M LOVELL, KL AF MOLLER, JR SASAKI, M LOVELL, KL TI MESSENGER-RNA LEVELS OF MBP, PLP AND MAG IN CAPRINE BETA-MANNOSIDOSIS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,LMCN,DEMYELINATING DISORDERS UNIT,BETHESDA,MD 20892. MICHIGAN STATE UNIV,DEPT PATHOL,E LANSING,MI 48824. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S4 EP S4 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900016 ER PT J AU PURDON, AD JONES, C SMITH, QR RAPOPORT, SI AF PURDON, AD JONES, C SMITH, QR RAPOPORT, SI TI ISOLATION OF ACYL-COA FROM RAT-BRAIN SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S75 EP S75 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900299 ER PT J AU SHETTY, HU PURDON, AD RAPOPORT, SI AF SHETTY, HU PURDON, AD RAPOPORT, SI TI ARACHIDONATE MOLECULAR-SPECIES OF RAT-BRAIN PC AND PI SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S75 EP S75 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900296 ER PT J AU SMITH, CB SUN, Y DEIBLER, GE AF SMITH, CB SUN, Y DEIBLER, GE TI EFFECTS OF AGING ON LEUCINE RECYCLING IN PROTEIN-PRECURSOR POOL SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract ID DEGRADATION; RATES C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 3 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S108 EP S108 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900428 ER PT J AU STOLL, J AF STOLL, J TI REDUCED NUMBER OF VOLTAGE-DEPENDENT SODIUM-CHANNELS IN CULTURED MOUSE TRISOMY-16 HIPPOCAMPAL-NEURONS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S103 EP S103 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900408 ER PT J AU TANIWAKI, T BECERRA, SP CHADER, GJ SCHWARTZ, JP AF TANIWAKI, T BECERRA, SP CHADER, GJ SCHWARTZ, JP TI NEUROTROPHIC EFFECTS OF PIGMENT EPITHELIUM-DERIVED FACTOR ON CEREBELLAR GRANULE CELLS IN CULTURE SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,CLIN NEUROSCI CLIN,BETHESDA,MD 20892. NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S13 EP S13 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900050 ER PT J AU TZENG, SF DEIBLER, GE DEVRIES, GH AF TZENG, SF DEIBLER, GE DEVRIES, GH TI MBP INTERACTS WITH GANGLIOSIDE GM1 AND FGF RECEPTOR TO CAUSE SCHWANN-CELL PROLIFERATION SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RP TZENG, SF (reprint author), VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S6 EP S6 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900022 ER PT J AU WILLIAMS, WM CHANG, MCJ RAPOPORT, SI AF WILLIAMS, WM CHANG, MCJ RAPOPORT, SI TI INCORPORATION OF RADIOLABELED FATTY-ACID INTO RAT-BRAIN MICROVESSELS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S18 EP S18 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900069 ER PT J AU YANG, XJ KAUFMAN, S AF YANG, XJ KAUFMAN, S TI DELETION MUTAGENESIS ANALYSIS OF HUMAN BRAIN TRYPTOPHAN-HYDROXYLASE EXPRESSED IN ESCHERICHIA-COLI SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,NEUROCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S96 EP S96 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900382 ER PT J AU BEHAR, TN SCHAFFNER, AE COLTON, CA SOMOGYI, R OLAH, Z LEHEL, C BARKER, JL AF BEHAR, TN SCHAFFNER, AE COLTON, CA SOMOGYI, R OLAH, Z LEHEL, C BARKER, JL TI GABA-INDUCED CHEMOKINESIS AND NGF-INDUCED CHEMOTAXIS OF EMBRYONIC SPINAL-CORD NEURONS SO JOURNAL OF NEUROSCIENCE LA English DT Article DE MIGRATION; DEVELOPMENT; CNS; CHEMOATTRACTANT; MOTILITY; RAT ID NERVE GROWTH-FACTOR; TRK PROTOONCOGENE PRODUCT; TYROSINE KINASE; FACTOR RECEPTOR; CELL-MIGRATION; RAT-BRAIN; BINDING; SYSTEM; IMMUNOREACTIVITY; EXPRESSION AB During CNS development, neuroblasts proliferate within germinal zones of the neuroepithelium, and then migrate to their final positions. Although many neurons are thought to migrate along processes of radial glial fibers, increasing evidence suggests environmental factors also influence nerve cell movement. Extracellular matrix molecules are thought to be involved in guiding neuronal migration, and molecules such as NGF and GABA exert trophic effects on immature neurons. The nature of the signals that initiate and direct neuroblast migration, however, is unknown. In vitro, NGF and GABA promote neurite outgrowth from cultured cells, and NGF induces axonal chemotaxis (directed migration along a chemical gradient). At earlier developmental stages, these molecules could influence neuroblast movement. Therefore, we investigated whether these molecules induce embryonic neuronal migration. Using an in vitro microchemotaxis assay, we show that rat embryonic spinal cord neurons migrate toward picomolar NGF and femtomolar GABA beginning at embryonic day 13 (E13). Cells exhibit chemotactic responses to NGF while GABA stimulates chemokinesis (increased random movement). GABA effects are mimicked by muscimol and inhibited by bicuculline and picrotoxin, suggesting GABA motility signals are mediated by GABA receptor proteins. Expression of GABA receptors by embryonic cord cells has been previously reported (Mandler et al., 1990; Walton et al., 1993). We used polymerase chain reaction analysis to demonstrate the presence of NGF and trk mRNA in E13 and E14 cord cells, indicating the cells express message for both NGF and high-affinity NGF receptors. Immunohistochemistry of E13 spinal cord sections indicates that NGF and GABA colocalize in fibers close to the target destinations of migrating neurons, suggesting diffusible gradients of these molecules provide chemoattractant signals to migratory cells. Thus, in vitro, neuroblast migration is induced by specific signaling molecules that are present in the developing spinal cord, and may stimulate migration of embryonic neurons prior to synaptogenesis. C1 GEORGETOWN UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,WASHINGTON,DC 20007. NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. RP BEHAR, TN (reprint author), NINCDS,NEUROPHYSIOL LAB,BLDG 36,ROOM 2C02,BETHESDA,MD 20892, USA. NR 44 TC 151 Z9 151 U1 0 U2 3 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD JAN PY 1994 VL 14 IS 1 BP 29 EP 38 PG 10 WC Neurosciences SC Neurosciences & Neurology GA MQ118 UT WOS:A1994MQ11800004 PM 8283236 ER PT J AU NIKODIJEVIC, B NIKODIJEVICKEDEVA, D OSHIMA, M PAIGE, B GUROFF, G AF NIKODIJEVIC, B NIKODIJEVICKEDEVA, D OSHIMA, M PAIGE, B GUROFF, G TI THE LONG-TERM DOWN-REGULATION OF DIHYDROPYRIDINE RECEPTORS BY BAY K-8644 IN PC12 CELLS SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE PC12; BAY K 8644; CALCIUM; DIHYDROPYRIDINE ID CALCIUM CHANNELS; CA-2+ CHANNELS; INCREASE; BINDING; K-8644 AB Treatment of PC12 cells with Bay K 8644 for 12 hr or more leads to an almost 80% decrease in the subsequent ability of Bay K 8644 to stimulate the uptake of radioactive calcium into the cells. This effect is a property of the S(-)isomer of Bay K 8644; pre-treatment with the R(+)isomer, now known to be a calcium channel blocker, has the opposite effect. This treatment is specific in that it does not interfere with the stimulation of calcium uptake by potassium, ATP, or nerve growth factor. Such treatment is accompanied by a 90% decrease in the ability of Bay K 8644 to stimulate the release of norepinephrine. The characteristics of the binding of [H-3]isradipine to control and to treated cells indicates that the decrease in the effect of dihydropyridines is accompanied by a marked decrease in the number of dihydropyridine binding sites with no apparent change in the affinity of the remaining sites. The continued ability of depolarizing levels of potassium to stimulate calcium uptake and the induction of the protooncogene c-fos in Bay K 8644-treated cells indicates that the L-type calcium channels are still intact, but are simply unresponsive to dihydropyridine agonists. (C) 1994 Wiley-Liss, Inc.