FN Thomson Reuters Web of Science™ VR 1.0 PT J AU CALLAHAN, R CROPP, CS MERLO, GR LISCIA, DS CAPPA, APM LIDEREAU, R AF CALLAHAN, R CROPP, CS MERLO, GR LISCIA, DS CAPPA, APM LIDEREAU, R TI SOMATIC MUTATIONS AND HUMAN BREAST-CANCER - A STATUS-REPORT SO CANCER LA English DT Article; Proceedings Paper CT WORKSHOP ON MOLECULAR MARKERS IN THE CLASSIFICATION AND STAGING OF CANCER CY DEC 13-14, 1990 CL ATLANTA, GA SP AMER CANC SOC, AMER JOINT COMM CANC ID TUMOR SUPPRESSOR GENES; RETINOBLASTOMA SUSCEPTIBILITY GENE; TRANSGENIC MICE; CELL-CYCLE; NEU ONCOGENE; OVARIAN-CANCER; MAMMARY-TUMORS; GROWTH-FACTORS; RAS ONCOGENE; INT-2 GENE AB A systematic study of primary human breast tumor DNA demonstrated that three proto-oncogenes or regions of the genome (c-myc, int-2, and c-erbB2) are frequently amplified and that there is loss of heterozygosity (LOH) on chromosomes 1p(37%), 1q(20%), 3p(30%), 7(41%), 11p(20%), 13q(30%), 17p(49%), 17q(29%), and 18q(34%). Specific subsets of tumors can be defined based on the particular collection of mutations they contain. For instance, LOH on chromosomes 11p, 17p, and 18q frequently occurs in the same tumor. A search for putative tumor suppressor genes within the regions of the genome affected by LOH has been started. In a comprehensive molecular analysis of the p53 gene on chromosome 17p, 46% of the tumors contained a point mutation in the p53 gene. C1 S GIOVANNI HOSP,ANAT PATHOL SECT,TURIN,ITALY. CTR RENE HUGUENIN,ST CLOUD,FRANCE. RP CALLAHAN, R (reprint author), NCI,BETHESDA,MD 20892, USA. NR 92 TC 110 Z9 110 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1992 VL 69 IS 6 SU S BP 1582 EP 1588 DI 10.1002/1097-0142(19920315)69:6+<1582::AID-CNCR2820691313>3.0.CO;2-Y PG 7 WC Oncology SC Oncology GA HJ806 UT WOS:A1992HJ80600012 PM 1540899 ER PT J AU GAZDAR, AF AF GAZDAR, AF TI MOLECULAR MARKERS FOR THE DIAGNOSIS AND PROGNOSIS OF LUNG-CANCER SO CANCER LA English DT Article; Proceedings Paper CT WORKSHOP ON MOLECULAR MARKERS IN THE CLASSIFICATION AND STAGING OF CANCER CY DEC 13-14, 1990 CL ATLANTA, GA SP AMER CANC SOC, AMER JOINT COMM CANC ID SMALL-CELL-CARCINOMA; RETINOBLASTOMA SUSCEPTIBILITY GENE; MULTIDRUG RESISTANCE GENE; POLYMERASE CHAIN-REACTION; ENVELOPE-RELATED MARKERS; L-DOPA DECARBOXYLASE; K-RAS ONCOGENE; P53 GENE; SQUAMOUS DIFFERENTIATION; ACTIVATING MUTATIONS AB Molecular probes for lung cancer have greatly increased the understanding of the biology of this disease and the preneoplastic changes that precede it. They have confirmed and extended the clinical, pathologic, and biologic reasons for the primary division of lung cancers into small cell and non-small cell lung cancer types. Many molecular changes are present in lung cancers and involve dominant oncogenes and recessive growth regulatory genes. Clinical application of these markers will aid diagnosis, classification, and clinical management. C1 NCI,USN HOSP,MED ONCOL BRANCH,BETHESDA,MD 20892. NR 89 TC 46 Z9 46 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1992 VL 69 IS 6 SU S BP 1592 EP 1599 DI 10.1002/1097-0142(19920315)69:6+<1592::AID-CNCR2820691315>3.0.CO;2-R PG 8 WC Oncology SC Oncology GA HJ806 UT WOS:A1992HJ80600014 PM 1311627 ER PT J AU HENSON, DE AF HENSON, DE TI FUTURE-DIRECTIONS FOR THE AMERICAN-JOINT-COMMITTEE-ON-CANCER SO CANCER LA English DT Article; Proceedings Paper CT WORKSHOP ON MOLECULAR MARKERS IN THE CLASSIFICATION AND STAGING OF CANCER CY DEC 13-14, 1990 CL ATLANTA, GA SP AMER CANC SOC, AMER JOINT COMM CANC ID DNA FLOW-CYTOMETRY; PRIMARY BREAST-CANCER; PROGNOSTIC FACTORS; SOLID TUMORS; COLORECTAL-CARCINOMA; SURVIVAL; ONCOGENE; AMPLIFICATION; INDEX; COLON AB This report summarizes future directions for the American Joint Committee on Cancer (AJCC). It was presented at the Workshop on Molecular Markers in the Classification and Staging of Cancer that was sponsored by the AJCC and supported by a grant from the American Cancer Society. RP HENSON, DE (reprint author), NCI,EARLY DETECT BRANCH,BETHESDA,MD 20892, USA. NR 48 TC 9 Z9 10 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1992 VL 69 IS 6 SU S BP 1639 EP 1644 DI 10.1002/1097-0142(19920315)69:6+<1639::AID-CNCR2820691320>3.0.CO;2-N PG 6 WC Oncology SC Oncology GA HJ806 UT WOS:A1992HJ80600019 PM 1540905 ER PT J AU STRICKLAND, JE UEDA, M HENNINGS, H YUSPA, SH AF STRICKLAND, JE UEDA, M HENNINGS, H YUSPA, SH TI A MODEL FOR INITIATED MOUSE SKIN - SUPPRESSION OF PAPILLOMA BUT NOT CARCINOMA FORMATION BY NORMAL EPIDERMAL-CELLS IN GRAFTS ON ATHYMIC NUDE-MICE SO CANCER RESEARCH LA English DT Article ID GROWTH FACTOR-ALPHA; TERMINAL DIFFERENTIATION; JUNCTIONAL COMMUNICATION; HUMAN KERATINOCYTES; EPITHELIAL-CELLS; TUMOR PROMOTERS; INHIBITION; INDUCTION; ONCOGENE; 12-O-TETRADECANOYLPHORBOL-13-ACETATE AB The availability of a skin grafting system on nude mouse hosts and of epidermal cell lines which form papillomas when grafted has made possible the creation of a model for initiated skin in vivo from cultured cells. When grafted with 6-8 x 10(6) primary dermal fibroblasts, 10 x 10(6) primary epidermal cells form an apparently normal skin, and cell line Sp-1 (0.5 x 10(6) cells) forms papillomas. Cell line SP-1 was derived from papillomas produced on SENCAR mice by initiation with 7,12-dimethylbenz[a]anthracene and promotion with 12-O-tetradecanoylphorbol-13-acetate. Grafting of 0.5 x 10(6) SP-1 cells along with 10 x 10(6) SENCAR newborn primary epidermal cells resulted in a 90% reduction in the average papilloma volume per mouse compared to controls without primary epidermal cells. Suppression occurred specifically with epidermal cells, either cultured or freshly prepared, and was not seen when an equivalent number of SENCAR primary dermal fibroblasts was grafted in place of epidermal cells. Nor did suppression occur when primary epidermal cells were replaced with a carcinogen-altered cell line, SCR722.SCR722 cells have a normal-skin phenotype when grafted. Furthermore, suppression of tumor formation did not occur when a malignant variant of SP-1 cells replaced benign SP-1 cells in grafts. Repeated treatment of suppressed grafts with 12-O-tetradecanoylphorbol-13-acetate resulted in an increased number of mice with papillomas and a larger mean papilloma volume per mouse compared to controls treated with solvent alone, whereas treatment of nonsuppressed grafts of papilloma cells with promoter produced no change in tumor size. These results support the concepts that normal epidermal cells suppress the growth of initiated cells and that repeated treatment with phorbol ester tumor promoters overcomes the suppression, leading to benign tumor formation. RP STRICKLAND, JE (reprint author), NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BLDG 37,ROOM 3B25,BETHESDA,MD 20892, USA. NR 48 TC 30 Z9 30 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1992 VL 52 IS 6 BP 1439 EP 1444 PG 6 WC Oncology SC Oncology GA HJ145 UT WOS:A1992HJ14500011 PM 1540951 ER PT J AU LATIF, F FIVASH, M GLENN, G TORY, K ORCUTT, ML HAMPSCH, K DELISIO, J LERMAN, M COWAN, J BECKETT, M WEICHSELBAUM, R AF LATIF, F FIVASH, M GLENN, G TORY, K ORCUTT, ML HAMPSCH, K DELISIO, J LERMAN, M COWAN, J BECKETT, M WEICHSELBAUM, R TI CHROMOSOME-3P DELETIONS IN HEAD AND NECK CARCINOMAS - STATISTICAL ASCERTAINMENT OF ALLELIC LOSS SO CANCER RESEARCH LA English DT Article ID NATURAL-POPULATIONS; LINES; HETEROZYGOSITY; FRAGMENTS; CANCER; TUMORS; CELLS AB Loss of function of tumor suppressor genes is important in the origin and progression of common adult tumors. Loss of heterozygosity indicating allelic loss has been used to detect chromosomal regions that harbor these genes. Using over 20 restriction fragment length polymorphism markers spaced throughout the entire length of chromosome 3p, we have generated 3p allelotypes for 18-26 head and neck squamous cell carcinoma cell lines. We then estimated the average heterozygosity over 19 loci for a random sample drawn from natural populations to be 7.80 and that for the tumor lines to be 1.65, indicating a gross reduction of heterozygosity, presumably due to allelic loss. Further comparison of per locus heterozygosity in normal and tumor DNAs showed which loci contributed to the general loss of heterozygosity. We showed that the commonly deleted region of 3p probably lies telomeric to D3S3 (3p14) and centromeric to RAF1 (3p25). This large region includes several putative tumor suppressor genes involved in multiple common tumor types of lung, breast, kidney, ovary, and cervix. The data demonstrate that chromosome 3p allelic loss is a common event in head and neck cancers and suggest that chromosome 3p tumor suppressor genes contribute to the pathogenesis of these tumors. C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,BLDG 560,ROOM 12-71,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DATA MANAGEMENT SERV INC,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702. UNIV CHICAGO,MED CTR,DEPT RADIAT ONCOL,CHICAGO,IL 60637. FU NCI NIH HHS [CA 41068, N01-CO-74102, N01-CO-74103] NR 24 TC 88 Z9 88 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1992 VL 52 IS 6 BP 1451 EP 1456 PG 6 WC Oncology SC Oncology GA HJ145 UT WOS:A1992HJ14500013 PM 1540952 ER PT J AU ANDERSON, LM KOSENIAUSKAS, R BURAK, ES MOSKAL, TJ GOMBAR, CT PHILLIPS, JM SANSONE, EB KEIMIG, S MAGEE, PN RICE, JM HARRINGTON, GW AF ANDERSON, LM KOSENIAUSKAS, R BURAK, ES MOSKAL, TJ GOMBAR, CT PHILLIPS, JM SANSONE, EB KEIMIG, S MAGEE, PN RICE, JM HARRINGTON, GW TI REDUCED BLOOD CLEARANCE AND INCREASED URINARY-EXCRETION OF N-NITROSODIMETHYLAMINE IN PATAS MONKEYS EXPOSED TO ETHANOL OR ISOPROPYL-ALCOHOL SO CANCER RESEARCH LA English DT Article ID HUMAN-LIVER MICROSOMES; RAT-LIVER; NITROSAMINE METABOLISM; HUMAN CANCER; INHIBITION; DEMETHYLASE; DIMETHYLNITROSAMINE; PHARMACOKINETICS; PURIFICATION; DISPOSITION AB Low concentrations of N-nitrosodimethylamine are metabolized in rodent and human liver by cytochrome P450IIE1, an activity competitively inhibitable by ethanol. In rodents coadministration of ethanol with N-nitrosodimethylamine results in increased tumorigenicity in extrahepatic organs, probably as a result of reduced hepatic clearance. To test this concept in a primate, the effects of ethanol cotreatment on the pharmacokinetics of N-nitrosodimethylamine were measured in male patas monkeys. Ethanol, 1.2 g/kg given p.o. before i.v. N-nitrosodimethylamine (1 mg/kg) or concurrently with an intragastric dose resulted in a 10-50-fold increase in the area under the blood concentration versus time curves and a 4-13-fold increase in mean residence times for N-nitrosodimethylamine. Isopropyl alcohol, 3.2 g/kg 24 h before N-nitrosodimethylamine, also increased these parameters 7-10-fold; this effect was associated with persistence of isopropyl alcohol and its metabolic product acetone, both IIE1 inhibitors, in the blood. While no N-nitrosodimethylamine was detected in expired air, trace amounts were found in urine. Ethanol and isopropyl alcohol pretreatment increased the maximum urinary N-nitrosodimethylamine concentration 15-50-fold and the percentage of the dose excreted in the urine by 100-800-fold. Thus ethanol and isopropyl alcohol greatly increase systemic exposure of extrahepatic organs to N-nitrosodimethylamine in a primate. C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP PROGRAM RESOURCES INC,FREDERICK,MD 21702. TEMPLE UNIV,DEPT CHEM,PHILADELPHIA,PA 19122. SMITHKLINE BEECHAM PHARMACEUT,DEPT DRUG METAB & PHARMACOKINET,KING OF PRUSSIA,PA 19406. SEMA INC,ROCKVILLE,MD 20850. TEMPLE UNIV,HLTH SCI CTR,SCH MED,FELS RES INST,PHILADELPHIA,PA 19140. RP ANDERSON, LM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,BLDG 538,FT DETRICK,FREDERICK,MD 21702, USA. FU NCI NIH HHS [CA-43342, N01-CP-71079] NR 48 TC 21 Z9 21 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1992 VL 52 IS 6 BP 1463 EP 1468 PG 6 WC Oncology SC Oncology GA HJ145 UT WOS:A1992HJ14500015 PM 1540953 ER PT J AU MANCHESTER, DK BOWMAN, ED PARKER, NB CAPORASO, NE WESTON, A AF MANCHESTER, DK BOWMAN, ED PARKER, NB CAPORASO, NE WESTON, A TI DETERMINANTS OF POLYCYCLIC AROMATIC HYDROCARBON-DNA ADDUCTS IN HUMAN PLACENTA SO CANCER RESEARCH LA English DT Article ID BENZOPYRENE DIOL EPOXIDE; MONOCLONAL-ANTIBODIES; LUNG-CANCER; FLUORESCENCE; LYMPHOCYTES; METABOLISM; SMOKING; HYDROXYLASE; CARCINOGENESIS; QUANTITATION AB To determine the relative contributions of tobacco smoking and P-450 metabolism (cytochrome P-450IA1) in the formation of benzo(a)pyrene-diol-epoxide and other polycyclic aromatic hydrocarbon-DNA adducts in vivo, 16 human placentas were assayed for aryl hydrocarbon hydroxylase activity and (+/-)r-7,t-8-dihydroxy-c-9,10-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene-DNA adduct levels. Immunoaffinity chromatography columns, conjugated with monoclonal antibodies raised against benzo(a)pyrene-diol-epoxide-deoxyguanosine, were used to concentrate polycyclic aromatic hydrocarbon-DNA adducted nucleotides, and synchronous fluorescence spectroscopy was used specifically to detect r-7,t-8,t-9,c-10-tetrahydroxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BP-tetrol) extracted from acid hydrolysates of immunoconcentrated materials. Data were analyzed for associations with maternal dietary and smoking habits, umbilical cord blood cotinine levels, and placental aryl hydrocarbon hydroxylase levels. Complex mixtures of fluorescent materials were present in organic solvent extracts of acid hydrolysates of immunoconcentrated nucleotide-adducts from all placentas with patterns of fluorescence that may be associated with tobacco smoking determined by generation of spectral fluorescence excitation-emission matrices. BP-tetrols were detected in extracts from 8 placentas: 5 of 7 from smokers and 3 of 9 from nonsmokers. Placental aryl hydrocarbon hydroxylase activity was significantly higher in placentas from which BP-tetrols were extracted 113.0 +/- 4.0 (mean +/- SE) pmol 3-hydroxybenzo(a)pyrene mg protein-1 min-1], than among placentas from which BP-tetrols were not extracted (1.3 +/- 3.7 pmol 3-hydroxybenzo(a)pyrene mg protein-1 min-1) (P = 0.03, Student's t test). This association was independent of maternal smoking or umbilical cord blood cotinine levels. These results indicate that while maternal tobacco smoking is associated with the accumulation of putative, but as yet unidentified, polycyclic aromatic hydrocarbon-DNA adducts in placenta, metabolic capacity appears to be the principal determinant for the (+/-)r-7,t-8-dihydroxy-c-9,10 epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene-DNA adduct levels detected. C1 NCI,HUMAN CARCINOGENESIS LAB,ROOM 2C16,BLDG 37,BETHESDA,MD 20892. NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. UNIV COLORADO,CHILDRENS HOSP KEMPE RES CTR,SCH MED,DEPT PEDIAT,DENVER,CO 80218. UNIV COLORADO,CHILDRENS HOSP KEMPE RES CTR,SCH MED,DEPT PHARMACOL,DENVER,CO 80218. FU NCRR NIH HHS [RR-69] NR 44 TC 63 Z9 63 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1992 VL 52 IS 6 BP 1499 EP 1503 PG 5 WC Oncology SC Oncology GA HJ145 UT WOS:A1992HJ14500020 PM 1540958 ER PT J AU DEMETER, LM STOLER, MH SOBEL, ME BROKER, TR CHOW, LT AF DEMETER, LM STOLER, MH SOBEL, ME BROKER, TR CHOW, LT TI EXPRESSION OF HIGH-AFFINITY LAMININ RECEPTOR MESSENGER-RNA CORRELATES WITH CELL-PROLIFERATION RATHER THAN INVASION IN HUMAN PAPILLOMAVIRUS-ASSOCIATED CERVICAL NEOPLASMS SO CANCER RESEARCH LA English DT Article ID INSITU HYBRIDIZATION; UTERINE CERVIX; CARCINOMA-CELLS; BINDING PROTEIN; ACTIVATED RAS; TRANSFORMATION; TYPE-11; ADENOCARCINOMA; METASTASIS; ONCOGENE AB Induction of the expression of the M(r) 67,000 high-affinity laminin receptor gene has been postulated as playing a role in the progression of human tumors to invasive cancers. We tested this hypothesis by examining histopathological sections of a large number of epithelial lesions of the genital tract associated with human papillomaviruses. In situ hybridization was performed with a riboprobe generated from a laminin receptor complementary DNA. Laminin receptor mRNA was expressed primarily in the less differentiated cells in normal squamous tissues and in a spectrum of squamous neoplasms. There was no net induction of mRNA per cell in intraepithelial or invasive squamous neoplasms relative to normal tissue. In contrast, laminin receptor mRNA was not expressed at a detectable level in normal glands of the uterine cervix but was dramatically induced in morphologically abnormal, human papillomavirus-positive glands, irrespective of the genotype of human papillomaviruses present. The induction occurred before any evidence of invasion, and there was no further increase during the transition from adenocarcinoma in situ to invasive carcinoma. We conclude that induction of high-affinity laminin receptor gene expression is associated with the development of malignancies of cervical glandular epithelia, but the increased expression appears to correlate with the proliferative rather than the invasive properties of these cells. C1 UNIV ROCHESTER,SCH MED & DENT,DEPT BIOCHEM,601 ELMWOOD AVE,ROCHESTER,NY 14642. UNIV ROCHESTER,SCH MED & DENT,DEPT MED,INFECT DIS UNIT,ROCHESTER,NY 14642. CLEVELAND CLIN FDN,DEPT PATHOL,CLEVELAND,OH 44195. NCI,DIV CANC BIOL & DIAG,PATHOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA36200, CA43629]; NIAID NIH HHS [AI-07169] NR 34 TC 31 Z9 31 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1992 VL 52 IS 6 BP 1561 EP 1567 PG 7 WC Oncology SC Oncology GA HJ145 UT WOS:A1992HJ14500031 PM 1311633 ER PT J AU SATO, T SAITO, H SWENSEN, J OLIFANT, A WOOD, C DANNER, D SAKAMOTO, T TAKITA, K KASUMI, F MIKI, Y SKOLNICK, M NAKAMURA, Y AF SATO, T SAITO, H SWENSEN, J OLIFANT, A WOOD, C DANNER, D SAKAMOTO, T TAKITA, K KASUMI, F MIKI, Y SKOLNICK, M NAKAMURA, Y TI THE HUMAN PROHIBITIN GENE LOCATED ON CHROMOSOME-17Q21 IS MUTATED IN SPORADIC BREAST-CANCER SO CANCER RESEARCH LA English DT Note ID NEUROFIBROMATOSIS TYPE-1 GENE; GTPASE-ACTIVATING PROTEIN; HIGH-RISK FAMILIES; SACCHAROMYCES-CEREVISIAE; RAS; MUTATIONS; ENCODES; GAP; SEGREGATION; INHERITANCE AB A gene called "prohibitin" was isolated as a candidate antiproliferating gene in rat liver cells. We have isolated the human homologue of the rat prohibitin gene and mapped it to chromosome 17q12-21 where a gene responsible for hereditary breast cancer was localized. DNA sequence analysis of 2 exons in this gene in 23 sporadic breast cancers, which showed loss of heterozygosity on the long arm of chromosome 17 or developed in patients 35 years old or younger, identified 4 cases of somatic mutation; 2 of these were missense mutations; 1 showed a 2-base deletion resulting in truncation of the gene product due to a frame shift; the other had a C to T transition in an intron adjacent to an intron-exon boundary. These results suggest that this gene may be a tumor suppressor gene and is associated with tumor development and/or progression of at least some breast cancers. C1 JAPANESE FDN CANC RES,INST CANC,DEPT BIOCHEM,1-37-1 KAMI IKEBUKURO,TOSHIMA KU,TOKYO 170,JAPAN. JAPANESE FDN CANC RES,INST CANC,DEPT SURG,TOSHIMA KU,TOKYO 170,JAPAN. UNIV UTAH,DEPT MED INFORMAT,SALT LAKE CITY,UT 84108. NIA,MOLEC GENET LAB,BALTIMORE,MD 21224. FU NCI NIH HHS [CA-48711] NR 25 TC 145 Z9 156 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1992 VL 52 IS 6 BP 1643 EP 1646 PG 4 WC Oncology SC Oncology GA HJ145 UT WOS:A1992HJ14500045 PM 1540973 ER PT J AU HAMASAKI, DI SATOH, H SUNIL, S SHINOHARA, T AF HAMASAKI, DI SATOH, H SUNIL, S SHINOHARA, T TI PROGRESSIVE PHYSIOLOGICAL ALTERATION OF THE RETINA DURING THE COURSE OF EXPERIMENTAL AUTOIMMUNE UVEITIS IN RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MIAMI,SCH MED,BASCOM PALMER EYE INST,MIAMI,FL 33152. NEI,RETINAL CELL & MOLEC 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 743 EP 743 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500255 ER PT J AU PERCOPO, C DETRICK, B EVANS, C HOOKS, JJ AF PERCOPO, C DETRICK, B EVANS, C HOOKS, JJ TI THE CYTOKINE, LEUKOREGULIN, INHIBITS HSV-1 REPLICATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,WASHINGTON,DC. GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 787 EP 787 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500473 ER PT J AU RODRIGUEZ, IR AGUIRRE, G MAZURUK, K CHADER, GJ AF RODRIGUEZ, IR AGUIRRE, G MAZURUK, K CHADER, GJ TI SELECTIVE CLONING OF RETINAL SPECIFIC GENES LOCATED ON THE HUMAN X-CHROMOSOME SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 791 EP 791 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500496 ER PT J AU BRADY, J PIATIGORSKY, J AF BRADY, J PIATIGORSKY, J TI ISOLATION AND CHARACTERIZATION OF ZINC FINGER CDNAS FROM THE NEWBORN MOUSE LENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 MAR 15 PY 1992 VL 33 IS 4 BP 793 EP 793 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500508 ER PT J AU DANCIGER, M KOZAK, CA FARBER, DB AF DANCIGER, M KOZAK, CA FARBER, DB TI CHROMOSOMAL MAPPING IN THE MOUSE OF 3 RETINAL GENES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,JULES STEIN EYE INST,LOS ANGELES,CA 90024. LOYOLA MARYMOUNT UNIV,LOS ANGELES,CA 90045. NIAID,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 793 EP 793 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500507 ER PT J AU GOPALSRIVASTAVA, R PIATIGORSKY, J AF GOPALSRIVASTAVA, R PIATIGORSKY, J TI REGULATION OF MURINE ALPHA-B-CRYSTALLIN GENE-EXPRESSION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 793 EP 793 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500509 ER PT J AU SHINOHARA, T BREITMAN, M KIKUCHI, T AF SHINOHARA, T BREITMAN, M KIKUCHI, T TI S-ANTIGEN (ARRESTIN) PROMOTER ACTIVITY INVITRO AND IN TRANSGENIC MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI, RES CORNEA MOLEC BIOL LAB, BETHESDA, MD 20892 USA. MT SINAI HOSP, DIV MOLEC & DEV BIOL, TORONTO M5G 1X5, ONTARIO, CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 EI 1552-5783 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 794 EP 794 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500511 ER PT J AU WARWAR, RE KIM, RY WISTOW, GJ ZELENKA, PS AF WARWAR, RE KIM, RY WISTOW, GJ ZELENKA, PS TI THE TAU-CRYSTALLIN ALPHA-ENOLASE GENE - A CANDIDATE FOR REGULATION BY C-MYC SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 794 EP 794 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500510 ER PT J AU DEBARGER, LR CHAN, CC CASPI, RR HARNING, R NUSSENBLATT, RB WHITCUP, SM AF DEBARGER, LR CHAN, CC CASPI, RR HARNING, R NUSSENBLATT, RB WHITCUP, SM TI EXPRESSION OF CELL-ADHESION MOLECULES IN MICE WITH EXPERIMENTAL AUTOIMMUNE UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. ROBERTS PHARMACEUT CORP,EATONTOWN,NJ. NR 0 TC 2 Z9 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 796 EP 796 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500525 ER PT J AU WHITCUP, SM DEBARGE, LR ROSEN, H NUSSENBLATT, RB CHAN, CC AF WHITCUP, SM DEBARGE, LR ROSEN, H NUSSENBLATT, RB CHAN, CC TI MONOCLONAL-ANTIBODY AGAINST MAC-1 (CD11B CD18) INHIBITS ENDOTOXIN INDUCED UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. MERCK SHARP & DOHME LTD,RAHWAY,NJ 07065. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 796 EP 796 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500523 ER PT J AU RAO, CM ZIGLER, JS AF RAO, CM ZIGLER, JS TI LEVEL OF REDUCED NUCLEOTIDES AND LENS PHOTODAMAGE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 799 EP 799 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500539 ER PT J AU ZHAO, JL SASTRY, SM SPERDUTO, RD CHEW, EY AF ZHAO, JL SASTRY, SM SPERDUTO, RD CHEW, EY TI ARTERIOVENOUS CROSSING PATTERN IN BRANCH RETINAL VEIN OCCLUSION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 805 EP 805 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500564 ER PT J AU LI, A LANE, WS JOHNSON, LV CHADER, GJ TOMBRANTINK, J AF LI, A LANE, WS JOHNSON, LV CHADER, GJ TOMBRANTINK, J TI NEURON-SPECIFIC ENOLASE - AN INTERPHOTORECEPTOR MATRIX (IPM) COMPONENT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. HARVARD UNIV,CAMBRIDGE,MA 02138. UNIV SO CALIF,SCH MED,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90033. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 815 EP 815 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500613 ER PT J AU HAYDEN, BJ SCHOEN, TJ WALDBILLIG, RJ CHADER, GJ AF HAYDEN, BJ SCHOEN, TJ WALDBILLIG, RJ CHADER, GJ TI DIFFERENTIAL REGULATION OF INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEINS IN Y-79 RETINOBLASTOMA CELLS BY DIFFERENTIATING AGENTS AND GROWTH-FACTORS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 818 EP 818 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500629 ER PT J AU BECERRA, SP STEELE, F TINK, J CHADER, GJ AF BECERRA, SP STEELE, F TINK, J CHADER, GJ TI RECOMBINANT HUMAN FETAL RETINAL-PIGMENT EPITHELIUM-DERIVED FACTOR (PEDF) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 823 EP 823 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500657 ER PT J AU TOMBRANTINK, J PAWAR, H ANDERSON, L SWAROOP, A STEELE, F RODRIGUEZ, I CHADER, GJ AF TOMBRANTINK, J PAWAR, H ANDERSON, L SWAROOP, A STEELE, F RODRIGUEZ, I CHADER, GJ TI MOLECULAR-CLONING AND CHROMOSOMAL LOCALIZATION OF THE GENE FOR HUMAN PIGMENT EPITHELIUM-DERIVED FACTOR (PEDF) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV MICHIGAN,SCH MED,DEPT OPHTHALMOL,ANN ARBOR,MI 48104. UNIV MICHIGAN,SCH MED,DEPT HUMAN GENET,ANN ARBOR,MI 48104. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 828 EP 828 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500679 ER PT J AU NAGINENI, C DETRICK, B HOOKS, JJ AF NAGINENI, C DETRICK, B HOOKS, JJ TI CYTOKINES ACTIVATE AND ARE PRODUCED BY HUMAN RPE CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. NR 0 TC 2 Z9 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 829 EP 829 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500685 ER PT J AU SCHOEN, TJ WALDBILLIG, RJ BEEBE, D POTTS, J CHADER, G RODRIGUEZ, IR AF SCHOEN, TJ WALDBILLIG, RJ BEEBE, D POTTS, J CHADER, G RODRIGUEZ, IR TI DISTRIBUTION OF MESSENGER-RNA AND CLONING OF INSULIN-LIKE GROWTH-FACTOR BINDING PROTEIN-2 (IGFBP-2) IN DEVELOPING CHICK OCULAR TISSUE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT ANAT & CELL BIOL,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 U1 0 U2 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 829 EP 829 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500684 ER PT J AU WALDBILLIG, RJ SCHOEN, TJ JONES, BE LEROITH, T CHADER, GJ AF WALDBILLIG, RJ SCHOEN, TJ JONES, BE LEROITH, T CHADER, GJ TI VITREOUS-HUMOR CONTAINS 2 HIGHLY SPECIFIC PROTEASES FOR INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEINS (IGFBPS) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 829 EP 829 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500683 ER PT J AU HIKITA, N LOPEZ, JS DESMET, MD CHAN, CC MOCHIZUKI, M NUSSENBLATT, RB AF HIKITA, N LOPEZ, JS DESMET, MD CHAN, CC MOCHIZUKI, M NUSSENBLATT, RB TI USE OF TOPICAL FK-506 IN THE CORNEAL GRAFT-REJECTION MODEL IN LEWIS RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. KURUME UNIV,SCH MED,DEPT OPHTHALMOL,KURUME,FUKUOKA 830,JAPAN. NR 0 TC 2 Z9 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 832 EP 832 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500697 ER PT J AU EGWUAGU, CE SZTEIN, J REID, W CHAN, CC MAHDI, R NUSSENBLATT, RB CHEPELINSKY, AB AF EGWUAGU, CE SZTEIN, J REID, W CHAN, CC MAHDI, R NUSSENBLATT, RB CHEPELINSKY, AB TI GAMMA-INTERFERON GENE-EXPRESSION IN THE LENS OF TRANSGENIC MICE DIRECTED BY THE ALPHA-A-CRYSTALLIN GENE PROMOTER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LABS,BETHESDA,MD 20892. NEI,MOLEC & DEV BIOL LABS,BETHESDA,MD 20892. RI Sztein, Jorge/B-7165-2012 NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 846 EP 846 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500769 ER PT J AU YAMAMOTO, JH MOCHIZUKI, M MINAMI, M NUMAGA, J FUJINO, Y HAYASHI, K MASUDA, K DESMET, M GERY, I NUSSENBLATT, RB AF YAMAMOTO, JH MOCHIZUKI, M MINAMI, M NUMAGA, J FUJINO, Y HAYASHI, K MASUDA, K DESMET, M GERY, I NUSSENBLATT, RB TI BEHCETS PATIENTS WITHOUT OCULAR INVOLVEMENT DO NOT RESPOND WELL TO RETINAL ANTIGENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV TOKYO,DEPT OPHTHALMOL,TOKYO 113,JAPAN. UNIV TOKYO,DEPT TRANSFUS MED & IMMUNOHEMATOL,TOKYO 113,JAPAN. KURUME UNIV,DEPT OPHTHALMOL,KURUME,FUKUOKA 830,JAPAN. NEI,BETHESDA,MD 20892. RI Yamamoto, Joyce/B-6192-2015 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 846 EP 846 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500767 ER PT J AU LI, Q ABE, T KIKUCHI, T NUSSENBLATT, RB SHINOHARA, T CHAN, CC AF LI, Q ABE, T KIKUCHI, T NUSSENBLATT, RB SHINOHARA, T CHAN, CC TI CORTICOSTEROIDS INDUCE HIGHER LEVEL OF S-ANTIGEN MESSENGER-RNA IN THE OCULAR TISSUE OF LEWIS RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NEI,RETINAL CELL & MOLEC 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 852 EP 852 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500806 ER PT J AU VINORES, SA VANNEIL, E CAMPOCHIARO, PA HERMAN, MM HOOKS, JJ DETRICK, B AF VINORES, SA VANNEIL, E CAMPOCHIARO, PA HERMAN, MM HOOKS, JJ DETRICK, B TI DOUBLE-LABELING ELECTRON-MICROSCOPIC IMMUNOCYTOCHEMISTRY FOR CELL IDENTIFICATION IN EPIRETINAL MEMBRANES - NEW ANSWERS, NEW DILEMMAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,DEPT OPHTHALMOL,BALTIMORE,MD 21218. UNIV VIRGINIA,DEPT OPHTHALMOL,CHARLOTTESVILLE,VA 22903. UNIV VIRGINIA,DEPT PATHOL,CHARLOTTESVILLE,VA 22903. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 857 EP 857 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500823 ER PT J AU KADOR, PF TAKAHASHI, Y WYMAN, M AF KADOR, PF TAKAHASHI, Y WYMAN, M TI RETINAL VESSEL CHANGES IN GALACTOSE-FED DOGS - INTERVENTION STUDIES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. OHIO STATE UNIV,COLL VET MED,COLUMBUS,OH 43210. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 878 EP 878 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500931 ER PT J AU ROBISON, WG LAVER, N KADOR, PF AF ROBISON, WG LAVER, N KADOR, PF TI MEAGER DELAY OF SUGAR CATARACTS AND PRE-PROLIFERATIVE RETINOPATHY IN GALACTOSE-FED RATS BY THE ARI PONALRESTAT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 878 EP 878 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500929 ER PT J AU ROY, MS ROY, A GALLUCCI, W COLLIER, B KIM, Y CHROUSOS, G AF ROY, MS ROY, A GALLUCCI, W COLLIER, B KIM, Y CHROUSOS, G TI DYSREGULATION OF THE HYPOTHALAMIC PITUITARY-ADRENAL AXIS IN TYPE-I DIABETICS - RELATIONSHIP TO DIABETIC-RETINOPATHY AND GLYCEMIC CONTROL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 RUTGERS STATE UNIV,NEWARK,NJ 07102. HILLSIDE HOSP,GLEN OAKS,NY. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 879 EP 879 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500936 ER PT J AU UNGERLEIDER, LG AF UNGERLEIDER, LG TI SEGREGATION OF OBJECT VISION AND SPATIAL VISION PROCESSING IN THE CORTEX OF MONKEYS AND HUMANS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIMH,NEUROPSYCHOL 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 901 EP 901 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501046 ER PT J AU TSILOU, ET HAMEL, CP HARRIS, EW DETRICK, B HOOKS, JJ REDMOND, TM AF TSILOU, ET HAMEL, CP HARRIS, EW DETRICK, B HOOKS, JJ REDMOND, TM TI PARTIAL-PURIFICATION, CHARACTERIZATION AND CLONING OF A RPE-SPECIFIC PROTEIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 914 EP 914 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501107 ER PT J AU BLAKE, DA VOGEL, T ROBERTS, DD WHIKEHART, DR AF BLAKE, DA VOGEL, T ROBERTS, DD WHIKEHART, DR TI CORNEAL ENDOTHELIAL-CELL CHEMOTAXIS TOWARDS SUGARS IS RELATED TO NA+,K+ ATPASE ACTIVITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 BIOTECHNOL GEN LTD,REHOVOT,ISRAEL. MEHARRY MED COLL,NASHVILLE,TN 37208. NCI,PATHOL LAB,BETHESDA,MD 20892. UNIV ALABAMA,BIRMINGHAM,AL 35294. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 924 EP 924 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501162 ER PT J AU SHAH, DN PIACENTINI, MA BURNIER, MN MCLEAN, IW NUSSENBLATT, RB CHAN, CC AF SHAH, DN PIACENTINI, MA BURNIER, MN MCLEAN, IW NUSSENBLATT, RB CHAN, CC TI INFLAMMATORY CELLULAR SUBSETS IN SYMPATHETIC OPHTHALMIA - CORRELATION WITH THE DISEASE KINETICS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOPATHOL LAB,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 929 EP 929 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501184 ER PT J AU DESMET, MD DYAN, M CASPI, R HAFLER, DA GERY, I NUSSENBLATT, RB AF DESMET, MD DYAN, M CASPI, R HAFLER, DA GERY, I NUSSENBLATT, RB TI DETERMINATION OF THE PRECURSOR FREQUENCY OF RESPONSE TO S-AG IN UVEITIS PATIENTS AND CONTROLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. BRIGHAM & WOMENS HOSP,CTR NEUROL DIS,BOSTON,MA 02115. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 930 EP 930 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501191 ER PT J AU SINGH, VK NITYANAND, S SHINOHARA, T PAUL, AK SINGH, V AGARWAL, PK AGARWAL, SS AF SINGH, VK NITYANAND, S SHINOHARA, T PAUL, AK SINGH, V AGARWAL, PK AGARWAL, SS TI CELLULAR IMMUNE-RESPONSE OF UVEITIS PATIENTS TO PEPTIDE-M, A FRAGMENT OF S-ANTIGEN, AND ITS HOMOLOGOUS MICROBIAL PEPTIDE YEAST HISTONE H3 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 SITAPUR EYE HOSP,SITAPUR,INDIA. SGPGI,DEPT IMMUNOL,LUCKNOW,INDIA. KING GEORGE V MEM HOSP,DEPT OPHTHALMOL,LUCKNOW 226003,UTTAR PRADESH,INDIA. NEI,RETINAL CELL & MOLEC BIOL LAB,MOLEC BIOL SECT,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 930 EP 930 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501190 ER PT J AU ETO, K SANTHANAKRISHNAN, S SUZUKI, S SHINOHARA, T AF ETO, K SANTHANAKRISHNAN, S SUZUKI, S SHINOHARA, T TI AUTOIMMUNE INFLAMMATION INDUCED BY MICROORGANISMS POSSESSING CROSS-REACTIVE ANTIGENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 931 EP 931 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501197 ER PT J AU YU, S SANTHANAKRISHNAN, S ETO, K USUKURA, J SHINOHARA, T AF YU, S SANTHANAKRISHNAN, S ETO, K USUKURA, J SHINOHARA, T TI MYCOBACTERIUM-TUBERCULOSIS INDUCED EXPERIMENTAL ADJUVANT RETINOUVEITIS (EAR) IN THE BALB/C MOUSE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 931 EP 931 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501195 ER PT J AU SAVION, S GROVER, S KAWANO, Y CASPI, RR AF SAVION, S GROVER, S KAWANO, Y CASPI, RR TI UVEITOGENICITY OF T-CELL LINES IN THE RAT DOES NOT CORRELATE WITH THEIR PRODUCTION OF TNF, IFN-GAMMA OR IL-3 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 8 Z9 8 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 MAR 15 PY 1992 VL 33 IS 4 BP 932 EP 932 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501204 ER PT J AU GROSSMAN, S LOPEZ, JS SHAH, DN RUBIN, B ALTMAN, D REZNIK, R TESTA, D FELDMAN, J CHAN, CC NUSSENBLATT, RB AF GROSSMAN, S LOPEZ, JS SHAH, DN RUBIN, B ALTMAN, D REZNIK, R TESTA, D FELDMAN, J CHAN, CC NUSSENBLATT, RB TI INHIBITION OF ENDOTOXIN-INDUCED UVEITIS (EIU) IN LEWIS RATS BY AA-313 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. BAR ILAN UNIV,RAMAT GAN,ISRAEL. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 933 EP 933 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501208 ER PT J AU LOPEZ, JS LI, O CASPI, RR NUSSENBLATT, RB KADOR, P CHAN, CC AF LOPEZ, JS LI, O CASPI, RR NUSSENBLATT, RB KADOR, P CHAN, CC TI USE OF ORAL CGS-13080 TO SUPPRESS THE DEVELOPMENT OF EXPERIMENTAL AUTOIMMUNE UVEITIS IN THE LEWIS RAT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MECHANISMS OCULAR DIS LAB,BETHESDA,MD 20892. NEI,IMMUNOL 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 933 EP 933 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501209 ER PT J AU MASTORAKOS, G SILVER, PB BOUZAS, EA CASPI, RR CHAN, CC CHROUSOS, GP AF MASTORAKOS, G SILVER, PB BOUZAS, EA CASPI, RR CHAN, CC CHROUSOS, GP TI IMMUNOREACTIVE CORTICOTROPIN RELEASING HORMONE IN EXPERIMENTAL UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NEI,OCULAR GENET BRANCH,BETHESDA,MD 20892. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 933 EP 933 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501207 ER PT J AU ROBERGE, FG CHEN, HF CHAN, CC XU, DS AF ROBERGE, FG CHEN, HF CHAN, CC XU, DS TI RAPAMYCIN TREATMENT OF AUTOIMMUNE UVEORETINITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NOTRE DAME RES CTR,MONTREAL,QUEBEC,CANADA. NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 933 EP 933 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501210 ER PT J AU KASNER, L CHAN, CC WHITCUP, SM CORDELLAMIELE, E GERY, I AF KASNER, L CHAN, CC WHITCUP, SM CORDELLAMIELE, E GERY, I TI THE EFFECT OF CHLORPROMAZINE (CPZ) ON ENDOTOXIN INDUCED UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NICHHD,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 934 EP 934 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501214 ER PT J AU MARTIN, DF DEBARGE, LR DESMET, M NUSSENBLATT, RB ROBERGE, FG AF MARTIN, DF DEBARGE, LR DESMET, M NUSSENBLATT, RB ROBERGE, FG TI SYNERGISTIC EFFECT OF RAPAMYCIN AND CYCLOSPORINE-A - SUPPRESSION OF LYMPHOCYTE-RESPONSE TO RETINAL S-ANTIGEN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 934 EP 934 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501211 ER PT J AU RUBIN, BI NAJAFIAN, F CASPI, RR SEHGAL, SN NUSSENBLATT, RB AF RUBIN, BI NAJAFIAN, F CASPI, RR SEHGAL, SN NUSSENBLATT, RB TI SYNERGISTIC INTERACTIONS OF CYCLOSPORINE AND RAPAMYCIN TO INHIBIT EAU IN THE LEWIS RAT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 WYETH AYERST LABS,PRINCETON,NJ. NEI,IMMUNOL LAB,BETHESDA,MD 20892. HOWARD UNIV,WASHINGTON,DC 20059. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 934 EP 934 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501212 ER PT J AU FENTON, RM SOYLU, M DESMET, MD CHAN, CC NUSSENBLATT, RB AF FENTON, RM SOYLU, M DESMET, MD CHAN, CC NUSSENBLATT, RB TI THE USE OF INDIRECT IMMUNOFLUORESCENCE TESTING AND GUINEA-PIG LIP MUCOSA FOR THE EVALUATION OF BEHCET AND NON-BEHCET UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract ID ANTIBODIES; DISEASE C1 UNIV CUKUROVA,ADANA,TURKEY. NEI,IMMUNOPATHOL LAB,BETHESDA,MD 20892. NR 2 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 942 EP 942 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501253 ER PT J AU JOBIN, DC KAZATCHKINE, MD CHAN, CC HOANG, PL AF JOBIN, DC KAZATCHKINE, MD CHAN, CC HOANG, PL TI USE OF INTRAVENOUS IMMUNOGLOBULINS (IVIG) IN THE TREATMENT OF BIRDSHOT RETINOCHOROIDOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 INSERM,U28,F-75005 PARIS,FRANCE. NEI,IMMUNOL LAB,BETHESDA,MD 20892. HOP PITIE,DEPT OPHTHALMOL,F-75651 PARIS 13,FRANCE. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 942 EP 942 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501254 ER PT J AU OTOUSA, JE STEELE, F RIEGER, R WASHBURN, T AF OTOUSA, JE STEELE, F RIEGER, R WASHBURN, T TI RETINAL DEGENERATION IN DROSOPHILA RDGC RESULTS FROM DEFECTIVE NOVEL SERINE/THREONINE PROTEIN PHOSPHATASE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV NOTRE DAME,NOTRE DAME,IN 46556. NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 946 EP 946 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501272 ER PT J AU BOUZAS, EA CARUSO, RC BANKIEWICZ, MA KAISERKUPFER, MI AF BOUZAS, EA CARUSO, RC BANKIEWICZ, MA KAISERKUPFER, MI TI 2 DIFFERENT VEP PATTERNS DEMONSTRATED IN ALBINISM UNRELATED TO CLINICAL TYPE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 964 EP 964 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501356 ER PT J AU FLIESLER, SJ WELPLY, JK DUFFIN, KL FLORMAN, R OBRIEN, PJ PITTLER, SJ AF FLIESLER, SJ WELPLY, JK DUFFIN, KL FLORMAN, R OBRIEN, PJ PITTLER, SJ TI OLIGOSACCHARIDE STRUCTURE AND GLYCOSYLATION SITE SEQUENCES OF FROG RHODOPSIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 ST LOUIS UNIV,SCH MED,BETHESDA EYE INST,ST LOUIS,MO 63104. MONSANTO CO,ST LOUIS,MO 63166. NEI,BETHESDA,MD 20892. BAYLOR COLL MED,CULLEN EYE INST,HOUSTON,TX 77030. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1002 EP 1002 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501553 ER PT J AU ABE, T ABE, T KIKUCHI, T SHINOHARA, T AF ABE, T ABE, T KIKUCHI, T SHINOHARA, T TI A FAMILY OF MULTIPLE PHOSDUCIN GENES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI, LRCMB, BETHESDA, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1005 EP 1005 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501572 ER PT J AU GALLO, S JONES, BE THOMPSON, E MOSHAYEDI, P CHADER, G WALDBILLIG, R AF GALLO, S JONES, BE THOMPSON, E MOSHAYEDI, P CHADER, G WALDBILLIG, R TI CHARACTERIZATION OF AN INTERPHOTORECEPTOR MATRIX (IPM) METALLOPROTEINASE-TIMP-LIKE INHIBITOR SYSTEM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. RI Thompson, Erik/A-1425-2009 OI Thompson, Erik/0000-0002-9723-4924 NR 0 TC 5 Z9 5 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 MAR 15 PY 1992 VL 33 IS 4 BP 1010 EP 1010 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501600 ER PT J AU SANTHANAKRISHNAN, S ETO, K SHINOHARA, T AF SANTHANAKRISHNAN, S ETO, K SHINOHARA, T TI IMMUNOGENIC DETERMINANTS BETWEEN SELF AND NONSELF CROSS-REACTIVE ANTIGENS IN EAU SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1023 EP 1023 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501659 ER PT J AU MAHDI, RM CASPI, RR TSAI, L NUSSENBLATT, RB GERY, I EGWUAGU, CE AF MAHDI, RM CASPI, RR TSAI, L NUSSENBLATT, RB GERY, I EGWUAGU, CE TI T-CELL RECEPTOR V-BETA GENE USAGE IN EXPERIMENTAL AUTOIMMUNE UVEORETINITIS (EAU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1024 EP 1024 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501662 ER PT J AU HARA, Y CASPI, R WIGGERT, B STREILEIN, JW AF HARA, Y CASPI, R WIGGERT, B STREILEIN, JW TI ANALYSIS OF AN INVITRO-CREATED ACAID-INDUCING SIGNAL THAT PREVENTS IRBP-SPECIFIC EXPERIMENTAL AUTOIMMUNE UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MIAMI,SCH MED,DEPT MICROBIOL & IMMUNOL,MIAMI,FL 33152. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NEI,RETINAL CELL & MOLEC 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1025 EP 1025 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501671 ER PT J AU KOZHICH, AT VISTICA, BP GERY, I BERZOFSKY, JA WAUBEN, M VANEDEN, W AF KOZHICH, AT VISTICA, BP GERY, I BERZOFSKY, JA WAUBEN, M VANEDEN, W TI INHIBITION OF EXPERIMENTAL AUTOIMMUNE UVEORETINITIS (EAU) BY SYNTHETIC PEPTIDES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MM SHEMYAKIN BIOORGAN CHEM INST,MOSCOW 117312,USSR. NEI,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. UNIV UTRECHT,UTRECHT,NETHERLANDS. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1025 EP 1025 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501670 ER PT J AU SASAMOTO, Y SHIRKEY, BL KAWANO, YI WIGGERT, B CHADER, GJ GERY, I AF SASAMOTO, Y SHIRKEY, BL KAWANO, YI WIGGERT, B CHADER, GJ GERY, I TI INDUCTION OF UNRESPONSIVENESS INVITRO TOWARD A UVEITOGENIC IRBP-DERIVED PEPTIDE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. HOWARD HUGHES MED INST,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 1025 EP 1025 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501668 ER PT J AU SANDELL, JH JACOBOWITZ, DM AF SANDELL, JH JACOBOWITZ, DM TI THE DISTRIBUTION OF CALRETININ-LIKE IMMUNOREACTIVITY AND CORRELATION WITH MESSENGER-RNA EXPRESSION IN THE RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,BOSTON,MA 02118. NIMH,BETHESDA,MD 20892. NR 0 TC 6 Z9 6 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 MAR 15 PY 1992 VL 33 IS 4 BP 1032 EP 1032 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501706 ER PT J AU KIDD, GL RUSSELL, P AF KIDD, GL RUSSELL, P TI HOW DIFFERENTIATED ARE LENTOID BODIES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1038 EP 1038 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501732 ER PT J AU TUMMINIA, SJ RAO, PV ZIGLER, JS RUSSELL, P AF TUMMINIA, SJ RAO, PV ZIGLER, JS RUSSELL, P TI ZETA-CRYSTALLIN IS PRESENT IN CULTURED MOUSE LENS EPITHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1039 EP 1039 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501738 ER PT J AU LAVER, N ROBISON, WG CALVIN, HI FU, SCJ AF LAVER, N ROBISON, WG CALVIN, HI FU, SCJ TI EARLY LESIONS IN CATARACTS OF GSH-DEPLETED MOUSE PUPS RETARDED BY ASCORBATE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV MED & DENT NEW JERSEY,DEPT BIOCHEM & MOLEC BIOL,NEWARK,NJ 07103. NR 1 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 1041 EP 1041 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501752 ER PT J AU DREW, LR PISANO, MM CHEPELINSKY, AB AF DREW, LR PISANO, MM CHEPELINSKY, AB TI CAT GENE-EXPRESSION IN TRANSGENIC MICE DIRECTED BY THE HUMAN MIP GENE PROMOTER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 MAR 15 PY 1992 VL 33 IS 4 BP 1043 EP 1043 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501761 ER PT J AU LI, X CUTHBERTSON, RA ZELENKA, PS NORMAN, B PIATIGORSKY, J AF LI, X CUTHBERTSON, RA ZELENKA, PS NORMAN, B PIATIGORSKY, J TI EXPRESSION OF DELTA-1-CRYSTALLIN AND DELTA-2-CRYSTALLIN IN LENS, RETINA AND CORNEA OF THE CHICKEN EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 1 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 1043 EP 1043 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501759 ER PT J AU TOMAREV, S ZINOVIEVA, R PIATIGORSKY, J AF TOMAREV, S ZINOVIEVA, R PIATIGORSKY, J TI STRUCTURE AND EXPRESSION OF CRYSTALLIN GENES OF CEPHALOPODS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 MAR 15 PY 1992 VL 33 IS 4 BP 1043 EP 1043 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501758 ER PT J AU ZIGLER, JS GONZALEZ, P RAO, PV AF ZIGLER, JS GONZALEZ, P RAO, PV TI COMPARATIVE-STUDY OF ZETA-CRYSTALLIN GENE FROM DIFFERENT SPECIES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1043 EP 1043 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501760 ER PT J AU HOPE, JN HEJTMANCIK, JF AF HOPE, JN HEJTMANCIK, JF TI EXPRESSION OF THE MOUSE BETA-A3/A1-CRYSTALLIN IN A BACULOVIRUS SYSTEM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LMOD,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1044 EP 1044 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501765 ER PT J AU KIM, RY WISTOW, GJ AF KIM, RY WISTOW, GJ TI EXPRESSION OF THE DUCK TAU-CRYSTALLIN/ALPHA-ENOLASE GENE IN TRANSGENIC MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 MAR 15 PY 1992 VL 33 IS 4 BP 1044 EP 1044 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501764 ER PT J AU JONES, BE WALDBILLIG, RJ SCHOEN, TJ HODOS, W CHADER, GJ AF JONES, BE WALDBILLIG, RJ SCHOEN, TJ HODOS, W CHADER, GJ TI EXTRACELLULAR-MATRIX METALLOPROTEINASES AND INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEIN (IGFBP) ARE ALTERED IN EXPERIMENTAL MYOPIA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV MARYLAND,DEPT PSYCHOL,COLLEGE PK,MD 20742. NR 0 TC 3 Z9 4 U1 0 U2 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 1054 EP 1054 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501811 ER PT J AU USUKURA, J SAI, S BREITMAN, M SHINOHARA, T AF USUKURA, J SAI, S BREITMAN, M SHINOHARA, T TI PHOTORECEPTOR CELL-DIFFERENTIATION IN THE TRANSGENIC MOUSE WITH OPSIN PROMOTER AND DIPHTHERIA-TOXIN FUSION GENE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NAGOYA UNIV, SCH MED, NAGOYA, AICHI 466, JAPAN. MT SINAI HOSP, TORONTO M5G 1X5, ONTARIO, CANADA. NEI, LMDB, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 EI 1552-5783 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1060 EP 1060 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501836 ER PT J AU SMITH, SB WIGGERT, B DUNCAN, T AF SMITH, SB WIGGERT, B DUNCAN, T TI RETINAL DEGENERATION IN THE C57VIT/VIT MOUSE - MORPHOMETRIC EVALUATION AND BIOCHEMICAL-STUDIES OF RHODOPSIN AND RETINOIDS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MED COLL GEORGIA,AUGUSTA,GA 30912. NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 1066 EP 1066 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501873 ER PT J AU GAUDET, SJ CHADER, GJ AF GAUDET, SJ CHADER, GJ TI ARYLAMINE N-ACETYLTRANSFERASE (NAT) - PARTIAL-PURIFICATION AND CHARACTERIZATION IN THE BOVINE RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1067 EP 1067 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501876 ER PT J AU GENTLEMAN, S LLOYD, R CHO, J CHADER, GJ AF GENTLEMAN, S LLOYD, R CHO, J CHADER, GJ TI STUDIES OF ALPHA-TUBULIN ACETYLTRANSFERASE IN BOVINE RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract ID PIGMENTOSA; AXONEMES C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 4 TC 0 Z9 0 U1 0 U2 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 1067 EP 1067 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501875 ER PT J AU WANG, Y PERCOPO, C DETRICK, B HOOKS, JJ AF WANG, Y PERCOPO, C DETRICK, B HOOKS, JJ TI CORONAVIRUS REPLICATION WITHIN THE RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1069 EP 1069 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501883 ER PT J AU BANKIEWICZ, MA CARUSO, RC BOUZAS, EA KAISERKUPFER, M AF BANKIEWICZ, MA CARUSO, RC BOUZAS, EA KAISERKUPFER, M TI ARE THE ELECTRORETINOGRAM AND THE ELECTROOCULOGRAM INDEPENDENT TESTS OF RETINAL FUNCTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1074 EP 1074 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501912 ER PT J AU REUTER, LM CARUSO, RC MERCER, PA KAISERKUPFER, MI AF REUTER, LM CARUSO, RC MERCER, PA KAISERKUPFER, MI TI THE INFLUENCE OF OCULAR LENGTH ON THE HUMAN GANZFELD ELECTRORETINOGRAM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1074 EP 1074 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501913 ER PT J AU CARUSO, RC KAISERKUPFER, MI BANKIEWICZ, MA AF CARUSO, RC KAISERKUPFER, MI BANKIEWICZ, MA TI STILES-CRAWFORD EFFECT AND INCREMENT THRESHOLD MEASUREMENTS IN GYRATE ATROPHY OF THE CHOROID AND RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1075 EP 1075 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501917 ER PT J AU MAGNO, BV DATILES, MB LASA, SM AF MAGNO, BV DATILES, MB LASA, SM TI ONE-YEAR CATARACT PROGRESSION RATES IN AN ALL-CATARACT POPULATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1096 EP 1096 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502018 ER PT J AU FITZGIBBON, EJ ZEE, DS OPTICAN, LM AF FITZGIBBON, EJ ZEE, DS OPTICAN, LM TI A MODEL OF SACCADE-VERGENCE INTERACTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1101 EP 1101 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502039 ER PT J AU KERTZMAN, C CURRIE, JN RAMSDEN, BM JACKSON, CL HALLETT, M FITZGIBBON, EJ AF KERTZMAN, C CURRIE, JN RAMSDEN, BM JACKSON, CL HALLETT, M FITZGIBBON, EJ TI PET SCAN STUDY OF REFLEXIVE, MEMORY GUIDED AND ANTISACCADES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. MENTAL HLTH RES INST,MELBOURNE,AUSTRALIA. NR 0 TC 3 Z9 3 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 MAR 15 PY 1992 VL 33 IS 4 BP 1153 EP 1153 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502311 ER PT J AU SCHWARZ, U FITZGIBBON, EJ AF SCHWARZ, U FITZGIBBON, EJ TI EYE-MOVEMENTS DURING COMPUTER-SIMULATED OPTICAL-FLOW AND TARGET MOTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LSR,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1153 EP 1153 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502306 ER PT J AU ZADUNAISKY, JA SPRING, K SELLERS, J ROBISON, WG AF ZADUNAISKY, JA SPRING, K SELLERS, J ROBISON, WG TI CONTRACTION AND DRUG SENSITIVITY OF CULTURED HUMAN TRABECULAR MESHWORK CELLS IN NORMAL AND GLAUCOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NYU,NEW YORK,NY 10003. NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 1163 EP 1163 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502355 ER PT J AU KAHN, CR LEE, IH RHIM, JS AF KAHN, CR LEE, IH RHIM, JS TI GENERATION AND MORPHOLOGICAL CHARACTERIZATION OF HUMAN CORNEAL EPITHELIAL PRIMARY CULTURES AND IMMORTALIZED CELL-LINES IN SERUM FREE MEDIUM - POTENTIAL MODEL FOR OCULAR STUDIES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. GILLETTE MED EVALUAT LABS,GAITHERSBURG,MD 20879. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1176 EP 1176 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502419 ER PT J AU REDMOND, TM NICKERSON, JM AF REDMOND, TM NICKERSON, JM TI RETINOID BINDING TO A RECOMBINANT CENTRAL 2-REPEAT SEGMENT OF IRBP SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. EMORY UNIV,ATLANTA,GA 30322. NR 0 TC 3 Z9 3 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 MAR 15 PY 1992 VL 33 IS 4 BP 1181 EP 1181 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502442 ER PT J AU DUNCAN, TE KUTTY, G PUTILINA, T CHADER, GJ WIGGERT, B AF DUNCAN, TE KUTTY, G PUTILINA, T CHADER, GJ WIGGERT, B TI LIGAND-BINDING BY A RETINOID-BINDING GLYCOPROTEIN FROM DROSOPHILA-MELANOGASTER HEADS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 1 TC 2 Z9 2 U1 0 U2 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 1182 EP 1182 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502450 ER PT J AU OKAJIMA, TI WIGGERT, B CHADER, GJ PEPPERBERG, DR AF OKAJIMA, TI WIGGERT, B CHADER, GJ PEPPERBERG, DR TI RETINOID PROCESSING IN THE RPE-EYECUP PROBED WITH ALL-TRANS (H-3) RETINOL AND IRBP SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV ILLINOIS,COLL MED,DEPT OPHTHALMOL,CHICAGO,IL 60680. UNIV ILLINOIS,COLL MED,DEPT VISUAL SCI,CHICAGO,IL 60680. NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1183 EP 1183 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502452 ER PT J AU HESS, HH AF HESS, HH TI EFFECT OF NUTRITIONAL FACTORS ON RETINAL DEGENERATION AND CATARACTS IN PINK-EYED TAN-HOODED ROYAL-COLLEGE-OF-SURGEONS (RCS) RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1186 EP 1186 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502466 ER PT J AU JUN, L GENTLEMAN, S WETZEL, MG OBRIEN, P CHADER, GJ AF JUN, L GENTLEMAN, S WETZEL, MG OBRIEN, P CHADER, GJ TI STUDIES ON THE DOCOSAHEXAENOIC ACID (DHA) BINDING-PROTEINS IN RETINA CYTOSOL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV KANSAS,MED CTR,KANSAS CITY,KS 66103. HLTH RES ASSOCIATES,ROCKVILLE,MD. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1189 EP 1189 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502482 ER PT J AU PIACENTINI, MA SHAH, DN CHAN, CC NUSSENBLATT, RB MCLEAN, IW BURNIER, MN AF PIACENTINI, MA SHAH, DN CHAN, CC NUSSENBLATT, RB MCLEAN, IW BURNIER, MN TI THE ORBITAL PSEUDOTUMOR SPECTRUM - AN IMMUNOPATHOLOGICAL STUDY OF 40 CASES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOPATHOL LAB,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NR 0 TC 2 Z9 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 1196 EP 1196 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502509 ER PT J AU BURNIER, MN PIACENTINI, MA SHAH, DN CHAN, CC NUSSENBLATT, RB MCLEAN, IW AF BURNIER, MN PIACENTINI, MA SHAH, DN CHAN, CC NUSSENBLATT, RB MCLEAN, IW TI DIFFERENTIATION BETWEEN BENIGN AND MALIGNANT ORBITAL LYMPHOCYTIC LESIONS - THE USE OF PROLIFERATING CELL NUCLEAR ANTIGEN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOPATHOL LAB,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NR 1 TC 2 Z9 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 1245 EP 1245 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502757 ER PT J AU OLD, SE CARPER, DA HOHMAN, TC AF OLD, SE CARPER, DA HOHMAN, TC TI EXPRESSION OF NA+,K+-ATPASE IN PRIMARY DOG LENS EPITHELIAL-CELLS AFTER OSMOTIC-STRESS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. WYETH AYERST LAB,PRINCETON,NJ. NR 0 TC 1 Z9 1 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 MAR 15 PY 1992 VL 33 IS 4 BP 1249 EP 1249 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502776 ER PT J AU FREDERIKSE, P CVEKL, A PIATIGORSKY, J AF FREDERIKSE, P CVEKL, A PIATIGORSKY, J TI REGULATION OF ALPHA-B-CRYSTALLIN GENE-EXPRESSION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 MAR 15 PY 1992 VL 33 IS 4 BP 1251 EP 1251 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502786 ER PT J AU HAWKINS, BS FINE, SL STRAATSMA, BR MOWERY, RL EARLE, JD AF HAWKINS, BS FINE, SL STRAATSMA, BR MOWERY, RL EARLE, JD TI 5-YEAR PROGRESS REPORT FROM THE COLLABORATIVE OCULAR MELANOMA STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV HOSP,WILMER OPHTHALMOL INST,BALTIMORE,MD 21205. UNIV PENN,SCHEIE EYE INST,PHILADELPHIA,PA 19104. JULES STEIN EYE INST,LOS ANGELES,CA. NEI,BETHESDA,MD 20892. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1254 EP 1254 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502803 ER PT J AU SUH, ED SASAMOTO, Y VISTICA, BP WIGGERT, B NUSSENBLATT, RB GERY, I AF SUH, ED SASAMOTO, Y VISTICA, BP WIGGERT, B NUSSENBLATT, RB GERY, I TI MECHANISM AND SPECIFICITY OF ORAL TOLERANCE IN EXPERIMENTAL AUTOIMMUNE UVEORETINITIS (EAU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1285 EP 1285 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502954 ER PT J AU CHINTALAGIRI, S DATILES, MB VIVINO, M TRUS, B MAGNO, BV LASA, SM AF CHINTALAGIRI, S DATILES, MB VIVINO, M TRUS, B MAGNO, BV LASA, SM TI STUDIES ON SCHEIMPFLUG CATARACT IMAGES - AUTOMATED DETECTION OF REGION BOUNDARIES AND THE AXIAL CENTER OF A LENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NIH,DIV COMP RES & TECHNOL,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1300 EP 1300 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503021 ER PT J AU DATILES, MB HERNANDEZ, E LASA, MS PODGOR, M MAGNO, BV AF DATILES, MB HERNANDEZ, E LASA, MS PODGOR, M MAGNO, BV TI RETROILLUMINATION PHOTOGRAPHY FOR CORTICAL CATARACT - IMAGE-ANALYSIS USING PLANIMETRY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1300 EP 1300 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503022 ER PT J AU LASA, MSM DATILES, MB CARUSO, RC MAGNO, BV AF LASA, MSM DATILES, MB CARUSO, RC MAGNO, BV TI GLARE SENSITIVITY IN EARLY CATARACTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1301 EP 1301 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503029 ER PT J AU ABREU, MT BURNIER, MN GAZINELLI, R LOPEZ, JS MARTINS, MC SILVEIRA, C BELFORT, R NUSSENBLATT, RB AF ABREU, MT BURNIER, MN GAZINELLI, R LOPEZ, JS MARTINS, MC SILVEIRA, C BELFORT, R NUSSENBLATT, RB TI EXPERIMENTAL-MODEL OF OCULAR TOXOPLASMOSIS USING THE OH3 AND S11 STRAINS FROM SOUTHERN BRAZIL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 CLIN SILVEIRA,EREXIM,RS,BRAZIL. NEI,BETHESDA,MD 20892. ESCOLA PAULISTA MED SCH,BR-04023 SAO PAULO,BRAZIL. RI Belfort Jr, Rubens/E-2252-2012 OI Belfort Jr, Rubens/0000-0002-8422-3898 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1320 EP 1320 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503131 ER PT J AU BREZIN, AP GAZZINELLI, R LI, Q NUSSENBLATT, RB CHAN, CC AF BREZIN, AP GAZZINELLI, R LI, Q NUSSENBLATT, RB CHAN, CC TI EXPERIMENTAL REACTIVATION OF CHRONIC TOXOPLASMOSIS - STAGE-SPECIFIC INSITU HYBRIDIZATION, DNA AMPLIFICATION AND IMMUNOHISTOCHEMISTRY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 1320 EP 1320 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503132 ER PT J AU CHAN, CC LI, Q BREZIN, AP WHITCUP, SM EGWAGU, C OTTESEN, EA NUSSENBLATT, RB AF CHAN, CC LI, Q BREZIN, AP WHITCUP, SM EGWAGU, C OTTESEN, EA NUSSENBLATT, RB TI DETECTION OF IL-2 AND IL-4 MESSENGER-RNA IN THE CONJUNCTIVA OF PATIENTS WITH ONCHOCERCIASIS BY INSITU HYBRIDIZATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NIAID,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1320 EP 1320 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503133 ER PT J AU REMALEY, NA MILTON, RC AF REMALEY, NA MILTON, RC TI EFFECTS OF INTERPOLATION IN CLINICAL GRADING SCALES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1324 EP 1324 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503150 ER PT J AU LIN, LR GIBLIN, FJ REDDY, VN KADOR, PF KINOSHITA, JH LOU, M AF LIN, LR GIBLIN, FJ REDDY, VN KADOR, PF KINOSHITA, JH LOU, M TI THE EFFICACY OF ALDOSE REDUCTASE INHIBITORS ON POLYOL ACCUMULATION IN HUMAN LENS AND RETINAL-PIGMENT EPITHELIUM IN TISSUE-CULTURE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 OAKLAND UNIV,EYE RES INST,ROCHESTER,MI 48063. NEI,BETHESDA,MD 20892. ALCON LABS INC,FT WORTH,TX 76101. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1376 EP 1376 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503409 ER PT J AU SATO, S AF SATO, S TI NAPHTHALENE DIOL DEHYDROGENASE AND ALDOSE REDUCTASE IN RAT LENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1376 EP 1376 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503408 ER PT J AU MORI, K VONKIENLIN, M BALABAN, R KADOR, PF AF MORI, K VONKIENLIN, M BALABAN, R KADOR, PF TI INVIVO MEASUREMENT OF ALDOSE REDUCTASE-ACTIVITY IN THE RABBIT LENS BY F-19 NMR-SPECTROSCOPY WITH 3-DEOXY-3-FLUOROGLUCOSE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NHLBI,INVIVO NMR RES CTR,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1377 EP 1377 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503411 ER PT J AU SCHAFFHAUSER, M SATO, S TERADA, T KADOR, PF AF SCHAFFHAUSER, M SATO, S TERADA, T KADOR, PF TI NADPH-DEPENDENT REDUCTASES IN DOG LENS, RETINA AND THYROID - THE PRESENCE A 3RD ENZYME GLYCERALDEHYDE REDUCTASE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1377 EP 1377 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503410 ER PT J AU TAKAHASHI, Y WYMAN, M KADOR, PF AF TAKAHASHI, Y WYMAN, M KADOR, PF TI POSTERIOR MIGRATION OF LENS EPITHELIAL-CELLS IN CATARACTS OF GALACTOSE-FED DOGS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. OHIO STATE UNIV,COLL VET MED,COLUMBUS,OH 43210. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1377 EP 1377 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503413 ER PT J AU YOKOYAMA, T LIN, LR CHAKRAPANI, B CARPER, D REDDY, VN AF YOKOYAMA, T LIN, LR CHAKRAPANI, B CARPER, D REDDY, VN TI THE ROLE OF NA+-K+ATPASE IN THE INCREASED ACCUMULATION OF MYOINOSITOL AND TAURINE IN CULTURED HUMAN LENS EPITHELIAL-CELLS UNDER HYPERTONIC STRESS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 OAKLAND UNIV,EYE RES INST,ROCHESTER,MI 48063. NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1378 EP 1378 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503417 ER PT J AU BERNSTEIN, SL NICKERSON, J AF BERNSTEIN, SL NICKERSON, J TI RIBOZYME-MEDIATED CLEAVAGE OF INTERPHOTORECEPTOR RETINOID BINDING-PROTEIN (IRBP) MESSENGER-RNA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. EMORY UNIV,DEPT OPHTHALMOL,ATLANTA,GA 30322. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1399 EP 1399 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503528 ER PT J AU BORST, DE SI, JS NICKERSON, JM AF BORST, DE SI, JS NICKERSON, JM TI FUNCTIONAL COMPARISON OF THE MOUSE IRBP PROMOTER IN Y-79 CELLS AND TRANSGENIC MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. EMORY UNIV,DEPT OPHTHALMOL,ATLANTA,GA 30322. NR 0 TC 6 Z9 6 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 MAR 15 PY 1992 VL 33 IS 4 BP 1399 EP 1399 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503525 ER PT J AU KUTTY, G VANVEEN, T NICKERSON, J SI, JS CHADER, GJ WIGGERT, B AF KUTTY, G VANVEEN, T NICKERSON, J SI, JS CHADER, GJ WIGGERT, B TI EFFECT OF LIGHT DEPRIVATION ON IRBP GENE-EXPRESSION IN THE MOUSE EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. GOTHENBURG UNIV,DEPT ZOOL,S-41124 GOTHENBURG,SWEDEN. EMORY UNIV,ATLANTA,GA 30322. NR 1 TC 0 Z9 0 U1 0 U2 2 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 MAR 15 PY 1992 VL 33 IS 4 BP 1399 EP 1399 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503529 ER PT J AU NICKERSON, JM BORST, DE SI, JS AF NICKERSON, JM BORST, DE SI, JS TI CIS-ELEMENTS AND TRANS-FACTORS IN THE IRBP GENE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 EMORY UNIV,DEPT OPHTHALMOL,ATLANTA,GA 30322. NEI,LRCMB,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1399 EP 1399 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503526 ER PT J AU DAVIS, JL WINWARD, KR LONARDO, EC LEE, TD PFLUGFELDER, SC NUSSENBLATT, RB MEISLER, DM AF DAVIS, JL WINWARD, KR LONARDO, EC LEE, TD PFLUGFELDER, SC NUSSENBLATT, RB MEISLER, DM TI ASSOCIATION OF P-ACNES ENDOPHTHALMITIS WITH HLA TYPE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MIAMI,MIAMI,FL 33152. CLEVELAND CLIN EDUC FDN,CLEVELAND,OH 44106. AMER RED CROSS,ROCKVILLE,MD. NEI,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1421 EP 1421 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503634 ER PT J AU FAZIOLI, F BOTTARO, DP MINICHIELLO, L AURICCHIO, A WONG, WT SEGATTO, O DIFIORE, PP AF FAZIOLI, F BOTTARO, DP MINICHIELLO, L AURICCHIO, A WONG, WT SEGATTO, O DIFIORE, PP TI IDENTIFICATION AND BIOCHEMICAL-CHARACTERIZATION OF NOVEL PUTATIVE SUBSTRATES FOR THE EPIDERMAL GROWTH-FACTOR RECEPTOR KINASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PHOSPHOLIPASE-C-GAMMA; PDGF BETA-RECEPTOR; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION; EGF RECEPTOR; INSULIN-RECEPTOR; PROTEIN; DOMAINS; CELLS; GAP AB To gain insight into the mechanisms which control the mitogenic response to epidermal growth factor (EGF), we have partially purified and characterized several intracellular proteins which are phosphorylated on tyrosine residues following activation of the epidermal growth factor receptor (EGFR). Partial purification was achieved by immunoaffinity chromatography using immobilized anti-phosphotyrosine antibodies. Antisera generated against the partially purified proteins were used to identify at least five novel EGFR putative substrates, designated, on the basis of their apparent molecular weight, p97, p68, p61, p56, and p23. All of these proteins became specifically phosphorylated on tyrosine after EGF treatment of intact cells, as assessed by phosphoamino acid analysis, and none of them represented an EGFR degradation product. The phosphorylation of these proteins appeared to be relatively specific for the EGFR. In particular, an EGFR-related kinase, erbB-2 was much less efficient than EGFR at phosphorylating p97, p56, and p23 and incapable of phosphorylating p68. The identification of these novel EGFR putative substrates should lead to a better understanding of the mechanisms controlling the specificity of EGFR-mediated mitogenic signaling. C1 NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,RM 1D23,BETHESDA,MD 20892. RI Bottaro, Donald/F-8550-2010; Di Fiore, Pier Paolo/K-2130-2012; OI Bottaro, Donald/0000-0002-5057-5334; Di Fiore, Pier Paolo/0000-0002-2252-0950; AURICCHIO, Alberto/0000-0002-0832-2472 NR 46 TC 35 Z9 35 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1992 VL 267 IS 8 BP 5155 EP 5161 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700026 PM 1347529 ER PT J AU DONOHUE, SJ ROSEBOOM, PH KLEIN, DC AF DONOHUE, SJ ROSEBOOM, PH KLEIN, DC TI BOVINE HYDROXYINDOLE-O-METHYLTRANSFERASE - SIGNIFICANT SEQUENCE REVISION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article AB Hydroxyindole-O-methyltransferase (HIOMT) catalyzes the final step in melatonin synthesis. The nucleotide and deduced amino acid sequences of bovine HIOMT have been reported. Our laboratory recently isolated a cDNA clone encoding human HIOMT. Comparison of the human and bovine nucleotide sequences revealed several discrepancies which prevented perfect alignment and produced defined regions of virtually no homology in the deduced amino acid sequence. Consequently, we repeated sequence analysis of the original bovine HIOMT cDNA clone, the results of which are reported here. The revised nucleotide sequence includes 23 differences from the published sequence. This completely changes the deduced amino acid sequence in two regions, encompassing a total of 96 residues, or 28% of the protein. The revised deduced amino acid sequence predicts different post-translational modifications as compared to that of the original deduced sequence. This information will make it possible in future investigations of HIOMT to design improved polymerase chain reaction primers, peptides for the generation of antisera, and probes for various types of analysis and screening of libraries. C1 NICHHD,NEUROENDOCRINOL SECT,DEV NEUROBIOL LAB,BLDG 36,ROOM 4A07,BETHESDA,MD 20892. NR 3 TC 18 Z9 19 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1992 VL 267 IS 8 BP 5184 EP 5185 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700030 PM 1544900 ER PT J AU OGASAHARA, K HIRAGA, K ITO, W MILES, EW YUTANI, K AF OGASAHARA, K HIRAGA, K ITO, W MILES, EW YUTANI, K TI ORIGIN OF THE MUTUAL ACTIVATION OF THE ALPHA-SUBUNIT AND BETA-2-SUBUNIT IN THE ALPHA-2-BETA-2-COMPLEX OF TRYPTOPHAN SYNTHASE - EFFECT OF ALANINE OR GLYCINE SUBSTITUTIONS AT PROLINE RESIDUES IN THE ALPHA-SUBUNIT SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; BETA-SUBUNIT; PYRIDOXAL-PHOSPHATE; CATALYTIC RESIDUE; L-SERINE; MECHANISM; BINDING; COMPLEX; SYNTHETASE AB To understand how the alpha and beta-2 subunits of tryptophan synthase from Escherichia coli interact to form an alpha-2-beta-2 complex and undergo mutual activation, we have investigated alpha-subunits with single amino acid replacements at conserved proline residues. Although the activities of alpha-2-beta-2 complexes that contain wild type alpha-subunit or alpha-subunits substituted at positions 28, 62, 96, and 207 are similar, the activities of alpha-2-beta-2 complexes that contain alpha-subunits substituted at positions 57 and 132 are remarkably altered. Whereas the latter enzymes have greatly reduced activities in the individual half-reactions, they have considerably higher activities in the overall reaction. These remarkable activity results are explained by a decrease in the affinity of these mutant alpha-subunits for the beta-2 subunit and by an increase in the affinity in the combined presence of ligands of both the alpha-subunit and the beta-2 subunit. Isothermal calorimetric titrations of wild type beta-2 subunit with wild type alpha-subunit and a mutant alpha-subunit containing a substitution of glycine for proline at position 132 show that both the affinity and the exothermic association enthalpy are greatly reduced in the mutant alpha-subunit although the stoichiometry of association is unchanged. The affinity of the mutant alpha-subunit for the beta-2 subunits is greatly increased in the presence of an alpha-subunit ligand, alpha-glycerol phosphate. We conclude that proline 132 plays a critical role in subunit interaction and in mutual subunit activation. C1 OSAKA UNIV, INST PROT RES, 3-2 YAMADAOKA, SUITA, OSAKA 565, JAPAN. NIH, BETHESDA, MD 20892 USA. NR 42 TC 32 Z9 32 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1992 VL 267 IS 8 BP 5222 EP 5228 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700037 PM 1544905 ER PT J AU MAUNE, JF KLEE, CB BECKINGHAM, K AF MAUNE, JF KLEE, CB BECKINGHAM, K TI CA2+ BINDING AND CONFORMATIONAL CHANGE IN 2 SERIES OF POINT MUTATIONS TO THE INDIVIDUAL CA2+-BINDING SITES OF CALMODULIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BOVINE BRAIN CALMODULIN; CALCIUM-BINDING; TROPONIN-C; TRYPTIC FRAGMENTS; PROTEIN ACTIVATOR; ESCHERICHIA-COLI; EXPRESSION; H-1-NMR; GENE; PHOSPHODIESTERASE AB Two series of site-directed mutations to the individual Ca2+-binding sites of Drosophila melanogaster calmodulin have been generated and studied. In each mutant, a conserved glutamic acid residue at position 12 in all of the Ca2+-binding loops has been mutated in one site. In one series the residue is changed to glutamine; in the second series the change is to lysine. The Ca2+-binding properties of these mutants and the wild-type protein under pseudo-physiological conditions are presented. In addition, Ca2+-induced changes to the environment of the single tyrosine residue (Tyr-138) have been studied for some of the mutants. Ca2+ binding to the wild-type protein is best modeled as two pairs of sites with a higher affinity pair that shows strong cooperativity. For all but one of these eight mutant proteins, only three Ca2+-binding events can be detected. In three of the amino-terminal mutants, the three residual sites are (i) a pair of relatively high affinity sites and (ii) a weakened low affinity site. For all four carboxyl-terminal mutations, the residual sites are three relatively low affinity sites. In general, mutations to sites 2 and 4 prove more deleterious than mutations to sites 1 and 3. The Ca2+-induced conformational changes in the vicinity of Tyr-138 are relatively undisturbed by mutations of site 1. However, the changes to Tyr-138 in the carboxyl-terminal site mutants indicate that upon disruption of the cooperative binding at the high affinity sites, conformational change in the carboxyl terminus occurs in two phases. It appears that binding of Ca2+ to either carboxyl-terminal site can elicit the first phase of the response but the second phase is almost abolished when site 4 is the mutated site. The final conformations of site 3 and 4 mutants are thus significantly different. C1 RICE UNIV,DEPT BIOCHEM & CELL BIOL,HOUSTON,TX 77251. NCI,BIOCHEM LAB,BETHESDA,MD 20205. FU NIGMS NIH HHS [GM37214] NR 55 TC 195 Z9 195 U1 0 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1992 VL 267 IS 8 BP 5286 EP 5295 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700046 PM 1544911 ER PT J AU PETERKOFSKY, B PRATHER, W AF PETERKOFSKY, B PRATHER, W TI A POSTTRANSLATIONAL MODIFICATION, UNRELATED TO HYDROXYLATION, IN THE COLLAGENOUS DOMAIN OF NONHELICAL PRO-ALPHA-2(I) PROCOLLAGEN CHAINS SECRETED BY CHEMICALLY TRANSFORMED HAMSTER FIBROBLASTS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PERINATAL OSTEOGENESIS IMPERFECTA; I COLLAGEN; TISSUE; HYDROXYLYSINE; DEGRADATION; METABOLISM; PROTEINS; CELLS; GENE AB Transformed Syrian hamster embryo (NQT-SHE) fibroblasts do not synthesize the pro-alpha-1 subunit of type I procollagen, but secrete two modified forms of the pro-alpha-2(I) subunit that migrate more slowly than the normal chain during gel electrophoresis (Peterkofsky, B., and Prather, W. (1986) J. Biol. Chem. 261, 16818-16826). By electrophoretic analysis of cyanogen bromide and V8 protease-derived peptides from the collagenous domains of intra- and extracellular pro-alpha-2(1) chains, we find that the modification occurs almost exclusively in secreted molecules, is located in the region spanned by the cyanogen bromide peptide CB3,5, and persists when hydroxylation is inhibited. Thus, modification is due to a post-translational reaction other than hydroxylation. The modified chains appear to be secreted in the denatured state since: 1) helical structures formed at 4-degrees-C under acidic conditions were unstable under neutral conditions at 37-degrees-C; 2) conditions that destabilize the type I procollagen helix and thus inhibit its secretion, i.e. inhibition of proline hydroxylation or incorporation of the proline analog cis-hydroxyproline, did not affect secretion of the modified chains. The time courses for secretion of nonhelical modified chains from NQT-SHE and of hydroxylated helical procollagen I from control cells, as a proportion of total collagen synthesized, were similar. Although cis-hydroxyproline did not inhibit the secretion of the modified chains, it induced their rapid intracellular degradation. RP PETERKOFSKY, B (reprint author), NCI,BIOCHEM LAB,BLDG 37,RM 4C18,BETHESDA,MD 20892, USA. NR 29 TC 8 Z9 8 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1992 VL 267 IS 8 BP 5388 EP 5395 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700060 PM 1312089 ER PT J AU STEPHAN, V BENHAMOU, M GUTKIND, JS ROBBINS, KC SIRAGANIAN, RP AF STEPHAN, V BENHAMOU, M GUTKIND, JS ROBBINS, KC SIRAGANIAN, RP TI FC-EPSILON-RI-INDUCED PROTEIN TYROSINE PHOSPHORYLATION OF PP72 IN RAT BASOPHILIC LEUKEMIA-CELLS (RBL-2H3) - EVIDENCE FOR A NOVEL SIGNAL TRANSDUCTION PATHWAY UNRELATED TO G-PROTEIN ACTIVATION AND PHOSPHATIDYLINOSITOL HYDROLYSIS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PHOSPHOLIPASE-C; HISTAMINE-RELEASE; MAST-CELLS; INOSITOL TRISPHOSPHATE; SYNERGISTIC SIGNALS; MEDIATED ACTIVATION; KINASE-C; RECEPTOR; SECRETION; INHIBITION AB Recently, we demonstrated that aggregation of the high affinity IgE receptor in rat basophilic leukemia (RBL-2H3) cells results in rapid tyrosine phosphorylation of a 72-kDa protein (pp72). Here we investigated the relationship of pp72 phosphorylation to guanine nucleotide-binding protein (G protein) activation and phosphatidylinositol hydrolysis. The activation of G proteins by NaF in intact cells or by guanosine 5'-O-(3-thiotriphosphate) in streptolysin 0-permeabilized cells induced both phosphatidylinositol hydrolysis and histamine release without tyrosine phosphorylation of pp72. Similarly, in RBL-2H3 cells expressing the G protein-coupled muscarinic acetylcholine receptor, carbachol activated phospholipase C and induced secretion without concomitant pp72 phosphorylation. Therefore, pp72 phosphorylation was not induced by G protein activation or as a consequence of phosphatidylinositol hydrolysis. To investigate whether pp72 tyrosine phosphorylation precedes the activation of phospholipase C, we studied the effect of the tyrosine kinase inhibitor genistein. Preincubation of cells with genistein decreased, in parallel, antigen-induced tyrosine phosphorylation of pp72 (IC50 = 34-mu-g/ml) and histamine release (IC50 = 31-mu-g/ml). However, genistein at concentrations of up to 60-mu-g/ml did not inhibit phosphatidylinositol hydrolysis nor did it change the amount of the secondary messenger inositol (1,4,5)-triphosphate. Previous observations showed that there was no pp72 tyrosine phosphorylation after activation of protein kinase C or after an increase in intracellular calcium. Taken together, these results suggest that pp72 tyrosine phosphorylation represents a distinct, independent signaling pathway induced specifically by aggregation of the Fc-epsilon-RI. C1 NIDR,IMMUNOL LAB,BLDG 10,RM 1N 106,BETHESDA,MD 20892. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. RI Gutkind, J. Silvio/A-1053-2009 NR 44 TC 69 Z9 69 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1992 VL 267 IS 8 BP 5434 EP 5441 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700066 PM 1372002 ER PT J AU PARKER, KC CARRENO, BM SESTAK, L UTZ, U BIDDISON, WE COLIGAN, JE AF PARKER, KC CARRENO, BM SESTAK, L UTZ, U BIDDISON, WE COLIGAN, JE TI PEPTIDE BINDING TO HLA-A2 AND HLA-B27 ISOLATED FROM ESCHERICHIA-COLI - RECONSTITUTION OF HLA-A2 AND HLA-B27 HEAVY-CHAIN BETA-2-MICROGLOBULIN COMPLEXES REQUIRES SPECIFIC PEPTIDES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CLASS-I MOLECULES; TOXIC LYMPHOCYTES-T; HISTOCOMPATIBILITY ANTIGENS; MONOCLONAL-ANTIBODY; IMMUNOGENIC PEPTIDES; CELL RECOGNITION; MHC RESTRICTION; VIRAL PEPTIDES; PROTEINS; ASSOCIATION AB The specificity of peptide binding by human leukocyte antigen (HLA) class I molecules was investigated in a cell-free direct-binding assay. Peptides were assessed for binding to HLA-A2 and HLA-B27 by measuring the formation of heterotrimeric HLA complexes that consisted of iodinated beta-2-microglobulin, HLA heavy chain fragments isolated from the Escherichia coli cytoplasm, and peptide. In this system, no detectable HLA heavy chain-beta-2-microglobulin complexes were formed unless appropriate peptides were intentionally added to the reconstitution solution. Analysis with monoclonal antibodies demonstrated that these heterotrimeric complexes were correctly folded. Five nonhomologous peptides, known to form complexes with HLA-A2 or HLA-B27 from T-cell functional studies, were tested for their capacity to bind to HLA-A2 and HLA-B27 using the reconstitution assay. Four of the peptides bound to the appropriate class I molecule only. One peptide and some (but not all) substitution analogs of it bound to both HLA-A2 and HLA-B27. The effect of peptide length on binding to HLA-B27 was studied, and it was found that the optimal length was 9 or 10 amino acid residues; however, one peptide that bound to HLA-B27 was 15 amino acids long. All peptides that bound to HLA-B27 in the direct-binding assay also competed with antigenic peptides for binding to HLA-B27 on the surface of intact cells, as determined by a standard cytotoxic T-lymphocyte functional assay. Thus, we conclude that HLA-A2 and HLA-B27 bind distinct but partially overlapping sets of peptides and that, at least in vitro, the assembly of HLA heavy chain-beta-2-microglobulin complexes requires specific peptides. C1 NINCDS,NEUROIMMUNOL BRANCH,MOLEC IMMUNOL SECT,BETHESDA,MD 20892. RP PARKER, KC (reprint author), NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892, USA. OI Parker, Kenneth/0000-0002-6282-2478 NR 62 TC 55 Z9 56 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1992 VL 267 IS 8 BP 5451 EP 5459 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700069 PM 1544922 ER PT J AU MAUVIEL, A KAHARI, VM EVANS, CH UITTO, J AF MAUVIEL, A KAHARI, VM EVANS, CH UITTO, J TI TRANSCRIPTIONAL ACTIVATION OF FIBROBLAST COLLAGENASE GENE-EXPRESSION BY A NOVEL LYMPHOKINE, LEUKOREGULIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NECROSIS-FACTOR-ALPHA; MESSENGER-RNA; C-JUN; GLUCOCORTICOID RECEPTOR; SYNOVIAL FIBROBLASTS; TISSUE INHIBITOR; PROTEIN; DNA; PROCOLLAGENASE; INTERLEUKIN-1 AB Leukoregulin (LR) is a novel T-cell derived cytokine with unique anti-tumor properties. We have recently demonstrated that LR is also able to modulate the biosynthetic repertoire of normal human skin fibroblasts in culture (Mauviel, A., Redini, F., Hartmann, D. J., Pujol, J.-P., and Evans, C. H. (1991) J. Cell Biol. 113, 1455-1462). In this study, we have examined in detail the effects of LR on collagenase gene expression in human skin fibroblast cultures. The results indicated time- and dose-dependent induction of collagenase mRNA steady-state levels, the maximum elevation being approximately 35-fold. In contrast, the mRNA levels for tissue inhibitor of metalloproteases remained unchanged in the same RNA preparations. The enhancement of collagenase mRNA levels was shown to be dependent on protein synthesis, and it could be counteracted by dexamethasone or all-trans-retinoic acid. Transient transfections of cultured fibroblasts with a human collagenase promoter/reporter gene construct indicated up-regulation of the promoter activity, which could be blocked by dexamethasone and all-trans-retinoic acid. The observation suggested regulation at the transcriptional level of collagenase gene expression. LR was also shown to induce the mRNA levels for junB, suggesting possible involvement of the AP-1 complex in the regulation. The ability of LR to selectively induce collagenase gene expression in skin fibroblasts suggests that this cytokine may significantly contribute to the degradation of the extracellular matrix in physiological situations, such as tissue development and repair, and in diseases characterized by excessive degradation and turnover of collagen. C1 NCI,DIV CANC ETIOL,BIOL LAB,TUMOR BIOL SECT,BETHESDA,MD 20892. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,JEFFERSON INST MOLEC MED,DEPT BIOCHEM & MOLEC BIOL,PHILADELPHIA,PA 19107. RI MAUVIEL, Alain/F-6251-2013 FU NIAMS NIH HHS [T32-AR-0751, R01-AR35297] NR 36 TC 21 Z9 21 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1992 VL 267 IS 8 BP 5644 EP 5648 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700096 PM 1372007 ER PT J AU FIELD, MJ AF FIELD, MJ TI TIME-DEPENDENT HARTREE-FOCK SIMULATIONS OF THE DYNAMICS OF POLYATOMIC-MOLECULES SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID APPROXIMATION; PRINCIPLE; SURFACES AB The use of the time-dependent Hartree-Fock method for performing molecular-dynamics simulations of polyatomic systems is explored. The theory is outlined for closed-shell restricted Hartree-Fock wave functions which employ the neglect of diatomic differential overlap approximation. The motions of the nuclei are treated classically. If the starting electronic wave function for a simulation obeys the time-independent variational principle then trajectories calculated with the algorithm stay very close to those obtained with a method in which the wave function obeys the time-independent variational principle at all times. RP FIELD, MJ (reprint author), NIH,DIV COMP RES & TECHNOL,BLDG 12A,BETHESDA,MD 20892, USA. NR 40 TC 23 Z9 23 U1 1 U2 2 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0021-9606 J9 J CHEM PHYS JI J. Chem. Phys. PD MAR 15 PY 1992 VL 96 IS 6 BP 4583 EP 4590 DI 10.1063/1.462794 PG 8 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA HK019 UT WOS:A1992HK01900056 ER PT J AU SEDER, RA BOULAY, JL FINKELMAN, F BARBIER, S BENSASSON, SZ LEGROS, G PAUL, WE AF SEDER, RA BOULAY, JL FINKELMAN, F BARBIER, S BENSASSON, SZ LEGROS, G PAUL, WE TI CD8+ T-CELLS CAN BE PRIMED INVITRO TO PRODUCE IL-4 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MONOCLONAL-ANTIBODY; GROWTH-FACTOR; TH2 CELLS; IFN-GAMMA; INTERLEUKIN-2; CLONES; IDENTIFICATION; ANTIGEN; COEXPRESSION; LYMPHOKINES AB IL-4 production by T lymphocytes from naive mice in response to stimulation by plate-bound anti-CD3 is concentrated among CD4+ T cells. In vitro stimulation of lymph node T cells with anti-CD3 plus IL-2 and IL-4 strikingly increases the frequency of cells that produce IL-4 in response to subsequent stimulation with anti-CD3 plus IL-2. Separation of these primed cell populations into CD4+ and CD8+ T cell by cell sorting reveals that the frequency of IL-4-producing cells in both population is similar. Verification that CD8+ T cells produce IL-4 is provided by the capacity of anti-IL-4 mAb to inhibit the response of the indicator cell line to the growth factor produced by the primed cells and by detection of IL-4 by an IL-4-specific ELISA. The in vitro "priming" of CD8+ T cells to produce IL-4 is not dependent on the presence of CD4+ T cells because highly purified CD8+ T cells can be stimulated to develop into cells capable of producing IL-4 by culture with plate-bound anti-CD3 plus IL-2 and IL-4. C1 NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. HEBREW UNIV JERUSALEM,HADASSAH MED CTR,LAUTENBERG CTR TUMOR IMMUNOL,JERUSALEM,ISRAEL. RP SEDER, RA (reprint author), NIAID,IMMUNOL LAB,BLDG 10,RM 11N311,BETHESDA,MD 20892, USA. RI Le Gros, Graham/C-6725-2011 NR 35 TC 201 Z9 206 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 15 PY 1992 VL 148 IS 6 BP 1652 EP 1656 PG 5 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600008 PM 1347305 ER PT J AU SHIRAI, M PENDLETON, CD BERZOFSKY, JA AF SHIRAI, M PENDLETON, CD BERZOFSKY, JA TI BROAD RECOGNITION OF CYTOTOXIC T-CELL EPITOPES FROM THE HIV-1 ENVELOPE PROTEIN WITH MULTIPLE CLASS-I HISTOCOMPATIBILITY MOLECULES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MHC CLASS-II; TOXIC LYMPHOCYTES-T; TRANSPLANTATION ANTIGENS; VIRUS-REPLICATION; FINE SPECIFICITY; PEPTIDES; DETERMINANT; MOUSE; COMPLEX; ASSOCIATION AB A few cases have been described of antigenic determinants that are broadly presented by multiple class II MHC molecules, especially murine I-E or human DR, in which polymorphism is limited to the beta-chain, and the a chain is conserved. However, no similar cases have been studied for presentation by class I MHC molecules. Because both domains of the MHC peptide binding site are polymorphic in class I molecules, exploring permissiveness in class I presentation would be of interest, and also such broadly presented antigenic determinants would clearly be useful for vaccine development. We had defined an immunodominant determinant, P18, of the HIV-1 gpl60 envelope protein recognized by human and murine CTL. To determine the range of class I MHC molecules that could present this peptide and to determine whether two HIV-1 gpl60 Th cell determinants, T1 and HP53, could also be presented by class I MHC molecules, we attempted to generate CTL specific for these three peptides in 10 strains of B10 congenic mice, representing 10 MHC types, and BALB/c mice. P18 was presented by at least four different class I MHC molecules from independent haplotypes (H-2d,p,u, and q to CD8+ CTL. In H-2d and H-2q the presentation was mapped to the D-end class I molecule, and for D(d), a requirement for both the alpha-1 and alpha-2 domains of D(d), not L(d), was found. HP53 was also presented by the same four different class I MHC molecules to CD8+ CTL although at higher concentrations. T1 was presented by class I molecules in three different strains of distinct MHC types (B10.M, H-2f; B10.A, H-2a; and B10, H-2b) to CTL. The CTL specific for P18 and HP53 were shown to be CD8+ and CD4- and to kill targets expressing endogenously synthesized whole gpl60 as well as targets pulsed with the corresponding peptide. To compare the site within each peptide presented by the different class I molecules, we used overlapping and substituted peptides and found that the critical regions of each peptide are the similar for all four MHC molecules. Thus, antigenic sites are broadly or permissively presented by class I MHC molecules even without a nonpolymorphic domain as found in DR and I-E, and these sequences may be of broad usefulness in a synthetic vaccine. C1 NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BLDG 10,RM 6B-12,BETHESDA,MD 20892. NR 52 TC 104 Z9 104 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 MAR 15 PY 1992 VL 148 IS 6 BP 1657 EP 1667 PG 11 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600009 PM 1371784 ER PT J AU SPECTOR, NL SAMSON, W RYAN, C GRIBBEN, J URBA, W WELCH, WJ NADLER, LM AF SPECTOR, NL SAMSON, W RYAN, C GRIBBEN, J URBA, W WELCH, WJ NADLER, LM TI GROWTH ARREST OF HUMAN LYMPHOCYTES-B IS ACCOMPANIED BY INDUCTION OF THE LOW-MOLECULAR-WEIGHT MAMMALIAN HEAT-SHOCK PROTEIN (HSP28) SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL-CYCLE PROGRESSION; SACCHAROMYCES-CEREVISIAE; RESTRICTED ANTIGEN; PHORBOL ESTER; TUMOR-ANTIGEN; EXPRESSION; ACTIVATION; GENE; PHOSPHORYLATION; STIMULATION AB A large number of protein and molecular markers have been identified that delineate the early stages of human B cell activation and proliferation. In contrast, few if any molecules are transiently expressed precisely as activated B cells stop proliferating and undergo growth arrest. We demonstrate that the low molecular weight heat shock protein (hsp28) exhibits unique induction kinetics that specifically demarcates this interval. After mitogenic activation of unstimulated splenic B cells, hsp28 protein and phosphorylation transiently increase coinciding precisely with the peak of cellular proliferation and the onset of growth arrest. Although most neoplastic B cells constitutively express hsp28, three cell lines were identified that were hsp28-. No differences in phenotype or growth kinetics were detected between hsp28+ and hsp28- neoplastic B cells demonstrating that hsp28 expression is not essential for cell growth. However, when treated with phorbol ester or heat shock, these hsp28- cell lines synthesize hsp28 followed by the onset growth arrest. The consistency with which hsp28 induction transiently delineates the interval from peak proliferation to the onset of growth arrest suggests hsp28 itself is likely to be involved in regulating this process. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL,SAN FRANCISCO,CA 94110. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94110. RP SPECTOR, NL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [1F32CA08954-01, CA-40216-06] NR 35 TC 82 Z9 82 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 MAR 15 PY 1992 VL 148 IS 6 BP 1668 EP 1673 PG 6 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600010 PM 1541812 ER PT J AU HARA, Y CASPI, RR WIGGERT, B CHAN, CC WILBANKS, GA STREILEIN, JW AF HARA, Y CASPI, RR WIGGERT, B CHAN, CC WILBANKS, GA STREILEIN, JW TI SUPPRESSION OF EXPERIMENTAL AUTOIMMUNE UVEITIS IN MICE BY INDUCTION OF ANTERIOR CHAMBER-ASSOCIATED IMMUNE DEVIATION WITH INTERPHOTORECEPTOR RETINOID-BINDING PROTEIN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; S-ANTIGEN; SOLUBLE-ANTIGEN; CELL-LINE; UVEORETINITIS; RESPONSES; UNRESPONSIVENESS; IMMUNIZATION; LYMPHOCYTES AB Immunization with bovine interphotoreceptor retinoid-binding protein induces autoimmune uveitis in B10.A mice. We have examined whether this soluble retina-specific Ag can induce anterior chamber-associated immune deviation when injected into the anterior chamber (AC) of the eye, and whether this deviant immune response has any effect on uveitis in susceptible mice. The results of these experiments indicate that interphotoreceptor retinoid-binding protein (IRBP) injected intracamerally altered the subsequent immune response of B10.A mice such that a) they were not able to develop IRBP-specific delayed hypersensitivity, nor (b) were they able to express significant autoimmune uveitis following a uveitogenic regimen. Moreover, spleen cells from mice that received IRBP in the AC suppressed uveitis when adoptively transferred into naive recipients. The splenic suppressor cells were able to prevent autoimmune uveitis in recipient mice when administered after the uveitogenic regimen. Most important, IRBP-specific splenic cells from mice treated with IRBP in the AC when injected into mice with established uveitis caused an abrupt cessation of the intraocular inflammation. The ability of intracamerally-injected soluble Ag to induce suppressor T cells that act on the efferent limb of the immune response suggests that the anterior-chamber-associated immune deviation phenomenon may have physiologic relevance in terms of preservation of the integrity of ocular tissue and renders this approach particularly suitable for treating already established experimental autoimmune diseases of this type. These results are discussed in terms of other methods that have been devised experimentally to suppress and prevent autoimmune uveitis and encephalomyelitis. C1 UNIV MIAMI,SCH MED,DEPT MICROBIOL & IMMUNOL,POB 016960 R-138,MIAMI,FL 33136. UNIV MIAMI,SCH MED,DEPT OPHTHALMOL,MIAMI,FL 33136. NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. FU NEI NIH HHS [EY05678] NR 45 TC 75 Z9 78 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 MAR 15 PY 1992 VL 148 IS 6 BP 1685 EP 1692 PG 8 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600012 PM 1531843 ER PT J AU MURAKAWA, Y MINAMI, Y STROBER, W JAMES, SP AF MURAKAWA, Y MINAMI, Y STROBER, W JAMES, SP TI ASSOCIATION OF HUMAN LYMPH-NODE HOMING RECEPTOR (LEU-8) WITH THE TCR/CD3 COMPLEX SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL RECEPTOR; ANTIGEN RECEPTOR; ZETA-CHAIN; LYMPHOCYTES-T; TYROSINE PHOSPHORYLATION; MEDIATED ACTIVATION; ADHESION MOLECULES; SUB-POPULATIONS; ETA-CHAIN; SURFACE AB Cross-linking of the human homologue of the murine MEL-14 lymph node homing receptor (Selectin-1, LECAM-1, Leu 8) on both T and B cells results in modification of cell function. To investigate this phenomenon, we performed studies to determine if the Leu 8 molecule influences T cell activation via the TCR/CD3 complex. In initial studies, we treated T cells with immobilized anti-CD3 (OKT3 mAb) in the presence or absence of immobilized Leu 8 mAb. We found that although Leu 8 mAb alone had no effect on T cell proliferation, this antibody markedly augmented immobilized OKT3 mAb-induced proliferation. In further studies, we immunoprecipitated surface radioiodinated T cell lysates with OKT3 and Leu 8 mAb to determine if molecules in the TCR/CD3 complex associate with Leu 8 molecules. Although Leu 8 mAb immunoprecipitated only a single protein of approximately 80 kDa from T cell lysates treated with Nonidet P-40 under reducing condition, it coimmunoprecipitated additional proteins of 48, 42, 28, 24, and 22 kDa from T cell lysates treated with 3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulfonate. These additional proteins were identified as the alpha-, beta-, gamma-, delta-, and epsilon-chains of the TCR/CD3 complex by one-dimensional and two-dimensional diagonal SDS-PAGE. Densitometric scanning showed that, on average, 18% of the TCR/CD3 complex associates with Leu 8. In a final study, we showed by immunoblotting analysis using anti-zeta-peptide antibody that Leu 8 mAb coimmunoprecipitates the zeta-chain of CD3. These results indicate that the human lymph node homing receptor homologue (Leu 8) participates in the activation of T cells, probably via its association with the TCR/CD3 complex. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. RP MURAKAWA, Y (reprint author), NIAID,MUCOSAL IMMUN SECT,CLIN INVEST LAB,BLDG 10,ROOM 11N-250,BETHESDA,MD 20892, USA. NR 39 TC 42 Z9 42 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 MAR 15 PY 1992 VL 148 IS 6 BP 1771 EP 1776 PG 6 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600025 PM 1371790 ER PT J AU GAZZINELLI, RT OSWALD, IP JAMES, SL SHER, A AF GAZZINELLI, RT OSWALD, IP JAMES, SL SHER, A TI IL-10 INHIBITS PARASITE KILLING AND NITROGEN-OXIDE PRODUCTION BY IFN-GAMMA-ACTIVATED MACROPHAGES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; INTERFERON-GAMMA; MURINE MACROPHAGES; TOXOPLASMA-GONDII; CYTO-TOXICITY; L-ARGININE; T-CELLS; CYTOKINES; DISEASE AB IL-10, a cytokine produced by CD4+ T lymphocytes belonging to the Th-2 subset, has previously been shown to inhibit the synthesis of IFN-gamma by both T cells and NK cells. We now demonstrate that IL-10 can also down-regulate IFN-gamma-dependent immunity by blocking the ability of that lymphokine to activate macrophages. Thus, IL-10, in a dose-dependent manner, inhibits the microbicidal activity of IFN-gamma-treated inflammatory macrophages against intracellular Toxoplasma gondii as well as the extracellular killing of schistosomula of Schistosoma mansoni. This suppression correlates with the inhibition by IL-10 of IFN-gamma-induced production of toxic nitrogen oxide metabolites, an effector mechanism previously implicated in the killing by macrophages of both parasite targets. IL-10 inhibition of nitric oxide production was shown to occur when the cytokine is given before or together with the IFN-gamma-activating stimulus, but not after its removal from the cultures and to require 12 h of contact for maximal suppressive effect on macrophage function. These results, taken together with previous findings on the down-regulation of Th1 lymphokine production by IL-10, indicate that the induction of IL-10 may be an important strategy by which parasites evade IFN-gamma-dependent, cell-mediated immune destruction. RP GAZZINELLI, RT (reprint author), NIAID,IMMUNOL & CELL BIOL SECT,PARASIT DIS LAB,RM 126,BETHESDA,MD 20892, USA. RI OSWALD, Isabelle/A-8497-2013 NR 38 TC 580 Z9 588 U1 3 U2 12 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 15 PY 1992 VL 148 IS 6 BP 1792 EP 1796 PG 5 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600028 PM 1541819 ER PT J AU MANGAN, DF ROBERTSON, B WAHL, SM AF MANGAN, DF ROBERTSON, B WAHL, SM TI IL-4 ENHANCES PROGRAMMED CELL-DEATH (APOPTOSIS) IN STIMULATED HUMAN MONOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INTERFERON-GAMMA; IFN-GAMMA; MONONUCLEAR-CELLS; FACTOR-I; B-CELLS; INTERLEUKIN-4; EXPRESSION; RECEPTOR; PROSTAGLANDIN-E2; RECOGNITION AB Because IL-4 down-regulates several proinflammatory functions associated with human monocytes/macrophages, we explored the possibility that IL-4 also decreases monocyte survival. IL-4 caused a concentration-dependent decrease in viability of IL-1 or LPS stimulated, but not unstimulated, monocytes. Nonviable cells demonstrated classic features of programmed cell death or apoptosis, in that they were condensed and contained oligonucleosome-sized (200 bp) DNA fragments. When compared with several other cytokines commonly associated with inflammatory lesions, IL-4 was uniquely effective in enhancing cell death. We found that IL-4 enhanced death more quickly in IL-1-stimulated cells than in LPS-stimulated cells, that stimulated monocytes did not become resistant to the effects of IL-4 during culture, and that the effects of IL-4 on viability were antagonized by IFN-gamma. Enhanced cell death was stimulus-specific in that monocyte viability maintained by certain activating agents, such as Con A or CSF, was unaffected by IL-4. These findings represent the first evidence of cytokine-enhanced programmed cell death in monocytes and suggest that the antiinflammatory effects of IL-4 are mediated in part by reducing survival of stimulated monocytes in chronic lesions. RP MANGAN, DF (reprint author), NIDR,CELLULAR IMMUNOL SECT,IMMUNOL LAB,BLDG 30,ROOM 329,BETHESDA,MD 20892, USA. FU NIDCR NIH HHS [DE05576] NR 37 TC 136 Z9 136 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 15 PY 1992 VL 148 IS 6 BP 1812 EP 1816 PG 5 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600031 PM 1541822 ER PT J AU SANDERS, VM POWELLOLIVER, FE AF SANDERS, VM POWELLOLIVER, FE TI BETA-2-ADRENOCEPTOR STIMULATION INCREASES THE NUMBER OF ANTIGEN-SPECIFIC PRECURSOR LYMPHOCYTES-B THAT DIFFERENTIATE INTO IGM-SECRETING CELLS WITHOUT AFFECTING BURST SIZE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTIBODY-RESPONSE INVITRO; HELPER T-CELLS; MURINE LYMPHOCYTES; GROWTH-FACTOR; FACTOR-I; NOREPINEPHRINE; ACTIVATION; INDUCTION; INNERVATION; ENUMERATION AB Previous studies have shown that early addition of a beta-2-adrenergic agonist to whole splenocyte cultures immunized with SRBC induced an increase in the number of cells secreting Ag-specific antibody. Because of the low frequency of Ag-specific B lymphocytes in these cultures, it has been difficult to determine the cellular mechanism by which this increase is produced. To gain insight into this cellular mechanism, the present study was designed to evaluate the responsiveness of TNP-specific B lymphocytes cultured at both high density and limiting dilution with keyhole limpet hemocyanin (KLH)-specific, IL-4-producing Th lymphocytes, TNP-KLH, and the beta-2-adrenergic agonist, terbutaline. The results showed that a maximal twofold increase in both the number of anti-TNP IgM-secreting cells and the amount of anti-TNP IgM secretion occurred in terbutaline-exposed lymphocytes after 5 days of bulk culture. This response occurred in a concentration-dependent manner and was inhibited by concomitant culture with beta-adrenoceptor antagonists. No appreciable change was measured in the level of either IgG1 secretion in terbutaline plus Ag-exposed bulk cultures or MHC class II expression on terbutaline plus Ag-exposed TNP-specific B lymphocytes as compared with Ag alone. These data raised the possibility that beta-2-adrenoceptor stimulation induced either the differentiation of a larger proportion of TNP-specific B lymphocyte precursors into anti-TNP IgM-secreting cells, or the extensive proliferation of a constant number of TNP-specific B lymphocyte precursors, or both. Limiting dilution results showed that beta-2-adrenoceptor stimulation induced a twofold increase in the number of TNP-specific B lymphocyte precursors, that differentiated into anti-TNP IgM-secreting cells, without affecting the number of anti-TNP IgM-secreting cells produced by each precursor clone. RP SANDERS, VM (reprint author), NIEHS,MAIL DROP C1-04,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 42 TC 58 Z9 58 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 15 PY 1992 VL 148 IS 6 BP 1822 EP 1828 PG 7 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600033 PM 1311733 ER PT J AU MIYAZAWA, M NISHIO, J WEHRLY, K DAVID, CS CHESEBRO, B AF MIYAZAWA, M NISHIO, J WEHRLY, K DAVID, CS CHESEBRO, B TI SPONTANEOUS-RECOVERY FROM FRIEND RETROVIRUS-INDUCED LEUKEMIA - MAPPING OF THE RFV-2-GENE IN THE Q/TL REGION OF MOUSE MHC SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; HOST GENETIC-CONTROL; T-CELL RECEPTOR; VIRUS LEUKEMIA; IDENTIFICATION; ANTIGENS; DELTA; ERYTHROLEUKEMIA; RECOMBINANT; INFECTION AB The Rfv-2 gene that influences the rate of spontaneous recovery from erythroleukemia induced by a low dose of Friend retrovirus complex was mapped to the Q/TL region of mouse MHC. Rfv-2 was physically and functionally distinct from the I-A-linked Ir gene that has been shown to control the responsiveness of Th cells to the envelope glycoprotein of Friend murine leukemia helper virus. The negative effect of the Rfv-2s allele was overcome by the B10.D2-H-2dm1 mutation of the D-L genes of H-2, suggesting functional similarities between the D-L and Q/TL genes in influencing resistance against Friend murine leukemia retrovirus complex infection or possible modification of Q/TL expression by genes in the D-L region. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,903 S 4TH ST,HAMILTON,MT 59840. MAYO CLIN & MAYO FDN,DEPT IMMUNOL,ROCHESTER,MN 55905. NR 30 TC 19 Z9 19 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 MAR 15 PY 1992 VL 148 IS 6 BP 1964 EP 1967 PG 4 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600053 PM 1541833 ER PT J AU PERRONEFILARDI, P BACHARACH, SL DILSIZIAN, V BONOW, RO AF PERRONEFILARDI, P BACHARACH, SL DILSIZIAN, V BONOW, RO TI EFFECTS OF REGIONAL SYSTOLIC ASYNCHRONY ON LEFT-VENTRICULAR GLOBAL DIASTOLIC FUNCTION IN PATIENTS WITH CORONARY-ARTERY DISEASE SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID ISOVOLUMIC RELAXATION PERIOD; RADIONUCLIDE ANGIOGRAPHY; HYPERTROPHIC CARDIOMYOPATHY; TIME CONSTANT; NORMAL HEART; NONUNIFORMITY; PRESSURE; CONTRACTION; MOTION; DOG AB Patients with coronary artery disease often have impaired left ventricular diastolic filling despite normal global systolic function. The influence of regional systolic asynchrony on diastolic function was assessed by radionuclide angiography in 60 patients with coronary artery disease and normal ejection fraction at rest: group 1 (n = 30) with normal wall motion at rest and group 2 (n = 30) with abnormal wall motion. Data were compared with those obtained from 19 normal volunteers. Age, heart rate, ejection fraction and echocardiographic end-diastolic dimension did not differ among the three groups. Peak filling rate in group 1 and group 2 was similar (2.5 +/- 0.5 and 2.3 +/- 0.6 end-diastolic counts/s, respectively) and significantly lower than that in the normal subjects (2.8 +/- 0.7 end-diastolic counts/s; p < 0.01 vs. group 2, p < 0.05 vs. group 1). Time to peak filling rate was prolonged in group 2 (184 +/- 27 ms) compared with that in normal subjects (162 +/- 19 ms; p < 0.01) and group 1 (172 +/- 15 ms; p < 0.05). Left ventricular end-diastolic pressure was significantly higher in group 2 than in group 1 (14 +/- 7 vs. 10 +/- 5 mm Hg, respectively; p < 0.05). Asynchrony was assessed by sector analysis of the radionuclide left ventricular region of interest. Diastolic asynchrony was similar in the two patient groups (30 +/- 23 ms in group 2, 26 +/- 16 ms in group 1) and was higher in both groups than in the normal subjects (16 +/- 8 ms; p < 0.01). However, systolic asynchrony was higher in group 2 (32 +/- 15 ms) than in both group 1 (14 +/- 6 ms; p < 0.01) and the normal group (9 +/- 6 ms; p < 0.01). In the total group of patients with coronary artery disease, systolic asynchrony correlated with global time to peak filling rate (r = 0.53; p < 0.001). This correlation became stronger when only group 2 was considered (r = 0.62; p < 0.001). Moreover, in group 2 systolic asynchrony correlated with the duration of the isovolumetric relaxation period (r = 0.58; p < 0.001) and the isovolumetric relaxation period, in turn, correlated with global time to peak filling rate (r = 0.72; p < 0.001). Thus, left ventricular systolic asynchrony affects both the relaxation and filling phases of diastole, thereby contributing to the impairment of diastolic function commonly observed in patients with coronary artery disease. C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 28 TC 31 Z9 32 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 15 PY 1992 VL 19 IS 4 BP 739 EP 744 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HJ636 UT WOS:A1992HJ63600003 PM 1312099 ER PT J AU GRANT, AJ ROESSLER, E JU, G TSUDO, M SUGAMURA, K WALDMANN, TA AF GRANT, AJ ROESSLER, E JU, G TSUDO, M SUGAMURA, K WALDMANN, TA TI THE INTERLEUKIN-2 RECEPTOR (IL-2R) - THE IL-2R ALPHA SUBUNIT ALTERS THE FUNCTION OF THE IL-2R BETA SUBUNIT TO ENHANCE IL-2 BINDING AND SIGNALING BY MECHANISMS THAT DO NOT REQUIRE BINDING OF IL-2 TO IL-2R ALPHA SUBUNIT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AFFINITY CONVERSION; INTER-CHAIN INTERACTIONS; LEUKEMIA ID NATURAL-KILLER CELLS; MONOCLONAL-ANTIBODIES; ANTI-TAC; CHAIN; DISTINCT; LYMPHOCYTES; SUPERFAMILY; ACTIVATION; GENERATION; PEPTIDE AB Interleukin 2 (IL-2)-mediated signaling through its high-affinity receptor involves a complex interrelationship between IL-2 and two IL-2-binding chains, IL-2R-alpha and beta-chains. Previously with the reagents available it was difficult to define functional interactions between these two IL-2R subunits involved in IL-2 binding and signal transduction. To extend our understanding of the interplay between the two binding subunits we have done studies with the monoclonal antibody HIEI, which interferes with interaction of IL-2R-alpha and beta-chains (IL-2R-alpha and IL-2R-beta, respectively). Furthermore, we used two forms of IL-2, recombinant native IL-2 and F42A, an IL-2 analog (Phe-42 --> Ala substitution) that binds only to IL-2R-beta. Analog F42A manifested 75-100% of the bioactivity of wild-type IL-2. This observation is inconsistent with the strict hierarchical IL-2-binding affinity conversion model previously proposed by Saito and coworkers [Saito Y., Sabe, H., Suzuki, N., Kondo, S., Ogura, T., Shimizu, A. & Honjo, T. (1988) J. Exp. Med. 168, 1563-1572] that predicted an ordered sequence of events in which IL-2 must first bind to IL-2R-alpha before its interaction with IL-2R-beta. Previous investigations using IL-2 variants were interpreted to show that IL-2R-alpha merely acts to concentrate IL-2 to the cell surface and that no other meaningful interaction occurred between IL-2R-alpha and IL-2R-beta. However, our data are inconsistent with this view. We draw this conclusion on the basis of our observation that antibody HIEI, which reacts with an epitope of IL-2R-alpha and interferes with interaction of this chain and IL-2R-beta, inhibits the IL-2-dependent proliferative effects mediated by analog F42A. Furthermore, by blocking interaction of IL-2R-alpha and IL-2R-beta with the antibody HIEI, a decrease in the affinity of radiolabeled analog F42A for IL-2R-beta was seen. In our proposed model IL-2R-alpha contributes several functions to IL-2-mediated signaling through the high-affinity IL-2R. These functions include concentration of IL-2 within the two-dimensional surface of the plasma membrane as well as alteration of the functional capacity of IL-2R-beta, an effect that does not require prior binding of IL-2 to IL-2R-alpha. The IL-2R-alpha-mediated augmentation of IL-2R-beta functions involves affinity conversion of IL-2R-beta, increasing its affinity for IL-2, and may involve facilitation of IL-2-mediated signaling after binding of IL-2 to this IL-2R-beta. C1 UNITIKA CENT HOSP,KYOTO 611,JAPAN. TOHOKU UNIV,SCH MED,SENDAI,MIYAGI 980,JAPAN. HOFFMANN LA ROCHE INC,ROCHE RES CTR,DEPT MOLEC GENET,NUTLEY,NJ 07110. RP GRANT, AJ (reprint author), NCI,METAB BRANCH,BETHESDA,MD 20892, USA. NR 28 TC 53 Z9 53 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2165 EP 2169 DI 10.1073/pnas.89.6.2165 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300035 PM 1549576 ER PT J AU JOHNSON, PR MONTEFIORI, DC GOLDSTEIN, S HAMM, TE ZHOU, J KITOV, S HAIGWOOD, NL MISHER, L LONDON, WT GERIN, JL ALLISON, A PURCELL, RH CHANOCK, RM HIRSCH, VM AF JOHNSON, PR MONTEFIORI, DC GOLDSTEIN, S HAMM, TE ZHOU, J KITOV, S HAIGWOOD, NL MISHER, L LONDON, WT GERIN, JL ALLISON, A PURCELL, RH CHANOCK, RM HIRSCH, VM TI INACTIVATED WHOLE-VIRUS VACCINE DERIVED FROM A PROVIRAL DNA CLONE OF SIMIAN IMMUNODEFICIENCY VIRUS INDUCES HIGH-LEVELS OF NEUTRALIZING ANTIBODIES AND CONFERS PROTECTION AGAINST HETEROLOGOUS CHALLENGE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DEPENDENT ENHANCEMENT; RHESUS MACAQUES; INFECTION; PLASMA; HIV-1 AB We tested the ability of macaques vaccinated with inactivated whole simian immunodeficiency virus (SIV) to resist challenge with either homologous or heterologous cell-free uncloned SIV administered by the intravenous route. The vaccine virus was derived from a proviral DNA clone and thus was considered genetically homogeneous. Sixteen macaques received either hepatitis B surface antigen (n = 6) or the inactivated whole-SIV vaccine (n = 10) at weeks 0, 4, and 49 of the study. All SIV vaccine recipients developed high levels of homologous and heterologous neutralizing antibodies in response to vaccination. At the time of challenge (week 53), vaccinees were further stratified to receive either homologous (n = 10) or heterologous (n = 6) uncloned live SIV. The envelope glycoproteins of the homologous and heterologous challenge viruses were 94% and 81% identical to the vaccine virus, respectively. Regardless of challenge inoculum, all vaccinees in the control group (hepatitis B surface antigen) became infected, whereas all SIV vaccinees were protected against detectable infection. These data support the concept that an efficacious vaccine for HIV might be possible, and suggest that genetic variation of HIV might not be an insurmountable obstacle for vaccine development. C1 GEORGETOWN UNIV,DEPT MICROBIOL,DIV MOLEC VIROL & IMMUNOL,ROCKVILLE,MD 20852. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. VANDERBILT UNIV,DEPT PATHOL,NASHVILLE,TN 37232. CHIRON CORP,EMERYVILLE,CA 94608. SYNTEX INC,PALO ALTO,CA 94303. RI Johnson, Philip/A-6892-2009 FU NIAID NIH HHS [N01-AI-72623] NR 29 TC 71 Z9 71 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2175 EP 2179 DI 10.1073/pnas.89.6.2175 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300037 PM 1549578 ER PT J AU RIBAS, JC WICKNER, RB AF RIBAS, JC WICKNER, RB TI RNA-DEPENDENT RNA-POLYMERASE CONSENSUS SEQUENCE OF THE L-A DOUBLE-STRANDED-RNA VIRUS - DEFINITION OF ESSENTIAL DOMAINS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID SACCHAROMYCES-CEREVISIAE; NUCLEOTIDE-SEQUENCE; DNA-POLYMERASE; YEAST; GENES; TRANSCRIPTASE; MUTAGENESIS; REPLICASE; ENCAPSIDATION; EXPRESSION AB The L-A double-stranded RNA virus of Saccharomyces cerevisiae makes a gag-pol fusion protein by a - 1 ribosomal frameshift. The pol amino acid sequence includes consensus patterns typical of the RNA-dependent RNA polymerases (EC 2.7.7.48) of (+) strand and double-stranded RNA viruses of animals and plants. We have carried out "alanine-scanning mutagenesis" of the region of L-A including the two most conserved polymerase motifs, SG...T...NT..N (. = any amino acid) and GDD. By constructing and analyzing 46 different mutations in and around the RNA polymerase consensus regions, we have precisely defined the extent of domains and specific residues essential for viral replication. Assuming that this highly conserved region has a common secondary structure among different viruses, we predict a largely beta-sheet structure. RP RIBAS, JC (reprint author), NIDDKD,GENET SIMPLE EUKARYOTES SECT,BIOCHEM PHARMACOL LAB,BLDG 8,ROOM 207,BETHESDA,MD 20892, USA. RI Ribas, Juan/C-9864-2015 OI Ribas, Juan/0000-0001-6430-0895 NR 40 TC 48 Z9 50 U1 1 U2 2 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2185 EP 2189 DI 10.1073/pnas.89.6.2185 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300039 PM 1549580 ER PT J AU BOYD, LF KOZLOWSKI, S MARGULIES, DH AF BOYD, LF KOZLOWSKI, S MARGULIES, DH TI SOLUTION BINDING OF AN ANTIGENIC PEPTIDE TO A MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I MOLECULE AND THE ROLE OF BETA-2-MICROGLOBULIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE H-2LD; MURINE CYTOMEGALOVIRUS; EQUILIBRIUM; KINETICS; LIGAND PROGRAM ID T-CELL RECOGNITION; HLA MOLECULES; LYMPHOCYTE-T; IMMUNOGENIC PEPTIDES; INFLUENZA PEPTIDES; LIGAND; ASSOCIATION; MEMBRANES; RECEPTOR; SURFACE AB The major histocompatibility complex-encoded class I molecule, a noncovalent dimer of a polymorphic 45-kDa heavy chain and a nonpolymorphic 12-kDa beta-2-microglobulin (beta-2m) light chain, binds peptide antigen prior to its interaction with T-cell antigen receptors. We report here that the binding in aqueous solution at 37-degrees-C of a soluble purified murine major histocompatibility complex class I protein, H-2L(s)d (a soluble analogue of H-2L(d) consisting of the alpha-1 and alpha-2 domains of H-2L(d), the alpha-3 domain and the C terminus of Q10b), to an antigenic peptide is controlled by the light-chain subunit beta-2m. Analysis of the equilibrium binding data favors a model in which two classes of peptide binding sites exist, the high-affinity class having an equilibrium constant for dissociation, K(H), of 3.7 x 10(-7) M and accounting for 12% of the theoretically available sites. Studies of binding in the presence of excess beta-2m indicate that this increases the concentration of available high-affinity sites. These data are consistent with a ternary model in which high-affinity sites are generated by the interaction Of beta-2m With the peptide-binding class I heavy chain. RP BOYD, LF (reprint author), NIAID,MOLEC BIOL SECT,IMMUNOL LAB,BETHESDA,MD 20892, USA. RI Margulies, David/H-7089-2013; Ain, Kenneth/A-5179-2012; OI Ain, Kenneth/0000-0002-2668-934X; Margulies, David/0000-0001-8530-7375 NR 43 TC 64 Z9 64 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2242 EP 2246 DI 10.1073/pnas.89.6.2242 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300051 PM 1549590 ER PT J AU NEGRO, F PACCHIONI, D SHIMIZU, Y MILLER, RH BUSSOLATI, G PURCELL, RH BONINO, F AF NEGRO, F PACCHIONI, D SHIMIZU, Y MILLER, RH BUSSOLATI, G PURCELL, RH BONINO, F TI DETECTION OF INTRAHEPATIC REPLICATION OF HEPATITIS-C VIRUS-RNA BY INSITU HYBRIDIZATION AND COMPARISON WITH HISTOPATHOLOGY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CHIMPANZEE ANIMAL MODEL; VIRAL MORPHOGENESIS; VIRAL PATHOGENESIS; DIGOXIGENIN-LABELED OLIGONUCLEOTIDE PROBE ID NON-B-HEPATITIS; POLYMERASE CHAIN-REACTION; NON-A-HEPATITIS; CHIMPANZEES; INTERFERON; SEQUENCES; ANTIBODIES; ANTIGEN; GENOME; CELLS AB A nonisotopic in situ hybridization (NISH) assay was used to detect hepatitis C virus (HCV) RNA. A synthetic oligonucleotide complementary to bases 252-301 of the highly conserved 5' noncoding region of the HCV genome was end-labeled by terminal deoxynucleotidyltransferase using digoxigenin-conjugated dUTP. The hybridized oligomer was revealed by an immunohistochemical reaction after incubation with an alkaline phosphatase-conjugated anti-digoxigenin antibody and subsequent amplification with a complex of alkaline phosphatase and anti-alkaline phosphatase antibodies. The intracellular distribution of HCV RNA was monitored in the livers of two chimpanzees experimentally infected with the H strain of HCV and compared with the serum alanine aminotransferase activity, serum HCV RNA, and liver histopathology. Most cells were stained in the cytoplasm as early as 2 days after inoculation, 1 and 2 days, respectively, before the appearance of viral RNA in the serum. The time course of HCV RNA replication was correlated with increases in serum alanine aminotransferase. However, neither one paralleled the appearance of liver cell necrosis nor showed any correlation with the inflammatory response. The NISH signal was not found in liver biopsy specimens taken from these two animals before inoculation with HCV, from chimpanzees with acute hepatitis type A, B, or delta, or from two animals never experimentally infected with any hepatitis agent; moreover, it disappeared when the positive specimens were predigested with RNase and it was not observed after hybridization of positive controls with a labeled oligomer unrelated to HCV RNA. Thus, detection of liver HCV RNA by NISH is a sensitive and specific method for studying HCV replication at the cellular level. Intracellular replication of HCV did not appear to be associated with histopathologic changes in the liver, although the correlation with increases of liver enzyme activity in the serum suggested possible damage to the liver cell membrane. C1 UNIV TURIN,SCH MED,DEPT BIOMED SCI & HUMAN ONCOL,I-10126 TURIN,ITALY. NATL INST HLTH,DEPT ENTEROVIRUSES,MUSASHIMURAYAMA,TOKYO 19012,JAPAN. NIAID,HEPATITIS VIRUSES SECT,INFECT DIS LAB,BETHESDA,MD 20892. RP NEGRO, F (reprint author), OSPED MOLINETTE,DEPT GASTROENTEROL,CORSO BRAMANTE 88,TURIN,ITALY. RI Negro, Francesco/E-2183-2012; OI Bonino, Ferruccio/0000-0001-9942-0328 NR 33 TC 151 Z9 151 U1 0 U2 3 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2247 EP 2251 DI 10.1073/pnas.89.6.2247 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300052 PM 1312716 ER PT J AU ALBINI, A NOONAN, DM MELCHIORI, A FASSINA, GF PERCARIO, M GENTLEMAN, S TOFFENETTI, J CHADER, GJ AF ALBINI, A NOONAN, DM MELCHIORI, A FASSINA, GF PERCARIO, M GENTLEMAN, S TOFFENETTI, J CHADER, GJ TI LAMININ-INDUCED RETINOBLASTOMA CELL-DIFFERENTIATION - POSSIBLE INVOLVEMENT OF A 100-KDA CELL-SURFACE LAMININ-BINDING PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID RETINAL CELLS; MESSENGER-RNA; FIBRONECTIN; ATTACHMENT; IRBP; ADHESION; INVITRO; IDENTIFICATION; SUBSTRATA; RECEPTORS AB Gene and protein expression of Y-79 retinoblastoma cells growing on poly(D-lysine) is switched from a photoreceptor-like to a conventional neuron-like pathway by the basement membrane glycoprotein laminin. Unlike other cell systems where laminin influences differentiation, Y-79 cells can neither attach to nor chemotactically respond to laminin. However, laminin increases attachment to poly(D-lysine). The laminin effects therefore seem to occur via an adhesion- and chemotaxis-independent mechanism. Moreover, these tumor cells do not exhibit high-affinity laminin binding, having only a single binding site of intermediate affinity. Laminin-Sepharose affinity chromatography of Y-79 cell surface proteins labeled with I-125 revealed a single major radiolabeled 100-kDa protein eluted by 20 mM EDTA, with an electrophoretic behavior different from that of integrins. No other proteins were eluted under more stringent conditions. This material, which we call LBM-100 (100-kDa laminin-binding molecule), may be a "differentiative" laminin-binding protein through which laminin influences gene expression and development independently of attachment. C1 CNR,CTR STUDIO NEUROFISIOL CEREBRALE,I-16132 GENOA,ITALY. NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. RP ALBINI, A (reprint author), IST NAZL RIC CANC,VIALE BENEDETTO XV 10,I-16132 GENOA,ITALY. RI Noonan, Douglas/A-8620-2010 OI Noonan, Douglas/0000-0001-8058-0719 NR 33 TC 29 Z9 30 U1 2 U2 3 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2257 EP 2261 DI 10.1073/pnas.89.6.2257 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300054 PM 1532253 ER PT J AU DONOVAN, DM TAKEMURA, M OHARA, BF BRANNOCK, MT UHL, GR AF DONOVAN, DM TAKEMURA, M OHARA, BF BRANNOCK, MT UHL, GR TI PREPROENKEPHALIN PROMOTER CASSETTE CONFERS BRAIN EXPRESSION AND SYNAPTIC REGULATION IN TRANSGENIC MICE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HALOPERIDOL; STRIATUM; DORSAL HORN; SEIZURE; PAIN ID PROENKEPHALIN MESSENGER-RNA; RAT SPINAL-CORD; GENE-EXPRESSION; C-FOS; CHLORAMPHENICOL ACETYLTRANSFERASE; NERVOUS-SYSTEM; CYCLIC AMP; ENKEPHALIN; PRODYNORPHIN; NEURONS AB The preproenkephalin A gene is a neurotransmitter gene whose expression can be modulated "transsynaptically" by changes in neuronal activity. DNA sequences lying within 200 base pairs of this gene's transcription start site resemble consensus binding sites for several transcription factor families. In nonneuronal cell cultures, this promoter region is sufficient to mediate gene responses to depolarization, phorbol esters, adenylate cyclase, and calcium fluxes. To assess the role that these cis-acting elements could play in preproenkephalin expression and regulation in vivo, the expression of a construct containing this 200-base-pair region fused to the chloramphenicol acetyltransferase gene was examined in transgenic mice. This promoter confers modest expression in brain, adrenal, and small intestine, with substantially higher levels in testis. These elements confer trans-synaptic regulation in two well-studied models of trans-synaptic preproenkephalin upregulation but not in a third system, underscoring the specificity of the regulatory sequence elements implicated in the synaptic regulation of neuronal genes. C1 NIDA, ADDICT RES CTR, MOLEC NEUROBIOL LAB, BALTIMORE, MD 21224 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROL, BALTIMORE, MD 21205 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROSCI, BALTIMORE, MD 21205 USA. NR 58 TC 28 Z9 28 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2345 EP 2349 DI 10.1073/pnas.89.6.2345 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300072 PM 1372443 ER PT J AU SHERMAN, A RINZEL, J AF SHERMAN, A RINZEL, J TI RHYTHMOGENIC EFFECTS OF WEAK ELECTROTONIC COUPLING IN NEURONAL MODELS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GAP JUNCTIONS; BURSTING OSCILLATIONS; COUPLED OSCILLATORS ID OSCILLATORS; CHANNEL; CELLS AB Strong gap-junctional coupling can synchronize the electrical oscillations of cells, but we show, in a theoretical model, that weak coupling can phase lock two cells 180-degrees out-of-phase. Antiphase oscillations can exist in parameter regimes where in-phase oscillations break down. Some consequences are (i) coupling two excitable cells leads to pacemaking, (ii) coupling two pacemaker cells leads to bursting, and (iii) coupling two bursters increases burst period. The latter shows that details of the fast spikes can affect macroscopic properties of the slow bursts. These effects hold in other models for bursting and may play a role in the collective behavior of cellular ensembles. RP SHERMAN, A (reprint author), NIDDKD,MATH RES BRANCH,BLDG 31,ROOM 4B-54,BETHESDA,MD 20892, USA. NR 21 TC 221 Z9 222 U1 0 U2 7 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2471 EP 2474 DI 10.1073/pnas.89.6.2471 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300098 PM 1549611 ER PT J AU LARUELLE, M JASKIW, GE LIPSKA, BK KOLACHANA, B CASANOVA, MF KLEINMAN, JE WEINBERGER, DR AF LARUELLE, M JASKIW, GE LIPSKA, BK KOLACHANA, B CASANOVA, MF KLEINMAN, JE WEINBERGER, DR TI D1 AND D2 RECEPTOR MODULATION IN RAT STRIATUM AND NUCLEUS-ACCUMBENS AFTER SUBCHRONIC AND CHRONIC HALOPERIDOL TREATMENT SO BRAIN RESEARCH LA English DT Article DE DOPAMINE-D1 RECEPTOR; DOPAMINE-D2 RECEPTOR; HALOPERIDOL; LIMBIC SYSTEM, ANTIPSYCHOTIC TREATMENT ID CHRONIC NEUROLEPTIC TREATMENT; DOPAMINE-RECEPTORS; D2-DOPAMINE RECEPTORS; REDUCED HALOPERIDOL; CLINICAL POTENCY; BINDING; BRAIN; D-1; SCHIZOPHRENIA; ANTAGONISTS AB The antipsychotic effects of neuroleptic drugs are believed to be achieved by chronic blockade of dopaminergic transmission in the limbic system. Nevertheless, the effects of chronic (3-12 months) haloperidol administration on the dopaminergic transmission in the nucleus accumbens of rodents remains poorly understood. Studies of spontaneous locomotor activity (SLA), a behavioral measure related to limbic dopamine transmission, and of dopamine D2 receptor density in the nucleus accumbens after chronic oral haloperidol treatment have yielded conflicting results. We evaluated these indices after 8 months of parenteral administration of haloperidol decanoate. We report here that, after 8 months of parenteral treatment, SLA stays significantly decreased and D2 receptors in the nucleus accumbens exhibit the same up-regulation as in the striatum (about 50%). These results fail to support the notion of a different pattern of D2 receptor adaptation to neuroleptic treatment between the nucleus accumbens and the striatum. In contrast, dopamine D1 receptors were found to be unaffected in the nucleus accumbens but decreased in the striatum by 22% after 8 months of treatment. This observation could be relevant to the pathogenesis of tardive dyskinesia. C1 NIMH,NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,IRP,WASHINGTON,DC 20032. RI Lipska, Barbara/E-4569-2017 NR 48 TC 52 Z9 52 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 13 PY 1992 VL 575 IS 1 BP 47 EP 56 DI 10.1016/0006-8993(92)90421-5 PG 10 WC Neurosciences SC Neurosciences & Neurology GA HK630 UT WOS:A1992HK63000007 PM 1387032 ER PT J AU COLEMAN, MH YAMAGUCHI, SI ROGAWSKI, MA AF COLEMAN, MH YAMAGUCHI, SI ROGAWSKI, MA TI PROTECTION AGAINST DENDROTOXIN-INDUCED CLONIC SEIZURES IN MICE BY ANTICONVULSANT DRUGS SO BRAIN RESEARCH LA English DT Note DE DENDROTOXIN; K+ CHANNEL BLOCKER; ANTICONVULSANT DRUG; SEIZURE; EPILEPSY ID DENDROASPIS-ANGUSTICEPS VENOM; CELL DEGRANULATING PEPTIDE; POTASSIUM CHANNELS; EPILEPTIFORM ACTIVITY; RECEPTOR ANTAGONISTS; INHIBITOR HOMOLOGS; SNAKE TOXINS; K+ CHANNEL; RAT-BRAIN; 4-AMINOPYRIDINE AB Various anticonvulsant drugs were evaluated for their ability to protect against clonic seizures induced in mice by intraventricular injection of the K+ channel blocking peptide dendrotoxin (DTX). Phenytoin, the phenytoin-like anticonvulsant carbamazepine and the broad spectrum drug valproate were effective in this model, whereas the GABA-enhancers diazepam and tiagabine, the NMDA antagonists (+/-)-CPP and (+)-MK-801, the AMPA antagonist NBQX, the antiabsence drug ethosuximide and the Ca2+ channel antagonist nimodipine were inactive. In contrast to the lack of activity of other NMDA antagonists, phencyclidine and ADCI [(+/-)-aminocarbonyl-10,11-dihydro-5H-dibenzo [a,d]cyclohepten-5,10-imine] were potent antagonists of DTX-induced seizures. C1 NINCDS,EPILEPSY RES BRANCH,NEURONAL EXCITABIL SECT,NIH BLDG 10,BETHESDA,MD 20892. RI Rogawski, Michael/B-6353-2009 OI Rogawski, Michael/0000-0002-3296-8193 NR 41 TC 27 Z9 27 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 13 PY 1992 VL 575 IS 1 BP 138 EP 142 DI 10.1016/0006-8993(92)90433-A PG 5 WC Neurosciences SC Neurosciences & Neurology GA HK630 UT WOS:A1992HK63000019 PM 1504773 ER PT J AU HEALY, B AF HEALY, B TI WOMEN IN SCIENCE - FROM PANES TO CEILINGS SO SCIENCE LA English DT Editorial Material RP HEALY, B (reprint author), NIH,BETHESDA,MD 20892, USA. NR 1 TC 11 Z9 11 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 13 PY 1992 VL 255 IS 5050 BP 1333 EP 1333 DI 10.1126/science.1542782 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HH744 UT WOS:A1992HH74400001 PM 1542782 ER PT J AU NAIR, BC DEVICO, AL NAKAMURA, S COPELAND, TD CHEN, Y PATEL, A ONEIL, T OROSZLAN, S GALLO, RC SARNGADHARAN, MG AF NAIR, BC DEVICO, AL NAKAMURA, S COPELAND, TD CHEN, Y PATEL, A ONEIL, T OROSZLAN, S GALLO, RC SARNGADHARAN, MG TI IDENTIFICATION OF A MAJOR GROWTH-FACTOR FOR AIDS KAPOSIS-SARCOMA CELLS AS ONCOSTATIN-M SO SCIENCE LA English DT Article ID YOUNG HOMOSEXUAL MEN; LONG-TERM CULTURE; REGULATOR; LESIONS; PROTEIN AB Conditioned medium from human T cell leukemia virus type 2 (HTLV-II)-infected T cells supports the growth and long-term culture of cells derived from acquired immunodeficiency syndrome (AIDS)-associated Kaposi's sarcoma lesions (AIDS-KS cells). A protein of 30 kilodaltons was purified from conditioned medium that supports the growth of AIDS-KS cells. The amino-terminal sequence of this protein was identical to the amino-terminal sequence of Oncostatin M, a glycoprotein that inhibits the growth of a variety of cancer cells. Oncostatin M from conditioned medium stimulated a twofold increase in the growth of AIDS-KS cells at a concentration of less than 1 nanogram of the protein per milliliter of medium. C1 ADV BIOSCIENCE LABS INC,DEPT CELL BIOL,KENSINGTON,MD 20895. NCI,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LABS,BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [N01-CP-73723, N01-CO-74101] NR 16 TC 217 Z9 219 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 13 PY 1992 VL 255 IS 5050 BP 1430 EP 1432 DI 10.1126/science.1542792 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HH744 UT WOS:A1992HH74400055 PM 1542792 ER PT J AU NAKAMURA, S SAKURADA, S SALAHUDDIN, SZ OSADA, Y TANAKA, NG SAKAMOTO, N SEKIGUCHI, M GALLO, RC AF NAKAMURA, S SAKURADA, S SALAHUDDIN, SZ OSADA, Y TANAKA, NG SAKAMOTO, N SEKIGUCHI, M GALLO, RC TI INHIBITION OF DEVELOPMENT OF KAPOSIS-SARCOMA RELATED LESIONS BY A BACTERIAL-CELL WALL COMPLEX SO SCIENCE LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; LONG-TERM CULTURE; HOMOSEXUAL MEN; ANGIOGENESIS; THERAPY; GROWTH AB In vitro and in vivo model systems for the study of human immunodeficiency virus (HIV-associated Kaposi's sarcoma (KS) were used to evaluate compounds for their potential as therapeutic agents. A sulfated polysaccharide-peptidoglycan compound (SP-PG) produced by bacteria controlled the in vitro growth of acquired immunodeficiency syndrome (AIDS)-associated, KS-derived spindle-shaped cells (AIDS-KS cells) at noncytotoxic concentrations. Angiogenesis induced by AIDS-KS cells in the chicken chorioallantoic membrane assay was blocked by SP-PG, which also inhibited the vascular hyperpermeability response and the angiogenesis associated with the induction of KS-like lesions that develop after subcutaneous inoculation of AIDS-KS cells into nude mice. Suramin, pentosan polysulfate, and interferon-alpha, which are currently in use for therapy of KS, were either less effective than SP-PG or much more cytotoxic, or both. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV SO CALIF,DEPT INTERNAL MED,LOS ANGELES,CA 90089. DAIICHI PHARMACEUT CO LTD,TOKYO 103,JAPAN. HUNTINGTON MEM HOSP,INST MOLEC MED & TECHNOL,PASADENA,CA 91105. NR 23 TC 84 Z9 84 U1 2 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 13 PY 1992 VL 255 IS 5050 BP 1437 EP 1440 DI 10.1126/science.1371891 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HH744 UT WOS:A1992HH74400058 PM 1371891 ER PT J AU JUCKER, M WALKER, LC MARTIN, LJ KITT, CA KLEINMAN, HK INGRAM, DK PRICE, DL AF JUCKER, M WALKER, LC MARTIN, LJ KITT, CA KLEINMAN, HK INGRAM, DK PRICE, DL TI AGE-ASSOCIATED INCLUSIONS IN NORMAL AND TRANSGENIC MOUSE-BRAIN SO SCIENCE LA English DT Article ID DISEASE; MICE C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,NEUROPATHOL LAB,BALTIMORE,MD 21205. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. RI Walker, L/J-6541-2015 OI Walker, L/0000-0001-9166-3261 NR 16 TC 52 Z9 52 U1 1 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 13 PY 1992 VL 255 IS 5050 BP 1443 EP 1445 DI 10.1126/science.1542796 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HH744 UT WOS:A1992HH74400060 PM 1542796 ER PT J AU MORGAN, PF NADI, NS KARANIAN, J LINNOILA, M AF MORGAN, PF NADI, NS KARANIAN, J LINNOILA, M TI MAPPING RAT-BRAIN STRUCTURES ACTIVATED DURING ETHANOL WITHDRAWAL - ROLE OF GLUTAMATE AND NMDA RECEPTORS SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION LA English DT Article DE ETHANOL; C-FOS; GLUTAMATE; NMDA (N-METHYL-D-ASPARTATE); HYBRIDIZATION (INSITU) ID C-FOS PROTEIN; MESSENGER-RNA; MOUSE-BRAIN; AP-1; TRANSCRIPTION; EXPRESSION; SEIZURES; NEURONS; COMPLEX; ALCOHOL AB Brain structures activated during ethanol withdrawal have been mapped by visualizing c-fos mRNA expression. The regional distribution of c-fos mRNA in brain during ethanol withdrawal can be mimicked by acute injection of N-methyl-D-aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK-801. The findings reveal that the dentate gyrus and piriform cortex are selectively activated during ethanol withdrawal and suggest that this may be mediated by glutamate activation of NMDA receptors. C1 NINCDS,MED NEUROL BRANCH,BETHESDA,MD 20892. RP MORGAN, PF (reprint author), NIAAA,CLIN STUDIES LAB,BLDG 10,ROOM 3C-102,BETHESDA,MD 20892, USA. NR 37 TC 69 Z9 69 U1 0 U2 0 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 MAR 12 PY 1992 VL 225 IS 3 BP 217 EP 223 DI 10.1016/0922-4106(92)90023-O PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HK530 UT WOS:A1992HK53000005 PM 1355445 ER PT J AU VUKICEVIC, S SOMOGYI, L MARTINOVIC, I ZIC, R KLEINMAN, HK MARUSIC, M AF VUKICEVIC, S SOMOGYI, L MARTINOVIC, I ZIC, R KLEINMAN, HK MARUSIC, M TI RECONSTITUTED BASEMENT-MEMBRANE (MATRIGEL) PROMOTES THE SURVIVAL AND INFLUENCES THE GROWTH OF MURINE TUMORS SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID LAMININ; CELLS; METASTASIS; IDENTIFICATION; ATTACHMENT; COMPONENTS; DOMAINS; IV AB The effects of reconstituted basement membrane (Matrigel) on in vivo survival and growth of several murine tumors were studied. Survival of tumor cells was enhanced in all experiments which resulted in increased incidence and/or in increased tumor mass. While basement membrane enhanced the in vivo growth of B16F6 melanoma cells, survival of these mice was prolonged. Basement membrane increased the incidence but reduced the growth of Ehrlich ascites tumor. Walker-256 hypercalcemic breast carcinosarcoma growth was enhanced and glandular-like structures were observed when grown on Matrigel. The results indicate that the enhanced survival of tumor cells in the presence of basement membrane is not unequivocally linked with increased malignancy. C1 UNIV ZAGREB,SCH MED,DEPT PHYSIOL,YU-41000 ZAGREB,YUGOSLAVIA. CTR BIOMED INVEST,ZAGREB,YUGOSLAVIA. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. RP VUKICEVIC, S (reprint author), UNIV ZAGREB,SCH MED,DEPT ANAT,SALATA 11,POB 978,YU-41000 ZAGREB,YUGOSLAVIA. OI Marusic, Matko/0000-0001-5562-1777 NR 23 TC 19 Z9 19 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD MAR 12 PY 1992 VL 50 IS 5 BP 791 EP 795 DI 10.1002/ijc.2910500521 PG 5 WC Oncology SC Oncology GA HJ376 UT WOS:A1992HJ37600020 PM 1544713 ER PT J AU PENG, CK BULDYREV, SV GOLDBERGER, AL HAVLIN, S SCIORTINO, F SIMONS, M STANLEY, HE AF PENG, CK BULDYREV, SV GOLDBERGER, AL HAVLIN, S SCIORTINO, F SIMONS, M STANLEY, HE TI LONG-RANGE CORRELATIONS IN NUCLEOTIDE-SEQUENCES SO NATURE LA English DT Article ID PIECES; GENES AB DNA SEQUENCES have been analysed using models, such as an n-step Markov chain, that incorporate the possibility of short-range nucleotide correlations 1. We propose here a method for studying the stochastic properties of nucleotide sequences by constructing a 1:1 map of the nucleotide sequence onto a walk, which we term a 'DNA walk'. We then use the mapping to provide a quantitative measure of the correlation between nucleotides over long distances along the DNA chain. Thus we uncover in the nucleotide sequence a remarkably long-range power law correlation that implies a new scale-invariant property of DNA. We find such long-range correlations in intron-containing genes and in nontranscribed regulatory DNA sequences, but not in complementary DNA sequences or intron-less genes. C1 BOSTON UNIV,DEPT PHYS,BOSTON,MA 02215. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV CARDIOVASC,BOSTON,MA 02215. NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. RP PENG, CK (reprint author), BOSTON UNIV,CTR POLYMER STUDIES,BOSTON,MA 02215, USA. RI Peng, Chung-Kang/E-1489-2011; Sciortino, Francesco/B-4768-2012; Simons, Michael/G-8553-2014; Buldyrev, Sergey/I-3933-2015 OI Peng, Chung-Kang/0000-0003-3666-9833; Simons, Michael/0000-0003-0348-7734; NR 11 TC 922 Z9 956 U1 2 U2 30 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 12 PY 1992 VL 356 IS 6365 BP 168 EP 170 DI 10.1038/356168a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HH731 UT WOS:A1992HH73100065 PM 1301010 ER PT J AU FLOETER, MK AF FLOETER, MK TI CAROTID ENDARTERECTOMY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP FLOETER, MK (reprint author), NIH,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 12 PY 1992 VL 326 IS 11 BP 763 EP 763 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HH064 UT WOS:A1992HH06400012 PM 1738385 ER PT J AU HEALY, B AF HEALY, B TI HELPING CHILDREN INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP HEALY, B (reprint author), NIH,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 11 PY 1992 VL 267 IS 10 BP 1319 EP 1319 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HG678 UT WOS:A1992HG67800004 PM 1740841 ER PT J AU KASLOW, RA AF KASLOW, RA TI CURRENT PERSPECTIVE ON LYME BORRELIOSIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID ERYTHEMA MIGRANS BORRELIOSIS; DISEASE SPIROCHETE; MANIFESTATIONS; ABNORMALITIES; BURGDORFERI RP KASLOW, RA (reprint author), NIAID,DIV MICROBIOL & INFECT DIS,EPIDEMIOL & BIOMETRY BRANCH,BETHESDA,MD 20892, USA. NR 26 TC 8 Z9 8 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 11 PY 1992 VL 267 IS 10 BP 1381 EP 1383 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA HG678 UT WOS:A1992HG67800034 PM 1740862 ER PT J AU RABEN, N BORRIELLO, F AMIN, J HORWITZ, R FRASER, D PLOTZ, P AF RABEN, N BORRIELLO, F AMIN, J HORWITZ, R FRASER, D PLOTZ, P TI HUMAN HISTIDYL-TRANSFER RNA-SYNTHETASE - RECOGNITION OF AMINO-ACID SIGNATURE REGIONS IN CLASS-2A AMINOACYL-TRANSFER RNA-SYNTHETASES SO NUCLEIC ACIDS RESEARCH LA English DT Article ID HUMAN-GENE; AUTOANTIBODIES; MYOSITIS; CLONING; POLYMYOSITIS; AUTOIMMUNITY; CEREVISIAE; SEQUENCE AB We have determined the sequence of cDNA for the human histidyl-tRNA synthetase (HRS) in a hepatoma cell line and confirmed it in fetal myoblast and fibroblast cell lines. The newly determined sequence differs in 48 places, including insertions and deletions, from a previously published sequence. By sequence specific probing and by direct sequencing, we have established that only the newly determined sequence is present in genomic DNA and we have sequenced 500 hundred bases upstream of the translation start site. The predicted amino acid sequence now clearly demonstrates all three motifs recognized in class 2 aminoacyl-tRNA synthetases. Alignment of E. coli, yeast, and when available, mammalian predicted amino acid sequences for three of the four members of the class 2a subgroup (his, pro, ser, and thr) shows strong preservation of amino acid specific signature regions proximal to motif 2 and proximal to motif 3. These probably represent the active site binding regions for the proximal acceptor stem and for the amino acid. The first two exons of human HRS contain a 32 amino acid helical motif, first described in human QRS, a class 1 synthetase, which is found also in a yeast RNA polymerase, a rabbit termination factor, and both bovine and human WRS, suggesting that it may be an RNA binding motif. RP RABEN, N (reprint author), NATL INST ARTHRITIS & MUSCULOSKELETAL & SKIN DIS,CONNECT TISSUE DIS SECT,BETHESDA,MD 20892, USA. NR 36 TC 40 Z9 44 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAR 11 PY 1992 VL 20 IS 5 BP 1075 EP 1081 DI 10.1093/nar/20.5.1075 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK001 UT WOS:A1992HK00100016 PM 1549469 ER PT J AU KOONIN, EV AF KOONIN, EV TI ARCHAEBACTERIAL VIRUS SSV1 ENCODES A PUTATIVE DNAA-LIKE PROTEIN SO NUCLEIC ACIDS RESEARCH LA English DT Note ID SEQUENCE; GENES RP KOONIN, EV (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BLDG 38A,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 10 TC 20 Z9 22 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAR 11 PY 1992 VL 20 IS 5 BP 1143 EP 1143 DI 10.1093/nar/20.5.1143 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK001 UT WOS:A1992HK00100030 PM 1549481 ER PT J AU CHOI, MG PROCHAZKA, M THUILLEZ, P LILLOJA, S AF CHOI, MG PROCHAZKA, M THUILLEZ, P LILLOJA, S TI A NEW TAQL ALLELE DETECTED BY THE CRI-R227 (D4S101) PROBE IN PIMA-INDIANS SO NUCLEIC ACIDS RESEARCH LA English DT Note RP CHOI, MG (reprint author), NATL INST DIABET & DIGEST & KIDNEY DIS,CLIN DIABET & NUTR SECT,4212 N 16TH ST,ROOM 541,PHOENIX,AZ 85016, USA. RI Lillioja, Stephen/A-8185-2012 NR 3 TC 1 Z9 1 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAR 11 PY 1992 VL 20 IS 5 BP 1157 EP 1157 DI 10.1093/nar/20.5.1157-a PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK001 UT WOS:A1992HK00100044 PM 1347923 ER PT J AU RUVINOV, SB MILES, EW AF RUVINOV, SB MILES, EW TI SUBUNIT COMMUNICATION IN THE TRYPTOPHAN SYNTHASE ALPHA-2-BETA-2 COMPLEX - EFFECTS OF BETA-SUBUNIT LIGANDS ON PROTEOLYTIC CLEAVAGE OF A FLEXIBLE LOOP IN THE ALPHA-SUBUNIT SO FEBS LETTERS LA English DT Article DE TRYPTOPHAN SYNTHASE; SUBUNIT COMMUNICATION; ALLOSTERIC MECHANISM; PROTEIN LOOP; PROTEOLYSIS; LIGAND BINDING ID SALMONELLA-TYPHIMURIUM; ESCHERICHIA-COLI; SITE AB To probe the structural basis for ligand-mediated communication between the alpha and beta-subunits in the tryptophan synthase alpha-2-beta-2 complex. we have determined the effects of ligands of the alpha and beta-subunits on proteolysis of a flexible loop in the alpha-subunit. We find that addition of a ligand of the beta-subunit (L-serine, D-tryptophan, or L-tryptophan) in combination with a ligand of the a subunit (alpha-glycerol 3-phosphate) almost completely prevents the tryptic cleavage of the alpha-subunit loop. Thus. the binding of a ligand to the beta-site affects the conformation of the alpha-subunit 25-30 angstrom distant. C1 NIDDKD,BIOCHEM PHARMACOL LAB,BLDG 8,ROOM 225,BETHESDA,MD 20892. NR 17 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAR 9 PY 1992 VL 299 IS 2 BP 197 EP 200 DI 10.1016/0014-5793(92)80246-D PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA HH970 UT WOS:A1992HH97000019 PM 1544494 ER PT J AU TOMBRANTINK, J LI, A JOHNSON, MA JOHNSON, LV CHADER, GJ AF TOMBRANTINK, J LI, A JOHNSON, MA JOHNSON, LV CHADER, GJ TI NEUROTROPHIC ACTIVITY OF INTERPHOTORECEPTOR MATRIX ON HUMAN Y79 RETINOBLASTOMA CELLS SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE RETINA; DEVELOPMENT; NEURON; TISSUE CULTURE; DIFFERENTIATION ID RETINOID-BINDING PROTEIN; PIGMENT-EPITHELIUM; PHOTORECEPTOR DEVELOPMENT; EXPLANTS INVITRO; RDS MUTANT; DIFFERENTIATION; ATTACHMENT; LAMININ; CONE; IRBP AB A neurotrophic activity of adult monkey and bovine interphotoreceptor matrix (IPM) was examined by using cultured human Y79 retinoblastoma cells as a model system. The cells were stimulated for 7 days in suspension culture with soluble IPM components and then attached to poly-D-lysine substratum. IPMs from both species induced greater than 80% neuronal differentiation of Y79 cell aggregates after 11 days of attachment as adjudged morphologically by the extension of lengthy, neurite-like processes. Immunocytochemical studies indicate that differentiated Y79 cells had an increased level of expression of neuron-specific enolase and a concomitant decreased expression of glial fibrillary acidic protein. This neurotrophic activity cannot be ascribed to nerve growth factor, platelet-derived growth factor, fibroblast growth factor, epidermal growth factor, or transforming growth factor beta. Although the nature of the factor and its cellular source have yet to be characterized, it may be related to a recently described neurotrophic protein secreted by human fetal retinal pigment epithelial cells in culture. Our findings provide evidence supporting the neuroblastic potential of the Y79 cell line and indicate that the IPM contains a potent neurotrophic activity. Such factors may be important to normal differentiation and maintenance of function of the neural retina. C1 UNIV SO CALIF,SCH MED,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90033. HOWARD HUGHES MED INST,BETHESDA,MD 20814. RP TOMBRANTINK, J (reprint author), NEI,RETINAL CELL & MOLEC BIOL,BETHESDA,MD 20892, USA. NR 51 TC 24 Z9 25 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD MAR 8 PY 1992 VL 317 IS 2 BP 175 EP 186 DI 10.1002/cne.903170206 PG 12 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA HF669 UT WOS:A1992HF66900005 PM 1573062 ER PT J AU VAHAKANGAS, KH SAMET, JM METCALF, RA WELSH, JA BENNETT, WP LANE, DP HARRIS, CC AF VAHAKANGAS, KH SAMET, JM METCALF, RA WELSH, JA BENNETT, WP LANE, DP HARRIS, CC TI MUTATIONS OF P53 AND RAS GENES IN RADON-ASSOCIATED LUNG-CANCER FROM URANIUM MINERS SO LANCET LA English DT Article ID POINT MUTATIONS; RISK; CARCINOMA; EXPOSURE; FREQUENT; CELLS AB Radon increases the risk of lung cancer in smoking and non-smoking underground miners. To investigate the mutational spectrum associated with exposure to high levels of radon, we sequenced exons 5-9 of the p53 tumour suppressor gene and codons 12-13 of the Ki-ras protooncogene in 19 lung cancers from uranium miners exposed to radon and tobacco smoke. Mutations were not found in Ki-ras, but 9 p53 mutations, including 2 deletions, were found in 7 patients by direct DNA sequencing after polymerase chain reaction amplification of DNA from formalin-fixed, paraffin-embedded tissue. In tumours from 5 patients, the mutation produced an aminoacid change and an increased nuclear content of p53 protein. The tumours with either a stop codon or frame-shift deletion in the p53 gene were negative by immunohistochemistry. None of the mutations were G:C to T:A transversions in the coding strand of the p53 gene, which are the most frequent base substitutions associated with tobacco smoking, and none were found at the hotspot codons described in lung cancer. The observed differences from the usual lung cancer mutational spectrum may reflect the genotoxic effects of radon. C1 NCI,HUMAN CARCINOGENESIS LAB,BLDG 37,ROOM 2C05,BETHESDA,MD 20892. UNIV DUNDEE,DEPT BIOCHEM,DUNDEE DD1 4HN,SCOTLAND. UNIV NEW MEXICO,MED CTR,CTR CANC,NEW MEXICO TUMOR REGISTRY,ALBUQUERQUE,NM 87131. UNIV NEW MEXICO,MED CTR,DEPT MED,ALBUQUERQUE,NM 87131. RI Lane, David/C-4920-2008 FU NCI NIH HHS [N01 CN-55426] NR 30 TC 288 Z9 294 U1 0 U2 12 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD MAR 7 PY 1992 VL 339 IS 8793 BP 576 EP 580 DI 10.1016/0140-6736(92)90866-2 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HH075 UT WOS:A1992HH07500004 PM 1347094 ER PT J AU TUDORWILLIAMS, G STCLAIR, MH MCKINNEY, RE MAHA, M WALTER, E SANTACROCE, S MINTZ, M ODONNELL, K RUDOLL, T VAVRO, CL CONNOR, EM WILFERT, CM AF TUDORWILLIAMS, G STCLAIR, MH MCKINNEY, RE MAHA, M WALTER, E SANTACROCE, S MINTZ, M ODONNELL, K RUDOLL, T VAVRO, CL CONNOR, EM WILFERT, CM TI HIV-1 SENSITIVITY TO ZIDOVUDINE AND CLINICAL OUTCOME - REPLY SO LANCET LA English DT Letter ID THERAPY RP TUDORWILLIAMS, G (reprint author), NIH,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, USA. NR 3 TC 2 Z9 2 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD MAR 7 PY 1992 VL 339 IS 8793 BP 627 EP 627 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HH075 UT WOS:A1992HH07500062 ER PT J AU GOEDERT, JJ AF GOEDERT, JJ TI HIV-EXPOSED TWINS - REPLY SO LANCET LA English DT Letter RP GOEDERT, JJ (reprint author), NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD MAR 7 PY 1992 VL 339 IS 8793 BP 628 EP 628 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HH075 UT WOS:A1992HH07500065 ER PT J AU FATATIS, A HOLTZCLAW, L PAYZA, K RUSSELL, JT AF FATATIS, A HOLTZCLAW, L PAYZA, K RUSSELL, JT TI SECRETION FROM RAT NEUROHYPOPHYSEAL NERVE-TERMINALS (NEUROSECRETOSOMES) RAPIDLY INACTIVATES DESPITE CONTINUED ELEVATION OF INTRACELLULAR CA2+ SO BRAIN RESEARCH LA English DT Article DE NEUROSECRETOSOME; NEUROHYPOPHYSIS; NERVE TERMINAL; CALCIUM IMAGING; CYTOPLASMIC FREE CALCIUM ID SYNAPTIC TRANSMITTER RELEASE; HORMONE-RELEASE; CALCIUM CURRENTS; VASOPRESSIN RELEASE; MUSCLE-CELLS; ENDINGS; NEURONS; CHANNELS; MECHANISMS; POTASSIUM AB Cytoplasmic calcium concentration was measured in neurosecretory nerve terminals (neurosecretosomes) isolated from rat neurohypophyses by fura-2 fluorescence measurements and digital video microscopy. Hormone release and cytoplasmic calcium concentration were measured during depolarizations induced by elevated extracellular potassium concentration. During prolonged depolarizations with 55 mM [K+]o, the cytoplasmic calcium concentration remained elevated as long as depolarization persisted, while secretion inactivated after the initial sharp rise. The amplitude and duration of the increase in [Ca2+]i was dependent on the degree of depolarization such that upon low levels of depolarizations (12.5 mM or 25 mM [K+]o), the calcium responses were smaller and relatively transient, and with higher levels of depolarization (55 mM [K+]o) the responses were sustained and were higher in amplitude. Responses to low levels of depolarization were less sensitive to the dihydropyridine calcium channel blocker, nimodipine, while the increase in [Ca2+]i induced by 55 mM [K+]o became transient, and was significantly smaller. These observations suggest that these peptidergic nerve terminals possess at least two different types of voltage-gated calcium channels. Removal of extracellular sodium resulted in a significant increase in [Ca2+]i and secretion in the absence of depolarizing stimulus, suggesting that sodium-calcium exchange mechanism is operative in these nerve terminals. Although the [Ca2+]i increase was of similar magnitude to the depolarization-induced changes, the resultant secretion was 10-fold lower, but the rate of inactivation of secretion, however, was comparable. C1 NICHHD,DEV NEUROBIOL LAB,NEURONAL SECRETORY SYST SECT,BLDG 36,RM B-316,BETHESDA,MD 20892. NAPLES UNIV,SCH MED 2,DEPT PHARMACOL,I-80138 NAPLES,ITALY. NR 48 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 6 PY 1992 VL 574 IS 1-2 BP 33 EP 41 DI 10.1016/0006-8993(92)90796-C PG 9 WC Neurosciences SC Neurosciences & Neurology GA HK089 UT WOS:A1992HK08900005 PM 1638405 ER PT J AU AZARI, NP RAPOPORT, SI GRADY, CL DECARLI, C HAXBY, JV SCHAPIRO, MB HORWITZ, B AF AZARI, NP RAPOPORT, SI GRADY, CL DECARLI, C HAXBY, JV SCHAPIRO, MB HORWITZ, B TI GENDER DIFFERENCES IN CORRELATIONS OF CEREBRAL GLUCOSE METABOLIC RATES IN YOUNG NORMAL ADULTS SO BRAIN RESEARCH LA English DT Article DE HUMAN; GENDER; POSITRON EMISSION TOMOGRAPHY; CORRELATION; CEREBRAL METABOLISM; BRAIN; GLUCOSE ID HUMAN CORPUS-CALLOSUM; SEX-RELATED DIFFERENCES; BRAIN-REGIONS; TRANSMISSION MEASUREMENTS; ALZHEIMER TYPE; BLOOD-FLOW; INTERCORRELATIONS; ORGANIZATION; DIMORPHISM; HANDEDNESS AB Correlational analysis of normalized regional cerebral metabolic data obtained by positron emission tomography, in healthy subjects in the 'resting' state (eyes covered, ears plugged) using [F-18]2-fluoro-2-deoxy-D-glucose, demonstrated gender differences in patterns of functional associations. Fifteen women and 18 men (< 40 yr) were scanned with a Scanditronix PC1024-7B tomograph. The brain was divided into 65 regions of interest (ROIs). There were no differences between men and women in global or regional metabolic rates, or in metabolic right-left asymmetries. Although the total number of significant correlations did not differ between men and women, patterns differed: female correlations r(F) were more positive than male correlations r(M) more often than r(M) > r(F); and most r(F) > r(M) cases involved left frontal and sensorimotor ROIs, whereas most r(M) > r(F) cases involved right sensorimotor and occipital ROIs. The findings demonstrate gender differences in the pattern of functional neocortical interactions at the 'resting' state. RP AZARI, NP (reprint author), NIA,NEUROSCI LAB,BLDG 10,ROOM 6C414,BETHESDA,MD 20892, USA. RI DeCarli, Charles/B-5541-2009 FU NINDS NIH HHS [R01 NS017950] NR 70 TC 48 Z9 50 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 6 PY 1992 VL 574 IS 1-2 BP 198 EP 208 DI 10.1016/0006-8993(92)90817-S PG 11 WC Neurosciences SC Neurosciences & Neurology GA HK089 UT WOS:A1992HK08900026 PM 1638393 ER PT J AU MURRAY, EA RAUSCH, DM LENDVAY, J SHARER, LR EIDEN, LE AF MURRAY, EA RAUSCH, DM LENDVAY, J SHARER, LR EIDEN, LE TI COGNITIVE AND MOTOR IMPAIRMENTS ASSOCIATED WITH SIV INFECTION IN RHESUS-MONKEYS SO SCIENCE LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; AIDS DEMENTIA COMPLEX; VIRUS-INFECTION; MEMORY AB Cognitive and motor deficits are now recognized as significant clinical features of infection with the human immunodeficiency virus (HIV). Juvenile rhesus macaques infected with simian immunodeficiency virus (SIV) were found to exhibit cognitive and motor deficits characteristic of HIV infection. Impairment on a motor skill task was the most reliable indicator of infection. Various cognitive impairments were also evident. These deficits were related to SIV infection of the brain but not to inflammatory lesions at a particular locus. The results suggest that the SIV-infected rhesus macaque is a valuable model for understanding the cause of HIV-associated central nervous system dysfunction and for developing a treatment. C1 NIMH,CELL BIOL LAB,MOLEC & CELLULAR NEUROBIOL UNIT,BETHESDA,MD 20892. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT LAB MED & PATHOL,NEWARK,NJ 07103. RP MURRAY, EA (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 9,ROOM 1E104,BETHESDA,MD 20892, USA. OI Eiden, Lee/0000-0001-7524-944X; Murray, Elisabeth/0000-0003-1450-1642 NR 21 TC 145 Z9 147 U1 1 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 6 PY 1992 VL 255 IS 5049 BP 1246 EP 1249 DI 10.1126/science.1546323 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HG677 UT WOS:A1992HG67700040 PM 1546323 ER PT J AU HUNT, DF HENDERSON, RA SHABANOWITZ, J SAKAGUCHI, K MICHEL, H SEVILIR, N COX, AL APPELLA, E ENGELHARD, VH AF HUNT, DF HENDERSON, RA SHABANOWITZ, J SAKAGUCHI, K MICHEL, H SEVILIR, N COX, AL APPELLA, E ENGELHARD, VH TI CHARACTERIZATION OF PEPTIDES BOUND TO THE CLASS-I MHC MOLECULE HLA-A2.1 BY MASS-SPECTROMETRY SO SCIENCE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; ANTIGEN PRESENTATION; LYMPHOCYTE-T; PROTEIN; PATHWAY; GENE AB Antigens recognized by T cells are expressed as peptides bound to major histocompatibility complex (MHC) molecules. Microcapillary high-performance liquid chromatography - electrospray ionization-tandem mass spectrometry was used to fractionate and sequence subpicomolar amounts of peptides isolated from the MHC molecule HLA-A2.1. Of 200 different species quantitated, eight were sequenced and four were found in cellular proteins. All were nine residues long and shared a distinct structural motif. The sensitivity and speed of this approach should enhance the analysis of peptides from small quantities of virally infected and transformed cells as well as those associated with autoimmune disease states. C1 UNIV VIRGINIA,SCH MED,DEPT MICROBIOL,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,SCH MED,BEIRNE CARTER CTR IMMUNOL RES,CHARLOTTESVILLE,VA 22908. NCI,CELL BIOL LAB,BETHESDA,MD 20892. RP HUNT, DF (reprint author), UNIV VIRGINIA,DEPT CHEM,CHARLOTTESVILLE,VA 22903, USA. RI Hunt, Donald/I-6936-2012 OI Hunt, Donald/0000-0003-2815-6368 FU NIAID NIH HHS [AI20963]; NIGMS NIH HHS [GM37537] NR 30 TC 967 Z9 981 U1 3 U2 36 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 6 PY 1992 VL 255 IS 5049 BP 1261 EP 1263 DI 10.1126/science.1546328 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HG677 UT WOS:A1992HG67700045 PM 1546328 ER PT J AU HENDERSON, RA MICHEL, H SAKAGUCHI, K SHABANOWITZ, J APPELLA, E HUNT, DF ENGELHARD, VH AF HENDERSON, RA MICHEL, H SAKAGUCHI, K SHABANOWITZ, J APPELLA, E HUNT, DF ENGELHARD, VH TI HLA-A2.1-ASSOCIATED PEPTIDES FROM A MUTANT-CELL LINE - A 2ND PATHWAY OF ANTIGEN PRESENTATION SO SCIENCE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-I MOLECULES; VIRAL PEPTIDES; LYMPHOCYTE-T; PROTEIN; BINDING; INVITRO; GENE AB Peptides extracted from HLA-A2.1 class I major histocompatibility complex (MHC) molecules expressed on the antigen processing mutant CEMx721.174.T2 were characterized by electrospray ionization-tandem mass spectrometry. Only seven dominant peptides were found, in contrast to over 200 associated with HLA-A2.1 on normal cells. These peptides were derived from the signal peptide domains of normal cellular proteins, were usually larger than nine residues, and were also associated with HLA-A2.1 in normal cells. These results suggest that proteolysis of signal peptide domains in the endoplasmic reticulum is a second mechanism for processing and presentation of peptides for association with class I molecules. C1 UNIV VIRGINIA,SCH MED,BEIRNE CARTER CTR IMMUNOL RES,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,DEPT CHEM,CHARLOTTESVILLE,VA 22903. NCI,CELL BIOL LAB,BETHESDA,MD 20892. RP HENDERSON, RA (reprint author), UNIV VIRGINIA,SCH MED,DEPT MICROBIOL,CHARLOTTESVILLE,VA 22908, USA. RI Hunt, Donald/I-6936-2012 OI Hunt, Donald/0000-0003-2815-6368 FU NIAID NIH HHS [AI20963]; NIGMS NIH HHS [GM37537] NR 32 TC 477 Z9 480 U1 0 U2 8 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 6 PY 1992 VL 255 IS 5049 BP 1264 EP 1266 DI 10.1126/science.1546329 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HG677 UT WOS:A1992HG67700046 PM 1546329 ER PT J AU SPANDE, TF GARRAFFO, HM DALY, JW TOKUYAMA, T SHIMADA, A AF SPANDE, TF GARRAFFO, HM DALY, JW TOKUYAMA, T SHIMADA, A TI IDENTIFICATION OF HISTRIONICOTOXINS BY GC-MS AND GC-FTIR - PHOTO-ARTIFACTS AND CHEMICAL-ARTIFACTS AND REVISED C-13 NMR ASSIGNMENTS SO TETRAHEDRON LA English DT Article ID FROG AB GC-mass and GC-FTIR spectral data together permit the rapid identification of the histrionicotoxin (HTX) alkaloids. C-13-NMR chemical shifts (delta-c) are reported for HTX 235A and revised delta-c are tabulated for nine HTXs and a perhydro-derivative. A butylboronic acid HTX derivative offers GC-MS and GC-FTIR advantages. Artefactual trans diene photoisomers of the HTX class are described as are formaldehyde condensation products. Two new HTX alkaloids 261 and 265E, are characterized by mass and FTIR spectra. C1 OSAKA CITY UNIV,FAC SCI,OSAKA 558,JAPAN. RP SPANDE, TF (reprint author), NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD 20892, USA. NR 12 TC 19 Z9 19 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4020 J9 TETRAHEDRON JI Tetrahedron PD MAR 6 PY 1992 VL 48 IS 10 BP 1823 EP 1836 DI 10.1016/S0040-4020(01)88508-2 PG 14 WC Chemistry, Organic SC Chemistry GA HH251 UT WOS:A1992HH25100005 ER PT J AU RAO, P ZIGLER, JS AF RAO, P ZIGLER, JS TI QUINONE INDUCED STIMULATION OF HEXOSE-MONOPHOSPHATE SHUNT ACTIVITY IN THE GUINEA-PIG LENS - ROLE OF ZETA-CRYSTALLIN SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE ZETA-CRYSTALLIN; HEXOSE MONOPHOSPHATE SHUNT; LENS; QUINONE OXIDOREDUCTASE; NADP NADPH ID RABBIT LENS; H2O2; DETOXIFICATION AB The response of the hexose monophosphate shunt (HMS) in organ-cultured guinea pig lens to 1,2-naphthoquinone and 5-hydroxy-1,4-naphthoquinone (juglone) has been investigated. Both these compounds, which are substrates of guinea pig lens zeta-crystallin (NADPH:quinone oxidoreductase), were found to cause increases in the rate of (CO2)-C-14 production from 1-C-14-labelled glucose. Exposure of lenses to 15-mu-M 1,2-naphthoquinone or 20-mu-M juglone yielded 5.9- and 7-fold stimulation of HMS activity, respectively. Unlike hydrogen peroxide-induced stimulation of HMS activity, these effects were not abolished by preincubation with the glutathione reductase inhibitor, 1,3-bis(2-chloroethyl)-1 nitrosourea (BCNU). While hydrogen peroxide produced substantial decrements in lens glutathione (GSH) levels, incubation with quinones was not associated with a similar reduction in GSH concentration. Protein-bound NADPH content in quinone-exposed guinea pig lenses was decreased, with a concomitant increase in the amounts of free NADP+. This finding supported the involvement of zeta-crystallin bound NADPH in the in vivo enzymic reduction of quinones. Hydrogen peroxide, on the other hand, caused decreases in the level of free NADPH alone, serving to confirm our earlier inference that quinone stimulated increases in the guinea pig lens HMS could be mediated through zeta-crystallin NADPH:quinone oxidoreductase activity. C1 NEI,MECHANISMS OCULAR DIS LAB,BLDG 6,ROOM 237,BETHESDA,MD 20892. NR 15 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD MAR 5 PY 1992 VL 1116 IS 1 BP 75 EP 81 DI 10.1016/0304-4165(92)90131-D PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HK095 UT WOS:A1992HK09500012 PM 1540627 ER PT J AU PIATIGORSKY, J AF PIATIGORSKY, J TI INNOVATION ASSOCIATED WITH CHANGES IN GENE-REGULATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID ALPHA-A-CRYSTALLIN; TISSUE-SPECIFIC EXPRESSION; CHICKEN DELTA-1-CRYSTALLIN GENE; VERTEBRATE LENS CRYSTALLINS; NON-LENTICULAR TISSUES; X-RAY-ANALYSIS; GAMMA-CRYSTALLIN; TRANSGENIC MICE; B-CRYSTALLIN; EYE LENS RP NEI, MOLEC & DEV BIOL LAB, BETHESDA, MD 20892 USA. NR 106 TC 136 Z9 136 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4277 EP 4280 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200001 PM 1537817 ER PT J AU KUBOTA, S TASHIRO, K YAMADA, Y AF KUBOTA, S TASHIRO, K YAMADA, Y TI SIGNALING SITE OF LAMININ WITH MITOGENIC ACTIVITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID BASEMENT-MEMBRANE COMPONENTS; GROWTH-FACTOR; SYNTHETIC PEPTIDE; CELL ATTACHMENT; PROTO-ONCOGENE; FOS PROTEINS; C-FOS; BINDING; JUN; RECEPTOR AB Laminin, a basement membrane glycoprotein, has diverse biological activities including cell adhesion, growth, and differentiation. However, little is known concerning the signal transduction and active site involved in cell growth. In this study, we have shown that laminin and a 19-mer peptide (PA22-2) from the carboxyl-terminal end of the long arm of the laminin A chain, which was previously shown to promote cell adhesion and neurite outgrowth, stimulate thymidine incorporation and cell growth of PC12 cells. Laminin and PA22-2 (PA) were also found to induce a rapid and transient mRNA expression of c-fos and c-jun protooncogenes in PC12 cells. Further, both laminin and PA stimulated the DNA binding activity of c-Fos and c-Jun protein complex to the AP-1 site. We have also found that there is a correlation between cell growth, c-fos expression, and the ability of cell attachment to laminin or to PA in different cell types. These results suggest that the PA sequence is a potent site in laminin for both signal transduction and cell growth. C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 34 TC 52 Z9 52 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4285 EP 4288 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200003 PM 1537819 ER PT J AU JOHNSON, RL VANHAASTERT, PJM KIMMEL, AR SAXE, CL JASTORFF, B DEVREOTES, PN AF JOHNSON, RL VANHAASTERT, PJM KIMMEL, AR SAXE, CL JASTORFF, B DEVREOTES, PN TI THE CYCLIC-NUCLEOTIDE SPECIFICITY OF 3 CAMP RECEPTORS IN DICTYOSTELIUM SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELL-SURFACE; DISCOIDEUM CELLS; DEVELOPMENTAL REGULATION; AMP RECEPTOR; BINDING; EXPRESSION; ACTIVATION; PROTEIN; LIGAND; DIFFERENTIATION AB cAMP receptors mediate signal transduction pathways during development in Dictyostelium. A cAMP receptor (cAR1) has been cloned and sequenced (Klein, P., Sun, T. J., Saxe, C. L., Kimmel, A. R., Johnson, R. L., and Devreotes, P. N. (1988) Science 241, 1467-1472) and recently several other cAR genes have been identified (Saxe, C. L., Johnson, R., Devreotes, P. N., and Kimmel, A. R. (1991a) Dev. Genet. 12, 6-13; Saxe, C. L., Johnson, R. L., Devreotes, P. N., and Kimmel, A. R. (1991b) Genes Dev. 5, 1-8). We have expressed three receptor subtypes, cAR1, cAR2, and cAR3, in growing cells and have investigated their affinity and pharmacological specificity in a series of [H-3]cAMP binding studies. In phosphate buffer, there were two affinity states of about 30 and 300 nM for cAR1 and 20 and 500 nM for cAR3 but no detectable affinity for cAR2. In the presence of 3 M ammonium sulfate, there was one affinity state of 4 nM for cAR1 and 11 nM for cAR2 and two affinity states of approximately 4 and 200 nM for cAR3. The relative affinities of 14 cyclic nucleotide derivatives were tested for each cAR in ammonium sulfate. These studies suggest a model (Van Haastert, P. J. M., and Kien, E. (1983) J. Biol. Chem. 258, 9636-9642) in which cAMP binds to all three receptor subtypes by maintaining hydrogen bond interactions at the N6 and O3' positions. Interactions at the exocyclic oxygens of cAMP varied between the receptors; cAR2 and cAR3 lacked a stereoselective interaction at the axial oxygen which was present in cAR1. The cleft, which binds the adenine ring of cAMP, was hydrophobic in cAR1 and cAR3 but relatively polar in cAR2. The analog specificity of cAR1 and cAR3 in phosphate buffer was similar to that measured in ammonium sulfate though the derivatives' relative affinity to cAMP was reduced. We conclude that these cAMP receptor subtypes can be distinguished by distinct pharmacological properties which will allow selective activation of each cAR during development. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21205. UNIV GRONINGEN,DEPT BIOCHEM,9747 AG GRONINGEN,NETHERLANDS. NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. UNIV BREMEN,INST ORGAN CHEM,W-280 BREMEN,GERMANY. FU NIGMS NIH HHS [GM34933, GM28007] NR 47 TC 79 Z9 79 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4600 EP 4607 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200050 PM 1537842 ER PT J AU SHAPIRO, SD GRIFFIN, GL GILBERT, DJ JENKINS, NA COPELAND, NG WELGUS, HG SENIOR, RM LEY, TJ AF SHAPIRO, SD GRIFFIN, GL GILBERT, DJ JENKINS, NA COPELAND, NG WELGUS, HG SENIOR, RM LEY, TJ TI MOLECULAR-CLONING, CHROMOSOMAL LOCALIZATION, AND BACTERIAL EXPRESSION OF A MURINE MACROPHAGE METALLOELASTASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN ALVEOLAR MACROPHAGES; HUMAN FIBROBLAST COLLAGENASE; HUMAN SYNOVIAL-CELLS; STIMULATES COLLAGENASE; ELASTIN DEGRADATION; CATHEPSIN-G; HUMAN-LUNG; INHIBITOR; GENE; METALLOPROTEINASE AB Murine macrophages have previously been shown to secrete a zinc-dependent proteinase that can degrade elastin. In this report, we identify murine macrophage elastase (MME) cDNA and show that it is a distinct member of the metalloproteinase gene family. Small amounts of MME were purified to homogeneity, and N-terminal amino acid sequence was obtained. This sequence was used to obtain a partial cDNA clone by the polymerase chain reaction; a cDNA library derived from a mouse macrophage-like cell line (P388D1) was screened with this probe. A full-length MME cDNA spanning approximately 1.8 kilobases contained an open reading frame of 1386 base pairs; the predicted molecular mass of the MME proenzyme is 53 kDa. The gene encoding MME is represented only once in the mouse genome and is located on chromosome 9. Despite a size that is similar to other metalloproteinases, MME is distinct, sharing only 33-48% amino acid homology with other metalloproteinases. In contrast to other metalloenzymes, MME appears to be rapidly processed to an active truncated form (N-terminal and C-terminal cleavage). We expressed recombinant MME in Escherichia coli and demonstrated that it has significant elastolytic activity that is specifically inhibited by the tissue inhibitor of metalloproteinases. MME is therefore a true metalloproteinase that may be involved in tissue injury and remodeling. C1 NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. WASHINGTON UNIV,JEWISH HOSP ST LOUIS,MED CTR,DEPT GENET,DIV DERMATOL,ST LOUIS,MO 63110. WASHINGTON UNIV,JEWISH HOSP ST LOUIS,MED CTR,DEPT MED,DIV HEMATOL ONCOL,ST LOUIS,MO 63110. RP SHAPIRO, SD (reprint author), WASHINGTON UNIV,JEWISH HOSP ST LOUIS,MED CTR,DIV RESP & CRIT CARE,ST LOUIS,MO 63110, USA. FU NCI NIH HHS [CA49712, N01-CO-74101]; NHLBI NIH HHS [HL29594] NR 52 TC 184 Z9 189 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4664 EP 4671 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200060 PM 1537850 ER PT J AU SARKADI, B PRICE, EM BOUCHER, RC GERMANN, UA SCARBOROUGH, GA AF SARKADI, B PRICE, EM BOUCHER, RC GERMANN, UA SCARBOROUGH, GA TI EXPRESSION OF THE HUMAN MULTIDRUG RESISTANCE CDNA IN INSECT CELLS GENERATES A HIGH-ACTIVITY DRUG-STIMULATED MEMBRANE ATPASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BACTERIAL TRANSPORT PROTEINS; P-GLYCOPROTEIN GENE; HAMSTER OVARY CELLS; MUTANTS; BINDING; PERMEABILITY; PURIFICATION; VINBLASTINE; COLCHICINE; ANTIBODIES AB Drug-resistant tumor cells actively extrude a variety of chemotherapeutic agents by the action of the multidrug resistance (MDR1) gene product, the plasma membrane P-glycoprotein. In this report we show that the expression of the human MDR1 gene in cultured Sf9 insect cells via a baculovirus vector generates a high activity vanadate-sensitive membrane ATPase. This ATPase is markedly stimulated by drugs known to interact with the P-glycoprotein, such as vinblastine and verapamil, and the ability of the various drugs to stimulate the ATPase corresponds to their previously observed affinity for this transporter. The drug-stimulated ATPase is not present in uninfected or mock-infected Sf9 cells, and its appearance correlates with the appearance of the MDR1 gene product detected with a monoclonal anti-MDR protein antibody and by labeling with 8-azido-ATP. The drug-induced ATPase requires magnesium ions, does not utilize ADP or AMP as substrates, exhibits a half-maximal activation at about 0.5 mM MgATP, and its maximal activity (about 3-5-mu-mol/mg MDR protein/min) approaches that of the well characterized ion transport ATPases. These results provide the first direct demonstration of a high capacity drug-stimulated ATPase activity of the human multidrug resistance protein and offer a new and simple assay for the investigation of functional interactions of various drugs with this clinically important enzyme. C1 UNIV N CAROLINA,DEPT PHARMACOL,CB 7365 FLOB,CHAPEL HILL,NC 27599. NATL INST HAEMATOL & BLOOD TRANSFUS,BUDAPEST,HUNGARY. NCI,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT MED,CHAPEL HILL,NC 27599. RI Sarkadi, Balazs/I-5024-2013 NR 36 TC 541 Z9 548 U1 4 U2 15 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4854 EP 4858 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200084 PM 1347044 ER PT J AU KENNEDY, ICS JUNE, CH OSHEA, JJ AF KENNEDY, ICS JUNE, CH OSHEA, JJ TI EXPRESSION OF THE HUMAN EPIDERMAL GROWTH-FACTOR RECEPTOR IN A MURINE T-CELL HYBRIDOMA - A TRANSMEMBRANE PROTEIN TYROSINE KINASE CAN SYNERGIZE WITH THE T-CELL ANTIGEN RECEPTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN LYMPHOCYTES-T; PHOSPHOLIPASE C-II; SIGNAL TRANSDUCTION; ONCOGENE PRODUCTS; CD4 RECEPTOR; SRC FAMILY; ZETA-CHAIN; PHOSPHORYLATION; ACTIVATION; STIMULATION AB Although the T-cell receptor for antigen (TCR) lacks intrinsic kinase activity, stimulation of this receptor induces tyrosine phosphorylation of multiple substrates. In contrast, the epidermal growth factor receptor (EGFR) has intrinsic cytoplasmic tyrosine kinase catalytic activity that is activated upon EGF binding. To compare the functional effects of the TCR and a transmembrane protein tyrosine kinase (PTK), we used retrovirus-mediated gene transduction to express the human c-erbB proto-oncogene, encoding the EGFR, in a murine T-cell hybridoma. Tyrosine phosphorylation induced by the TCR and the EGFR occurred on substrates unique to each receptor as well as on several shared substrates, including the zeta-chain of the TCR. Stimulation of the EGFR induced calcium ion flux in these cells, suggesting that the heterologous tyrosine kinase can couple to the T-cell phospholipase signal transduction pathway, but this stimulus did not lead to interleukin 2 production. However, EGF stimulation of transduced cells significantly enhanced TCR signaling, as assessed by interleukin 2 production, indicating that cross talk can occur between the TCR and a transmembrane PTK. C1 USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20892. RP KENNEDY, ICS (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,EXPTL IMMUNOL LAB,FREDERICK,MD 21702, USA. NR 60 TC 7 Z9 7 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4924 EP 4929 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200094 PM 1537871 ER PT J AU BRZESKA, H MARTIN, B KULESZALIPKA, D BAINES, I KORN, ED AF BRZESKA, H MARTIN, B KULESZALIPKA, D BAINES, I KORN, ED TI PREPARATION OF A PHOSPHOLIPID-INSENSITIVE, AUTOPHOSPHORYLATION-ACTIVATED CATALYTIC FRAGMENT OF ACANTHAMOEBA MYOSIN-I HEAVY-CHAIN KINASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-KINASE; MICROGRAM QUANTITIES; SYNTHETIC PEPTIDES; COFACTOR PROTEIN; ACTIN ACTIVATION; AMINO-ACID; RAT-BRAIN; C FAMILY; PURIFICATION; CASTELLANII AB The actin-activated Mg2+-ATPase activity of Acanthamoeba myosin I depends on phosphorylation of its single heavy chain. The activity of the myosin I heavy chain kinase is increased about 50-fold by autophosphorylation, and the rate of kinase autophosphorylation is enhanced about 20-fold by acidic phospholipids independent of the presence of Ca2+ (Brzeska, H., Lynch, T. J., and Korn, E. D. (1990) J. Biol. Chem. 265, 3591-3594). In this paper, we show that chymotryptic digestion of the kinase produces a 54-kDa fragment which contains three to four of the approximately 11 original phosphorylation sites and whose activity is greatly stimulated by autophosphorylation. However, both the rate of autophosphorylation and the kinase activity of the 54-kDa fragment are independent of phospholipid and comparable to those of intact kinase in the presence of phospholipid. These data imply that the (probably NH2-terminal) region(s) removed by proteolysis is necessary for phospholipid-sensitive inhibition of autophosphorylation of sites residing within the (probably COOH-terminal) 54-kDa fragment. The 54-kDa fragment contains the catalytic site of the kinase as well as three to four sites whose phosphorylation is necessary for full expression of kinase activity. The middle region of the kinase molecule contains proline-rich regions that are similar to the COOH-terminal tail of the kinase substrate, Acanthamoeba myosin I. C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. RP BRZESKA, H (reprint author), NHLBI,CELL BIOL LAB,BETHESDA,MD 20892, USA. RI Korn, Edward/F-9929-2012 NR 46 TC 12 Z9 12 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4949 EP 4956 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200097 PM 1311323 ER PT J AU CHIANG, PK BURBELO, PD BRUGH, SA GORDON, RK FUKUDA, K YAMADA, Y AF CHIANG, PK BURBELO, PD BRUGH, SA GORDON, RK FUKUDA, K YAMADA, Y TI ACTIVATION OF COLLAGEN-IV GENE-EXPRESSION IN F9 TERATOCARCINOMA CELLS BY 3-DEAZAADENOSINE ANALOGS - INDIRECT INHIBITORS OF METHYLATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID S-ADENOSYLHOMOCYSTEINE HYDROLASE; DNA METHYLATION; DIFFERENTIATION; ALPHA-1(IV); PROMOTER; POTENT AB 3-Deazaadenosine analogs can function as inhibitors and also as alternative substrates of S-adenosylhomocysteine (AdoHcy) hydrolase. In cells treated with the analogs, AdoHcy invariably accumulates, leading to inhibition of cellular methylation. F9 teratocarcinoma cells, stably transfected with two collagen (IV) promoter-enhancer-CAT constructs and treated with 10-mu-M 3-deazaadenosine, 3-deaza-(+/-)-aristeromycin or 3-deazaneplanocin, showed a strong induction of CAT activities without affecting differentiation. In comparison, the same 3-deaza analogs did not affect the CAT activity in F9 cells transfected with the beta-actin promoter-CAT construct. Furthermore, Northern blot analysis of endogenous mRNA from wild-type F9 cells treated with the 3-deaza nucleosides all showed an induction of the collagen alpha-1(IV) chain mRNA. Thus, the 3-deaza analogs most likely affect DNA methylation because their results are consistent with the previous observation that the integrated collagen alpha-1(IV) promoter-enhancer constructs were activated with 5 azacytidine. C1 NIDA,BETHESDA,MD 20892. RP CHIANG, PK (reprint author), WALTER REED ARMY MED CTR,APPL BIOCHEM BRANCH,WASHINGTON,DC 20307, USA. RI Burbelo, Peter/B-1027-2009 NR 29 TC 31 Z9 31 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4988 EP 4991 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200103 PM 1537874 ER PT J AU CHAO, FF BLANCHETTEMACKIE, EJ TERTOV, VV SKARLATOS, SI CHEN, YJ KRUTH, HS AF CHAO, FF BLANCHETTEMACKIE, EJ TERTOV, VV SKARLATOS, SI CHEN, YJ KRUTH, HS TI HYDROLYSIS OF CHOLESTERYL ESTER IN LOW-DENSITY-LIPOPROTEIN CONVERTS THIS LIPOPROTEIN TO A LIPOSOME SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN ATHEROSCLEROTIC LESIONS; RICH LIPID PARTICLES; HUMAN AORTIC INTIMA; UNESTERIFIED CHOLESTEROL; DIFFERENT MECHANISMS; PLASMA-LIPOPROTEINS; CA++ ANTAGONISTS; PURIFICATION; HYDROLASE; LOCALIZATION AB Previously, we isolated and characterized unique liposomal-like, cholesterol-rich lipid particles that accumulate in human atherosclerotic lesions. Human plasma low density lipoprotein (LDL) has a molar ratio of total cholesterol to phospholipid (3:1) similar to that of this lesion cholesterol-rich lipid particle. However, LDL is enriched in cholesteryl ester while the lesion lipid particle is enriched in unesterified cholesterol. To examine a possible precursor-product relationship between LDL and the lesion lipid particle, we hydrolyzed the cholesteryl ester core of LDL with cholesterol esterase. Cholesteryl ester hydrolysis occurred only after LDL was treated with trypsin. Trypsin pretreatment was not required for cholesteryl ester hydrolysis of LDL oxidized with copper, a treatment that also degrades apolipoprotein B, the major protein moiety in LDL. In contrast to greater than 90% hydrolysis of cholesteryl ester in trypsin-cholesterol esterase-treated or copper-oxidized LDL, there was only 18% hydrolysis of cholesteryl ester in similarly treated high density lipoprotein. With a limited 10-min hydrolysis of LDL cholesteryl ester, LDL-sized particles and newly formed larger flattened films or discs were present. With complete hydrolysis of LDL cholesteryl ester, LDL particles converted to complex multilamellar, liposomal-like, structures with sizes approximately five times larger than native LDL. These liposomal-like particles derived from LDL were chemically and structurally similar to unesterified cholesterol-rich lipid particles that accumulate in atherosclerotic lesions. C1 NHLBI,MOLEC DIS BRANCH,EXPTL ATHEROSCLEROSIS SECT,BLDG 10,RM 5N-113,BETHESDA,MD 20892. NIADDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. USSR CARDIOL RES CTR,INST EXPTL CARDIOL,MOSCOW,USSR. NR 43 TC 50 Z9 50 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4992 EP 4998 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200104 PM 1537875 ER PT J AU KAWABATA, S HIGGINS, GA GORDON, JW AF KAWABATA, S HIGGINS, GA GORDON, JW TI ALZHEIMERS RETRACTION SO NATURE LA English DT Letter C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. CUNY MT SINAI SCH MED,DEPT GERIATR & ADULT DEV,NEW YORK,NY 10029. RP KAWABATA, S (reprint author), YAMANOUCHI PHARMACEUT CO LTD,TOKYO 103,JAPAN. NR 1 TC 25 Z9 25 U1 2 U2 9 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 5 PY 1992 VL 356 IS 6364 BP 23 EP 23 DI 10.1038/356023b0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HG602 UT WOS:A1992HG60200036 PM 1538775 ER PT J AU URBA, WJ LONGO, DL AF URBA, WJ LONGO, DL TI MEDICAL PROGRESS - HODGKINS-DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID BONE-MARROW TRANSPLANTATION; COMBINED MODALITY THERAPY; CHEMOTHERAPY PLUS RADIOTHERAPY; STEM-CELL TRANSPLANTATION; SOUTHWEST-ONCOLOGY-GROUP; FIELD RADIATION-THERAPY; 2ND MALIGNANT NEOPLASMS; HIGH-DOSE CHEMOTHERAPY; CLINICAL STAGE-I; TERM FOLLOW-UP C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. RP URBA, WJ (reprint author), DYNCORP,PROGRAM RESOURCES INC,CLIN IMMUNOL SERV,BLDG 560,RM 11-62,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 152 TC 227 Z9 227 U1 0 U2 4 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 5 PY 1992 VL 326 IS 10 BP 678 EP 687 DI 10.1056/NEJM199203053261006 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA HG117 UT WOS:A1992HG11700006 PM 1736106 ER PT J AU PANZA, JA EPSTEIN, SE QUYYUMI, AA AF PANZA, JA EPSTEIN, SE QUYYUMI, AA TI CIRCADIAN VARIATION IN VASCULAR TONE - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID ANGINA-PECTORIS; EXERCISE; CONSTRICTION; DISEASE RP PANZA, JA (reprint author), NHLBI,BETHESDA,MD 20892, USA. NR 9 TC 0 Z9 0 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 5 PY 1992 VL 326 IS 10 BP 710 EP 711 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HG117 UT WOS:A1992HG11700022 ER PT J AU WHELTON, PK APPEL, L CHARLESTON, J DALCIN, AT EWART, C FRIED, L KAIDY, D KLAG, MJ KUMANYIKA, S STEFFEN, L WALKER, WG OBERMAN, A COUNTS, K HATAWAY, H RACZYNSKI, J RAPPAPORT, N WEINSIER, R BORHANI, NO BERNAUER, E BORHANI, P DELACRUZ, C ERTL, A HEUSTIS, D LEE, M LOVELACE, W OCONNOR, E PEEL, L SUGARS, C TAYLOR, JO CORKERY, BW EVANS, DA KEOUGH, ME MORRIS, MC PISTORINO, E SACKS, F CAMERON, M CORRIGAN, S WRIGHT, NK APPLEGATE, WB BREWER, A GOODWIN, L MILLER, S MURPHY, J RANDLE, J SULLIVAN, J LASSER, NL BATEY, DM DOLAN, L HAMILL, S KENNEDY, P LASSER, VI KULLER, LH CAGGIULA, AW MILAS, NC YAMAMOTO, ME VOGT, TM GREENLICK, MR HOLLIS, J STEVENS, V COHEN, JD MATTFELDTBEMAN, M BRINKMANN, C ROTH, K SHEPEK, L HENNEKENS, CH BURING, J COOK, N DANIELSON, E EBERLEIN, K GORDON, D HEBERT, P MACFADYEN, J MAYRENT, S ROSNER, B SATTERFIELD, S TOSTESON, H VANDENBURGH, M CUTLER, JA BRITTAIN, E FARRAND, M KAUFMANN, P LAKATOS, E OBARZANEK, E BELCHER, J DOMMEYER, A MILLS, I NEIBLING, P WOODS, M GOLDMAN, BJK BLETHEN, E SACKS, F AF WHELTON, PK APPEL, L CHARLESTON, J DALCIN, AT EWART, C FRIED, L KAIDY, D KLAG, MJ KUMANYIKA, S STEFFEN, L WALKER, WG OBERMAN, A COUNTS, K HATAWAY, H RACZYNSKI, J RAPPAPORT, N WEINSIER, R BORHANI, NO BERNAUER, E BORHANI, P DELACRUZ, C ERTL, A HEUSTIS, D LEE, M LOVELACE, W OCONNOR, E PEEL, L SUGARS, C TAYLOR, JO CORKERY, BW EVANS, DA KEOUGH, ME MORRIS, MC PISTORINO, E SACKS, F CAMERON, M CORRIGAN, S WRIGHT, NK APPLEGATE, WB BREWER, A GOODWIN, L MILLER, S MURPHY, J RANDLE, J SULLIVAN, J LASSER, NL BATEY, DM DOLAN, L HAMILL, S KENNEDY, P LASSER, VI KULLER, LH CAGGIULA, AW MILAS, NC YAMAMOTO, ME VOGT, TM GREENLICK, MR HOLLIS, J STEVENS, V COHEN, JD MATTFELDTBEMAN, M BRINKMANN, C ROTH, K SHEPEK, L HENNEKENS, CH BURING, J COOK, N DANIELSON, E EBERLEIN, K GORDON, D HEBERT, P MACFADYEN, J MAYRENT, S ROSNER, B SATTERFIELD, S TOSTESON, H VANDENBURGH, M CUTLER, JA BRITTAIN, E FARRAND, M KAUFMANN, P LAKATOS, E OBARZANEK, E BELCHER, J DOMMEYER, A MILLS, I NEIBLING, P WOODS, M GOLDMAN, BJK BLETHEN, E SACKS, F TI THE EFFECTS OF NONPHARMACOLOGIC INTERVENTIONS ON BLOOD-PRESSURE OF PERSONS WITH HIGH NORMAL LEVELS - RESULTS OF THE TRIALS OF HYPERTENSION PREVENTION, PHASE-I SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID DOUBLE-BLIND; FISH-OIL; CALCIUM SUPPLEMENTATION; ORAL CALCIUM; MAGNESIUM; CROSSOVER; MILD AB Objective.-To test the short-term feasibility and efficacy of seven nonpharmacologic interventions in persons with high normal diastolic blood pressure. Design.-Randomized control multicenter trials. Setting.-Volunteers recruited from the community, treated and followed up at special clinics. Participants.-Of 16 821 screenees, 2182 men and women, aged 30 through 54 years, with diastolic blood pressure from 80 through 89 mm Hg were selected. Of these, 50 did not return for follow-up blood pressure measurements. Interventions.-Three life-style change groups (weight reduction, sodium reduction, and stress management) were each compared with unmasked nonintervention controls over 18 months. Four nutritional supplement groups (calcium, magnesium, potassium, and fish oil) were each compared singly, in double-blind fashion, with placebo controls over 6 months. Main Outcome Measures.-Primary: change in diastolic blood pressure from baseline to final follow-up, measured by blinded observers. Secondary: changes in systolic blood pressure and intervention compliance measures. Results.-Weight reduction intervention produced weight loss of 3.9 kg (P < .01), diastolic blood pressure change of - 2.3 mm Hg (P < .01), and systolic blood pressure change of -2.9 mmHg (P < .01). Sodium reduction interventions lowered urinary sodium excretion by 44 mmol/24 h (P < .01), diastolic blood pressure by 0.9 mm Hg (P < .05), and systolic blood pressure by 1.7 mm Hg (P < .01). Despite good compliance, neither stress management nor nutritional supplements reduced diastolic blood pressure or systolic blood pressure significantly (P > .05). Conclusions.-Weight reduction is the most effective of the strategies tested for reducing blood pressure in normotensive persons. Sodium reduction is also effective. The long-term effects of weight reduction and sodium reduction, alone and in combination, require further evaluation. C1 NHLBI, ROOM 604, FED BLDG, BETHESDA, MD 20892 USA. JOHNS HOPKINS UNIV, SCH HYG & PUBL HLTH, BALTIMORE, MD 21218 USA. UNIV ALABAMA, BIRMINGHAM, AL 35294 USA. UNIV CALIF DAVIS, DAVIS, CA 95616 USA. E BOSTON NEIGHBORHOOD HLTH CTR, BOSTON, MA USA. UNIV MISSISSIPPI, JACKSON, MS 39216 USA. UNIV TENNESSEE CTR HLTH SCI, MEMPHIS, TN 38163 USA. UNIV MED & DENT NEW JERSEY, NEW JERSEY MED SCH, NEWARK, NJ 07103 USA. UNIV PITTSBURGH, PITTSBURGH, PA 15260 USA. KAISER PERMANENTE CTR HLTH RES, PORTLAND, OR USA. ST LOUIS UNIV, SCH MED, ST LOUIS, MO 63104 USA. BRIGHAM & WOMENS HOSP, CHANNING LAB, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. UNIV MINNESOTA, MINNEAPOLIS, MN 55455 USA. TUFTS UNIV, BOSTON, MA 02111 USA. NR 36 TC 357 Z9 363 U1 0 U2 11 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 4 PY 1992 VL 267 IS 9 BP 1213 EP 1220 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA HF439 UT WOS:A1992HF43900022 ER PT J AU GLENN, GM LINEHAN, WM HOSOE, S LATIF, F YAO, M CHOYKE, P GORIN, MB CHEW, E OLDFIELD, E MANOLATOS, C ORCUTT, ML WALTHER, MM WEISS, GH TORY, K JENSSON, O LERMAN, MI ZBAR, B AF GLENN, GM LINEHAN, WM HOSOE, S LATIF, F YAO, M CHOYKE, P GORIN, MB CHEW, E OLDFIELD, E MANOLATOS, C ORCUTT, ML WALTHER, MM WEISS, GH TORY, K JENSSON, O LERMAN, MI ZBAR, B TI SCREENING FOR VONHIPPEL-LINDAU DISEASE BY DNA POLYMORPHISM ANALYSIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID LINKAGE; MANIFESTATIONS; CHROMOSOME-3; MEMBERS; REGION; KIDNEY AB Objective.-Von Hippel-Lindau (VHL) disease is a rare, inherited multisystem neoplastic disorder. There is no biochemical test available to distinguish VHL disease gene carriers from their healthy siblings. We evaluated DNA polymorphism analysis as a method for identifying disease gene carriers. Design.-Prospective comparison of the results of DNA analysis with a comprehensive clinical screening examination. Setting.-The Clinical Center of the National Institutes of Health. Patients.-Blood was collected from 182 members of 16 families with VHL disease. Forty-eight asymptomatic individuals, at risk of developing this hereditary illness (with an affected parent or sibling), were examined for occult disease at the Clinical Center of the National Institutes of Health and tested by DNA polymorphism analysis. Results.-DNA polymorphism analysis predicted nine disease gene carriers and 33 individuals with the wild-type (normal) allele among the 48 individuals at risk of developing VHL disease; the test was not informative in six individuals. All nine individuals predicted to carry the VHL gene had evidence of occult disease on clinical examination. There was no clinical evidence of VHL disease in 32 of 33 individuals predicted to carry the wild-type allele. Conclusions.-DNA polymorphism analysis can identify individuals likely to carry the VHL disease gene among asymptomatic members of disease families. This technique serves to focus attention on those individuals who require periodic medical examination and may help to alleviate the morbidity and mortality associated with this disease. C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,BLDG 560,ROOM 12-71,FREDERICK,MD 21701. NCI,CANC DIAG BRANCH,FREDERICK,MD 21701. NCI,SURG BRANCH,FREDERICK,MD 21701. NEI,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. NEI,CTR CLIN,DEPT NURSING,BETHESDA,MD 20892. NEI,CLIN BRANCH,BETHESDA,MD 20892. NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. EYE & EAR INST,PITTSBURGH,PA. PROGRAM RESOURCES INC,FREDERICK,MD. NATL UNIV HOSP REYKJAVIK,BLOOD BANK,REYKJAVIK,ICELAND. FU Intramural NIH HHS [Z99 EY999999] NR 35 TC 71 Z9 71 U1 0 U2 5 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 4 PY 1992 VL 267 IS 9 BP 1226 EP 1231 DI 10.1001/jama.267.9.1226 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HF439 UT WOS:A1992HF43900024 PM 1347089 ER PT J AU CHROUSOS, GP GOLD, PW AF CHROUSOS, GP GOLD, PW TI THE CONCEPTS OF STRESS AND STRESS SYSTEM DISORDERS - OVERVIEW OF PHYSICAL AND BEHAVIORAL HOMEOSTASIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID CORTICOTROPIN-RELEASING-FACTOR; PITUITARY-ADRENAL AXIS; HORMONE-SECRETION INVITRO; LOCUS COERULEUS NEURONS; CENTRAL NERVOUS-SYSTEM; ACTIVATES NORADRENERGIC NEURONS; FACTOR-LIKE IMMUNOREACTIVITY; HYPOTHALAMIC BETA-ENDORPHIN; GROWTH-HORMONE; ANOREXIA-NERVOSA AB Objective.-This article defines stress and related concepts and reviews their historical development. The notion of a stress system as the effector of the stress syndrome is suggested, and its physiologic and pathophysiologic manifestations are described. A new perspective on human disease states associated with dysregulation of the stress system is provided. Data Sources.-Published original articles from human and animal studies and selected reviews. Literature was surveyed utilizing MEDLINE and the Index Medicus. Study Selection.-Original articles from the basic science and human literature consisted entirely of controlled studies based on verified methodologies and, with the exception of the most recent studies, replicated by more than one laboratory. Many of the basic science and clinical studies had been conducted in our own laboratories and clinical research units. Reviews cited were written by acknowledged leaders in the fields of neurobiology, endocrinology, and behavior. Data Extraction.-Independent extraction and cross-referencing by the authors. Data Synthesis.-Stress and related concepts can be traced as far back as written science and medicine. The stress system coordinates the generalized stress response, which takes place when a stressor of any kind exceeds a threshold. The main components of the stress system are the corticotropin-releasing hormone and locus ceruleus-norepinephrine/autonomic systems and their peripheral effectors, the pituitary-adrenal axis, and the limbs of the autonomic system, Activation of the stress system leads to behavioral and peripheral changes that improve the ability of the organism to adjust homeostasis and increase its chances for survival. There has been an exponential increase in knowledge regarding the interactions among the components of the stress system and between the stress system and other brain elements involved in the regulation of emotion, cognitive function, and behavior, as well as with the axes responsible for reproduction, growth, and immunity. This new knowledge has allowed association of stress system dysfunction, characterized by sustained hyperactivity and/or hypoactivity, to various pathophysiologic states that cut across the traditional boundaries of medical disciplines. These include a range of psychiatric, endocrine, and inflammatory disorders and/or susceptibility to such disorders. Conclusions.-We hope that knowledge from apparently disparate fields of science and medicine integrated into a working theoretical framework will allow generation and testing of new hypotheses on the pathophysiology and diagnosis of, and therapy for, a variety of human illnesses reflecting systematic alterations in the principal effectors of the generalized stress response. We predict that pharmacologic agents capable of altering the central apparatus that governs the stress response will be useful in the treatment of many of these illnesses. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RP CHROUSOS, GP (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10N262,BETHESDA,MD 20892, USA. NR 151 TC 2099 Z9 2181 U1 33 U2 344 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 4 PY 1992 VL 267 IS 9 BP 1244 EP 1252 DI 10.1001/jama.267.9.1244 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA HF439 UT WOS:A1992HF43900028 PM 1538563 ER PT J AU KANNEL, WB ANDERSON, K WILSON, PWF AF KANNEL, WB ANDERSON, K WILSON, PWF TI WHITE BLOOD-CELL COUNT AND CARDIOVASCULAR-DISEASE - INSIGHTS FROM THE FRAMINGHAM-STUDY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID MYOCARDIAL-INFARCTION; LEUKOCYTE COUNTS; CORONARY; PREDICTOR; MORTALITY; RISK AB Objective.-To examine the relation of white blood cell (WBC) count to the development of cardiovascular disease (CVD), including coronary heart disease, stroke, peripheral arterial disease, and cardiac failure. Traditional CVD risk factors, hematocrit, and vital capacity were considered. Design.-Prospective cohort analysis with one baseline examination of relevant risk factors and 12 years of follow-up for CVD. Participants and Methods.-A community-based sample (Framingham Offspring Study) of 1393 men and 1401 women who were free of CVD at the onset of the study and who were between the ages of 30 and 59 years at baseline. Time-dependent multiple variable logistic regression methods were used. Results.-There were 180 CVD events in men and 80 in women. The WBC count was correlated most strongly with the number of cigarettes smoked per day, hematocrit, and vital capacity. Among nonsmoking men with WBC counts within the normal range, the age-adjusted WBC count was significantly associated with CVD and coronary heart disease incidence. For each 1.0 x 10(9)/L-cell difference in WBC count, the CVD risk increased 32%. In women, each 1.0 x 10(9)/L-cell increment in WBC count was associated with a 17% increase in CVD risk, but only in smokers, and the relationship was not statistically significant after adjustment for relevant risk factors. Conclusions.