* C1 NICHHD,GROWTH FACTORS SECT,BETHESDA,MD 20892. NR 21 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 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD JAN 1 PY 1994 VL 37 IS 1 BP 71 EP 82 DI 10.1002/jnr.490370110 PG 12 WC Neurosciences SC Neurosciences & Neurology GA MR524 UT WOS:A1994MR52400008 PM 7511705 ER PT J AU ZHOU, R COPELAND, TD KROMER, LF SCHULZ, NT AF ZHOU, R COPELAND, TD KROMER, LF SCHULZ, NT TI ISOLATION AND CHARACTERIZATION OF BSK, A GROWTH-FACTOR RECEPTOR-LIKE TYROSINE KINASE ASSOCIATED WITH THE LIMBIC SYSTEM SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Note DE BRAIN-SPECIFIC KINASE; PROTEIN TYROSINE KINASE; HIPPOCAMPUS; IN SITU HYBRIDIZATION ID NEUROTROPHIC FACTOR PREVENTS; FACTOR PROMOTES SURVIVAL; NERVOUS-SYSTEM; CHOLINERGIC NEURONS; MOLECULAR-CLONING; MOTOR NEURONS; BRAIN; GENE; FAMILY; EXPRESSION AB Neuronal degeneration has been shown to be involved in various neurological disorders. Growth/trophic factors and their receptors are known to be important for the regeneration and survival of neurons. We report here the molecular cloning of a receptor-like protein tyrosine kinase, bsk, (for brain specific kinase). Bsk is highly related to the eph/elk receptorlike kinase family members. Northern blot analysis shows that it is expressed specifically in the brain, with no expression detected in adult heart, spleen, lung, liver, skeletal muscle, and kidney. In situ hybridization analysis of adult mouse brain sections indicates that bsk is expressed at high levels in the hippocampus, tenia tecta, indusium griseum, and the piriform cortex, major components of the limbic system that are important for learning and memory. In addition, elevated levels of expression are found in other areas of the limbic system such as the amygdala, medial septum, and nucleus of the diagonal band, and in the olfactory bulb, which has close connections to the limbic system. The highest level of expression is found in the CA3 region of the hippocampus and the pyramidal cell layer of the piriform cortex. In 16.5 day mouse embryos, bsk is expressed predominantly in the primordial cortex of the telencephalon. An antibody against a C-terminal peptide of bsk recognized a 105 kD protein in the 16.5 day embryonic head extract. Our analysis shows that bsk is a growth factor receptor-like protein tyrosine kinase and that its greatest expression in the adult brain is associated with components of the limbic system. (C) 1994 Wiley-Liss, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,FREDERICK,MD. GEORGETOWN UNIV,SCH MED,DEPT ANAT & CELL BIOL,WASHINGTON,DC 20007. RP ZHOU, R (reprint author), RUTGERS STATE UNIV,COLL PHARM,DEPT CHEM BIOL,CANC RES LAB,PISCATAWAY,NJ 08855, USA. FU NCI NIH HHS [N01-CO-74101] NR 48 TC 62 Z9 65 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD JAN 1 PY 1994 VL 37 IS 1 BP 129 EP 143 DI 10.1002/jnr.490370117 PG 15 WC Neurosciences SC Neurosciences & Neurology GA MR524 UT WOS:A1994MR52400015 PM 8145300 ER PT J AU OLDFIELD, EH MURASZKO, K SHAWKER, TH PATRONAS, NJ AF OLDFIELD, EH MURASZKO, K SHAWKER, TH PATRONAS, NJ TI PATHOPHYSIOLOGY OF SYRINGOMYELIA ASSOCIATED WITH CHIARI I MALFORMATION OF THE CEREBELLAR TONSILS - IMPLICATIONS FOR DIAGNOSIS AND TREATMENT SO JOURNAL OF NEUROSURGERY LA English DT Article DE SYRINGOMYELIA; CHIARI MALFORMATION; CEREBROSPINAL FLUID; INTRAOPERATIVE ULTRASONOGRAPHY; MAGNETIC RESONANCE IMAGING ID MAGNETIC-RESONANCE; THECOPERITONEAL SHUNT; SURGICAL-TREATMENT; SPINAL-CORD; CSF FLOW; CINE MR; PATHOGENESIS; HYDROMYELIA; EXPERIENCE; ADULTS AB The mechanisms previously proposed for the progression of syringomyelia associated with Chiari I malformation of the cerebellar tonsils are controversial, leave many clinical observations unexplained, and underlie the prevalence of different operations currently used as initial treatment. To explore the mechanism of syringomyelia progression in this setting, the authors used anatomical and dynamic (phase-contrast and phase-contrast cine) magnetic resonance (MR) imaging, and intraoperative ultrasonography to examine the anatomy and dynamics of movement of the cerebellar tonsils, the wall of the spinal cord surrounding the syrinx, and the movement of cerebrospinal fluid (CSF) and syrinx fluid at rest, during the respiratory and cardiac cycles, and during Valsalva maneuver in seven affected patients. In all patients the cerebellar tonsils occluded the subarachnoid space at the level of the foramen magnum. Syringomyelia extended from the cervical to the lower thoracic segment of the spinal cord. No patient had evidence of a patent communication between the fourth ventricle and the syrinx on anatomical MR images, dynamic MR images, or intraoperative ultrasound studies. Dynamic MR images of three patients revealed abrupt downward movement of the spinal CSF and the syrinx fluid during systole and upward movement during diastole, but limited movement of CSF across the foramen magnum during the cardiac cycle. Intraoperative ultrasound studies demonstrated abrupt downward movement of the cerebellar tonsils during systole that was synchronous with sudden constriction of the spinal cord and syrinx. Decompression of the foramen magnum was achieved via suboccipital craniectomy, laminectomy of C-1 and C-2, and dural grafting, leaving the arachnoid intact. Immediately after surgery, the pulsatile downward thrust of the tonsils and constriction of the spinal cord and syrinx disappeared. Syringomyelia resolved within 1 to 6 months after surgery in all patients. Observations by the authors suggest the following previously unrecognized mechanism for progression of syringomyelia associated with occlusion of the subarachnoid space at the foramen magnum. The brain expands as it fills with blood during systole, imparting a systolic pressure wave to the intracranial CSF that is accommodated in normal subjects by sudden movement of CSF from the basal cisterns to the upper portion of the spinal canal. With obstruction to rapid movement of CSF at the foramen magnum, the cerebellar tonsils, which plug the subarachnoid space posteriorly, move downward with each systolic pulse, acting as a piston on the partially isolated spinal CSF and producing a systolic pressure wave in the spinal CSF that acts on the surface of the spinal cord. This causes progression of syringomyelia by abruptly compressing the cord and propelling the fluid in the syrinx longitudinally with each pulse, and may be responsible for the origin and maintenance of syringomyelia by the pulsatile pressure waves forcing CSF into the cord through the perivascular and interstitial spaces. Effective treatment occurs when the systolic pressure wave transmitted by the cerebellar tonsils is eliminated by relieving the obstruction to rapid movement of subarachnoid CSF across the foramen magnum. The presence of this mechanism can be detected preoperatively on dynamic MR images and during surgery on ultrasound studies by the pulsatile excursion of the wall of the spinal cord surrounding the syrinx and by its immediate disappearance and the expansion of the syrinx during forced inspiration after decompression of the tonsils. Effective treatment is achieved with bone and dural decompression of the foramen magnum alone, without entering the arachnoid. C1 UNIV MICHIGAN,DEPT SURG,NEUROSURG SECT,ANN ARBOR,MI 48109. NIH,CTR CLIN,DEPT DIAGNOST RADIOL,BETHESDA,MD. RP OLDFIELD, EH (reprint author), NINCDS,SURG NEUROL BRANCH,BLDG 10,ROOM 5D37,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 67 TC 451 Z9 475 U1 0 U2 18 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD JAN PY 1994 VL 80 IS 1 BP 3 EP 15 DI 10.3171/jns.1994.80.1.0003 PG 13 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA MQ154 UT WOS:A1994MQ15400001 PM 8271018 ER PT J AU RAM, Z NIEMAN, LK CUTLER, GB CHROUSOS, GP DOPPMAN, JL OLDFIELD, EH AF RAM, Z NIEMAN, LK CUTLER, GB CHROUSOS, GP DOPPMAN, JL OLDFIELD, EH TI EARLY REPEAT SURGERY FOR PERSISTENT CUSHINGS-DISEASE SO JOURNAL OF NEUROSURGERY LA English DT Article DE CUSHINGS DISEASE; PITUITARY ADENOMA; TRANSSPHENOIDAL SURGERY ID CORTICOTROPIN-RELEASING HORMONE; TRANS-SPHENOIDAL SURGERY; PITUITARY-ADENOMAS; DIFFERENTIAL-DIAGNOSIS; STIMULATION TEST; IRRADIATION; MICROSURGERY; MANAGEMENT AB The potential efficacy of early repeat transsphenoidal surgery for persistent Cushing's disease has not previously been examined. On 222 patients with no prior pituitary treatment and a preoperative diagnosis of Cushing's disease, 29 (13%) remained hypercortisolemic after an initial transsphenoidal pituitary exploration. Seventeen of these 29 patients underwent further surgery 7 to 46 days after the initial transsphenoidal approach in order to completely excise suspected residual tumor. Patients were followed for 4 to 84 months (mean +/- standard deviation, 34 +/- 25 months) to document sustained remission or recurrence of Cushing's disease (a urine free cortisol level > 90 mu g/day was considered evidence of recurrence). Of the 17 patients with repeat surgery, 12 (71%) had resolution of hypercortisolism (morning plasma cortisol level < 5 mu g/dl); however, in three of these 12, hypercortisolism recurred 5, 12, and 24 months later. In 14 patients a lesion that appeared to be a tumor was identified during the initial procedure or on histological examination. Of these, 12 had immediate resolution of hypercortisolism and nine are still in remission. Three patients, in whom no adenoma could be identified during the initial surgery or an examination of the partial hypophysectomy specimen from the initial surgery, had persistent Cushing's syndrome after the second operation. Seven (41%) of the 17 patients developed hypopituitarism requiring treatment with thyroid hormone, gonadal steroid, or vasopressin replacement. The low incidence of identification of an adenoma on computerized tomography or magnetic resonance images (three of 17 patients), the failure to find a corticotrophic adenoma during the initial surgery (10 of 17 patients), and the failure of these 17 patients to respond to the initial transsphenoidal surgery suggest that they may comprise a subset of patients who are more difficult to treat successfully with surgery than most patients with Cushing's disease. Despite that, early reoperation induced immediate remission of hypercortisolism in 71% of cases, but did so at the expense of a high risk of hypopituitarism. However, since the alternative treatments (such as radiation therapy, long-term drug therapy, or bilateral adrenalectomy) also have potential adverse effects, early reoperation deserves consideration for the management of persistent Cushing's disease, especially when an adrenocorticotrophic hormone-secreting adenoma was partially excised during the first surgery. C1 NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. NICHHD,CTR CLIN,DEPT DIAGNOST RADIOL,BETHESDA,MD. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NR 28 TC 122 Z9 124 U1 0 U2 2 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD JAN PY 1994 VL 80 IS 1 BP 37 EP 45 DI 10.3171/jns.1994.80.1.0037 PG 9 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA MQ154 UT WOS:A1994MQ15400006 PM 8271020 ER PT J AU KIPPENHAN, JS BARKER, WW NAGEL, J GRADY, C DUARA, R AF KIPPENHAN, JS BARKER, WW NAGEL, J GRADY, C DUARA, R TI NEURAL-NETWORK CLASSIFICATION OF NORMAL AND ALZHEIMERS-DISEASE SUBJECTS USING HIGH-RESOLUTION AND LOW-RESOLUTION PET CAMERAS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE NEURAL NETWORK; ALZHEIMERS DISEASE; FLUORODEOXYGLUCOSE ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL GLUCOSE-METABOLISM; DEMENTIA; SCAN AB Neural-network classification methods were applied to studies of FDG-PET images of the brain acquired from a total of 77 ''probable'' Alzheimer's disease and 124 normal subjects at two different centers. Methods: Classification performances, as determined by relative-operating-characteristic (ROC) analyses of cross-validation experiments, were measured for FDG PET images obtained with either a 15-mm FWHM PETT V or a 6-mm FWHM Scanditronix PC-1024-78 camera for various methods of data representation. Neural networks were trained to distinguish between normal and abnormal subjects on the basis of regional metabolic patterns. For both databases, classification performance could be improved by increasing the ''resolution'' of the representation (decreasing the region size) and by normalizing the regional metabolic Values to the value of a reference region (occipital region). Results: The optimal classification performance for Scanditronix data (ROC area = 0.95) was higher than that for PETT V data (ROC area = 0.87). Under Bayesian theory, the classification performance with Scanditronix data corresponded to an ability to change a pre-test probability of disease of 50% to a post-test probability of either 90% for a positive classification or 10% for a negative classification. Conclusion: This classification can be used to either strongly confirm or rule out the presence of abnormalities. C1 UNIV MIAMI,DEPT BIOMED ENGN,CORAL GABLES,FL. UNIV MIAMI,DEPT RADIOL,CORAL GABLES,FL. UNIV MIAMI,DEPT NEUROL,CORAL GABLES,FL. NIA,NEUROSCI LAB,BETHESDA,MD 20892. RP KIPPENHAN, JS (reprint author), MT SINAI MED CTR,WIEN CTR,4300 ALTON RD,MIAMI BEACH,FL 33140, USA. NR 32 TC 36 Z9 36 U1 0 U2 1 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JAN PY 1994 VL 35 IS 1 BP 7 EP 15 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MW249 UT WOS:A1994MW24900010 PM 8271062 ER PT J AU ABRAMS, SA YERGEY, AL SCHANLER, RJ VIEIRA, NE WELCH, TR AF ABRAMS, SA YERGEY, AL SCHANLER, RJ VIEIRA, NE WELCH, TR TI HYPERCALCIURIA IN PREMATURE-INFANTS RECEIVING HIGH MINERAL-CONTAINING DIETS SO JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION LA English DT Article DE CALCIUM ABSORPTION; URINARY CALCIUM; PREMATURE INFANTS; MINERAL BALANCE ID BIRTH-WEIGHT INFANTS; URINARY CALCIUM EXCRETION; HUMAN-MILK; MOTHERS MILK; NUTRITIONAL BALANCE; FORMULA; PHOSPHORUS; SUPPLEMENTATION; ABSORPTION; RETENTION AB We evaluated urinary calcium excretion in 21 premature infants fed either a formula containing high concentrations of calcium (Ca) and phosphorus (P) or human milk fortified with a commercially available human milk fortifier. Dual-tracer stable-isotope Ca absorption studies were performed on all infants. Urinary Ca excretion was not significantly related to Ca or P intake or true Ca absorption. The recovery of the orally administered tracer in the urine was used to evaluate the source of calciuria in study subjects. In almost all subjects, tissue derived (V-bu), rather than diet-derived (V-ou), Ca was the principal source of urinary Ca. Hypercalciuric subjects demonstrated greater V-bu and V-ou than nonhypercalciuric subjects. Our data demonstrate that moderate hypercalciuria is common in premature infants whose diets are high in mineral content and that hypercalciuria is not related to inadequate mineral intake or Ca absorption but is related, instead, to losses of both tissue and dietary Ca. C1 TEXAS CHILDRENS HOSP,HOUSTON,TX. NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. UNIV CINCINNATI,COLL MED,DEPT PEDIAT,CINCINNATI,OH. RP ABRAMS, SA (reprint author), BAYLOR COLL MED,CHILDRENS NUTR RES CTR,USDA ARS,DEPT PEDIAT,1100 BATES ST,HOUSTON,TX 77030, USA. OI Abrams, Steven/0000-0003-4972-9233 FU NCRR NIH HHS [M01-RR-01188] NR 26 TC 12 Z9 12 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-2116 J9 J PEDIATR GASTR NUTR JI J. Pediatr. Gastroenterol. Nutr. PD