-The degree of elevation of WBC count within the normal range is a marker for increased risk of CVD that is partially explained by cigarette smoking. Future-studies should include differential WBC determinations to assess their association with CVD. C1 NHLBI,FRAMINGHAM HEART STUDY,5 THURBER ST,FRAMINGHAM,MA 01701. BOSTON UNIV,SCH MED,EVANS MEM RES FDN,DEPT MED,PREVENT MED & EPIDEMIOL SECT,BOSTON,MA 02118. CENTOCOR INC,MALVERN,PA. FU NHLBI NIH HHS [N01-HV-52971, N01-HV-92922] NR 13 TC 273 Z9 284 U1 0 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 4 PY 1992 VL 267 IS 9 BP 1253 EP 1256 DI 10.1001/jama.267.9.1253 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA HF439 UT WOS:A1992HF43900029 PM 1538564 ER PT J AU HOEL, DG DAVIS, DL MILLER, AB SONDIK, EJ SWERDLOW, AJ AF HOEL, DG DAVIS, DL MILLER, AB SONDIK, EJ SWERDLOW, AJ TI TRENDS IN CANCER MORTALITY IN 15 INDUSTRIALIZED COUNTRIES, 1969-1986 SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID BREAST-CANCER; WOMEN AB Background: Assessing trends in cancer provides a means for gauging progress against the disease, estimating future demands for care and treatment, and suggesting clues about shifting causal factors that may account for the more recent changes. Purpose: This study was designed to evaluate trends in the major sites of cancer associated with high mortality rates in 15 industrialized countries. To highlight differences among regions, we grouped these countries into six geographic areas: United States, Eastern Europe, Western Europe, East Asia, Oceania, and Nordic countries. In addition, cancer mortality trends in these regions were compared with incidence patterns in the United States. Methods: Data provided by the World Health Organization were used to evaluate age-specific mortality trends from 1969 through 1986 for lung, breast, prostate, stomach, and colorectal cancers and for all other sites considered as a group. We also assembled and analyzed data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute for the same sites and age groups from 1973 through 1986. Results: Over the period 1969 through 1986, recorded cancer mortality in persons aged 45 years and older in the six regions studied has increased for lung, breast, and prostate cancers in most age groups, while the decline in stomach cancer mortality is substantial. The increase in lung cancer deaths in men aged 45-54 years has slowed greatly or reversed in all areas except Eastern Europe and East Asia. Trends for intestinal cancer vary by age and region. For all other sites considered as a group, increases have occurred for persons older than 64 years in most regions. In Eastern Europe, there are disturbingly high rates and rapid increases for several of the major forms of cancer in persons aged 45-54 years. In general, trends for cancer incidence in the United States parallel those for mortality. For intestinal cancer, however, incidence has increased while mortality has declined. Conclusions: The trends we report cannot be explained solely by changes in cigarette smoking or aging. Other causes of changes in cancer incidence and mortality need to be determined. Implications: The increasing and decreasing trends in mortality from and incidence of cancer that we found are important for health care planning and may also suggest opportunities for research in cancer prevention. C1 OFF CENSUSES & POPULAT SURVEYS,LONDON,ENGLAND. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. UNIV LONDON LONDON SCH HYG & TROP MED,LONDON WC1E 7HT,ENGLAND. NATL RES COUNCIL,WASHINGTON,DC 20418. UNIV TORONTO,DEPT PREVENT MED & BIOSTAT,TORONTO M5S 1A1,ONTARIO,CANADA. WHO,CANC & PALLIAT CARE UNIT,CH-1211 GENEVA 27,SWITZERLAND. RP HOEL, DG (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 31 TC 87 Z9 89 U1 0 U2 1 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 4 PY 1992 VL 84 IS 5 BP 313 EP 320 DI 10.1093/jnci/84.5.313 PG 8 WC Oncology SC Oncology GA HU102 UT WOS:A1992HU10200012 PM 1738181 ER PT J AU TANGREA, JA EDWARDS, BK TAYLOR, PR HARTMAN, AM PECK, GL SALASCHE, SJ MENON, PA BENSON, PM MELLETTE, JR GUILL, MA ROBINSON, JK GUIN, JD STOLL, HL GRABSKI, WJ WINTON, GB AF TANGREA, JA EDWARDS, BK TAYLOR, PR HARTMAN, AM PECK, GL SALASCHE, SJ MENON, PA BENSON, PM MELLETTE, JR GUILL, MA ROBINSON, JK GUIN, JD STOLL, HL GRABSKI, WJ WINTON, GB TI LONG-TERM THERAPY WITH LOW-DOSE ISOTRETINOIN FOR PREVENTION OF BASAL-CELL CARCINOMA - A MULTICENTER CLINICAL-TRIAL SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID SKELETAL HYPEROSTOSIS DISH; 13-CIS-RETINOIC ACID; SPINAL HYPEROSTOSIS; ORAL ISOTRETINOIN; ICHTHYOSIS; TOXICITY; ACNE AB Background: High-dose isotretinoin has been reported to have a prophylactic effect on nonmelanoma skin cancer, although it is associated with significant toxicity. Purpose: To test the effectiveness of the long-term administration of low-dose isotretinoin in reducing the occurrence of basal cell carcinoma at a new site in patients with previously treated basal cell carcinomas and to measure the toxicity associated with this regimen, we conducted a clinical trial at eight cancer centers. Methods: Nine hundred and eighty-one patients with two or more previously confirmed basal cell carcinomas were randomly assigned to receive either 10 mg of isotretinoin or a placebo daily. Patients were followed for 36 months and monitored at 6-month intervals for skin cancer and toxic effects. Results: After 36 months of treatment, no statistically significant difference in either the cumulative percent of patients with an occurrence of basal cell carcinoma at a new site or the annual rate of basal cell carcinoma formation existed between patients receiving isotretinoin and those receiving the placebo. Elevated serum triglycerides, hyperostotic axial skeletal changes, and mucocutaneous reactions were more frequent in the group receiving isotretinoin than in the control group, and these differences were all statistically significant (P < .001). Conclusion: This low-dose regimen of isotretinoin not only is ineffective in reducing the occurrence of basal cell carcinoma at new sites in patients with two or more previously treated basal cell carcinomas but also is associated with significant adverse systemic effects. Implication: The toxicity associated with the long-term administration of isotretinoin, even at the low dose used in this trial, must be weighed in planning future prevention trials. C1 EISENHOWER ARMY MED CTR,AUGUSTA,GA. NORTHWESTERN UNIV,CHICAGO,IL 60611. UNIV ARKANSAS,LITTLE ROCK,AR 72204. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. USN HOSP,PORTSMOUTH,VA. FITZSIMONS ARMY MED CTR,AURORA,CO 80045. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. BROOKE ARMY MED CTR,SAN ANTONIO,TX. NR 35 TC 118 Z9 120 U1 0 U2 4 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 4 PY 1992 VL 84 IS 5 BP 328 EP 332 DI 10.1093/jnci/84.5.328 PG 5 WC Oncology SC Oncology GA HU102 UT WOS:A1992HU10200014 PM 1738183 ER PT J AU CITRON, M GRAVER, M SCHOENHAUS, M CHEN, S DECKER, R KLEYNERMAN, L KAHN, LB WHITE, A FORNACE, AJ YAROSH, D AF CITRON, M GRAVER, M SCHOENHAUS, M CHEN, S DECKER, R KLEYNERMAN, L KAHN, LB WHITE, A FORNACE, AJ YAROSH, D TI DETECTION OF MESSENGER-RNA FROM O6-METHYLGUANINE-DNA METHYLTRANSFERASE GENE MGMT IN HUMAN NORMAL AND TUMOR-TISSUES SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ESCHERICHIA-COLI; CELL STRAINS; REPAIR; O-6-METHYLGUANINE; DNA; MER+ AB Background: The level of the DNA repair protein O6-methylguanine-DNA methyltransferase is an important determinant of the response of tumor cells in culture to alkylating nitrosoureas. In these cells, the abundance of messenger RNA (mRNA) is directly correlated with repair activity. Purpose: Our purpose was to compare transferase mRNA levels with the repair activity in primary human tumors. Methods: Human transferase mRNA was measured in tissue samples from brain tumors, normal lung, lung tumors, ovarian tumors, and normal human liver by use of an RNA protection assay with an antisense probe prepared from the cloned gene. Results: Normal and tumor tissue samples from the same patient had similar transferase activity levels, but transferase expression varied widely among tissue samples from different patients. Brain and lung samples, on average, had transferase mRNA levels closer to those in liver samples than their transferase activity levels. In two cases, tissue samples which were transferase deficient by the activity assays were found to lack transferase mRNA. Conclusions: Deficiencies in transferase activity are due to reduced or absent mRNA transcription or processing. In brain and lung, there may be post-transcriptional control of mRNA expression. The wide interindividual variation in transferase expression is also seen at the transcription level. Implications: These are among the first measures of transferase mRNA expression in primary human tissue. More samples should be examined to extend these observations. C1 LONG ISL JEWISH MED CTR,DIV CARDIOTHORAC SURG,NEW HYDE PK,NY 11042. LONG ISL JEWISH MED CTR,DIV GYNECOL ONCOL,NEW HYDE PK,NY 11042. NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. APPL GENET INC,FREEPORT,NY. LONG ISL JEWISH MED CTR,DEPT NEUROSURG,NEW HYDE PK,NY 11042. LONG ISL JEWISH MED CTR,DEPT PATHOL,NEW HYDE PK,NY 11042. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. RP CITRON, M (reprint author), LONG ISL JEWISH MED CTR,DIV HEMATOL ONCOL,NEW HYDE PK,NY 11042, USA. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X FU NCI NIH HHS [N43-CM-O7360] NR 12 TC 45 Z9 47 U1 0 U2 1 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 4 PY 1992 VL 84 IS 5 BP 337 EP 340 DI 10.1093/jnci/84.5.337 PG 4 WC Oncology SC Oncology GA HU102 UT WOS:A1992HU10200016 PM 1738185 ER PT J AU LUBET, RA DRAGNEV, KH CHAUHAN, DP NIMS, RW DIWAN, BA WARD, JM JONES, CR RICE, JM MILLER, MS AF LUBET, RA DRAGNEV, KH CHAUHAN, DP NIMS, RW DIWAN, BA WARD, JM JONES, CR RICE, JM MILLER, MS TI A PLEIOTROPIC RESPONSE TO PHENOBARBITAL-TYPE ENZYME INDUCERS IN THE F344/NCR RAT - EFFECTS OF CHEMICALS OF VARIED STRUCTURE SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID LIVER MICROSOMAL CYTOCHROME-P-450; TUMOR-PROMOTING ACTIVITIES; MESSENGER-RNA; ALDEHYDE DEHYDROGENASE; N-NITROSODIETHYLAMINE; EPOXIDE HYDROLASE; TESTOSTERONE HYDROXYLATION; FLUOROMETRIC ASSAY; GENE-EXPRESSION; INDUCTION AB The effects of a number of phenobarbital-type inducers on selected drug-metabolizing enzymes in male F344/NCr rats were determined by measuring specific catalytic activities and/or by measuring the levels of RNA which hybridize with specific probes for the corresponding genes. The effects on hepatic CYP2B1 were assessed by measuring the levels of CYP2B1-specific RNA and benzyloxyresorufin O-dealkylase and testosterone 16-beta-hydroxylase activities. Levels of CYP3A were monitored by measuring the rate of hydroxylation of testosterone at the 6-beta-position. Microsomal epoxide hydrolase activity was determined by measurement of cellular RNA specific for this form and by assaying the hydrolysis of benzo[a]pyrene-4,5-oxide. UDP-glucuronyltransferase activity was assayed by measuring the glucuronidation of 3-hydroxybenz[a]anthracene. Levels of glutathione S-transferase Ya/Yc were measured by quantifying total cellular RNA coding for the proteins. When male F344/NCr rats were administered various doses of phenobarbital or dichlorodiphenyltrichloroethane (DDT), strong correlations between the induction of CYP2B1 and the induction of epoxide hydrolase or UDP-glucuronyltransferase activities were observed. Treatment of rats with barbiturates, hydantoins, halogenated pesticides such as DDT or alpha-hexachlorocyclohexane, 2,4,5,2',4',5'-hexachlorobiphenyl, CYP2B1 inhibitors such as clotrimazole or clonazepam, or such structurally-diverse compounds as 2-hexanone or diallyl sulfide resulted in induction of CYP2B1-mediated enzyme activity and induction of certain other forms of cytochrome P450, microsomal epoxide hydrolase, at least one form of UDP-glucuronyltransferase, and multiple forms of glutathione S-transferase. This suggests that, as a class, compounds which induce CYP2B1 also induce a coordinate hepatic pleiotropic response which includes induction of these other phase I and phase II drug-metabolizing enzymes. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RP LUBET, RA (reprint author), NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,BLDG 538,ROOM 205E,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 67 TC 97 Z9 97 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 3 PY 1992 VL 43 IS 5 BP 1067 EP 1078 DI 10.1016/0006-2952(92)90614-O PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HJ516 UT WOS:A1992HJ51600021 PM 1372805 ER PT J AU LUBET, RA NIMS, RW DRAGNEV, KH JONES, CR DIWAN, BA DEVOR, DE WARD, JM MILLER, MS RICE, JM AF LUBET, RA NIMS, RW DRAGNEV, KH JONES, CR DIWAN, BA DEVOR, DE WARD, JM MILLER, MS RICE, JM TI A MARKEDLY DIMINISHED PLEIOTROPIC RESPONSE TO PHENOBARBITAL AND STRUCTURALLY-RELATED XENOBIOTICS IN ZUCKER RATS IN COMPARISON WITH F344/NCR OR DA RATS SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID ARYL-HYDROCARBON HYDROXYLASE; MICROSOMAL-ENZYME INDUCTION; HEPATIC DRUG-METABOLISM; GENETICALLY-OBESE RATS; MESSENGER-RNAS; EPOXIDE HYDROLASE; CYTOCHROME-P-450 ISOZYMES; POLYHALOGENATED BIPHENYLS; N-NITROSODIETHYLAMINE; EXTRAHEPATIC TISSUES AB Phenobarbital (PB) and certain structurally-related compounds induce a variety of hepatic drug-metabolizing enzymes in many strains of rats. Thus, following administration of PB (300, 500 ppm), barbital (BB, 1500 ppm) or 5-ethyl-5-phenylhydantoin (EPH, 500 ppm), CYP2B1-mediated benzyloxyresorufin O-dealkylase activity and epoxide hydrolase activity were profoundly induced in female DA and F344/NCr rats. In contrast, outbred female lean and obese Zucker rats showed markedly reduced CYP2B1 responses (< 15% and < 5% of those observed in the female DA or F344/NCr rat) to PB (doses less-than-or-equal-to 300 ppm), BB (1500 ppm) OT EPH (500 ppm). In parallel studies, profound increases in RNA levels coding for CYP2B1, glutathione S-transferases Ya/Yc (alpha-subclass), or epoxide hydrolase were detected in the female F344/NCr rat following treatment with PB (300 ppm), BB (1500 ppm) or EPH (500 ppm). In contrast, lean Zucker rats showed a strong response only to the highest dose of PB (500 ppm), implying that the diminished response in the Zucker rats may occur at some pretranslational level. Similar studies with lower doses of PB, EPH or BB in male lean Zucker rats showed a decreased response, relative to that in male F344/NCr rats. However, this insensitivity was not as profound as that observed in the female Zucker rats. In fact, the response to PB-type inducers in male or female Zucker rats is probably most clearly explained as a shift of the dose-response curve sharply to the right (decreased responsiveness, compared to F344/NCr or DA rats of the same sex). This decreased responsiveness of female lean Zucker rats to induction of CYP2B1, relative to that of F344/NCr rats, was also observed with the structurally-diverse PB-type inducers clonazepam, clotrimazole and 2-hexanone. In contrast, the female Zucker rat (obese or lean) displayed a pronounced response to induction of CYP1A-mediated ethoxyresorufin O-deethylase activity by beta-naphthoflavone, a prototype inducer of CYP1A1 and CYP1A2. The Zucker rat would thus appear to represent a potentially exploitable genetic model for examining the mechanism of enzyme induction by the myriad xenobiotics which induce a PB-type response. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RP LUBET, RA (reprint author), NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,BLDG 538,ROOM 205E,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 55 TC 16 Z9 16 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 3 PY 1992 VL 43 IS 5 BP 1079 EP 1087 DI 10.1016/0006-2952(92)90615-P PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HJ516 UT WOS:A1992HJ51600022 PM 1554380 ER PT J AU DALY, JW PADGETT, WL AF DALY, JW PADGETT, WL TI AGONIST ACTIVITY OF 2-SUBSTITUTED AND 5'-SUBSTITUTED ADENOSINE-ANALOGS AND THEIR N6-CYCLOALKYL DERIVATIVES AT ADENOSINE-A1 AND ADENOSINE-A2 RECEPTORS COUPLED TO ADENYLATE-CYCLASE SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID RAT-BRAIN; 1,3-DIPROPYL-8-PHENYLXANTHINE; A2-RECEPTORS; ANTAGONISTS; SUBCLASSES; NUCLEOSIDE; MEMBRANES; RELEASE; LIGANDS; POTENT AB The activity of N6-cycloalkyl derivatives of adenosine, 2-chioroadenosine, 5'-chloroadenosine and N-ethylcarboximidoadenosine (NECA) and of 2-fluoroadenosine and 5-methylthioadenosines were compared at the A1-adenosine receptor inhibitory to adenylate cyclase in rat fat cell membranes and at the A2A-adenosine receptors stimulatory to adenylate cyclase in rat PC12 cell membranes. The N6-cycloalkyl derivatives in all cases were more potent (4- to 23-fold) than the parent compound at the A1 receptor, and were less potent (1.6- to 11-fold) than the parent compound at the A2A receptor. N6-Cyclopentyl-5'-chloroadenosine was the most selective agonist (900-fold) for the A1 receptor, while 2-fluoroadenosine was the only agonist with some selectivity (4.8-fold) for the A2A receptor. 5'-Methylthioadenosine was a weak agonist at both adenosine receptors. A 2-fluoro derivative of 5'methylthioadenosine was somewhat more potent, Affinities of these analogs for inhibition of binding of radioligands to rat brain A1 and A2A receptors are presented. RP DALY, JW (reprint author), NIDDKD,BIOORGAN CHEM LAB,BLDG 8,ROOM 1A17,BETHESDA,MD 20892, USA. NR 31 TC 41 Z9 42 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 3 PY 1992 VL 43 IS 5 BP 1089 EP 1093 DI 10.1016/0006-2952(92)90616-Q PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HJ516 UT WOS:A1992HJ51600023 PM 1554381 ER PT J AU BOJE, KM SKOLNICK, P AF BOJE, KM SKOLNICK, P TI NITRIC-OXIDE DOES NOT MEDIATE THE NEUROTROPHIC EFFECTS OF EXCITATORY AMINO-ACIDS IN CULTURED CEREBELLAR GRANULE NEURONS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE NITRIC OXIDE (NO); EXCITATORY AMINO ACIDS; NMDA (N-METHYL-D-ASPARTATE); CEREBELLAR GRANULE CELLS; S-NITROSO-N-ACETYLPENICILLAMINE; NEUROTROPHIC EFFECTS ID D-ASPARTATE PROMOTES; L-ARGININE; RELAXING FACTOR; NMDA RECEPTORS; VISUAL-CORTEX; CYTO-TOXICITY; CELLS; GLUTAMATE; SURVIVAL; DIFFERENTIATION AB Excitatory amino acids, such as N-methyl-D-aspartate (NMDA) and kainate, promote neuritogenesis and viability in primary cultures of cerebellar granule cells. In view of the recent demonstration that excitatory amino acids activate the synthesis of nitric oxide, the present study examined a potential role of nitric oxide in mediating the neurotrophic effects of excitatory amino acids. NMDA enhanced the viability of 8-day-old cerebellar granule cell cultures in a concentration-dependent fashion, whereas kainate showed a concentration-dependent biphasic effect. A specific inhibitor of nitric oxide synthase, N(G)-nitroarginine (0.5 mM), did not antagonize the neurotrophic effects of NMDA (0.5 mM) or kainate (0.05 mM). The concentration of N(G)-nitroarginine was sufficient to inhibit NMDA or kainate stimulated nitric oxide synthesis and was stable in the culture media throughout the 8-day culture period. Using a specific chemiluminescence detection method, endogenous nitric oxide was directly measured in the headspace gas phase of homogenized cultured cerebellar granule cells, and was not detected when homogenates were incubated with N(G)-nitroarginine (0.5 mM). Furthermore, addition of a nitric oxide precursor, S-nitroso-N-acetylpenicillamine (1-200-mu-M), was not neurotrophic, but rather, was neurotoxic in granule cells. These findings indicate that nitric oxide is not a neurotrophic factor in primary cultures of cerebellar granule cells. RP BOJE, KM (reprint author), NIDDKD,NEUROSCI LAB,BLDG 8,ROOM 111,BETHESDA,MD 20892, USA. NR 49 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD MAR 3 PY 1992 VL 212 IS 2-3 BP 151 EP 158 DI 10.1016/0014-2999(92)90323-V PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HK036 UT WOS:A1992HK03600004 PM 1318207 ER PT J AU ASHER, O FUCHS, S ZUK, D RAPAPORT, D BUONANNO, A AF ASHER, O FUCHS, S ZUK, D RAPAPORT, D BUONANNO, A TI CHANGES IN THE EXPRESSION OF MESSENGER-RNAS FOR MYOGENIC FACTORS AND OTHER MUSCLE-SPECIFIC PROTEINS IN EXPERIMENTAL AUTOIMMUNE MYASTHENIA-GRAVIS SO FEBS LETTERS LA English DT Article DE EXPERIMENTAL AUTOIMMUNE MYASTHENIA GRAVIS; DENERVATION; MYOGENIN, MYOD1; MRF4; ACETYLCHOLINE RECEPTOR MESSENGER RNA; MUSCLE CREATINE KINASE; ALPHA-ACTIN; MUSCLE DYSTROPHIN ID ACETYLCHOLINE-RECEPTOR GENES; MYOD1; ENHANCER; MEMBER; FAMILY; HOMOLOGY; ELEMENT; REGION; MRF4 AB The regulation of genes for acetylcholine receptor (AChR), myogenic factors and other muscle-specific proteins has been analyzed in experimental autoimmune myasthenia gravis (EAMG) and following denervation. The levels of the transcripts for the myogenic factors, MyoD1, myogenin and MRF4, were measured using Northern blot analysis. Myogenin and MRF4 transcript levels were observed to be 3.1- and 2.6-fold higher in muscle of rats with EAMG than in controls, respectively. MyoD1 levels, however, remained unchanged. The increases in AChR, myogenin and MRF4 mRNAs were one order of magnitude higher in 2-week denervated muscle than in the myasthenic muscle. The levels of muscle creatine kinase (MCK), alpha-actin and muscle dystrophin transcripts were also analyzed. Dystrophin levels were found to be 1.7- and 4.7-fold higher in EAMG and denervated muscle, respectively, than in controls; in contrast, MCK and alpha-actin levels remained unchanged. C1 WEIZMANN INST SCI,DEPT CELL BIOL,IL-76100 REHOVOT,ISRAEL. NICHHD,DEV NEUROBIOL LAB,MOLEC NEUROBIOL UNIT,BETHESDA,MD 20892. RP ASHER, O (reprint author), WEIZMANN INST SCI,DEPT CHEM IMMUNOL,IL-76100 REHOVOT,ISRAEL. NR 32 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAR 2 PY 1992 VL 299 IS 1 BP 15 EP 18 DI 10.1016/0014-5793(92)80089-Y PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA HH501 UT WOS:A1992HH50100004 PM 1312030 ER PT J AU CHIN, H SMITH, MA KIM, HL KIM, H AF CHIN, H SMITH, MA KIM, HL KIM, H TI EXPRESSION OF DIHYDROPYRIDINE-SENSITIVE BRAIN CALCIUM CHANNELS IN THE RAT CENTRAL-NERVOUS-SYSTEM SO FEBS LETTERS LA English DT Article DE CA2+-CHANNEL; INSITU HYBRIDIZATION; IMMUNOHISTOCHEMISTRY; BRAIN ID SKELETAL-MUSCLE; BINDING POLYPEPTIDE; RECEPTOR; SUBUNIT; CELL; BENZOTHIAZEPINE; IDENTIFICATION; LOCALIZATION; ANTIBODIES; BLOCKING AB We have localized dihydropyridine (DHP)-sensitive calcium channels in rat brain by in situ hybridization and immunohistochemistry. The mRNA for the dihydropyridine-sensitive calcium channel alpha-1 subunit (DHPR-B) is prominently localized in neuronal cells in the olfactory bulb, dentate gyrus, hippocampus, arcuate nucleus, paraventricular nucleus, ventromedial nucleus, cerebral cortex, superior colliculus and the cerebellar Purkinje cell layer. Strong expression of DHPR-B mRNA was also found in the pituitary and pineal glands. DHP-sensitive calcium channel alpha-1 subunit distribution has also been examined immunohistochemically with polyclonal antibodies raised against synthetic peptides specific for the DHPR-B alpha-1 subunit protein. The results from immunohistochemistry were in good agreement with those from in situ hybridization. Thus, regional distribution and localization of DHPR-B mRNA and alpha-1 subunit protein in rat brain suggest that this type of DHP-sensitive brain calcium channel may play an important role in excitation-secretion coupling functions in the neuroendocrine system. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RP CHIN, H (reprint author), NINCDS,MOLEC BIOL LAB,BLDG 36,ROOM 3D-02,BETHESDA,MD 20892, USA. NR 25 TC 62 Z9 63 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAR 2 PY 1992 VL 299 IS 1 BP 69 EP 74 DI 10.1016/0014-5793(92)80103-N PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA HH501 UT WOS:A1992HH50100018 PM 1312035 ER PT J AU PARKER, RI MCKEOWN, LP GALLIN, JI GRALNICK, HR AF PARKER, RI MCKEOWN, LP GALLIN, JI GRALNICK, HR TI ABSENCE OF THE LARGEST PLATELET-VONWILLEBRAND MULTIMERS IN A PATIENT WITH LACTOFERRIN DEFICIENCY AND A BLEEDING TENDENCY SO THROMBOSIS AND HAEMOSTASIS LA English DT Article ID VIII-RELATED ANTIGEN; THROMBIN-STIMULATED PLATELETS; IMMUNOFLUORESCENT LOCALIZATION; SHEAR RATE; DISEASE; RELEASE; COLLAGEN; ADHESION; BLOOD; SUBENDOTHELIUM AB We have studied a young male with lactoferrin deficiency and a bleeding tendency responsive to cryoprecipitate. This child has had increased bleeding following surgical procedures and a variably prolonged template bleeding time. The patient has a normal platelet count, normal in vitro platelet ATP secretion and aggregation in response to a variety of agonists, and normal concentration of plasma-von Willebrand factor ristocetin cofactor activity and antigen. Analysis of plasma-vWf multimers by agarose gel electrophoresis consistently demonstrated a subtle decrease in the largest vWf multimers. In contrast, analysis of the patient's platelet-vWf revealed normal vWf:Ag, decreased vWf ristocetin cofactor activity, and a striking absence of the high and intermediate size molecular weight vWf multimers. Analysis of surface bound platelet-vWf demonstrated normal amounts on the surface of unstimulated platelets, but after thrombin stimulation the platelet-vWf surface expression did not increase. This lack of increased platelet-vWf surface expression resulted from decreased binding of secreted platelet-vWf to be surface of stimulated platelets. These data suggest that the patient's bleeding tendency may be related to a defect in his platelet-vWf structure and/or mobilization. This case represents a unique demonstration of an abnormality of platelet-vWf in the presence of normal plasma-vWf, and supports the data indicating an important role for platelet-vWf in primary hemostasis. C1 NIAID,CTR CLIN,DEPT CLIN PATHOL,HEMATOL SERV,BETHESDA,MD 20892. NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 29 TC 14 Z9 14 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD MAR 2 PY 1992 VL 67 IS 3 BP 320 EP 324 PG 5 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA HH209 UT WOS:A1992HH20900008 PM 1641822 ER PT J AU HEALY, BP AF HEALY, BP TI BEYOND THE COLLEGE WALLS SO ACADEMIC MEDICINE LA English DT Article AB The author outlines historical and current reasons that the National Institutes of Health (NIH) and academic medicine are inherently political and are now facing expanding political exposure. She emphasizes especially the power of modern discoveries in biology; this power stems from the many practical benefits that these discoveries can bring and their economic implications, and the growing public awareness of these benefits and implications. She then discusses the political realities of the biomedical enterprise, illustrating them by describing the nature of issues surrounding (1) the NIH budget and (2) technology transfer. Discussion of the latter topic includes a detailed description of controversies about patents (which revolve around the issue of who owns and controls the distribution and use of scientific information) and several important policy issues that are raised by these controversies (e.g., should there be uniform international policies regarding intellectual property rights associated with discoveries of novel biologically expressed genes of uncertain in-vivo function, and if so, how is that achieved?). The author concludes by stating that these examples of the politics of knowledge and of the NIH are among many vital biomedical issues of American life (which she lists) that require the academic medicine community to look beyond its own walls and participate in the complex world of politics and public policy. RP HEALY, BP (reprint author), NIH,BLDG 1,ROOM 344,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 1 U2 4 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1040-2446 J9 ACAD MED JI Acad. Med. PD MAR PY 1992 VL 67 IS 3 BP 137 EP 141 DI 10.1097/00001888-199203000-00001 PG 5 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA HH852 UT WOS:A1992HH85200001 PM 1540263 ER PT J AU KAWANAMI, O MATSUDA, K YONEYAMA, H FERRANS, VJ CRYSTAL, RG AF KAWANAMI, O MATSUDA, K YONEYAMA, H FERRANS, VJ CRYSTAL, RG TI ENDOTHELIAL FENESTRATION OF THE ALVEOLAR CAPILLARIES IN INTERSTITIAL FIBROTIC LUNG-DISEASES SO ACTA PATHOLOGICA JAPONICA LA English DT Article DE ALVEOLAR CAPILLARY; DIAPHRAGMED FENESTRA; CAPILLARY ENDOTHELIUM; BRONCHIAL CIRCULATION; ENDOTHELIUM ID RESPIRATORY-DISTRESS SYNDROME; ANCHORING FIBRILS; GAS-EXCHANGE; PNEUMONITIS; LESIONS; DAMAGE; INJURY; RABBIT; CELLS AB A light and electron microscopy study was performed on endothelial cells of alveolar capillaries in biopsied lung tissues obtained from 28 patients with interstitial fibrotic lung diseases, including idiopathic pulmonary fibrosis, sarcoidosis, hypersensitivity pneumonitis, chronic eosinophilic pneumonia, collagen vascular diseases and acute interstitial pneumonia. In the relatively early stages of acute interstitial pneumonia, hypersensitivity pneumonitis and other diseases, the cytoplasms of the endothelial cells appeared swollen and electron-lucent and occasionally showed degeneration and necrosis. Although mitosis was not evident in the endothelium at any disease stage, some capillary endothelial cells showed regeneration. Furthermore, although rarely, they showed obvious phenotypic transformation into diaphragmed fenestrae in some limited segments of fibrotic lungs in the 20 of the 28 patients examined. The frequency of endothelial fenestration seemed to be correlated with the degree of interstitial fibrosis along the alveolar walls. In such fibrotic lung tissues, cuboidal metaplastic cells of bronchiolar origin proliferated on the luminal side. The mechanism of endothelial fenestration in the alveolar capillaries is assumed to be comparable with cuboidal metaplasia of alveolar epithelial cells. The alveolar capillary endothelium is recruited from the bronchiolar capillaries via bronchopulmonary anastomoses unless endothelial repair occurs in situ. Regenerating endothelial cells move into the alveolar capillary tubes along the remnant sleeves of the basement membrane. New endothelial processes finally display their original fenestrated structure while secreting irregular fragments of basement membrane during implantation in the capillary beds. C1 NHLBI,PATHOL BRANCH,ULTRASTRUCT SECT,BETHESDA,MD 20892. NHLBI,PULM BRANCH,BETHESDA,MD 20892. RP KAWANAMI, O (reprint author), NIPPON MED SCH HOSP 2,PATHOL & CLIN RES LAB,NAKAHARA KU,KAWASAKI 211,JAPAN. NR 30 TC 13 Z9 17 U1 0 U2 3 PU BLACKWELL SCIENCE PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON VICTORIA 3053, AUSTRALIA SN 0001-6632 J9 ACTA PATHOL JAPON PD MAR PY 1992 VL 42 IS 3 BP 177 EP 184 PG 8 WC Pathology SC Pathology GA HR419 UT WOS:A1992HR41900004 PM 1570740 ER PT J AU DIMITROV, DS HILLMAN, K MANISCHEWITZ, J BLUMENTHAL, R GOLDING, H AF DIMITROV, DS HILLMAN, K MANISCHEWITZ, J BLUMENTHAL, R GOLDING, H TI CORRELATION BETWEEN KINETICS OF SOLUBLE CD4 INTERACTIONS WITH HIV-1-ENV-EXPRESSING CELLS AND INHIBITION OF SYNCYTIA FORMATION - IMPLICATIONS FOR MECHANISMS OF CELL-FUSION AND THERAPY FOR AIDS SO AIDS LA English DT Article DE SCD4 BINDING; GP120 SHEDDING; SYNCYTIA INHIBITION; SCD4 TREATMENT OF AIDS; MEMBRANE FUSION ID HUMAN-IMMUNODEFICIENCY-VIRUS; ENVELOPE GLYCOPROTEIN; INFECTION; HIV-1; GP120; DISSOCIATION; MOLECULES; INVITRO; COMPLEX; TYPE-1 AB Objectives: To study the kinetics of the interactions between soluble (s) CD4 and HIV-1-Env-expressing cells in relation to subsequent events leading to cell fusion and inhibition of syncytia formation. Design: Vaccinia-HIV-1 (Env)-infected CD4- T-cells were used to study the kinetics of sCD4-gp120/41 interactions and syncytia formation (with CD4+ T-cells) under identical conditions. Methods: sCD4 association and dissociation rates for HIV-1-Env-expressing cells, and quantification of sCD4-induced gp120 shedding was determined by a quantitative flow cytometry assay. Syncytia inhibition was measured in the continuous presence of sCD4, or after washing of HIV-1-Env-expressing cells following pre-incubation with sCD4. Results: The kinetics of syncytia inhibition correlated with sCD4 binding when sCD4 was maintained during the culture. When Env-expressing cells, which had been pre-incubated with sCD4, were washed to remove unbound sCD4, no syncytia formation inhibition was observed, even following sCD4-induced shedding of > 50% of surface gp120 molecules. Conclusions: The lack of syncytia inhibition seen after removal of unbound sCD4, even after pre-incubation of cells under saturation and gp120 shedding conditions, indicated that sufficient numbers of fusogenic molecules remained on the sCD4-treated cells. In addition, fast dissociation of pre-bound sCD4 occurred in culture. These results are important for understanding HIV-1-Env-mediated cell fusion and AIDS therapy. C1 US FDA,CTR BIOL EVALUAT & RES,DIV VIROL,BETHESDA,MD 20892. NCI,MEMBRANE STRUCT & FUNCT SECT,BETHESDA,MD 20892. NR 29 TC 14 Z9 14 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD MAR PY 1992 VL 6 IS 3 BP 249 EP 256 DI 10.1097/00002030-199203000-00023 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA HM325 UT WOS:A1992HM32500001 PM 1348943 ER PT J AU GALLANT, JE SOMANI, J CHAISSON, RE STANTON, D SMITH, M QUINN, TC AF GALLANT, JE SOMANI, J CHAISSON, RE STANTON, D SMITH, M QUINN, TC TI DIAGNOSTIC-ACCURACY OF 3 CLINICAL CASE DEFINITIONS FOR ADVANCED HIV DISEASE SO AIDS LA English DT Article DE CASE DEFINITION; AIDS CLASSIFICATION; AIDS DIAGNOSIS; AIDS EPIDEMIOLOGY; HIV INFECTION; WORLD-HEALTH-ORGANIZATION; CARACAS DEFINITION; BRAZIL; POPULATION SURVEILLANCE ID AIDS; UGANDA AB Objective: To assess the accuracy of three clinical case definitions for advanced HIV disease: the World Health Organization (WHO) case definition, and the original and revised Caracas case definitions. Design: Retrospective chart review. Setting: A clinic for patients with all stages of HIV infection at the Johns Hopkins Hospital, Bethesda, Maryland, USA, a tertiary care university hospital. Patients, participants: Two hundred and twenty-four HIV-positive adults who underwent initial evaluation between 1 January 1990 and 31 December 1990. Main outcome measures: A score for each definition was assigned based on initial evaluation. The sensitivity, specificity, and predictive values were calculated using the Centers for Disease Control (CDC) staging criteria, and results were correlated with total CD4 cell counts. Results: The sensitivities of the WHO, and the original and revised Caracas definitions were 40, 67, and 60%, respectively, using CDC disease stage IV as a positive standard. Specificities were between 99 and 100%, using CDC stage II-III disease as a negative standard. Mean CD4 cell counts for patients with positive scores were 184, 160, and 158 x 10(6)/l, respectively, compared to 191 x 10(6)/l for CDC stage IV patients. Sensitivity was lower when the positive standard was expanded to include all patients with CD4 cell counts < 200 x 10(6)/l. Conclusions: In our study population, case definitions were specific, but only moderately sensitive for advanced HIV disease. Prospective studies should be conducted in diverse geographic regions, using lymphocyte or CD4 cell counts when possible. C1 JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,BALTIMORE,MD 21205. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 20 TC 9 Z9 9 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD MAR PY 1992 VL 6 IS 3 BP 295 EP 299 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA HM325 UT WOS:A1992HM32500006 PM 1348946 ER PT J AU JOHNSON, PR HIRSCH, VM AF JOHNSON, PR HIRSCH, VM TI GENETIC-VARIATION OF SIMIAN IMMUNODEFICIENCY VIRUSES IN NONHUMAN-PRIMATES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID AFRICAN-GREEN MONKEYS; MACAQUE MONKEYS; REVERSE-TRANSCRIPTASE; RHESUS-MONKEYS; HTLV-III; HIV-1; AIDS; RETROVIRUS; PROTEIN; TYPE-2 AB The generation of biologically active proviral DNA clones of simian immunodeficiency virus (SIV) that give rise to infectious virions has allowed the detailed examination of genetic variation in experimentally inoculated monkeys. Studies of nucleotide sequences derived directly from circulating leukocytes of infected monkeys show that the SIV genome undergoes rapid and dramatic variation during the course of infection. The env gene is a major site for variation, and within the Env protein, hypervariable regions analogous to those previously defined for the human immunodeficiency virus type 1 (HIV-1) env gene are apparent. A major exception is the region corresponding to the V3 domain in HIV-1, which has been highly conserved in all SIV studies to date. These data notwithstanding, the role of SIV genetic variation in the pathogenesis of AIDS in monkeys remains unclear. Genetic variation within the env gene does not appear to be sufficient for the development of AIDS since significant variation is observed in both pathogenic and nonpathogenic SIV infections. Furthermore, although it generally is believed that env gene variation might allow HIV and SIV to avoid recognition and elimination by host immune responses, this premise has not been rigorously proven. The use of molecularly cloned SIV in monkey models has provided important quantitative and qualitative information on in vivo sequence variation, and these data, in turn, have laid the groundwork for addressing the undoubtedly complex functional significance of this variation. C1 GEORGETOWN UNIV,DEPT MICROBIOL,DIV MOLEC VIROL & IMMUNOL,WASHINGTON,DC 20007. NIAID,INFECT DIS LAB,ROCKVILLE,MD. RP JOHNSON, PR (reprint author), OHIO STATE UNIV,CHILDRENS HOSP,WEXNER INST,DEPT PEDIAT,ROOM W309,700 CHILDRENS DR,COLUMBUS,OH 43205, USA. RI Johnson, Philip/A-6892-2009 NR 37 TC 20 Z9 20 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAR PY 1992 VL 8 IS 3 BP 367 EP 372 DI 10.1089/aid.1992.8.367 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA HK848 UT WOS:A1992HK84800006 PM 1571196 ER PT J AU COHEN, SG AF COHEN, SG TI DISCOVERY AND REDISCOVERY SO ALLERGY PROCEEDINGS LA English DT Article RP COHEN, SG (reprint author), NIAID,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 SN 1046-9354 J9 ALLERGY PROC JI Allergy Proc. PD MAR-APR PY 1992 VL 13 IS 2 BP 97 EP 104 DI 10.2500/108854192778878935 PG 8 WC Allergy SC Allergy GA HR495 UT WOS:A1992HR49500009 PM 1587472 ER PT J AU COHEN, SG AF COHEN, SG TI THE CHICKEN IN HISTORY AND IN THE SOUP .2. THANK-YOU COLUMBUS SO ALLERGY PROCEEDINGS LA English DT Editorial Material RP COHEN, SG (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 SN 1046-9354 J9 ALLERGY PROC JI Allergy Proc. PD MAR-APR PY 1992 VL 13 IS 2 BP 105 EP 112 DI 10.2500/108854192778878872 PG 8 WC Allergy SC Allergy GA HR495 UT WOS:A1992HR49500010 PM 1587465 ER PT J AU KALINER, MA AF KALINER, MA TI NONSEDATING ANTIHISTAMINES - PHARMACOLOGY, CLINICAL EFFICACY AND ADVERSE-EFFECTS SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Antihistamines are effective therapy for histamine-mediated conditions, including seasonal and perennial allergic rhinitis and chronic urticaria. Until recently, all antihistamines produced some degree of drowsiness, as well as anticholinergic side effects. Several nonsedating antihistamines have been developed. Two of these antihistamines-terfenadine and astemizole-are commercially available. The lack of central nervous system effects is attributed to the inability of these drugs to penetrate the blood-brain barrier. They also have no appreciable binding to cholinergic receptors. Clinical trials have demonstrated that the newer agents are as effective as classic antihistamines and that they have no greater incidence of central nervous system or anticholinergic side effects than placebo. RP KALINER, MA (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 0 TC 13 Z9 13 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD MAR PY 1992 VL 45 IS 3 BP 1337 EP 1342 PG 6 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA HH556 UT WOS:A1992HH55600027 PM 1347437 ER PT J AU CLEVIDENCE, BA JUDD, JT SCHATZKIN, A MUESING, RA CAMPBELL, WS BROWN, CC TAYLOR, PR AF CLEVIDENCE, BA JUDD, JT SCHATZKIN, A MUESING, RA CAMPBELL, WS BROWN, CC TAYLOR, PR TI PLASMA-LIPID AND LIPOPROTEIN CONCENTRATIONS OF MEN CONSUMING A LOW-FAT, HIGH-FIBER DIET SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE DIET; DIETARY FAT; DIETARY FIBER; BLOOD LIPIDS; LIPOPROTEINS; PLASMA CHOLESTEROL; HDL CHOLESTEROL; LDL CHOLESTEROL ID HIGH-DENSITY LIPOPROTEIN; CORONARY HEART-DISEASE; HYPERCHOLESTEROLEMIC MEN; OAT-BRAN; CHOLESTEROL; ACIDS; POPULATIONS; REGRESSION; FRAMINGHAM AB This study assessed the influence of a low-fat, high-fiber diet on blood lipid concentrations of 42 men with desirable or moderately elevated cholesterol concentrations. A low-fat diet (19% fat, 4% saturated fatty acids, 4.6 g fiber/MJ) was compared with a high-fat diet (41% fat, 15% saturated fatty acids, 2.0 g fiber/MJ) and with subjects' self-selected diets. Substituting the low-fat for the high-fat diet decreased total, low-density-lipoprotein, and high-density-lipoprotein cholesterol by 17-20%. Lipid changes between 6 and 10 wk were minor. A reduction in plasma cholesterol of > 0.52 mmol/L was achieved with the low-fat diet in 59% of men changing from their self-selected diets and in 79% changing from the high-fat diet. Percent reduction was independent of subjects' cholesterol classification. Results indicate that significant reductions in plasma cholesterol can be achieved by the majority of men committing to a low-fat, high-fiber diet. C1 NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,LIPID RES CLIN,WASHINGTON,DC 20052. RP CLEVIDENCE, BA (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE HUMAN NUTR RES CTR,LIPID NUTR LAB,BLDG 308,BELTSVILLE,MD 20705, USA. NR 35 TC 30 Z9 30 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD MAR PY 1992 VL 55 IS 3 BP 689 EP 694 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HG351 UT WOS:A1992HG35100013 PM 1312762 ER PT J AU EMANCIPATOR, K URANKARNAGY, N LEONARD, KA BRADFORD, G EMANCIPATOR, SN AF EMANCIPATOR, K URANKARNAGY, N LEONARD, KA BRADFORD, G EMANCIPATOR, SN TI IMMUNOHISTOLOGIC DEMONSTRATION OF MYOCARDIAL PROTEINS WITH APPLICATIONS SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE CREATINE KINASE MB ISOENZYME; MYOSIN LIGHT CHAIN-1; TERATOMA; RHABDOMYOSARCOMA; TUMOR MARKER; REGENERATIVE MUSCLE ID KINASE-MB ISOENZYME; CREATINE-KINASE; LUNG-CANCER; CK-MB; SERUM; PATIENT; RHABDOMYOSARCOMA; EXTRACTION; INFARCTION; TUMOR AB The authors used antibodies specific for creatine kinase MB isoenzyme (CK-MB) and myosin light chain-1 (MLC-1) for immunohistologic staining. At appropriate dilutions of antibody, frozen sections of human heart muscle were positive for both CK-MB and MLC-1, whereas sections of human skeletal muscle were negative for both proteins. Staining for both CK-MB and MLC-1 also was demonstrated in an immature teratoma. Furthermore, staining was localized to the rhabdomyosarcomatous elements within the teratoma; other components of the tumor did not stain for CK-MB or MLC-1. Biopsies of skeletal muscle revealed that regenerative, but not intact normal or degenerating, fibers also contained CK-MB and MLC-1. Immunohistologic stains for CK-MB and MLC-1 may be useful as tumor markers and as markers for regenerative muscle fibers. C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,BETHESDA,MD 20892. CASE WESTERN RESERVE UNIV,INST PATHOL,CLEVELAND,OH 44106. SUNY STONY BROOK,DEPT PATHOL,STONY BROOK,NY 11794. FU NIAID NIH HHS [AI-31230]; NIDDK NIH HHS [DK-38544] NR 16 TC 5 Z9 6 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD MAR PY 1992 VL 97 IS 3 BP 376 EP 380 PG 5 WC Pathology SC Pathology GA HG492 UT WOS:A1992HG49200015 PM 1371901 ER PT J AU SEIGEL, DG PODGOR, MJ REMALEY, NA AF SEIGEL, DG PODGOR, MJ REMALEY, NA TI ACCEPTABLE VALUES OF KAPPA FOR COMPARISON OF 2 GROUPS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Note DE BIAS; CLINICAL TRIALS; EPIDEMIOLOGIC METHODS; MODELS; STATISTICAL; ODDS RATIO; RELATIVE RISK; STATISTICS ID II LOCS-II; LENS OPACITIES AB A model was developed for a simple clinical trial in which graders had defined probabilities of misclassifying pathologic material to disease present or absent. The authors compared Kappa between graders, and efficiency and bias in the clinical trial in the presence of misclassification. Though related to bias and efficiency, Kappa did not predict these two statistics well. These results pertain generally to evaluation of systems for encoding medical information, and the relevance of Kappa in determining whether such systems are ready for use in comparative studies. The authors conclude that, by itself, Kappa is not informative enough to evaluate the appropriateness of a grading scheme for comparative studies. Additional, and perhaps difficult, questions must be addressed for such evaluation. RP SEIGEL, DG (reprint author), NEI,BIOMETRY & EPIDEMIOL PROGRAM,BLDG 31,ROOM 6A10,BETHESDA,MD 20892, USA. NR 8 TC 95 Z9 97 U1 0 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAR 1 PY 1992 VL 135 IS 5 BP 571 EP 578 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HR190 UT WOS:A1992HR19000013 PM 1570823 ER PT J AU RIEDEL, DA AF RIEDEL, DA TI HUMAN T-LYMPHOTROPIC VIRUS (HTLV-I) SEROPREVALENCE IN JAMAICA .1. DEMOGRAPHIC DETERMINANTS .2. GEOGRAPHIC AND ECOLOGIC DETERMINANTS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter RP RIEDEL, DA (reprint author), NCI,EXECUT PLAZA N,ROOM 418,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAR 1 PY 1992 VL 135 IS 5 BP 591 EP 591 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HR190 UT WOS:A1992HR19000021 PM 1570828 ER PT J AU BYRNE, J FEARS, TR GAIL, MH PEE, D CONNELLY, RR AUSTIN, DF HOLMES, GF HOLMES, FF LATOURETTE, HB MEIGS, JW STRONG, LC MYERS, MH MULVIHILL, JJ AF BYRNE, J FEARS, TR GAIL, MH PEE, D CONNELLY, RR AUSTIN, DF HOLMES, GF HOLMES, FF LATOURETTE, HB MEIGS, JW STRONG, LC MYERS, MH MULVIHILL, JJ TI EARLY MENOPAUSE IN LONG-TERM SURVIVORS OF CANCER DURING ADOLESCENCE SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE MENOPAUSE; CHILDHOOD CANCER; RADIATION; ALKYLATING AGENT; OVARIAN FAILURE; FOLLOW-UP STUDIES ID ACUTE LYMPHOBLASTIC-LEUKEMIA; HODGKINS-DISEASE; OVARIAN-FUNCTION; COMBINATION CHEMOTHERAPY; GONADAL DAMAGE; CHILDHOOD; WOMEN; FERTILITY; FAILURE; PUBERTY AB OBJECTIVE: We attempted to investigate the risk of early menopause after treatment for cancer during childhood or adolescence. STUDY DESIGN: We interviewed 1067 women in whom cancer was diagnosed before age 20, who were at least 5-year survivors, and who were still menstruating at age 21. Self-reported menopause status in survivors was compared with that in 1599 control women. RESULTS: Cancer survivors, with disease diagnosed between ages 13 and 19, had a risk of menopause four times greater than that of controls during the ages 21 to 25; the risk relative to controls declined thereafter. Significantly increased relative risks of menopause during the early 20s occurred after treatment with either radiotherapy alone (relative risk 3.7) or alkylating agents alone (relative risk 9.2). During ages 21 to 25 the risk of menopause increased 27-fold for women treated with both radiation below the diaphragm and alkylating agent chemotherapy. By age 31, 42% of these women had reached menopause compared with 5% for controls. CONCLUSION: Treatment for cancer during adolescence carries a substantial risk for early menopause among women still menstruating at age 21. Increasing use of radiation and chemotherapy, together with the continued trend toward delayed childbearing, suggests that these women should be made aware of their smaller window of fertility so that they can plan their families accordingly. C1 INFORMAT MANAGEMENT SERV INC, ROCKVILLE, MD USA. CALIF DEPT HLTH SERV, EMERYVILLE, CA USA. UNIV KANSAS, MED CTR, KANSAS CITY, KS 66103 USA. UNIV IOWA, IOWA CITY, IA 52242 USA. YALE UNIV, NEW HAVEN, CT 06520 USA. UNIV TEXAS, MD ANDERSON CANCER CTR, HOUSTON, TX 77030 USA. UNIV PITTSBURGH, DEPT HUMAN GENET, PITTSBURGH, PA 15260 USA. RP BYRNE, J (reprint author), NCI, CLIN EPIDEMIOL BRANCH, EPIDEMIOL & BIOSTAT PROGRAM, EPN 400, BETHESDA, MD 20892 USA. NR 26 TC 245 Z9 254 U1 1 U2 6 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9378 EI 1097-6868 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD MAR PY 1992 VL 166 IS 3 BP 788 EP 793 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA HJ885 UT WOS:A1992HJ88500003 PM 1550144 ER PT J AU HILLIER, SL KROHN, MA NUGENT, RP GIBBS, RS AF HILLIER, SL KROHN, MA NUGENT, RP GIBBS, RS TI CHARACTERISTICS OF 3 VAGINAL FLORA PATTERNS ASSESSED BY GRAM STAIN AMONG PREGNANT-WOMEN SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE BACTERIAL VAGINOSIS; VAGINAL FLORA ID LOW-BIRTH-WEIGHT; BACTERIAL VAGINOSIS; CHLAMYDIA-TRACHOMATIS; NONSPECIFIC VAGINITIS; RISK FACTOR; INFECTION; DIAGNOSIS; ENDOMETRITIS; ASSOCIATIONS; PREVALENCE AB This study was undertaken to define the characteristics and persistence of vaginal flora in 7918 pregnant women at 23 to 26 weeks' gestation. Vaginal smears were categorized as normal (predominant lactobacilli), intermediate (reduced lactobacilli), or positive for bacterial vaginosis. The women with normal flora were least likely to have elevated vaginal pH, amine odor, milky discharge, or colonization by Gardnerella, Bacteroides, or genital mycoplasmas. Women with intermediate vaginal flora had intermediate frequencies of these clinical signs and microorganisms. Group B streptococci and yeast were associated with normal or intermediate flora, whereas Neisseria gonorrhoeae and Chlamydia trachomatis were recovered more frequently from women with intermediate flora or bacterial vaginosis. Trichomonas vaginalis was most associated with intermediate flora. At follow-up, 81% of the women with normal flora had remained normal. Of the women with intermediate flora, 32% acquired bacterial vaginosis and 30% shifted to normal flora. Only 12% of the women with bacterial vaginosis had shifted to normal flora. We conclude that there are two primary stable vaginal flora patterns (normal flora or bacterial vaginosis) and a third less distinct transitional flora pattern between these two. C1 UNIV WASHINGTON, DEPT EPIDEMIOL, SEATTLE, WA 98195 USA. NICHHD, BETHESDA, MD 20892 USA. UNIV COLORADO, HLTH SCI CTR, DEPT OBSTET & GYNECOL, DENVER, CO 80262 USA. RP HILLIER, SL (reprint author), UNIV WASHINGTON, DEPT OBSTET & GYNECOL, RH20, SEATTLE, WA 98195 USA. FU NICHD NIH HHS [HD-3-2832, HD-3-2833, HD-3-2834] NR 25 TC 150 Z9 152 U1 0 U2 3 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9378 EI 1097-6868 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD MAR PY 1992 VL 166 IS 3 BP 938 EP 944 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA HJ885 UT WOS:A1992HJ88500036 PM 1372474 ER PT J AU PARKER, RI GREWAL, RP MCKEOWN, LP BARTON, NW AF PARKER, RI GREWAL, RP MCKEOWN, LP BARTON, NW TI EFFECT OF PLATELET COUNT ON THE DDAVP-INDUCED SHORTENING OF THE BLEEDING-TIME IN THROMBOCYTOPENIC GAUCHER PATIENTS SO AMERICAN JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY LA English DT Article DE VWF; PLATELET AGGREGATION; PLATELET FUNCTIONS ID 1-DESAMINO-8-D-ARGININE VASOPRESSIN DESMOPRESSIN; VIII-VONWILLEBRAND-FACTOR; CONTROLLED TRIAL; BLOOD-LOSS; DYSFUNCTION; DISEASE; SURGERY AB As part of an investigative protocol requiring serial liver biopsies in patients with Type I Gaucher's disease who were receiving enzyme replacement therapy, we gave 11 patients a total of 15 infusions of DDAVP (0.3-mu-g/kg IV) and measured the Simplate bleeding time pre- and postinfusion. All patients were thrombocytopenic (one patient 100-150,000; seven 66-99,000; and three 50-65,000/mu-l). Nine of 15 infusions resulted in at least a 2-min shortening of the bleeding time; in 6/11 infusions in which the platelet count was > 65,000, the bleeding time shortened to less-than-or-equal-to 10 min, in 1/11 it shortened greater-than-or-equal-to 2 min but not to less-than-or-equal-to 10 min. In only 2/4 infusions given to patients with platelet counts < 65,000 did the bleeding time demonstrate any significant shortening. None of the six liver biopsies performed in the patients whose bleeding time shortened to less-than-or-equal-to 10 min resulted in any significant bleeding; blood products were not transfused either pre- or postprocedure. These limited data demonstrate that a high percentage of patients with platelet counts of 65-100,000/mu-l can manifest a significant shortening of bleeding time following a standard infusion of DDAVP, and that in approximately half of these patients the bleeding time will shorten enough to safely allow the performance of a liver biopsy without the need for prophylactic transfusion of blood products. C1 NIH,CTR CLIN,DEPT CLIN PATHOL,HEMATOL SERV,BETHESDA,MD 20892. NINCDS,DMNB,BETHESDA,MD 20892. NR 17 TC 6 Z9 6 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-8562 J9 AM J PEDIAT HEMATOL PD SPR PY 1992 VL 14 IS 1 BP 39 EP 43 PG 5 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA GZ931 UT WOS:A1992GZ93100005 PM 1550261 ER PT J AU BABIJ, P KAWAMOTO, S WHITE, S ADELSTEIN, RS PERIASAMY, M AF BABIJ, P KAWAMOTO, S WHITE, S ADELSTEIN, RS PERIASAMY, M TI DIFFERENTIAL EXPRESSION OF SM1 AND SM2 MYOSIN ISOFORMS IN CULTURED VASCULAR SMOOTH-MUSCLE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GENE EXPRESSION; MOLECULAR; CARDIOVASCULAR; CELL GROWTH ID MESSENGER-RNA EXPRESSION; HEAVY-CHAIN ISOFORMS; ALPHA-ACTIN; CELLS; CLONING; RAT; HYPERTROPHY; DIVERSITY; PROTEINS; DENSITY AB Ribonuclease protection assays were used to measure expression of smooth muscle (SM) specific myosin heavy chain (MHC) isoforms SM1 (204 kDa) and SM2 (200 kDa) and also nonmuscle MHC-A in cultured smooth muscle cells isolated from rat aorta. In cells grown in 10% serum for 3-5 days until subconfluent, SM1 MHC mRNA decreased by 30% and SM2 MHC mRNA decreased by 80%. In cells grown in confluency for 7-11 days, SM1 MHC mRNA decreased by 45% and SM2 MHC mRNA decreased by 80%. Similar reductions were found in passaged cells. Serum withdrawal for 1-2 days from confluent cultures had little or no effect on SM1 or SM2 MHC mRNA levels. In contrast, nonmuscle MHC-A mRNA increased 10-fold in subconfluent cultures but increased only threefold higher than controls in quiescent cells. Myosin protein analysis using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting indicated that SM1 MHC protein was detectable at a reduced level in confluent cultured cells, whereas SM2 MHC protein was absent in confluent cells. The decrease in SM2 was much greater than SM1, indicating differential regulation. An apparently new isoform of SM1 MHC migrating with a mobility similar to SM2 type MHC was detected by immunoblot analysis in cultured cells. C1 UNIV VERMONT,COLL MED,DEPT PHYSIOL & BIOPHYS,GIVEN BLDG,BURLINGTON,VT 05405. UNIV VERMONT,COLL MED,DEPT MICROBIOL & MOLEC GENET,BURLINGTON,VT 05405. NHLBI,BETHESDA,MD 20892. FU PHS HHS [R29-38355] NR 25 TC 48 Z9 48 U1 0 U2 6 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP C607 EP C613 PN 1 PG 7 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200009 PM 1550206 ER PT J AU HOMSHER, E WANG, F SELLERS, JR AF HOMSHER, E WANG, F SELLERS, JR TI FACTORS AFFECTING MOVEMENT OF F-ACTIN FILAMENTS PROPELLED BY SKELETAL-MUSCLE HEAVY-MEROMYOSIN SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MOTILITY ASSAYS; MOTION ANALYSIS; SHORTENING VELOCITY ID MYOSIN STEP SIZE; SHORTENING VELOCITY; SMOOTH-MUSCLE; TEMPERATURE-DEPENDENCE; SLIDING MOVEMENT; INVITRO MOTILITY; IONIC-STRENGTH; FIBERS; PHOSPHATE; CONTRACTION AB The measurement of fluorescent-labeled actin filament movement driven by mechanoenzymes (e.g., myosin) is an important methodology for the study of molecular motors. It is assumed that the filament velocity (V(f)) is analogous to the unloaded shortening velocity (V(u)) seen in muscle fibers. Methods are described to reproducibly quantitate the movement of these filaments and to select uniformly moving filaments and specify their V(f). Use of these techniques allowed comparison of V(f) to literature values for V(u) with regard to [ATP], [ADP], [P(i)], pH, ionic strength (10-150 mM), and temperature (15-30-degrees-C). V(f) and V(u) are quantitatively similar with respect to the effects of substrate and product concentrations and temperatures > 20-degrees-C. However, V(f) is more sensitive to decreases in pH and temperatures < 20-degrees-C than V(u). At ionic strengths of 50-150 mM, V(f) and V(u) exhibit similar ionic strength dependencies (decreasing with ionic strength). At ionic strengths < 50 mM, V(f) is markedly reduced. Results of experiments using adenosine 5'-O-(3-thiotriphosphate) suggest that increasing the number of weakly bound cross bridges does not seriously affect V(f). Thus, although V(f) is a good analogue for V(u) under certain conditions (elevated ionic strength and temperatures > 20-degrees-C), under others it is not. The results of motility assays must be cautiously interpreted. C1 NHLBI,CELLULAR & MOLEC MOTIL SECT,MOLEC CARDIOL LAB,BETHESDA,MD 20892. RP HOMSHER, E (reprint author), UNIV CALIF LOS ANGELES,CTR HLTH SCI,SCH MED,DEPT PHYSIOL,LOS ANGELES,CA 90024, USA. FU NIAMS NIH HHS [AR-30988] NR 34 TC 121 Z9 121 U1 1 U2 6 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP C714 EP C723 PN 1 PG 10 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200023 PM 1550212 ER PT J AU SMARDO, FL BURG, MB GARCIAPEREZ, A AF SMARDO, FL BURG, MB GARCIAPEREZ, A TI KIDNEY ALDOSE REDUCTASE GENE-TRANSCRIPTION IS OSMOTICALLY REGULATED SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE OSMOTIC STRESS; OSMOLYTES; SORBITOL; BETAINE; STRESS PROTEINS ID RENAL MEDULLARY CELLS; ACTIVE RIBONUCLEIC-ACID; NACL; RNA; STRESS; INDUCTION AB Cells generally adapt to long-term hypertonic stress by accumulating organic osmolytes. PAP-HT25 renal medullary cells in hypertonic medium accumulate sorbitol through a reaction catalyzed by aldose reductase and betaine through osmotically regulated transport. Hypertonicity increases aldose reductase protein synthesis rate by elevating its mRNA abundance. To test whether the rise in aldose reductase mRNA is due to enhanced transcription, PAP-HT25 cells adapted to isotonic medium were switched to hypertonic medium, and transcription rate was measured by nuclear run-on. Aldose reductase transcription rate peaked at 17-fold the isotonic level after 12 h of hypertonicity. Then, transcription fell as sorbitol and betaine accumulated. Transcription stabilized at fivefold the isotonic level within days. Aldose reductase mRNA stability was not significantly different between the hypertonic and isotonic steady states. Thus aldose reductase mRNA is osmotically regulated through changes in its transcription. The osmotically induced rise in aldose reductase transcription is blunted by the accumulation of intracellular betaine and is exaggerated and prolonged by preventing the accumulation of both sorbitol (by aldose reductase inhibition) and betaine (by removal from the medium). This study presents the first description of osmoregulated gene transcription in animal cells. C1 NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BLDG 10,ROOM 6N307,BETHESDA,MD 20892. NR 23 TC 131 Z9 131 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP C776 EP C782 PN 1 PG 7 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200030 PM 1550215 ER PT J AU KIM, YA KING, MT TEAGUE, WE RUFO, GA VEECH, RL PASSONNEAU, JV AF KIM, YA KING, MT TEAGUE, WE RUFO, GA VEECH, RL PASSONNEAU, JV TI REGULATION OF THE PURINE SALVAGE PATHWAY IN RAT-LIVER SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PURINE METABOLISM; RIBOSE 5-PHOSPHATE AND PURINES; PHOSPHORIBOSYLPYROPHOSPHATE AND PURINES ID PHOSPHORIBOSYL PYROPHOSPHATE; NUCLEOTIDE PRODUCTION; HUMAN-ERYTHROCYTES; AD-LIBITUM; ETHANOL; PURIFICATION; HYPOXANTHINE; STIMULATION; SYNTHETASE; ACETATE AB The regulation of purine metabolism in rat liver has been examined under conditions that alter the flux through the pathway. Rats were given intraperitoneal injections of ethanol, sodium acetate, or sodium phosphate to attain body water concentrations of approximately 70, 20, and 10 mM, respectively. The livers were freeze-clamped after 30 min, and extracts were made for the analysis of metabolites, cofactors, purine bases, and nucleosides; homogenates were made for the measurement of the activities and kinetic parameters of seven enzymes that participate in purine salvage. The values of the equilibrium constants of nine reactions were determined in vitro and compared with the ratios of the reactants measured in liver. The changes in phosphoribosylpyrophosphate (PRPP), a key intermediate in both the de novo and salvage pathways of purine metabolism, were directly correlated with the changes in ribose 5-phosphate (ribose-5-P); ([PRPP] = 1.7[ribose-5-P] - 7.4-mu-mol/kg). Ribose-5-P concentrations in turn could be predicted from the liver content of fructose 6-phosphate and glyceraldehyde 3-phosphate by calculation from the known equilibria. The maximum velocities in the tissue of the seven enzymes measured were calculated from the measured substrate values in the liver and with consideration of other effectors of enzyme activity. PRPP synthetase was the least active of the enzymes measured, indicating a possible rate-limiting step. The DELTA-G of the enzyme steps differed from equilibrium values by factors ranging from 4 (nucleoside phosphorylase) to 10(5) (PRPP synthetase and purine transferase reactions). The regulation of purine salvage appeared to depend on the levels of PRPP and ribose-5-P. C1 NIAAA,METAB & MOLEC BIOL LAB,12501 WASHINGTON AVE,ROCKVILLE,MD 20852. NR 38 TC 26 Z9 26 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP E344 EP E352 PN 1 PG 9 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200048 PM 1372483 ER PT J AU GU, ZF PRADHAN, T COY, DH MANTEY, S BUNNETT, NW JENSEN, RT MATON, PN AF GU, ZF PRADHAN, T COY, DH MANTEY, S BUNNETT, NW JENSEN, RT MATON, PN TI ACTIONS OF SOMATOSTATINS ON GASTRIC SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ADENOSINE 3',5'-CYCLIC MONOPHOSPHATE; REGULATORY G-PROTEINS; MUSCLE CONTRACTION; VASOACTIVE INTESTINAL PEPTIDE; MUSCLE RELAXATION ID PITUITARY-TUMOR-CELLS; HORMONE-RELEASING FACTOR; GUINEA-PIG STOMACH; CYCLIC-AMP; GROWTH-HORMONE; ADENYLATE-CYCLASE; PERTUSSIS TOXIN; INHIBITION; SECRETION; RECEPTORS AB The effects of somatostatin-28, somatostatin-14, and a synthetic somatostatin octapeptide analogue, D-Phe-Cys-Tyr-D-Trp-Lys-Thr-Cys-Nal-NH2 (cyclo SS-8) were examined on contraction of dispersed gastric smooth muscle cells from guinea pigs. The somatostatins did not cause contraction of gastric smooth muscle cells, nor did they inhibit carbachol-stimulated contraction. However, they reversed vasoactive intestinal peptide (VIP)-induced inhibition (relaxation) of carbachol-stimulated contraction. Somatostatin-28 had a half-maximal effect (EC50) at 1.6 +/- 0.8 nM, cyclo SS-8 at 0.6 +/- 0.3 nM, but somatostatin-14 had no effect even when used in concentrations as high as 1-mu-M. Incubation of muscle cells with peptidase inhibitors phosphoramidon (1-mu-M) plus amastatin (10-mu-M) had no effect on the EC50 of somatostatin-28 or cyclo SS-8 but increased the potency of somatostatin-14 > 1,000-fold. When peptides were incubated with muscle cells and the products applied to high-performance liquid chromatography, cyclo SS-8 was not degraded, but somatostatin-14 was rapidly degraded when present alone, and the addition of peptidase inhibitors partially inhibited the degradation. Cyclo SS-8 had its maximal effect at 0.5-1 min and inhibited relaxation induced by VIP, isoproterenol, glucagon, or dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP). Cyclo SS-8 partially inhibited the increase in VIP-stimulated cAMP. Preincubation with pertussis toxin blocked the inhibitory action of cyclo SS-8 on VIP or DBcAMP-induced relaxation. These results indicate that gastric smooth muscle cells rapidly degrade somatostatin-14 and suggest that muscle cell peptidases could have a major effect on the actions of somatostatin-14. Furthermore, gastric muscle cells possess somatostatin receptors, occupation of which inhibits relaxation induced by a variety of agents. Somatostatins act both through the guanine nucleotide regulatory protein G(i) to inhibit adenylate cyclase and at sites distal to the generation of cAMP. C1 NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT SURG,SAN FRANCISCO,CA 94143. TULANE UNIV,MED CTR,DEPT MED,PEPTIDE RES LABS,NEW ORLEANS,LA 70112. FU NCI NIH HHS [CA-45153]; NIDDK NIH HHS [DK-39957] NR 35 TC 26 Z9 26 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP G432 EP G438 PN 1 PG 7 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200059 PM 1347975 ER PT J AU MELVIN, JE TURNER, RJ AF MELVIN, JE TURNER, RJ TI CL- FLUXES RELATED TO FLUID SECRETION BY THE RAT PAROTID - INVOLVEMENT OF CL--HCO3- EXCHANGE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE SALIVARY GLANDS; EXOCRINE SECRETION; ANION EXCHANGE; SODIUM-POTASSIUM-CHLORIDE COTRANSPORT ID RABBIT SALIVARY-GLAND; INDUCED INTRACELLULAR ACIDOSIS; BASOLATERAL MEMBRANE-VESICLES; ACINAR-CELLS; NA+/H+ EXCHANGE; ION-TRANSPORT; ACTIVATION; COTRANSPORT; MECHANISMS; CALCIUM AB Muscarinic-induced Cl-36- and Rb-86+ (K+ substitute) fluxes were studied in rat parotid acini. Stimulation resulted in a rapid [half time (t1/2) < 30 s] decrease in both Cl- and Rb+ content (approximately 50 and 30%, respectively) followed by a slower partial recovery (t1/2 approximately 3-4 min) to approximately 80% of resting levels for both ions. Cl- loss was inhibited by the venom of Leiurus quinquestriatus, which contains the maxi-K+ channel blocker charybdotoxin. Cl- recovery was blunted in the presence of bumetanide, an inhibitor of Na+-K+-Cl- co-transport, or on HCO3- removal and was completely blocked in the presence of bumetanide and 4,4' diisothiocyanostilbene-2,2' disulfonic acid (DIDS), an inhibitor of Cl--HCO3- exchange. In HCO3--containing medium a rapid (t1/2 < 1 min), DIDS-inhibitable cytoplasmic alkalinization (approximately 0.4 pH unit) was observed in acini switched to a Cl--free solution. This alkalinization was not seen in HCO3--free medium but persisted in the absence of Na+, consistent with the presence of a potent Na+-independent Cl--HCO3- exchanger. Kinetic studies indicated that the half-maximal effect of this exchanger for extracellular Cl- was approximately 18 mM. These results are consistent with the hypothesis that secretagogue-induced KCl loss by salivary acinar cells occurs via electrically coupled K+ and Cl- channels. In addition, they provide strong evidence that Cl- entry into, and thus fluid secretion by, these cells is mediated by both Cl--HCO3- exchange and Na+-K+-Cl- cotransport. C1 NIDR,CLIN INVEST,BETHESDA,MD 20892. UNIV ROCHESTER,DEPT NEUROBIOL & ANAT,ROCHESTER,NY 14642. NIDR,PATIENT CARE BRANCH,BETHESDA,MD 20892. RP MELVIN, JE (reprint author), UNIV ROCHESTER,DEPT DENT RES,601 ELMWOOD AVE,BOX 611,ROCHESTER,NY 14642, USA. FU NIDCR NIH HHS [R01 DE-09692, R01 DE-08921] NR 30 TC 38 Z9 39 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP G393 EP G398 PN 1 PG 6 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200054 PM 1312791 ER PT J AU ZHANG, L GU, ZF PRADHAN, T JENSEN, RT MATON, PN AF ZHANG, L GU, ZF PRADHAN, T JENSEN, RT MATON, PN TI CHARACTERIZATION OF OPIOID RECEPTORS ON SMOOTH-MUSCLE CELLS FROM GUINEA-PIG STOMACH SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE AGONIST; ANTAGONISTS; PEPTIDES; MUSCLE CONTRACTION ID SITE-DIRECTED ALKYLATION; CANINE SMALL-INTESTINE; OPIATE RECEPTORS; BINDING-SITES; KAPPA-SUBTYPE; BRAIN; CONTRACTION; ANTAGONISTS; SELECTIVITY; PEPTIDES AB On the basis of opioid-stimulated contraction of dispersed gastric smooth muscle cells it has been suggested that these cells possess opioid receptors of three subtypes: kappa (kappa), mu (mu), and delta (delta). We have used selective peptidase-resistant radioligands, agonists and antagonists, to examine receptor subtypes on dispersed gastric smooth muscle cells from guinea pigs prepared by collagenase digestion. The kappa-agonist U-50488H, the mu-agonist [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAGO), and the delta-agonist [D-Pen2,Pen5]enkephalin (DPDPE) each caused muscle contraction. The concentrations required to caused half-maximal contraction were U50488H (6 pM) > DAGO (13 pM) > DPDPE (6 nM). The abilities of these agonists to inhibit binding of [H-3]U-69593 (kappa-preferring) by 50% were U50488H (43 nM) > DAGO (43-mu-M) > DPDPE (200-mu-M). Their abilities to inhibit binding of [H-3]naloxone (mu-preferring) by 50% were DAGO (0.2-mu-M) > U50488H (10-mu-M) > DPDPE (> 100-mu-M). No binding could be detected with the delta-selective ligand [H-3]DPDPE. The kappa-preferring antagonist Mr2266 (10 nM) preferentially inhibited contraction stimulated by the kappa-agonist U50488H, and naltrexone (10 nM) (mu-selective antagonist) preferentially inhibited contraction stimulated by the mu-agonist DAGO. ICI 174864 (200-mu-M; delta-selective antagonist) had no effect on contraction stimulated by mu-, kappa-, or delta-agonists. Contraction stimulated by the delta-agonist DPDPE was inhibited by both kappa- and mu-receptor antagonists. Studies on the effect of the antagonists on binding of [H-3]naloxone and [H-3]-U69593 also provided evidence for kappa- and mu-sites but not for delta-sites. These data demonstrate that gastric smooth muscle cells possess kappa- and mu-receptors, occupation of which causes muscle contraction, but no delta-receptors could be detected by these methods. C1 NIDDK,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 37 TC 8 Z9 8 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP G461 EP G469 PN 1 PG 9 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200063 PM 1312793 ER PT J AU DENNIS, D JACOBSON, K BELARDINELLI, L AF DENNIS, D JACOBSON, K BELARDINELLI, L TI EVIDENCE OF SPARE ADENOSINE-A1-RECEPTORS IN GUINEA-PIG ATRIOVENTRICULAR NODE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ADENOSINE ANTAGONISTS; COUPLING MECHANISM; PHYSIOLOGICAL RESERVE ID A1 ADENOSINE RECEPTORS; RADIOLIGAND-BINDING; ADENYLATE-CYCLASE; BRAIN MEMBRANES; AGONIST; ACTIVATION; SOLUBILIZATION; ANTAGONISTS; CONDUCTION; MYOCYTES AB In normoxic, isolated perfused guinea pig hearts instrumented for measurement of atrioventricular nodal conduction time (AVCT), an analysis utilizing the irreversible A1-adenosine (Ado) antagonist, meta-1,3-phenylene diisothiocyanate xanthine amine cogener (m-DITC-XAC), a novel isothiocyanate derivative of 1,3-dialkylxanthine, was used to investigate whether spare A1-Ado receptors exist in the guinea pig atrioventricular (AV) node and the degree of amplification (reserve) between A1-Ado receptor occupancy and dromotropic response (e.g., AVCT slowing). The potency, dose dependency, and kinetic profile (time dependence of washout and washin) of m-DITC-XAC was determined and compared with those of known competitive (reversible) A1-Ado receptor antagonists. In the presence of m-DITC-XAC, Ado and N6-cyclopentyladenosine (CPA) produced submaximal dromotropic responses. In a series of 19 hearts, m-DITC-XAC caused 100% apparent antagonism of the effect of Ado on AVCT even after 60 min of washout. In contrast, > 90% of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) and XAC-induced antagonism of the effect of Ado on AVCT dissipated within 35 min. Unlike XAC, which caused maximal attenuation of Ado's AVCT effect within 5 min and remained constant thereafter, m-DITC-XAC showed marked time- and concentration-dependent behavior. It was found that 5 min of 0.5-mu-M m-DITC-XAC pretreatment irreversibly inactivated 72% of the A1-Ado receptors mediating the dromotropic effect, and the estimated agonist equilibrium dissociation constant for CPA was 84 +/- 4 nM. The percent of spare A1-Ado receptors at the EC50 and extrapolated maximal S-H interval prolongation levels was 20 and 54%, respectively, and the reserve (coupling amplification) varied from 1 to 2.3 within the 0-50% maximal response range. In summary, m-DITC-XAC appears to specifically and irreversibly antagonize the negative dromotropic effect of Ado and CPA, and guinea pig AV nodal tissue possesses spare A1-Ado receptors. C1 UNIV FLORIDA,COLL MED,DEPT MED,BOX J-277,JHMHC,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT PHARMACOL,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT ANESTHESIOL,GAINESVILLE,FL 32610. NIDDKD,CHEM LAB,BETHESDA,MD 20892. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU NHLBI NIH HHS [HL-35272] NR 33 TC 27 Z9 27 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP H661 EP H671 PN 2 PG 11 WC Physiology SC Physiology GA HK364 UT WOS:A1992HK36400007 PM 1558173 ER PT J AU GORDON, CT RAPOPORT, JL HAMBURGER, SD STATE, RC MANNHEIM, GB AF GORDON, CT RAPOPORT, JL HAMBURGER, SD STATE, RC MANNHEIM, GB TI DIFFERENTIAL RESPONSE OF 7 SUBJECTS WITH AUTISTIC DISORDER TO CLOMIPRAMINE AND DESIPRAMINE SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; CHILDREN AB Objective: Clomipramine, a serotonin reuptake blocker that has unique antiobsessional properties, was hypothesized to have a different effect from that of desipramine, a tricyclic antidepressant with selective adrenergic effects, for the stereotyped, repetitive behaviors in autism. Method: Seven subjects, ages 6-18 years, with autistic disorder completed a 10-week double-blind, crossover trial of clomipramine and desipramine following a 2-week single-blind, placebo phase. Results: Clomipramine was superior to desipramine and placebo, as indicated by standardized ratings of autism and anger as well as ratings of repetitive and compulsive behaviors. Clomipramine and desipramine were equally superior to placebo for ratings of hyperactivity. Parents of all seven subjects elected to have their children continue to take clomipramine after the study. Conclusions: Clomipramine and desipramine are differentially effective in treating the obsessive-compulsive and core symptoms in autistic disorder. Biological links between compulsions and stereotyped, repetitive behaviors in autistic disorder should be explored. RP GORDON, CT (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,RM 6N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 20 TC 75 Z9 75 U1 2 U2 5 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAR PY 1992 VL 149 IS 3 BP 363 EP 366 PG 4 WC Psychiatry SC Psychiatry GA HG195 UT WOS:A1992HG19500010 PM 1536276 ER PT J AU WILCOX, AJ SKJOERVEN, R AF WILCOX, AJ SKJOERVEN, R TI BIRTH-WEIGHT AND PERINATAL-MORTALITY - THE EFFECT OF GESTATIONAL-AGE SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article AB Background. The strong association between birth weight and perinatal mortality is due both to gestational age and to factors unrelated to gestational age. Conventional analysis obscures these separate contributions to perinatal mortality, and over-emphasizes the role of birth weight. An alternative approach is used here to separate gestational age from other factors. Methods. Data are from 400 000 singleton births in the Norwegian Medical Birth Registry. The method of Wilcox and Russell is used to distinguish the contributions to perinatal mortality made by gestational age and by relative birth weight at each gestational age. Results. Gestational age is a powerful predictor of birth weight and perinatal survival. After these effects of gestational age are controlled for, relative birth weight retains a strong association with survival. Conclusions. Current public health policies in the United States emphasize the prevention of low birth weight. The present analysis suggests that the prevention of early delivery would benefit babies of all birth weights. C1 UNIV BERGEN, MED INFORMAT & STAT SECT, N-5014 BERGEN, NORWAY. RP WILCOX, AJ (reprint author), NIEHS, EPIDEMIOL BRANCH, POB 12233, RES TRIANGLE PK, NC 27709 USA. OI Wilcox, Allen/0000-0002-3376-1311 NR 14 TC 147 Z9 153 U1 0 U2 1 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD MAR PY 1992 VL 82 IS 3 BP 378 EP 382 DI 10.2105/AJPH.82.3.378 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HL802 UT WOS:A1992HL80200009 PM 1536353 ER PT J AU OVERPECK, MD HOFFMAN, HJ PRAGER, K AF OVERPECK, MD HOFFMAN, HJ PRAGER, K TI THE LOWEST BIRTH-WEIGHT INFANTS AND THE UNITED-STATES INFANT-MORTALITY RATE - NCHS 1983 LINKED BIRTH INFANT DEATH DATA SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Note ID NEONATAL-MORTALITY; SURVEILLANCE; POPULATIONS; CALIFORNIA; GROWTH AB The National Center for Health Statistics Linked Birth and Infant Death Data Set, 1983 birth cohort, shows that infants weighing less than 750 g, comprising only 0.3% of all births, account for 25% of deaths in the first year of life and for 41% of deaths in the first week. If interventions had prevented the death of these very small babies, the infant mortality rate would have been 8.3 per 1000 live births instead of 10.9, and the Black/White mortality differential would have been reduced by 25%. C1 CTR DIS CONTROL, HYATTSVILLE, MD USA. RP OVERPECK, MD (reprint author), NICHHD, DIV EPIDEMIOL STAT & PREVENT RES, EXECUT PLAZA N, ROOM 640, BETHESDA, MD 20892 USA. NR 40 TC 35 Z9 35 U1 0 U2 1 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD MAR PY 1992 VL 82 IS 3 BP 441 EP 444 DI 10.2105/AJPH.82.3.441 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HL802 UT WOS:A1992HL80200023 PM 1536365 ER PT J AU MALLOY, MH KAO, TC LEE, YJ AF MALLOY, MH KAO, TC LEE, YJ TI ANALYZING THE EFFECT OF PRENATAL-CARE ON PREGNANCY OUTCOME - A CONDITIONAL APPROACH SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Note ID GESTATIONAL-AGE; BIRTH-WEIGHT AB We used vital statistics data to examine the effect of the time of entry into prenatal care relative to the gestational age of delivery on pregnancy outcome. Early entry into prenatal care was associated with better outcomes only in women who delivered at 37 through 42 weeks of gestation. We are concerned that the evaluation of the effect of prenatal care using vital statistics data may be questionable because of the problems inherent in the data. C1 NICHHD,DIV PREVENT RES,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT PREVENT MED & BIOMETR,BETHESDA,MD 20814. NR 9 TC 13 Z9 14 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD MAR PY 1992 VL 82 IS 3 BP 448 EP 450 DI 10.2105/AJPH.82.3.448 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HL802 UT WOS:A1992HL80200025 PM 1536367 ER PT J AU PATTERSON, BH BLOCK, G AF PATTERSON, BH BLOCK, G TI PATTERSON AND BLOCK RESPOND SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Letter RP PATTERSON, BH (reprint author), NCI,DIV CANC PREVENT & CONTROL,EXECUT PLAZA N,SUITE 344,BETHESDA,MD 20892, USA. RI Block, Gladys/E-3304-2010 NR 3 TC 3 Z9 3 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD MAR PY 1992 VL 82 IS 3 BP 466 EP 466 DI 10.2105/AJPH.82.3.466 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HL802 UT WOS:A1992HL80200035 ER PT J AU ABRUZZO, LV JAFFE, ES COTELINGAM, JD WHANGPENG, J DELDUCA, V MEDEIROS, LJ AF ABRUZZO, LV JAFFE, ES COTELINGAM, JD WHANGPENG, J DELDUCA, V MEDEIROS, LJ TI T-CELL LYMPHOBLASTIC LYMPHOMA WITH EOSINOPHILIA ASSOCIATED WITH SUBSEQUENT MYELOID MALIGNANCY SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE LYMPHOBLASTIC LYMPHOMA; EOSINOPHILIA; T-CELL