JAN PY 1994 VL 18 IS 1 BP 20 EP 24 DI 10.1097/00005176-199401000-00003 PG 5 WC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics SC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics GA MP534 UT WOS:A1994MP53400003 PM 8126613 ER PT J AU MAILLARD, MC NIKODIJEVIC, O LANOUE, KF BERKICH, D JI, XD BARTUS, R JACOBSON, KA AF MAILLARD, MC NIKODIJEVIC, O LANOUE, KF BERKICH, D JI, XD BARTUS, R JACOBSON, KA TI ADENOSINE RECEPTOR PRODRUGS - SYNTHESIS AND BIOLOGICAL-ACTIVITY OF DERIVATIVES OF POTENT, A(1)-SELECTIVE AGONISTS SO JOURNAL OF PHARMACEUTICAL SCIENCES LA English DT Article ID BRAIN; ANTAGONISTS; INHIBITION; MEMBRANES; SYSTEM AB 5'-Ester derivatives of the potent adenosine agonists N-6-[4-[[[[4-[[[(2-acetylaminoethyl) amino]carbonyl]methyl]anilino]carbonyl]methyl]phenyl]adenosine (N-AcADAC; 1) and N-6-cyclopentyladenosine (CPA; 2) were prepared as prodrugs. Both alkyl esters or carbonates (designed to enter the brain by virtue of increased lipophilicity) and 1,4-dihydro-1-methyl-3-[(pyridinylcarbonyl)oxy]esters designed to concentrate in the brain by virtue of a redox delivery system were synthesized. In the 5'-blocked form, the adenosine agonists displayed highly diminished affinity for rat brain A(1)-adenosine receptors in binding assays. The dihydropyridine prodrug 29 was active in an assay of locomotor depression in mice, in which adenosine agonists are highly depressant. The behavior depression was not reversible by peripheral administration of a non-central nervous system active adenosine antagonist. In an assay of the peripheral action of adenosine (i.e., the inhibition of lipolysis in rats), the parent compounds were highly potent and the dihydropyridine prodrug was much less potent. C1 PENN STATE UNIV,MILTON S HERSHEY MED CTR,HERSHEY,PA 17033. CORTEX PHARMACEUT INC,IRVINE,CA. RP MAILLARD, MC (reprint author), NIDDKD,MOLEC RECOGNIT SECT,BIOORGAN CHEM LAB,BLDG 8A,RM B1A-17,BETHESDA,MD 20892, USA. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999] NR 31 TC 16 Z9 16 U1 0 U2 1 PU AMER PHARMACEUTICAL ASSN PI WASHINGTON PA 2215 CONSTITUTION AVE NW, WASHINGTON, DC 20037 SN 0022-3549 J9 J PHARM SCI JI J. Pharm. Sci. PD JAN PY 1994 VL 83 IS 1 BP 46 EP 53 DI 10.1002/jps.2600830112 PG 8 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA MP535 UT WOS:A1994MP53500010 PM 8138909 ER PT J AU ABASSI, ZA KELLY, G GOLOMB, E KLEIN, H KEISER, HR AF ABASSI, ZA KELLY, G GOLOMB, E KLEIN, H KEISER, HR TI LOSARTAN IMPROVES THE NATRIURETIC RESPONSE TO ANF IN RATS WITH HIGH-OUTPUT HEART-FAILURE SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID CONVERTING-ENZYME-INHIBITION; ANGIOTENSIN-II; RENAL RESPONSES; SODIUM; PEPTIDE; DOGS; MECHANISM; PHARMACOLOGY; ACCUMULATION; ENDOTHELIN AB During severe congestive heart failure (CHF), a number of sodium-retaining and vasoconstricting mechanisms are activated, including the renin-angiotensin-aldosterone system. In CHF, the renal effects of atrial natriuretic factor (ANF) are attenuated. The interaction of these endocrine factors is a major determinant of the clinical course of CHF. This study was designed to evaluate the role of the renin-angiotensin-aldosterone system in the development of avid sodium retention in CHF, induced in rats by creation of an aorto-caval fistula. Rats with aorto-caval fistula either compensate and maintain a normal sodium balance (UNaV > 1400 mu Eq/day) or decompensate and develop severe sodium retention (UNaV < 200 mu Eq/day), which leads to severe CHF. Chronic treatment with losartan, an angiotensin II receptor blocker, 10 mg/day, resulted in dramatic natriuresis (UNaV > 1000 mu EQ/day) in decompensated rats, but not in compensated rats or controls. ANF infusion (50 mu g/kg/hr) increased fractional sodium excretion 46-fold in compensated rats, but only 18-fold in decompensated rats. A similar pattern of responsiveness to ANF was observed in urinary cyclic GMP excretion. Chronic losartan treatment restored the natriuretic and urinary cyclic GMP excretion responses of decompensated rats to ANF. The improvement in the natriuretic response after losartan treatment was associated with a suppression of the previously elevated plasma aldosterone. These results demonstrate the pivotal role of angiotensin II in the development of sodium retention and of the blunted renal response to ANF in CHF, and indicate why losartan is useful therapy for cardiac edema. RP ABASSI, ZA (reprint author), NHLBI,HYPERTENS ENDOCRINE BRANCH,BLDG 10,ROOM 8C103,BETHESDA,MD 20892, USA. NR 49 TC 33 Z9 33 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD JAN PY 1994 VL 268 IS 1 BP 224 EP 230 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY152 UT WOS:A1994MY15200033 PM 8301562 ER PT J AU RIEMANN, D HOHAGEN, F BAHRO, M LIS, S STADMULLER, G GANN, H BERGER, M AF RIEMANN, D HOHAGEN, F BAHRO, M LIS, S STADMULLER, G GANN, H BERGER, M TI CHOLINERGIC NEUROTRANSMISSION, REM-SLEEP AND DEPRESSION SO JOURNAL OF PSYCHOSOMATIC RESEARCH LA English DT Article ID ELECTROENCEPHALOGRAPHIC SLEEP; INDUCTION TEST; HEALTHY-SUBJECTS; EEG SLEEP; ALZHEIMERS-DISEASE; AGONIST RS-86; LATENCY; SCHIZOPHRENIA; AGE; METAANALYSIS AB It is known from animal experiments that the regulation of REM and Non-REM sleep is governed by cholinergic and serotonergic/adrenergic neurons in the brain stem. Cholinergic neurons in the gigantocellular field of the tegmentum seem to be responsible for the triggering and maintenance of REM sleep. These findings are of special interest for interpreting abnormalities of REM sleep in depression. Psychiatric sleep research in the last two decades has demonstrated that an early onset of REM sleep and heightened REM density frequently occurs in patients suffering from depression. Extrapolating from animal data on REM sleep regulation, the premature onset of REM sleep in depression may be interpreted as the consequence of a central nervous cholinergic overactivity or muscarinic supersensitivity. In our experimental work we have tested assumptions of the so-called reciprocal interaction model of NonREM and REM sleep by cholinergic/anticholinergic stimulation strategies of sleep in healthy subjects. Furthermore, the impact of cholinergic stimulation on sleep in depression, healthy control subjects and other psychopathological conditions was investigated. These studies demonstrated that the most pronounced REM sleep response to cholinergic stimulation occurred in depression. C1 NIMH,BETHESDA,MD 20892. CLIN BARMEN,DEPT NEUROL,WUPPERTAL,GERMANY. RP RIEMANN, D (reprint author), UNIV FREIBURG,PSYCHIAT CLIN,HAUPSTR 5,D-79104 FREIBURG,GERMANY. OI Riemann, Dieter/0000-0002-1968-6220; Lis, Stefanie/0000-0002-8051-2756 NR 49 TC 22 Z9 22 U1 4 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0022-3999 J9 J PSYCHOSOM RES JI J. Psychosomat. Res. PY 1994 VL 38 SU 1 BP 15 EP 25 DI 10.1016/0022-3999(94)90132-5 PG 11 WC Psychiatry SC Psychiatry GA PH237 UT WOS:A1994PH23700005 PM 7799246 ER PT J AU HAUSER, ST HUFFMAN, LC AF HAUSER, ST HUFFMAN, LC TI INTRODUCTION - AFFECTIVE PROCESSES IN ADOLESCENCE SO JOURNAL OF RESEARCH ON ADOLESCENCE LA English DT Article; Proceedings Paper CT Workshop on Affective Processes in Adolescence CY OCT 19-20, 1992 CL BETHESDA, MD SP NIMH AB This Special Issue represents a major product of a National Institute of Mental Health (NIMH) sponsored workshop, held October 19-20, 1992, in Bethesda, Maryland. Consistent with accelerating interest in the understanding of affective processes during the adolescent period, the Behavioral, Cognitive, and Social Processes Research Branch of NIMH generously supported several meetings to plan the workshop, the workshop itself, and the sustained subsequent efforts to transform the 2 days of talks and discussions into a coherent volume that could be distributed to our scientific colleagues. The major goal of the workshop, organized by Stuart Hauser and Lynne Huffman, was to explore multilevel approaches to research on affective processes during the adolescent period, including psychophysiological, behavioral, intrapsychic, interactional, and sociocultural perspectives. Experts and discussants were invited to discuss conceptual advances that might be facilitated by an integration and cross-fertilization of basic and clinical viewpoints. Workshop participants and observes were also encouraged of offer suggestions regarding critical future research questions. C1 NIMH,DIV NEUROSCI & BEHAV SCI,5600 FISHERS LANE,ROCKVILLE,MD 20857. HARVARD UNIV,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 1050-8392 J9 J RES ADOLESCENCE JI J. Res. Adolesc. PY 1994 VL 4 IS 4 BP 465 EP 467 DI 10.1207/s15327795jra0404_1 PG 3 WC Family Studies; Psychology, Developmental SC Family Studies; Psychology GA QL367 UT WOS:A1994QL36700001 ER PT J AU HUFFMAN, LC HAUSER, ST AF HUFFMAN, LC HAUSER, ST TI AFTERWORD - REFLECTIONS AND FUTURE-DIRECTIONS SO JOURNAL OF RESEARCH ON ADOLESCENCE LA English DT Article; Proceedings Paper CT Workshop on Affective Processes in Adolescence CY OCT 19-20, 1992 CL BETHESDA, MD SP NIMH AB The preceding articles reflect the continued and evolving interest of basic and clinical research scientists and the National Institute of Mental Health (NIMH) in the study of affective processes during the adolescent period. In this afterword, through drawing together a future research agenda, we integrate the contributions of the articles with the discussions among workshop participants that followed each presentation and continued throughout the 2-day workshop on affective processes in adolescence. C1 HARVARD UNIV,CAMBRIDGE,MA 02138. RP HUFFMAN, LC (reprint author), NIMH,DIV NEUROSCI & BEHAV SCI,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 3 TC 2 Z9 2 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 1050-8392 J9 J RES ADOLESCENCE JI J. Res. Adolesc. PY 1994 VL 4 IS 4 BP 657 EP 662 DI 10.1207/s15327795jra0404_13 PG 6 WC Family Studies; Psychology, Developmental SC Family Studies; Psychology GA QL367 UT WOS:A1994QL36700013 ER PT J AU GHARAVI, AE SAMMARITANO, LR WEN, JY MIYAWAKI, N MORSE, JH ZARRABI, MH LOCKSHIN, MD AF GHARAVI, AE SAMMARITANO, LR WEN, JY MIYAWAKI, N MORSE, JH ZARRABI, MH LOCKSHIN, MD TI CHARACTERISTICS OF HUMAN-IMMUNODEFICIENCY-VIRUS AND CHLORPROMAZINE-INDUCED ANTIPHOSPHOLIPID ANTIBODIES - EFFECT OF BETA(2), GLYCOPROTEIN-I ON BINDING TO PHOSPHOLIPID SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE ANTIPHOSPHOLIPID ANTIBODY; HUMAN IMMUNODEFICIENCY VIRUS; SYPHILIS; LUPUS ANTICOAGULANT; SYSTEMIC LUPUS ERYTHEMATOSUS; CHLORPROMAZINE ID ANTICARDIOLIPIN ANTIBODIES; LUPUS-ERYTHEMATOSUS; AUTOIMMUNE-DISEASE; APOLIPOPROTEIN-H; ANTICOAGULANT; COAGULATION; THROMBOSIS; INFECTION; COMPLEX; ANTIGEN AB Objective. To investigate the nature of the target epitope for human immunodeficiency virus (HIV) and chlorpromazine (CPZ) induced antiphospholipid antibodies (aPL) by evaluating the effect of the aPL cofactor (beta 2 glycoprotein I) on phospholipid binding and to compare this with known binding patterns of infection induced and autoimmune aPL. Methods. aPL positive sera from 17 patients with HIV and 16 patients with schizophrenia treated with CPZ were tested and compared with aPL positive sera from 20 patients with syphilis and 35 with autoimmune disease. Both the sera and either IgG fractions prepared by affinity chromatography or IgM fractions prepared by euglobulin precipitation and gel filtration were tested for binding to cardiolipin (CL) in ELISA in the presence and absence of purified human beta 2 glycoprotein I(beta 2-GPI). Competition studies evaluated biotinylated CPZ IgM aPL binding and the effect on this of added aPL, placental anticoagulant protein I - a phospholipid binding protein that inhibits autoimmune aPL - and CL vesicles. Results. HIV IgG aPL binding to CL was inhibited by beta 2-GPI (51-53%), like syphilis IgG aPL and in contrast to autoimmune IgG aPL. CPZ IgM aPL, like autoimmune IgM aPL, bound more efficiently in the presence of beta 2-GPI, with binding increases of 31-149%. Binding of biotinylated CPZ IgM aPL to CL was competitively inhibited by autoimmune IgG aPL (47%) and CPZ aPL (92%) but not by HIV IgG aPL or normal IgG. Placental anticoagulant protein I and CL vesicles completely prevented binding of CPZ IgM aPL to CL (100 and 96% inhibition, respectively). Conclusions. Findings indicate that CPZ aPL resembles the autoimmune aPL, whereas aPL found in HIV infection do not appear to be of autoimmune type. C1 CORNELL UNIV,HOSP SPECIAL SURG,MED CTR,NEW YORK,NY 10021. COLUMBIA UNIV,COLL PHYS & SURG,NEW YORK,NY. VET ADM MED CTR,NORTHPORT,NY. NIAMSD,DIV EXTRAMURAL,BETHESDA,MD. RP GHARAVI, AE (reprint author), LOUISIANA STATE UNIV,MED CTR,ANTIPHOSPHOLIPID RES LAB,1542 TULANE AVE,NEW ORLEANS,LA 70112, USA. FU NIAMS NIH HHS [AR32929] NR 24 TC 41 Z9 42 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD JAN PY 1994 VL 21 IS 1 BP 94 EP 99 PG 6 WC Rheumatology SC Rheumatology GA MT011 UT WOS:A1994MT01100020 PM 8151598 ER PT J AU ORTMANN, O MERELLI, F STOJILKOVIC, SS SCHULZ, KD EMONS, G CATT, KJ AF ORTMANN, O MERELLI, F STOJILKOVIC, SS SCHULZ, KD EMONS, G CATT, KJ TI MODULATION OF CALCIUM SIGNALING AND LH-SECRETION BY PROGESTERONE IN PITUITARY GONADOTROPHS AND CLONAL PITUITARY-CELLS SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article ID LUTEINIZING-HORMONE SECRETION; PROTEIN-KINASE-C; ESTRADIOL; CULTURE; RELEASE; RECEPTOR; OSCILLATIONS; ALPHA-T3-1; CA-2+; GNRH AB In estradiol-treated pituitary cells, progesterone enhances gonadotropin-releasing hormone (GnRH)-induced LH secretion from cultured rat pituitary cells during short-term treatment but attenuates this response during prolonged treatment. In the present study, the effects of gonadal steroids on GnRH-induced cytoplasmic calcium ([Ca2+](i)) responses in gonadotrophs were analyzed in rat pituitary cells and immortalized (alpha T3-1) murine gonadotrophs. Ca2+ responses were measured in cell suspensions and single gonadotrophs, loaded with Fura-2 or Indo-1, respectively, and pretreated for 48 h with 1 nM estradiol with or without 100 nM progesterone, or for 48 h with 1 nM estradiol and then for 3 h with 100 nM progesterone. In cells of the alpha T3-1 gonadotroph lineage, GnRH elicited biphasic Ca2+ signals composed of an initial peak response followed by a prolonged plateau phase. The amplitudes of both the extracellular Ca2+-independent spike phase and the extracellular Ca2+-dependent plateau phase were enhanced or inhibited by short- or long-term progesterone treatment, respectively. In single pituitary gonadotrophs, GnRH (0.5 nM) elicited oscillatory responses due to intermittent release and uptake of Ca2+ from intracellular stores. Treatment with progesterone shifted the oscillatory signal toward biphasic (3 h) or subthreshold (48 h) response profiles, revealing a steroid-induced change in the pattern of Ca2+ mobilization. In addition to these agonist-induced responses, the transient [Ca2+](i) responses of pituitary cells and individual gonadotrophs to high K+ were enhanced or inhibited after short- or long-term progesterone treatment, respectively. These actions were correlated with the effects of progesterone on K+-induced LH secretion. The [Ca2+](i) and LH secretory responses to phorbol ester treatment were also enhanced by short-term exposure of the cells to progesterone. The results demonstrate that the stimulatory and inhibitory effects of progesterone on agonist-induced Ca2+ signaling result from changes in Ca2+ mobilization and entry, and contribute to the modulatory actions of the steroid on GnRH-induced LH secretion. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. PHILIPPS UNIV,DEPT OBSTET & GYNECOL,W-3550 MARBURG,GERMANY. NR 29 TC 28 Z9 28 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-0760 J9 J STEROID BIOCHEM JI J. Steroid Biochem. Mol. Biol. PD JAN PY 1994 VL 48 IS 1 BP 47 EP 54 DI 10.1016/0960-0760(94)90249-6 PG 8 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA NA034 UT WOS:A1994NA03400005 PM 8136305 ER PT J AU SMACK, DP KORGE, BP JAMES, WD AF SMACK, DP KORGE, BP JAMES, WD TI KERATIN AND KERATINIZATION SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Review ID EPIDERMOLYSIS-BULLOSA SIMPLEX; HYPERPROLIFERATION-ASSOCIATED KERATINS; HUMAN EPIDERMAL-KERATINOCYTES; SQUAMOUS-CELL CARCINOMAS; HUMAN LORICRIN GENE; HUMAN-HAIR FOLLICLE; INTERMEDIATE FILAMENTS; CULTURED KERATINOCYTES; MONOCLONAL-ANTIBODIES; RETINOIC ACID AB A flood of new knowledge and discoveries in the basic science of keratins and keratinization has appeared in the past several years. This review summarizes this recent information with a focus on the epithelial keratin polypeptides, keratin intermediate filaments, keratohyaline granule proteins, cell envelope formation and cell envelope proteins, ''soft'' keratinization, true disorders of keratinization (i.e., epidermolysis bullosa simplex and epidermolytic hyperkeratosis), and disease and drug effects on keratinization. C1 NIAMSD,SKIN BIOL BRANCH,BETHESDA,MD. RP SMACK, DP (reprint author), WALTER REED ARMY MED CTR,DERMATOL SERV,WASHINGTON,DC 20307, USA. NR 117 TC 69 Z9 70 U1 0 U2 3 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD JAN PY 1994 VL 30 IS 1 BP 85 EP 102 PG 18 WC Dermatology SC Dermatology GA MR307 UT WOS:A1994MR30700012 PM 7506275 ER PT J AU BAUM, BJ AF BAUM, BJ TI ADVANCES IN SALIVARY AND SOFT-TISSUE MANAGEMENT SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article; Proceedings Paper CT Oral Pharmaceutical Symposium CY APR 23, 1993 CL BOSTON, MA ID INVIVO RP BAUM, BJ (reprint author), NIDR,BETHESDA,MD 20892, USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD JAN PY 1994 VL 125 SU S BP S26 EP S30 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MR848 UT WOS:A1994MR84800006 PM 8294672 ER PT J AU HAVAS, S HEIMENDINGER, J REYNOLDS, K BARANOWSKI, T NICKLAS, TA BISHOP, D BULLER, D SORENSEN, G BERESFORD, SAA COWAN, A DAMRON, D AF HAVAS, S HEIMENDINGER, J REYNOLDS, K BARANOWSKI, T NICKLAS, TA BISHOP, D BULLER, D SORENSEN, G BERESFORD, SAA COWAN, A DAMRON, D TI 5 A DAY FOR BETTER HEALTH - A NEW RESEARCH INITIATIVE SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID CANCER; VEGETABLES; FRUIT C1 NCI,5 A DAY BETTER HLTH PROGRAM,ROCKVILLE,MD 20892. UNIV ALABAMA,SCH PUBL HLTH,BIRMINGHAM,AL 35294. EMORY UNIV,SCH PUBL HLTH,ATLANTA,GA 30329. TULANE UNIV,MED CTR,SCH PUBL HLTH & TROP MED,NEW ORLEANS,LA 70112. MINNESOTA DEPT HLTH,HLTH BEHAV DEV EDUC SECT,MINNEAPOLIS,MN 55440. UNIV ARIZONA,SCH MED,TUCSON,AZ. HARVARD UNIV,SCH PUBL HLTH,CAMBRIDGE,MA 02138. UNIV WASHINGTON,SEATTLE,WA 98195. N CAROLINA DEPT ENVIRONM HLTH & NAT RESOURCES,DIV ADULT HLTH PROMOT,RALEIGH,NC 27611. RP HAVAS, S (reprint author), UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201, USA. FU NCI NIH HHS [R01 CA059805] NR 15 TC 145 Z9 146 U1 0 U2 4 PU AMER DIETETIC ASSN PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD JAN PY 1994 VL 94 IS 1 BP 32 EP 36 DI 10.1016/0002-8223(94)92037-0 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MR351 UT WOS:A1994MR35100011 PM 8270753 ER PT J AU PAHOR, M GURALNIK, JM CHRISCHILLES, EA WALLACE, RB AF PAHOR, M GURALNIK, JM CHRISCHILLES, EA WALLACE, RB TI USE OF LAXATIVE MEDICATION IN OLDER PERSONS AND ASSOCIATIONS WITH LOW SERUM-ALBUMIN SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID ACTIVE METABOLITE; RHEIN ANTHRONE; HEALTH-STATUS; AGE; PROSTAGLANDIN-E2; CONSTIPATION; MORTALITY; DISEASE; RATS; HOME AB Objective: To study laxative use among older persons and the association of laxative intake with hypoalbuminemia. Design: Cross-sectional study in a population-based cohort. Setting: Community and institutions in the Iowa and Washington counties, Iowa site of the Established Populations for Epidemiologic Studies of the Elderly. Participants: Persons aged 71 years or older, who were interviewed at the 6th year of follow-up and for whom drug intake information was obtained (n = 2,529). Main Outcome Measures: Laxative medication use and prevalence of hypoalbuminemia. Results: The prevalence rate of laxative use was 8.8% in the community and 74.6% in nursing homes. Increasing age was independently associated with laxative use (odds ratio [OR] = 1.66, 95% confidence interval [CI] = 1.33 to 2.07 for a 10-year increase), after adjusting for gender, institutionalization, disability in activities of daily living, body mass index, and use of the following drugs: furosemide, benzodiazepines, antidepressants, codeine, and calcium antagonists. Laxative use was independently associated with hypoalbuminemia (OR = 3.17, 95% CI = 1.42 to 7.08) after adjusting for age, gender, anemia, number of comorbid conditions, disability in activities of daily living, body mass index, use of furosemide, and institutionalization status. Compared with those who never used laxatives, those who took laxatives only at the 6th year of follow-up were at increased risk of hypoalbuminemia (OR = 2.65, 95% CI = 1.04 to 6.77), and those who used laxatives at both the 3rd and 6th years of follow-up were at greatest risk (OR = 4.02, 95% CI = 1.53 to 10.06). Conclusion: Laxatives are used by large numbers of older persons, and the investigation on unknown adverse effects is important. Prospective studies are needed to confirm the association of laxative use with hypoalbuminemia found in this study and to assess the mechanisms of this association. C1 NIA, EPIDEMIOL DEMOG & BIOMETRY PROGRAM, BETHESDA, MD 20892 USA. UNIV IOWA, DEPT PREVENT MED & ENVIRONM HLTH, IOWA CITY, IA 52242 USA. RP PAHOR, M (reprint author), UNIV CATTOLICA SACRO CUORE, CATTEDRA GERONTOL, LARGO F VITO 1, I-00168 ROME, ITALY. NR 26 TC 13 Z9 13 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JAN PY 1994 VL 42 IS 1 BP 50 EP 56 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA MQ714 UT WOS:A1994MQ71400010 PM 8277116 ER PT J AU DERENZO, EG AF DERENZO, EG TI FUNCTIONAL STATUS CARE CATEGORIES AND NATIONAL-HEALTH POLICY SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Letter RP DERENZO, EG (reprint author), NIH,BIOETH PROGRAM,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JAN PY 1994 VL 42 IS 1 BP 113 EP 113 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA MQ714 UT WOS:A1994MQ71400020 PM 8277106 ER PT J AU MCCRAY, AT SRINIVASAN, S BROWNE, AC AF MCCRAY, AT SRINIVASAN, S BROWNE, AC TI LEXICAL METHODS FOR MANAGING VARIATION IN BIOMEDICAL TERMINOLOGIES SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC ID SYSTEM AB Access to biomedical terminologies is hampered by the high degree of variability inherent in natural language terms and in the terminologies themselves. The lexicon, lexical programs, databases, and indexes included with the 1994 release of the UMLS(R) Knowledge Sources are designed to help users manage this variability. We describe these resources and illustrate their flexibility and usefulness in providing enhanced access to data in the UMLS Metathesaurus(R). RP MCCRAY, AT (reprint author), NATL LIB MED,BETHESDA,MD 20209, USA. NR 16 TC 5 Z9 5 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1994 SU S BP 235 EP 239 PG 5 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA QF216 UT WOS:A1994QF21600043 ER PT J AU RINDFLESCH, TC ARONSON, AR AF RINDFLESCH, TC ARONSON, AR TI AMBIGUITY RESOLUTION WITH MAPPING FREE-TEXT TO THE UMLS METATHESAURUS SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC AB We propose a method for resolving ambiguities encountered when mapping free text to the UMLS(R) Metathesarus. (R) Much of the research in medical informatics involves the manipulation of free text. The Metathesaurus contains extensive information which supports solutions to problems encountered while processing such text. After discussing the process of mapping free text to the Metathesaurus and describing the ambiguities which are often the result of such mapping, we provide examples of rules designed to eliminate mapping ambiguities. These rules refer to the context in which the ambiguity occurs and crucially depend on semantic types obtained from the Metathesaurus. We have conducted a preliminary test of the methodology and the results obtained indicate that the rules successfully resolve ambiguity around 80% of the time. RP RINDFLESCH, TC (reprint author), NATL LIB MED,BETHESDA,MD 20894, USA. NR 20 TC 1 Z9 1 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1994 SU S BP 240 EP 244 PG 5 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA QF216 UT WOS:A1994QF21600044 ER PT J AU ROMANO, CA AF ROMANO, CA TI PREDICTORS OF NURSE ADOPTION OF A COMPUTERIZED INFORMATION-SYSTEM AS AN INNOVATION SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC AB This descriptive study focused on factors that influence the diffusion and adoption of an innovation after it is first introduced to members of a social system. The purposes of the study were 1) to explore a set of individual, technological, and organizational characteristics as predictors of hospital nurse adoption of a computerized information system (CIS) as an innovation, and 2) to investigate the effect of the organizational position on innovation adoption. A computerized nursing information system for staffing, scheduling and productivity management was selected as the innovation. RP ROMANO, CA (reprint author), NIH,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 1 U2 1 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1994 SU S BP 961 EP 961 PG 1 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA QF216 UT WOS:A1994QF21600169 ER PT J AU BARNETT, O SHORTLIFFE, E CHUEH, H PIGGINS, J GREENES, R CIMINO, J MUSEN, M CLAYTON, P HUMPHREYS, B KINGSLAND, L AF BARNETT, O SHORTLIFFE, E CHUEH, H PIGGINS, J GREENES, R CIMINO, J MUSEN, M CLAYTON, P HUMPHREYS, B KINGSLAND, L TI PATIENT-CARE APPLICATIONS ON INTERNET SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC C1 NATL LIB MED,BETHESDA,MD 20209. RP BARNETT, O (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1994 SU S BP 1060 EP 1060 PG 1 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA QF216 UT WOS:A1994QF21600260 ER PT J AU SPIEGELHALTER, DJ FREEDMAN, LS PARMAR, MKB AF SPIEGELHALTER, DJ FREEDMAN, LS PARMAR, MKB TI BAYESIAN APPROACHES TO RANDOMIZED TRIALS SO JOURNAL OF THE ROYAL STATISTICAL SOCIETY SERIES A-STATISTICS IN SOCIETY LA English DT Article DE CLINICAL TRIALS; ETHICS; POWER; PREDICTION; PRIOR DISTRIBUTION; RANGE OF EQUIVALENCE; SHRINKAGE; STOPPING RULES; SUBJECTIVE PROBABILITIES ID MONITORING CLINICAL-TRIALS; GROUP SEQUENTIAL-METHODS; PREDICTIVE PROBABILITY; ADJUVANT THERAPY; INTERIM ANALYSIS; STOPPING RULES; FLUOROURACIL; STATISTICS; CARCINOMA; OPINION AB Statistical issues in conducting randomized trials include the choice of a sample size, whether to stop a trial early and the appropriate analysis and interpretation of the trial results. At each of these stages, evidence external to the trial is useful, but generally such evidence is introduced in an unstructured and informal manner. We argue that a Bayesian approach allows a formal basis for using external evidence and in addition provides a rational way for dealing with issues such as the ethics of randomization, trials to show treatment equivalence, the monitoring of accumulating data and the prediction of the consequences of continuing a study. The motivation for using this methodology is practical rather than ideological. C1 MRC, CANC TRIALS OFF, CAMBRIDGE, ENGLAND. NCI, BETHESDA, MD 20892 USA. RP SPIEGELHALTER, DJ (reprint author), INST PUBL HLTH, MRC, BIOSTAT UNIT, ROBINSON WAY, CAMBRIDGE CB2 2SR, ENGLAND. NR 69 TC 329 Z9 332 U1 2 U2 26 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0964-1998 EI 1467-985X J9 J R STAT SOC A STAT JI J. R. Stat. Soc. Ser. A-Stat. Soc. PY 1994 VL 157 BP 357 EP 387 DI 10.2307/2983527 PN 3 PG 31 WC Social Sciences, Mathematical Methods; Statistics & Probability SC Mathematical Methods In Social Sciences; Mathematics GA PX871 UT WOS:A1994PX87100004 ER PT J AU GRIEVE, AP POCOCK, SJ ABRAMS, K ASHBY, D HEALY, MJR JENNISON, C LEWIS, JA LINDLEY, DV MACHIN, D NEWMAN, GB BATHER, JA BAILEY, RA EVANS, SJW KEIDING, N MATTHEWS, JNS GORE, SM SENN, S HERSON, J TURNBULL, BW ALTMAN, DG ARMITAGE, P ATKINSON, AC BERRY, DA BUYSE, ME CARLIN, BP DEMETS, DL DEMPSTER, AP DUNSTAN, FDJ ELLENBERG, SS FAYERS, P GAIL, MH GEORGE, SL GREENHOUSE, JB WASSERMAN, LA HARRELL, FE JOSEPH, L SHAPIRO, SH KADANE, JB LEHMANN, HP MARUBINI, E MARIANI, L PATER, JL PETTIT, LI YOUNG, KDS ROSNER, GL WHITEHEAD, J WIEAND, HS AF GRIEVE, AP POCOCK, SJ ABRAMS, K ASHBY, D HEALY, MJR JENNISON, C LEWIS, JA LINDLEY, DV MACHIN, D NEWMAN, GB BATHER, JA BAILEY, RA EVANS, SJW KEIDING, N MATTHEWS, JNS GORE, SM SENN, S HERSON, J TURNBULL, BW ALTMAN, DG ARMITAGE, P ATKINSON, AC BERRY, DA BUYSE, ME CARLIN, BP DEMETS, DL DEMPSTER, AP DUNSTAN, FDJ ELLENBERG, SS FAYERS, P GAIL, MH GEORGE, SL GREENHOUSE, JB WASSERMAN, LA HARRELL, FE JOSEPH, L SHAPIRO, SH KADANE, JB LEHMANN, HP MARUBINI, E MARIANI, L PATER, JL PETTIT, LI YOUNG, KDS ROSNER, GL WHITEHEAD, J WIEAND, HS TI BAYESIAN APPROACHES TO RANDOMIZED TRIALS - DISCUSSION SO JOURNAL OF THE ROYAL STATISTICAL SOCIETY SERIES A-STATISTICS IN SOCIETY LA English DT Discussion ID SEQUENTIAL CLINICAL-TRIALS; PROGNOSTIC FACTORS; INTERIM ANALYSES; STOPPING RULES; OPINION; TESTS; ALLOCATION; DESIGN C1 UNIV LONDON LONDON SCH HYG & TROP MED, LONDON WC1E 7HT, ENGLAND. UNIV LEICESTER, LEICESTER LE1 7RH, ENGLAND. UNIV LIVERPOOL, LIVERPOOL L69 3BX, ENGLAND. INST EDUC, LONDON, ENGLAND. UNIV BATH, BATH BA2 7AY, AVON, ENGLAND. UNIV KENT, CANTERBURY CT2 7NZ, KENT, ENGLAND. MRC, CANC TRIALS OFF, CAMBRIDGE, ENGLAND. UNIV SUSSEX, BRIGHTON BN1 9RH, E SUSSEX, ENGLAND. GOLDSMITHS COLL, LONDON, ENGLAND. UNIV LONDON LONDON HOSP, COLL MED, LONDON E1 1BB, ENGLAND. UNIV COPENHAGEN, DK-1168 COPENHAGEN, DENMARK. UNIV NEWCASTLE UPON TYNE, NEWCASTLE UPON TYNE NE1 7RU, TYNE & WEAR, ENGLAND. MRC, BIOSTAT UNIT, CAMBRIDGE, ENGLAND. CIBA GEIGY AG, DIV PHARMACEUT, CH-4002 BASEL, SWITZERLAND. APPL LOG ASSOCIATES, HOUSTON, TX USA. CORNELL UNIV, ITHACA, NY 14853 USA. IMPERIAL CANC RES FUND, LONDON WC2A 3PX, ENGLAND. UNIV LONDON LONDON SCH ECON & POLIT SCI, LONDON WC2A 2AE, ENGLAND. DUKE UNIV, DURHAM, NC 27706 USA. INT INST DRUG DEV, BRUSSELS, BELGIUM. LIMBURGS UNIV CENTRUM, B-3610 DIEPENBEEK, BELGIUM. UNIV MINNESOTA, MINNEAPOLIS, MN 55455 USA. UNIV WISCONSIN, MADISON, WI 53706 USA. UNIV WASHINGTON, SEATTLE, WA USA. HARVARD UNIV, CAMBRIDGE, MA 02138 USA. UNIV WALES COLL MED, CARDIFF CF4 4XN, S GLAM, WALES. US FDA, ROCKVILLE, MD 20857 USA. NCI, BETHESDA, MD 20892 USA. DUKE UNIV, MED CTR, DURHAM, NC 27710 USA. MCGILL UNIV, MONTREAL, PQ H3A 2T5, CANADA. CARNEGIE MELLON UNIV, PITTSBURGH, PA 15213 USA. JOHNS HOPKINS UNIV, SCH MED, BALTIMORE, MD 21205 USA. UNIV MILAN, I-20122 MILAN, ITALY. QUEENS UNIV, KINGSTON, ON K7L 3N6, CANADA. GOLDSMITHS COLL, LONDON, ENGLAND. UNIV SURREY, GUILDFORD GU2 5XH, SURREY, ENGLAND. UNIV READING, READING RG6 2AH, BERKS, ENGLAND. MAYO CLIN & MAYO FDN, ROCHESTER, MN 55905 USA. RP GRIEVE, AP (reprint author), ZENECA PHARMACEUT, MACCLESFIELD, ENGLAND. RI Senn, Stephen/A-8101-2008; Fayers, Peter/A-5999-2010; Senn, Stephen/B-2903-2013; OI Senn, Stephen/0000-0002-7558-8473; Grieve, Andrew/0000-0003-3143-2554 NR 82 TC 2 Z9 2 U1 1 U2 3 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0964-1998 EI 1467-985X J9 J R STAT SOC A STAT JI J. R. Stat. Soc. Ser. A-Stat. Soc. PY 1994 VL 157 BP 387 EP 416 PN 3 PG 30 WC Social Sciences, Mathematical Methods; Statistics & Probability SC Mathematical Methods In Social Sciences; Mathematics GA PX871 UT WOS:A1994PX87100005 ER PT J AU BAWDON, RE GRAVELL, M HAMILTON, R SEVER, J MILLER, R GIBBS, CJ AF BAWDON, RE GRAVELL, M HAMILTON, R SEVER, J MILLER, R GIBBS, CJ TI STUDIES ON THE PLACENTAL-TRANSFER OF CELL-FREE HUMAN-IMMUNODEFICIENCY-VIRUS AND P24 ANTIGEN IN AN EX-VIVO HUMAN PLACENTAL MODEL SO JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION LA English DT Article DE HIV-1; P24 ANTIGEN; HUMAN PLACENTA; EX VIVO STUDIES OF HIV-1; TRANSPLACENTAL TRANSFER OF HIV-1 ID INFECTION AB OBJECTIVE: We studied whether the human placenta has the structural integrity to impede transplacental passage of cell-free human immunodeficiency virus (HIV/)-1 or p24 antigen from the maternal to the fetal circulation. METHODS: Nine term human placentas from uncomplicated vaginal or cesarean section deliveries were studied ex vivo with a placental perfusion apparatus to determine whether cell-free HIV/-1 at 200-2000 tissue culture infections dose (TCID50/mL) would pass to the fetal circulation. Passage of virus or p24 was assessed by infectivity titration and/or p24 antigen capture enzyme immunoassay. RESULTS: Infections HIV-1 was not detected in any of the fetal perfusate samples taken periodically during experiments. Low concentrations of HIV-1 p24 antigen, however, were detected in fetal perfusate samples from three placentas. CONCLUSIONS: The term human placenta effectively impedes passage of cell-free HIV-1 from the maternal to the fetal circulation. However, it may be permeable to passage of p24 antigen. C1 CHILDRENS NATL MED CTR, WASHINGTON, DC USA. NIH, BETHESDA, MD USA. NATL NAVAL MED CTR, BETHESDA, MD USA. RP BAWDON, RE (reprint author), UNIV TEXAS, SW MED CTR, DEPT OBSTET & GYNECOL, 5323 HARRY HINES BLVD, DALLAS, TX 75235 USA. NR 14 TC 9 Z9 9 U1 0 U2 1 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1071-5576 J9 J SOC GYNECOL INVEST JI J. Soc. Gynecol. Invest. PD JAN-MAR PY 1994 VL 1 IS 1 BP 45 EP 48 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA QB005 UT WOS:A1994QB00500009 PM 9419745 ER PT J AU PREWITT, TW MATTHEWS, W CHAUDHRI, G POGREBNIAK, HW PASS, HI MCKNEALLY, MF AF PREWITT, TW MATTHEWS, W CHAUDHRI, G POGREBNIAK, HW PASS, HI MCKNEALLY, MF TI TUMOR-NECROSIS-FACTOR INDUCES DOXORUBICIN RESISTANCE TO LUNG-CANCER CELLS IN-VITRO SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article; Proceedings Paper CT 73rd Annual Meeting of the American-Association-for-Thoracic-Surgery CY APR 25-28, 1993 CL CHICAGO, IL SP AMER ASSOC THORAC SURG ID HYDROXYL RADICAL FORMATION; CYCLE ARREST; FACTOR-ALPHA; PROLIFERATION; CYTOTOXICITY; ADRIAMYCIN; MECHANISMS; GROWTH; AGENTS; DNA AB Tumor necrosis factor can alter the cell cycle of tumor cells and protect hematopoietic stem cells from cell cycle-specific chemotherapy, but the ability of tumor necrosis factor to protect cancer cells from chemotherapy by manipulation of the cell cycle is unknown. Twenty-four-hour exposure of A549 human lung cancer cells to tumor necrosis factor shifted cells from S phase to G(0)/G(1) phase as determined by analysis of isolated cell nuclei with an FACScan Cell Sorter. This effect was not seen in cells exposed to interleukin-1 or interleukin-6. Growth assays demonstrated that tumor necrosis factor slowed the doubling time of A549 cells, confirming that tumor necrosis factor caused G(0)/G(1) arrest in these cells. Pretreatment with tumor necrosis factor rendered cells resistant to subsequent 1-hour exposure to doxorubicin, a chemotherapeutic agent active against S phase cells. Tumor necrosis factor did not protect cells against either cisplatin or mitomycin C, drugs not specific for S phase. Measurement of intracellular drug levels indicated that pretreatment with tumor necrosis factor did not affect doxorubicin uptake or efflux. These findings suggest that cells producing tumor necrosis factor within a tumor may render surrounding malignant cells resistant to cell cycle-specific chemotherapy, and this mechanism may explain failure of sequential immunotherapy-chemotherapy protocols. C1 NCI,SURG BRANCH,THORAC ONCOL SECT,BETHESDA,MD 20892. RI Chaudhri, Geeta/K-3290-2013 NR 34 TC 14 Z9 14 U1 0 U2 2 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD JAN PY 1994 VL 107 IS 1 BP 43 EP 49 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA MR275 UT WOS:A1994MR27500008 PM 8283917 ER PT J AU FRIEDMAN, RM LOPEZ, FJ TUCKER, JA KING, LR NEGROVILAR, A AF FRIEDMAN, RM LOPEZ, FJ TUCKER, JA KING, LR NEGROVILAR, A TI FERTILITY AFTER CRYPTORCHIDISM - A COMPARATIVE-ANALYSIS OF EARLY ORCHIDOPEXY WITH AND WITHOUT CONCOMITANT HORMONAL-THERAPY IN THE YOUNG MALE-RAT SO JOURNAL OF UROLOGY LA English DT Article DE CRYPTORCHIDISM; TESTIS; GONADORELIN; GONADOTROPINS, CHORIONIC ID HUMAN CHORIONIC-GONADOTROPIN; TESTICULAR DESCENT; SECRETION; ORCHIOPEXY; FLUTAMIDE; LHRH AB Infertility is common in patients with a history of bilateral cryptorchidism, even after successful prepubertal orchidopexy. Recent data suggest that this defect may be partially due to the existence of hormonal abnormalities in some forms of cryptorchidism. To analyze any potential benefit of hormonal therapy, we have evaluated the immediate and long-term effects of chronic hormonal therapy administered following surgical correction of cryptorchidism. First, using young male rats, we examined the effects of chronic human chorionic gonadotropin (HCG) and a luteinizing hormone-releasing hormone agonist (LHRH-A), alone or combined, on acute pituitary-gonadal axis responsiveness to LHRH administration. High doses of HCG and/or LHRH-A induced deleterious effects on the pituitary-testicular axis in terms of suppression of response to LHRH. Therefore, treatment with a low dose of HCG (50 U/kg./day) for 14 days was used, since it produced a significant increase in intratesticular testosterone (ITT). Second, we tested this hormonal regimen in a cryptorchid rat model. Bilateral cryptorchidism was produced by gubernaculum resection at 14 days of age. Early orchidopexy was performed at age 30 days, and HCG therapy was given from 31 to 44 days of age. Follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T) levels were determined before and immediately after hormonal therapy, and at sacrifice. Animals were sacrificed at 61 days of age for determination of serum and testicular hormone levels, accessory sex organ weights and testis histology. Five or six animals from each group were retained for breeding studies at the age of 90 days. Hormonal alterations noted immediately following treatment of cryptorchid animals with HCG are not lasting. The data reveal that the fertility defect in bilateral cryptorchidism is partially prevented by early orchidopexy and that adjunctive hormonal therapy is probably of little additional benefit. C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,REPROD NEUROENDOCRINOL SECT,RES TRIANGLE PK,NC 27709. UNIV SO ALABAMA,MED CTR,DEPT PATHOL,MOBILE,AL 36688. RP FRIEDMAN, RM (reprint author), DUKE UNIV,MED CTR,DIV UROL SURG,DURHAM,NC 27710, USA. NR 35 TC 13 Z9 13 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD JAN PY 1994 VL 151 IS 1 BP 227 EP 233 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA ML652 UT WOS:A1994ML65200075 PM 7902876 ER EF