IMMUNOPHENOTYPE; ACUTE MYELOID LEUKEMIA ID ACUTE MYELOBLASTIC-LEUKEMIA; COLONY-STIMULATING FACTOR; GENE; HETEROGENEITY; TRANSLOCATION; DISEASE AB Three patients with T-cell lymphoblastic lymphoma and peripheral blood eosinophilia are reported. At the time of diagnosis, all patients had lymphadenopathy, and one had a mediastinal mass. Lymph node biopsies revealed lymphoblastic lymphoma admixed with a variable number of mature eosinophils. Immunophenotypic studies demonstrated that each lymphoma had an immature T-cell immunophenotype. Bone marrow biopsies were hypercellular with myeloid hyperplasia and eosinophilia but were negative for lymphoma. All patients received multiagent chemotherapy; one patient achieved a complete remission, and two patients had partial remissions. All patients subsequently developed a myeloid malignancy. Two died of acute myeloid leukemia within 18 months of the diagnosis of lymphoblastic lymphoma. The third patient relapsed with a lymphoma that had histologic and immunophenotypic features of both T-cell lymphoblastic lymphoma and granulocytic sarcoma and also developed a poorly defined myeloproliferative disorder. These findings suggest that T-cell lymphoblastic lymphoma associated with eosinophilia may represent a distinct clinico-pathologic entity with a high risk of subsequent myeloid neoplasia. C1 NCI, PATHOL LAB, HEMATOPATHOL SECT, BLDG 10, ROOM 2N108, BETHESDA, MD 20892 USA. NCI, DIV CHEMOTHERAPY, MED BRANCH, BETHESDA, MD 20892 USA. NATL NAVAL MED CTR, DEPT LAB MED, BETHESDA, MD 20814 USA. MED CTR DELAWARE, DEPT HEMATOL, NEWARK, DE USA. NR 28 TC 83 Z9 89 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD MAR PY 1992 VL 16 IS 3 BP 236 EP 245 DI 10.1097/00000478-199203000-00003 PG 10 WC Pathology; Surgery SC Pathology; Surgery GA HF371 UT WOS:A1992HF37100003 PM 1599015 ER PT J AU CHANG, K PAI, LH PASS, H POGREBNIAK, HW TSAO, MS PASTAN, I WILLINGHAM, MC AF CHANG, K PAI, LH PASS, H POGREBNIAK, HW TSAO, MS PASTAN, I WILLINGHAM, MC TI MONOCLONAL-ANTIBODY K1 REACTS WITH EPITHELIAL MESOTHELIOMA BUT NOT WITH LUNG ADENOCARCINOMA SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE MESOTHELIOMA; MAB K1; ADENOCARCINOMA; LUNG ID MALIGNANT MESOTHELIOMA; CARCINOEMBRYONIC ANTIGEN; PULMONARY ADENOCARCINOMA; DISTINCTION; CARCINOMA; CHILDHOOD; FEATURES; TUMORS AB Immunoperoxidase histochemical staining of cryostat sections from human tumor tissues revealed that a murine monoclonal antibody (MAb), K1, can distinguish epithelia mesotheliomas from lung adenocarcinomas. All of 15 epithelial-type mesotheliomas and all four mixed type mesothelioma samples, but none of 23 lung adenocarcinomas with different degrees of histologic differentiation demonstrated reactivity with antibody K1. Of the cell populations in each mesothelioma tested, 80% to 100% showed strong and homogeneous staining with MAb K1. Immunofluorescence analysis of live cultured cells from an epithelioid mesothelioma (H-meso) and several lung carcinoma cell tines as well as a pleural effusion of a patient with mesothelioma also showed selective reactivity of K1 with the mesothelioma cells. These data indicate that K1 can be useful as a mesothelial cell marker for the differential pathological diagnosis of the epithelial form of mesothelioma; K1 may also be useful in the study of the pathogenesis, immunodiagnosis, and immunotherapy of epithelial-type and mixed-type human malignant mesothelioma. C1 NCI,MOLEC BIOL LAB,BLDG 37,ROOM 4E16,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. MONTREAL GEN HOSP,DEPT PATHOL,MONTREAL H3G 1A4,QUEBEC,CANADA. NR 35 TC 108 Z9 111 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD MAR PY 1992 VL 16 IS 3 BP 259 EP 268 DI 10.1097/00000478-199203000-00006 PG 10 WC Pathology; Surgery SC Pathology; Surgery GA HF371 UT WOS:A1992HF37100006 PM 1599018 ER PT J AU SANDER, CA JAFFE, ES GEBHARDT, FC YANO, T MEDEIROS, LJ AF SANDER, CA JAFFE, ES GEBHARDT, FC YANO, T MEDEIROS, LJ TI MEDIASTINAL LYMPHOBLASTIC LYMPHOMA WITH AN IMMATURE B-CELL IMMUNOPHENOTYPE SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE MEDIASTINUM; MALIGNANT LYMPHOMA; LYMPHOBLASTIC LYMPHOMA; B-CELL LINEAGE ID HUMAN THYMUS; T-CELL; LEUKEMIA; TRANSFERASE AB A 19-year-old woman presented with a large mediastinal mass, histologically shown to be malignant lymphoma of lymphoblastic type (LBL). Immunophenotypic and gene rearrangement analysis unequivocally demonstrated that the neoplasm was of B-cell lineage. The neoplastic cells expressed terminal deoxynucleotidyl transferase, the pan-B cell antigens CD19, CD20, and CD22, and were negative for immunoglobulins and numerous T-cell antigens tested. Southern blot analysis showed rearrangement of one allele of the immunoglobulin heavy chain gene while the immunoglobulin-kappa and T-cell receptor beta-chain genes were in the germline configuration. Thus, the immunophenotypic and molecular findings in this case correspond to an early stage of B-cell differentiation, the pre-pre B-cell stage as has been named by others. In contrast with LBL of immature T-cell lineage, precursor B-cell LBLs involving the mediastinum are truly rare. Occasional cases have been reported that have arisen elsewhere and subsequently involved the mediastinum at time of relapse or tumor progression. Well-documented examples of immature B-cell LBL arising in the mediastinum are virtually unreported. The site and cell population giving rise to this neoplasm is unknown. However, origin from precursors of normal thymic medullary B cells is proposed as one possibility. C1 FRANKLIN SQ HOSP,DEPT PATHOL,BALTIMORE,MD 21237. RP SANDER, CA (reprint author), NCI,PATHOL LAB,HEMATOPATHOL SECT,BLDG 10,ROOM 2N109,BETHESDA,MD 20892, USA. NR 20 TC 23 Z9 24 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD MAR PY 1992 VL 16 IS 3 BP 300 EP 305 DI 10.1097/00000478-199203000-00011 PG 6 WC Pathology; Surgery SC Pathology; Surgery GA HF371 UT WOS:A1992HF37100011 PM 1317999 ER PT J AU COSTA, PT AF COSTA, PT TI SHOCK,NATHAN,W. (1906-1989) - OBITUARY SO AMERICAN PSYCHOLOGIST LA English DT Item About an Individual RP COSTA, PT (reprint author), NIA,BALTIMORE,MD 21224, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0003-066X J9 AM PSYCHOL JI Am. Psychol. PD MAR PY 1992 VL 47 IS 3 BP 423 EP 423 PG 1 WC Psychology, Multidisciplinary SC Psychology GA HG479 UT WOS:A1992HG47900006 ER PT J AU CARIFIO, MS GRACE, WC AF CARIFIO, MS GRACE, WC TI IGNORED DATA ON THE DEVELOPMENT OF PSYCHOLOGY INTERNSHIPS SO AMERICAN PSYCHOLOGIST LA English DT Letter C1 NIDA,ROCKVILLE,MD. RP CARIFIO, MS (reprint author), BARRY UNIV,MIAMI,FL 33161, USA. NR 3 TC 5 Z9 5 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0003-066X J9 AM PSYCHOL JI Am. Psychol. PD MAR PY 1992 VL 47 IS 3 BP 428 EP 428 DI 10.1037//0003-066X.47.3.428.a PG 1 WC Psychology, Multidisciplinary SC Psychology GA HG479 UT WOS:A1992HG47900012 ER PT J AU HENSON, PM BARNES, PJ BANKSSCHLEGEL, SP AF HENSON, PM BARNES, PJ BANKSSCHLEGEL, SP TI PLATELET-ACTIVATING-FACTOR - ROLE IN PULMONARY INJURY AND DYSFUNCTION AND BLOOD ABNORMALITIES SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article C1 NHLBI,DIV LUNG DIS,WESTWOOD BLDG,ROOM 6A15,5333 WESTBARD AVE,BETHESDA,MD 20892. NR 0 TC 33 Z9 34 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD MAR PY 1992 VL 145 IS 3 BP 726 EP 731 PG 6 WC Respiratory System SC Respiratory System GA HH281 UT WOS:A1992HH28100041 PM 1312316 ER PT J AU HENDERSON, DK AF HENDERSON, DK TI THE HIV-INFECTED OR HBV-INFECTED HEALTH-CARE PROVIDER AND SOCIETY PERCEPTION OF RISK - SCIENCE, NONSCIENCE, AND NONSENSE SO ANNALS OF ALLERGY LA English DT Editorial Material RP HENDERSON, DK (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,BETHESDA,MD 20892, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY PI ARLINGTON HTS PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 SN 0003-4738 J9 ANN ALLERGY JI Ann. Allergy PD MAR PY 1992 VL 68 IS 3 BP 197 EP 199 PG 3 WC Allergy SC Allergy GA HK260 UT WOS:A1992HK26000001 PM 1546812 ER PT J AU GOLDFARB, LG BROWN, P HALTIA, M CATHALA, F MCCOMBIE, WR KOVANEN, J CERVENAKOVA, L GOLDIN, L NIETO, A GODEC, MS ASHER, DM GAJDUSEK, DC AF GOLDFARB, LG BROWN, P HALTIA, M CATHALA, F MCCOMBIE, WR KOVANEN, J CERVENAKOVA, L GOLDIN, L NIETO, A GODEC, MS ASHER, DM GAJDUSEK, DC TI CREUTZFELDT-JAKOB DISEASE COSEGREGATES WITH THE CODON-178ASN PRNP MUTATION IN FAMILIES OF EUROPEAN ORIGIN SO ANNALS OF NEUROLOGY LA English DT Article ID GERSTMANN-STRAUSSLER SYNDROME; PRION PROTEIN GENE; SCHEINKER SYNDROME; MISSENSE VARIANT; HUMAN-BRAIN; SCRAPIE; DIAGNOSIS; CODON-200; INSERTION; FRANCE AB We recently discovered an amino acid-altering heterozygous mutation in codon 178 of the PRNP amyloid precursor gene in patients with familial Creutzfeldt-Jakob disease. This mutation is now shown to be associated with the occurrence of disease in 7 unrelated families of Western European origin, among which a total ef 65 members are known to have died from Creutzfeldt-Jakob disease, The mutation was detected in each of 17 tested patients, including at least 1 affected member of each family, and in 16 of 36 of their first-degree relatives, but not in affected families with other mutations, patients with the nonfamilial form of the disease, or 83 healthy control individuals. Linkage analysis in two informative families yielded a lod score of 5.30, which, because no recombinants were found, strongly suggests that codon 178Asn is the actual disease mutation. C1 NINCDS,RECEPTOR BIOCHEM & MOLEC BIOL SECT,BETHESDA,MD 20892. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. UNIV HELSINKI,DEPT PATHOL,SF-00100 HELSINKI 10,FINLAND. UNIV HELSINKI,DEPT NEUROL,SF-00100 HELSINKI 10,FINLAND. HOP LA PITIE SALPETRIERE,NEUROVIROL LAB,F-75651 PARIS 13,FRANCE. RP GOLDFARB, LG (reprint author), NINCDS,CENT NERVOUS SYST STUDIES LAB,BLDG 36,ROOM 5B21,BETHESDA,MD 20892, USA. OI McCombie, W. Richard/0000-0003-1899-0682 NR 44 TC 82 Z9 82 U1 2 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD MAR PY 1992 VL 31 IS 3 BP 274 EP 281 DI 10.1002/ana.410310308 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA HQ121 UT WOS:A1992HQ12100007 PM 1353341 ER PT J AU HAMILTON, JM AF HAMILTON, JM TI BEST TREATMENT FOR COLORECTAL-CANCER AND CONFIRMATORY TRIALS - REPLY SO ANNALS OF ONCOLOGY LA English DT Letter RP HAMILTON, JM (reprint author), NCI,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD MAR PY 1992 VL 3 IS 3 BP 245 EP 246 PG 2 WC Oncology SC Oncology GA HK849 UT WOS:A1992HK84900021 ER PT J AU DEBOER, DA CLARK, RE AF DEBOER, DA CLARK, RE TI IRON CHELATION IN MYOCARDIAL PRESERVATION AFTER ISCHEMIA-REPERFUSION INJURY - THE IMPORTANCE OF PRETREATMENT AND TOXICITY SO ANNALS OF THORACIC SURGERY LA English DT Article ID FREE-RADICAL SCAVENGERS; SUPEROXIDE-DISMUTASE; HYDROXYL RADICALS; OXYGEN RADICALS; TISSUE-INJURY; RAT-HEART; DEFEROXAMINE; DESFERRIOXAMINE; CARDIOPLEGIA; PROTECTION AB Oxygen-derived free radicals have been implicated in myocardial ischemia-reperfusion injury. It has been proposed that deferoxamine, an iron chelator, improves myocardial preservation by reducing the iron-catalyzed production of the hydroxyl radical. The objectives of this study were to define the appropriate timing of iron chelation therapy and the dose-response properties of deferoxamine. Isolated working rat hearts were subjected to 25 minutes of normothermic global ischemia. Deferoxamine was given as pretreatment (n = 39; doses of 10 or 30 mg/kg), added to cardioplegic solution (n = 43; doses 0.46 to 1.90 mmol/L), or administered upon reperfusion (n = 52; doses 0.15 to 0.76 mmol/L) and compared with saline controls (n = 25). Deferoxamine pretreatment improved survival at each dose from a control value of 44% to 71% and 72% (p < 0.05), respectively. A cardioplegia dose of 0.46 mmol/L improved survival from 48% to 75%. Higher doses reduced survival and implied a toxic effect. Reperfusion therapy did not alter survival. Regardless of time of administration, deferoxamine did not improve ventricular function or adenosine triphosphate levels. Deferoxamine given as pretreatment 1 hour before ischemia at doses of 30 mg/kg, and perhaps as low as 10 mg/kg, significantly improved survival. The addition of deferoxamine to cardioplegic solution was safe and may be protective at approximately 0.50 mmol/L; however, toxicity should be considered at concentrations greater than 0.76 mmol/L. These data support the postulate that iron catalysis is involved in the production of oxygen-derived free radicals during ischemia-reperfusion injury. We conclude that pretreatment before ischemia is an important component of iron chelation therapy in myocardial preservation. C1 NHLBI,SURG BRANCH,BETHESDA,MD 20892. NR 29 TC 40 Z9 40 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD MAR PY 1992 VL 53 IS 3 BP 412 EP 418 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA HH119 UT WOS:A1992HH11900010 PM 1540057 ER PT J AU PECHEUX, MG RUEL, J BORNSTEIN, MH AF PECHEUX, MG RUEL, J BORNSTEIN, MH TI MOTHER AND INFANT IN THE 1ST YEAR - A LONGITUDINAL-STUDY OF 2 TYPES OF INTERACTION SO ANNEE PSYCHOLOGIQUE LA French DT Article DE MOTHER-INFANT INTERACTION; ATTENTION; SCAFFOLDING; SPECIFICITY ID ENVIRONMENTAL ACTION; PERFORMANCE; STABILITY AB Specific relations between some maternal and infant behaviors within the stream of interactions in normal settings are investigated. Dyadic activities, involving only the two interactants, are contrasted with extradyadic activities, involving physical objects. Thirty dyads were videorecorded at home, during common activities, when the infant was 5- and 8-months old. Frequencies of maternal and infant behaviors, directed towards their partners or objects, were derived from the recordings. At both ages maternal activities are organized around two basic behaviors : talk to baby and responsiveness to his behavior. Concerning the infant, his activity is rather global at 5 months but becomes differentiated later. Last, the focusing of infant's attention on objects at 5 months depends on the frequency of maternal attention mobilization, while 8-month-olds are still able to orient and sustain attention without maternal help. Results are discussed in relation with the specificity hypothesis ot maternal scaffolding of infant cognitive development. C1 CNRS,URA 1353,F-75005 PARIS,FRANCE. NICHHD,BETHESDA,MD 20892. RP PECHEUX, MG (reprint author), UNIV PARIS 05,PSYCHOL DEV & EDUC ENFANT LAB,41 RUE GAY LUSSAC,F-75005 PARIS,FRANCE. NR 27 TC 3 Z9 3 U1 0 U2 0 PU PRESSES UNIV FRANCE PI EVRY PA DEPT DES REVUES 14, AVENUE DU BOIS-DE-L'EPINE B.P. 90, 91003 EVRY, FRANCE SN 0003-5033 J9 ANN PSYCHOL JI Annee Psychol. PD MAR PY 1992 VL 92 IS 1 BP 45 EP 58 PG 14 WC Psychology, Multidisciplinary SC Psychology GA HY419 UT WOS:A1992HY41900003 ER PT J AU TAMURA, S KORZEKWA, KR KIMURA, S GELBOIN, HV GONZALEZ, FJ AF TAMURA, S KORZEKWA, KR KIMURA, S GELBOIN, HV GONZALEZ, FJ TI BACULOVIRUS-MEDIATED EXPRESSION AND FUNCTIONAL-CHARACTERIZATION OF HUMAN NADPH-P450 OXIDOREDUCTASE SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID CYTOCHROME P-450 REDUCTASE; NADPH-CYTOCHROME-P-450 OXIDOREDUCTASE; SACCHAROMYCES-CEREVISIAE; NUCLEOTIDE-SEQUENCE; CDNA; IDENTIFICATION; PROTEINS; DOMAIN C1 NCI,MOLEC CARCINOGENESIS LAB,BLDG 37,ROOM 3E24,BETHESDA,MD 20892. NR 21 TC 42 Z9 42 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 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD MAR PY 1992 VL 293 IS 2 BP 219 EP 223 DI 10.1016/0003-9861(92)90388-D PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HD330 UT WOS:A1992HD33000004 PM 1536559 ER PT J AU GOTO, Y SUMIDA, Y FLANAGAN, JE ROBINSON, FW SIMPSON, IA CUSHMAN, SW KONO, T AF GOTO, Y SUMIDA, Y FLANAGAN, JE ROBINSON, FW SIMPSON, IA CUSHMAN, SW KONO, T TI EFFECTS OF FLUORESCEIN ISOTHIOCYANATE ON INSULIN ACTIONS IN RAT ADIPOCYTES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID GLUCOSE-TRANSPORT ACTIVITY; FAT-CELLS; PLASMA-MEMBRANE; APPARENT TRANSLOCATION; EPIDIDYMAL ADIPOCYTES; POTENTIAL MECHANISM; PHOSPHODIESTERASE; STIMULATION; BINDING; ENERGY C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT MOLEC PHYSIOL & BIOPHYS,NASHVILLE,TN 37232. NIDDKD,EXPTL DIABET METAB & NUTR SECT,BETHESDA,MD 20892. FU NIDDK NIH HHS [DK 19925, DK 67025] NR 36 TC 8 Z9 8 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD MAR PY 1992 VL 293 IS 2 BP 224 EP 230 DI 10.1016/0003-9861(92)90389-E PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HD330 UT WOS:A1992HD33000005 PM 1536560 ER PT J AU STEVENS, JR AF STEVENS, JR TI ABNORMAL REINNERVATION AS A BASIS FOR SCHIZOPHRENIA - A HYPOTHESIS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Review ID ADRENAL-STEROID RECEPTORS; TEMPORAL-LOBE EPILEPSY; HORMONE TARGET SITES; POST-MORTEM BRAINS; DOPAMINE-RECEPTORS; NERVOUS-SYSTEM; KAINIC ACID; SYNAPTIC REORGANIZATION; ANATOMICAL DISTRIBUTION; PARAHIPPOCAMPAL GYRUS AB Neuropathologic and neuroimaging studies reveal atrophy or dystrophy of the hippocampal region and enlarged ventricles indicative of tissue loss in many patients with schizophrenia. It is now widely recognized that brain damage can provoke regenerative collateral sprouting of axons, synaptic proliferation, and reorganization, even in the adult mammalian brain. The functional consequences of these plastic regenerative changes are largely unknown; they could be adaptive or cause further impairment. There is evidence of lesion-provoked aberrant synaptic regeneration in epilepsy and Alzheimer's disease. Data suggest that anomalous reinnervation could also have a significant role in the pathophysiology of schizophrenia. Histologic methods to test this hypothesis are in progress. C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. NR 102 TC 114 Z9 115 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD MAR PY 1992 VL 49 IS 3 BP 238 EP 243 PG 6 WC Psychiatry SC Psychiatry GA HG925 UT WOS:A1992HG92500008 PM 1567277 ER PT J AU GOLDBERG, TE TORREY, EF AF GOLDBERG, TE TORREY, EF TI MATCHING FOR EDUCATION IN STUDIES OF SCHIZOPHRENIA - REPLY SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter ID MONOZYGOTIC TWINS DISCORDANT RP GOLDBERG, TE (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. NR 3 TC 5 Z9 5 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD MAR PY 1992 VL 49 IS 3 BP 246 EP 246 PG 1 WC Psychiatry SC Psychiatry GA HG925 UT WOS:A1992HG92500011 ER PT J AU GOLDBERG, TE TORREY, EF WEINBERGER, DR AF GOLDBERG, TE TORREY, EF WEINBERGER, DR TI NEUROPSYCHOLOGICAL PERFORMANCE IN THE UNAFFECTED TWIN - REPLY SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter RP GOLDBERG, TE (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. NR 3 TC 2 Z9 2 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD MAR PY 1992 VL 49 IS 3 BP 247 EP 247 PG 1 WC Psychiatry SC Psychiatry GA HG925 UT WOS:A1992HG92500013 ER PT J AU CHEW, EY WILLIAMS, GA BURTON, TC BARTON, FB REMALEY, NA FERRIS, FL AF CHEW, EY WILLIAMS, GA BURTON, TC BARTON, FB REMALEY, NA FERRIS, FL TI ASPIRIN EFFECTS ON THE DEVELOPMENT OF CATARACTS IN PATIENTS WITH DIABETES-MELLITUS - EARLY TREATMENT DIABETIC-RETINOPATHY STUDY REPORT .16. SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID SENILE CATARACTS AB The Early Treatment Diabetic Retinopathy Study, a randomized clinical trial supported by the National Eye Institute, was designed to assess the effect of photocoagulation and aspirin in 3711 patients with mild to severe nonproliferative or early proliferative diabetic retinopathy. Although the primary goal of the study was to evaluate the effect of photocoagulation and aspirin on diabetic retinopathy, the study also provided an opportunity to evaluate the effects of aspirin on the development of cataract. No evidence showed that aspirin use reduced the risk of development of cataract requiring extraction (4.1% vs 4.3% in patients assigned to aspirin or placebo treatment, respectively; Mantel-Cox P = .77; relative risk, 1.05; 99% confidence interval, 0.73 to 1.51). Aspirin use also did not reduce the risk of less extensive but visually significant lens opacities developing (29.6% vs 28.3%; Mantel-Cox P = .76; relative risk, 0.99; 99% confidence interval, 0.85 to 1.15). Early Treatment Diabetic Retinopathy Study results do not support the hypothesis that aspirin (at a dose of 650 mg/d) reduces the risk of cataract development in this diabetic population. C1 MARYLAND MED RES INST, BALTIMORE, MD USA. MICHIGAN STATE UNIV, E LANSING, MI 48824 USA. MED COLL WISCONSIN, MILWAUKEE, WI 53226 USA. RP CHEW, EY (reprint author), NEI, BIOMETRY & EPIDEMIOL PROGRAM, BLDG 31, ROOM 6A-24, BETHESDA, MD 20892 USA. FU Intramural NIH HHS [Z99 EY999999] NR 22 TC 24 Z9 27 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-9950 EI 1538-3601 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAR PY 1992 VL 110 IS 3 BP 339 EP 342 PG 4 WC Ophthalmology SC Ophthalmology GA HH279 UT WOS:A1992HH27900017 PM 1543449 ER PT J AU WILLIAMS, HJ WARD, JR READING, JC BROOKS, RH CLEGG, DO SKOSEY, JL WEISMAN, MH WILLKENS, RF SINGER, JZ ALARCON, GS FIELD, EH CLEMENTS, PJ RUSSELL, IJ HOCHMAN, RF BOUMPAS, DT MARBLE, DA AF WILLIAMS, HJ WARD, JR READING, JC BROOKS, RH CLEGG, DO SKOSEY, JL WEISMAN, MH WILLKENS, RF SINGER, JZ ALARCON, GS FIELD, EH CLEMENTS, PJ RUSSELL, IJ HOCHMAN, RF BOUMPAS, DT MARBLE, DA TI COMPARISON OF AURANOFIN, METHOTREXATE, AND THE COMBINATION OF BOTH IN THE TREATMENT OF RHEUMATOID-ARTHRITIS - A CONTROLLED CLINICAL-TRIAL SO ARTHRITIS AND RHEUMATISM LA English DT Article ID LOW-DOSE METHOTREXATE; D-PENICILLAMINE; DOUBLE-BLIND; COMBINED CYCLOPHOSPHAMIDE; PULSE METHOTREXATE; HYDROXYCHLOROQUINE; THERAPY; DISEASE; GOLD; SULPHASALAZINE AB Objective. To compare the relative safety and efficacy of auranofin (AUR), methotrexate (MTX), and the combination of both in the treatment of active rheumatoid arthritis (RA). Methods. Three hundred thirty-five patients with active RA were entered into a 48-week, prospective, controlled, double-blind, multicenter trial and were randomly assigned to 1 of 3 treatment groups. Results. Two hundred eleven patients completed the trial. No remissions were seen, and there were no statistically significant differences among the treatment groups in the clinical or laboratory variables measured. Patients taking AUR alone had a slower onset of response than did patients taking MTX alone or in combination. Withdrawals because of adverse drug reactions were slightly more common for those taking combination therapy, but the differences were not statistically significant. Withdrawals because of lack of response were more common for single-drug therapy, with the difference between AUR and the combination reaching statistical significance. No unexpected adverse drug effects were identified, and all reactions resolved without sequelae. Conclusion. Except for fewer withdrawals because of lack of response, combination therapy did not demonstrate any advantage in efficacy over single-drug treatment within the time frame of the study. C1 UNIV UTAH,SCH MED,DEPT INTERNAL MED,SALT LAKE CITY,UT 84112. UNIV UTAH,SCH MED,DEPT FAMILY & PREVENT MED,SALT LAKE CITY,UT 84112. VANDERBILT UNIV,DIV RHEUMATOL & IMMUNOL,NASHVILLE,TN 37240. UNIV ILLINOIS,RHEUMATOL SECT,CHICAGO,IL 60680. UNIV CALIF SAN DIEGO,DIV RHEUMATOL,SAN DIEGO,CA 92103. UNIV WASHINGTON,HARBORVIEW MED CTR,DIV ARTHRIT,SEATTLE,WA 98104. SUNY DOWNSTATE MED CTR,DEPT MED,BROOKLYN,NY 11203. UNIV ALABAMA,DIV CLIN IMMUNOL & RHEUMATOL,BIRMINGHAM,AL 35233. UNIV IOWA,COLL MED,DEPT MED,IOWA CITY,IA 52242. UNIV CALIF LOS ANGELES,SCH MED,DIV RHEUMATOL,LOS ANGELES,CA 90024. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. GUTHRIE CLIN,RHEUMATOL SECT,SAYRE,PA. NIAMSK,BETHESDA,MD. RP WILLIAMS, HJ (reprint author), UNIV UTAH,MED CTR,SCH MED,COOPERAT SYSTEMAT STUDIES RHEUMAT DIS PROGRAM,50 N MED RD,SALT LAKE CITY,UT 84132, USA. FU NIAMS NIH HHS [N01-AR1-2264] NR 52 TC 152 Z9 153 U1 0 U2 5 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD MAR PY 1992 VL 35 IS 3 BP 259 EP 269 DI 10.1002/art.1780350304 PG 11 WC Rheumatology SC Rheumatology GA HG482 UT WOS:A1992HG48200003 PM 1536666 ER PT J AU HIBBS, JR MITTLEMAN, B HILL, P MEDSGER, TA AF HIBBS, JR MITTLEMAN, B HILL, P MEDSGER, TA TI L-TRYPTOPHAN ASSOCIATED EOSINOPHILIC FASCIITIS PRIOR TO THE 1989 EOSINOPHILIA-MYALGIA-SYNDROME OUTBREAK SO ARTHRITIS AND RHEUMATISM LA English DT Article ID INGESTION AB Objective. To investigate the relationship between L-tryptophan (LT) ingestion and eosinophilic fasciitis (EF) occurring prior to the outbreak of eosinophilia-myalgia syndrome in 1989. Methods. Interviews and record reviews of 45 EF case-patients and 126 polymyositis patients (controls) diagnosed prior to 1988. Results. Nine case-patients (20%) and no controls recalled taking LT before onset of the disease (odds ratio = infinity, 95% confidence interval = 8.3-infinity). Among EF case-patients, LT ingestion was associated with dyspnea. Conclusion. LT ingestion was associated with EF prior to the 1989 outbreak of eosinophilia-myalgia syndrome. Lung abnormalities may be a distinguishing feature of LT-mediated illness. C1 UNIV PITTSBURGH,SCH MED,DEPT MED,DIV RHEUMATOL & CLIN IMMUNOL,PITTSBURGH,PA 15261. RP HIBBS, JR (reprint author), NHLBI,CHB,BLDG 10,ROOM 7C-103,BETHESDA,MD 20892, USA. FU NIADDK NIH HHS [AM-21393] NR 14 TC 28 Z9 28 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD MAR PY 1992 VL 35 IS 3 BP 299 EP 303 DI 10.1002/art.1780350308 PG 5 WC Rheumatology SC Rheumatology GA HG482 UT WOS:A1992HG48200007 PM 1536667 ER PT J AU FRIEDMAN, E GORDELADZE, JO GEJMAN, PV MURTAGH, JJ GERTCH, DS TU, T AF FRIEDMAN, E GORDELADZE, JO GEJMAN, PV MURTAGH, JJ GERTCH, DS TU, T TI HYPERTROPHIC CARDIOMYOPATHY - FAILURE TO DEMONSTRATE MUTATIONS IN EXON 13 OF THE CARDIAC BETA-MYOSIN HEAVY-CHAIN GENE SO BASIC RESEARCH IN CARDIOLOGY LA English DT Article DE HYPERTROPHIC CARDIOMYOPATHY; DENATURING GRADIENT GEL ELECTROPHORESIS; CARDIAC BETA-MYOSIN HEAVY CHAIN GENE; POLYMERASE CHAIN REACTION (PCR) ID GRADIENT GEL-ELECTROPHORESIS; SINGLE BASE CHANGES; MOLECULAR-BASIS; DNA; IDENTIFICATION AB Familial hypertrophic cardiomyopathy (FHCM) has been linked to the cardiac beta-myosin heavy-chain (MHC) genes on chromosome 14 (14q1), and a missense mutation within exon 13 of the beta-MHC gene has been implicated in the pathogenesis of the disease. To test whether this constitutional mutation occurs somatically in the myocardium of the sporadic form of the disease, we studied seven patients with familial (n = 3) or sporadic (n = 4) hypertrophic cardiomyopathy (HCM). Amplification of exon 13 of the beta-MHC from paraffin-embedded myocardium using the polymerase chain reaction (PCR) was performed and analysis of the amplified product for migration abnormalities using denaturing gradient gel electrophoresis (DGGE) and direct sequencing of the PCR product were used. Neither patients with HCM nor subjects with dilated cardiomyopathy (DCM) (n = 2) exhibited an aberration within exon 13 of the myocardial beta-MHC. It is concluded that a specific beta-MHC gene mutation is displayed only in a subset of patients with familial disease, thus further emphasizing the notion of genetic heterogeneity. In addition, in the sporadic form of the disease, somatically occurring mutations in this particular exon could not be demonstrated. C1 NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NHLBI,PATHOL BRANCH,BETHESDA,MD 20892. NR 18 TC 0 Z9 0 U1 0 U2 1 PU DR DIETRICH STEINKOPFF VERLAG PI BERLIN 33 PA C/O SPRINGER-VERLAG, HEIDELBERGER PLATZ 3, 1000 BERLIN 33, GERMANY SN 0300-8428 J9 BASIC RES CARDIOL JI Basic Res. Cardiol. PD MAR-APR PY 1992 VL 87 IS 2 BP 106 EP 112 DI 10.1007/BF00801958 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HV387 UT WOS:A1992HV38700002 PM 1590733 ER PT J AU MCMURRY, TJ BRECHBIEL, M KUMAR, K GANSOW, OA AF MCMURRY, TJ BRECHBIEL, M KUMAR, K GANSOW, OA TI CONVENIENT SYNTHESIS OF BIFUNCTIONAL TETRAAZA MACROCYCLES SO BIOCONJUGATE CHEMISTRY LA English DT Article ID MONOCLONAL-ANTIBODIES; LANTHANIDE COMPLEXES; CHELATING AGENT; FUNCTIONALIZED CYCLAM; COVALENT ATTACHMENT; METAL-COMPLEXES; ACETIC ACIDS; Y-90; MACROMOLECULES; CYCLIZATION AB A convenient synthesis of 4-nitrobenzyl-substituted macrocyclic tetraamines and their conversion to bifunctional poly(amino carboxylate) chelating agents is described. Cyclization of (4-nitrobenzyl)-ethylenediamine with appropriate BOC-protected amino disuccinimido esters in dioxane at 90-degrees-C resulted in the formation of 12- and 14-membered ring diamides in 40% and 44% yield, respectively. A 12-membered macrocyclic triamide was also prepared in 44% yield by cyclization of N-(2-aminoethyl)-4-nitrophenylalaninamide with disuccinimidyl N-(tert-butoxycarbonyl)iminodiacetate. Deprotection (HCl/dioxane) and reduction with borane gave the substituted macrocyclic amines which were then alkylated with either bromoacetic acid or tert-butyl bromoacetate. Preparation of the isothiocyanate derivatives and C-14 labeled chelating agents are described. Attempts to prepare a 9-membered macrocyclic diamide using this cyclization technique resulted instead in a 20% yield of a 10:1 mixture of isomeric fused 5,6 ring acylamidines. Deprotection (HCl/dioxane) and reduction with borane gave a substituted piperazine derivative in 55% yield. RP MCMURRY, TJ (reprint author), NCI,RADIAT ONCOL BRANCH,BLDG 10,ROOM B3-B69,BETHESDA,MD 20892, USA. NR 67 TC 111 Z9 112 U1 3 U2 15 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 1043-1802 J9 BIOCONJUGATE CHEM JI Bioconjugate Chem. PD MAR-APR PY 1992 VL 3 IS 2 BP 108 EP 117 DI 10.1021/bc00014a004 PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA HL948 UT WOS:A1992HL94800004 PM 1515464 ER PT J AU GERACIOTI, TD LOOSEN, PT GOLD, PW KLING, MA AF GERACIOTI, TD LOOSEN, PT GOLD, PW KLING, MA TI CORTISOL, THYROID-HORMONE, AND MOOD IN ATYPICAL DEPRESSION - A LONGITUDINAL CASE-STUDY SO BIOLOGICAL PSYCHIATRY LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; DIAGNOSIS; ILLNESS; STRESS C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT PSYCHIAT,NASHVILLE,TN 37232. NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RP GERACIOTI, TD (reprint author), VET ADM MED CTR,PSYCHIAT SERV 116A,1310 24TH AVE S,NASHVILLE,TN 37212, USA. RI Kling, Mitchel/F-4152-2010 OI Kling, Mitchel/0000-0002-2232-1409 NR 17 TC 9 Z9 9 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 1 PY 1992 VL 31 IS 5 BP 515 EP 519 DI 10.1016/0006-3223(92)90262-X PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA HP164 UT WOS:A1992HP16400007 PM 1581426 ER PT J AU HUGHES, MD FREEDMAN, LS POCOCK, SJ AF HUGHES, MD FREEDMAN, LS POCOCK, SJ TI THE IMPACT OF STOPPING RULES ON HETEROGENEITY OF RESULTS IN OVERVIEWS OF CLINICAL-TRIALS SO BIOMETRICS LA English DT Article DE HETEROGENEITY; METAANALYSIS; OVERVIEW; RANDOM EFFECTS; STOPPING RULES ID PUBLICATION BIAS; INTERIM ANALYSES; META-ANALYSIS; DESIGN AB This paper explores the extent to which application of statistical stopping rules in clinical trials can create an artificial heterogeneity of treatment effects in overviews (meta-analyses) of related trials. For illustration, we concentrate on overviews of identically designed group sequential trials, using either fixed nominal or O'Brien and Fleming two-sided boundaries. Some analytic results are obtained for two-group designs and simulation studies are otherwise used, with the following overall findings. The use of stopping rules leads to biased estimates of treatment effect so that the assessment of heterogeneity of results in an overview of trials, some of which have used stopping rules, is confounded by this bias. If the true treatment effect being studied is small, as is often the case, then artificial heterogeneity is introduced, thus increasing the Type I error rate in the test of homogeneity. This could lead to erroneous use of a random effects model, producing exaggerated estimates and confidence intervals. However, if the true mean effect is large, then between-trial heterogeneity may be underestimated. When undertaking or interpreting overviews, one should ascertain whether stopping rules have been used (either formally or informally) and should consider whether their use might account for any heterogeneity found. C1 NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,BETHESDA,MD 20892. RP HUGHES, MD (reprint author), UNIV LONDON LONDON SCH HYG & TROP MED,DEPT EPIDEMIOL & POPULAT SCI,MED STAT UNIT,KEPPEL ST,LONDON WC1E 7HT,ENGLAND. NR 12 TC 27 Z9 27 U1 1 U2 4 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 1992 VL 48 IS 1 BP 41 EP 53 DI 10.2307/2532737 PG 13 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA HR666 UT WOS:A1992HR66600004 PM 1581492 ER PT J AU TROPEA, JE NASHED, NT LOUIS, JM SAYER, JM JERINA, DM AF TROPEA, JE NASHED, NT LOUIS, JM SAYER, JM JERINA, DM TI EFFECT OF SALT ON THE KINETIC-PARAMETERS OF RETROVIRAL AND MAMMALIAN ASPARTIC-ACID PROTEASES SO BIOORGANIC CHEMISTRY LA English DT Article ID HIV-1 PROTEASE; SPECTROPHOTOMETRIC ASSAY; PEPSTATIN; PROTEINASES; INHIBITOR; COMPLEX; RESOLUTION C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. NR 27 TC 13 Z9 13 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0045-2068 J9 BIOORG CHEM JI Bioorganic Chem. PD MAR PY 1992 VL 20 IS 1 BP 67 EP 76 DI 10.1016/0045-2068(92)90027-Z PG 10 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA HK327 UT WOS:A1992HK32700007 ER PT J AU LEVY, A SHARMA, VS ZHANG, L RIFKIND, JM AF LEVY, A SHARMA, VS ZHANG, L RIFKIND, JM TI A NEW MODE FOR HEME HEME INTERACTIONS IN HEMOGLOBIN ASSOCIATED WITH DISTAL PERTURBATIONS SO BIOPHYSICAL JOURNAL LA English DT Article ID TERTIARY STRUCTURAL-CHANGE; CARBON-MONOXIDE BINDING; LIGAND-BINDING; QUATERNARY STRUCTURE; OXYGEN BINDING; MECHANISM; RESOLUTION; STEREOCHEMISTRY; KINETICS; IRON AB The distal side of the heme pocket, known to regulate ligand affinity, is shown to be directly involved in subunit interactions. Valency hybrids with oxygen or carbon monoxide bound to the reduced chain are used to model R-state hemoglobin with different distal perturbations, Electron paramagnetic resonance of the oxidized chains shows that the carbon monoxide perturbation is transmitted between subunits to the distal histidine and the oxidized iron center. A comparison of hybrids with only one type of chain oxidized and hybrids with a single alpha-beta dimer oxidized is consistent with this perturbation being transmitted across the alpha-1-beta-1 interface. This represents a new mode of subunit interactions in hemoglobin. C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. RP LEVY, A (reprint author), NIA,CELLULAR & MOLEC BIOL LAB,MOLEC DYNAM SECT,BALTIMORE,MD 21224, USA. NR 36 TC 32 Z9 32 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD MAR PY 1992 VL 61 IS 3 BP 750 EP 755 PG 6 WC Biophysics SC Biophysics GA HH578 UT WOS:A1992HH57800016 PM 1324020 ER PT J AU UYESAKA, N HASEGAWA, S ISHIOKA, N ISHIOKA, R SHIO, H SCHECHTER, AN AF UYESAKA, N HASEGAWA, S ISHIOKA, N ISHIOKA, R SHIO, H SCHECHTER, AN TI EFFECTS OF SUPEROXIDE ANIONS ON RED-CELL DEFORMABILITY AND MEMBRANE-PROTEINS SO BIORHEOLOGY LA English DT Article DE RED BLOOD CELLS (RBC); SUPEROXIDE ANION; DEFORMABILITY; MEMBRANE PROTEIN; BAND-3 PROTEIN ID PREDOMINANT TRANSMEMBRANE POLYPEPTIDE; HUMAN-ERYTHROCYTE-MEMBRANES; LIPID-PEROXIDATION; OXYGEN RADICALS; BAND 3; SKELETON; MALONYLDIALDEHYDE; PROTEOLYSIS; METABOLISM; DAMAGE AB The effect ot' superoxide anions (O2-) on red blood cells (RBC) deformability and membrane proteins was investigated using hypoxanthine-xanthine oxidase system. Exposure of RBC to O2-caused a marked decrease in RBC deformability with a concomitant increase in cell volume and shape changes. The RBC exposed to O2-also displayed pronounced degradation of membrane proteins such as band 3 protein and spectrin; new bands of low molecular weight products appeared as the original membrane proteins tended to diminish. without the appearance of high molecular weight products. Since the membrane proteins are involved in processes regulating membrane properties such as permeability and viscoelasticity, the decreased deformability induced by O2- may be attributable to changes in membrane proteins. Interestingly, resealed ghosts exposed to O2- did not show any significant change in membrane proteins, which suggests the existence of further generation of O2-and subsequent production of other active oxygen species mediated by O2--initiated autoxidation of hemoglobin in intact RBC. Furthermore, electrophoretic analysis suggested that active oxygens increased the endogenous proteolytic susceptibility of RBC. In conclusion. a close linkage was suggested between RBC deformability and the membrane proteins. C1 JIKEI UNIV,INST MED SCI,DIV BIOCHEM,TOKYO 105,JAPAN. KYOTO UNIV,FAC MED,DEPT NEUROL,KYOTO 606,JAPAN. NIDDKD,CHEM BIOL LAB,BETHESDA,MD. RP UYESAKA, N (reprint author), NIPPON MED COLL,DEPT PHYSIOL,SENDAGI 1-1-5,BUNKYO KU,TOKYO 113,JAPAN. OI Schechter, Alan N/0000-0002-5235-9408 NR 39 TC 68 Z9 70 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-355X J9 BIORHEOLOGY JI Biorheology PD MAR-JUN PY 1992 VL 29 IS 2-3 BP 217 EP 229 PG 13 WC Biophysics; Engineering, Biomedical; Hematology SC Biophysics; Engineering; Hematology GA JP002 UT WOS:A1992JP00200003 PM 1338497 ER PT J AU DUNBAR, CE STEWART, FM AF DUNBAR, CE STEWART, FM TI SEPARATING THE WHEAT FROM THE CHAFF - SELECTION OF BENIGN HEMATOPOIETIC-CELLS IN CHRONIC MYELOID-LEUKEMIA SO BLOOD LA English DT Editorial Material ID CHRONIC MYELOGENOUS LEUKEMIA; APPEARING PHILADELPHIA-CHROMOSOME; CHRONIC MYELOCYTIC-LEUKEMIA; MARROW; TRANSPLANTATION; INVITRO C1 UNIV VIRGINIA,MED CTR,SCH MED,DEPT MED,DIV HEMATOL & ONCOL,CHARLOTTESVILLE,VA 22901. NIH,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NR 40 TC 46 Z9 46 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1992 VL 79 IS 5 BP 1107 EP 1110 PG 4 WC Hematology SC Hematology GA HF638 UT WOS:A1992HF63800001 PM 1536939 ER PT J AU YANO, T VANKRIEKEN, JHJM MAGRATH, IT LONGO, DL JAFFE, ES RAFFELD, M AF YANO, T VANKRIEKEN, JHJM MAGRATH, IT LONGO, DL JAFFE, ES RAFFELD, M TI HISTOGENETIC CORRELATIONS BETWEEN SUBCATEGORIES OF SMALL NONCLEAVED CELL LYMPHOMAS SO BLOOD LA English DT Article ID NON-HODGKINS-LYMPHOMAS; CONSTANT REGION GENES; EPSTEIN-BARR VIRUS; C-MYC ONCOGENE; BURKITT-LYMPHOMA; FOLLICULAR LYMPHOMAS; CHROMOSOMAL BREAKPOINT; MOLECULAR ANALYSIS; UNITED-STATES; EPSILON-GENES C1 NCI,DIV CANC BIOL DIAG & CTR,PATHOL LAB,BLDG 10,ROOM 2N110,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,FREDERICK,MD 21701. RI van Krieken, Joannes/D-4138-2009 OI van Krieken, Joannes/0000-0001-6544-1040 NR 41 TC 77 Z9 78 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1992 VL 79 IS 5 BP 1282 EP 1290 PG 9 WC Hematology SC Hematology GA HF638 UT WOS:A1992HF63800025 PM 1311213 ER PT J AU APLAN, PD LOMBARDI, DP REAMAN, GH SATHER, HN HAMMOND, GD KIRSCH, IR AF APLAN, PD LOMBARDI, DP REAMAN, GH SATHER, HN HAMMOND, GD KIRSCH, IR TI INVOLVEMENT OF THE PUTATIVE HEMATOPOIETIC TRANSCRIPTION FACTOR SCL IN T-CELL ACUTE LYMPHOBLASTIC-LEUKEMIA SO BLOOD LA English DT Article ID DNA-BINDING MOTIF; CHROMOSOMAL TRANSLOCATION; GENE; LINE; RECOMBINATION; SEQUENCES; ENCODES; PROTEIN; LOCUS C1 CHILDRENS NATL MED CTR,DEPT HEMATOL ONCOL,WASHINGTON,DC. CHILDRENS CANC STUDY GRP,ARCADIA,CA. NCI,NAVY MED BRANCH,BETHESDA,MD 20892. NCI,PEDIAT ONCOL BRANCH,BETHESDA,MD 20892. RI Aplan, Peter/K-9064-2016 NR 27 TC 125 Z9 127 U1 2 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1992 VL 79 IS 5 BP 1327 EP 1333 PG 7 WC Hematology SC Hematology GA HF638 UT WOS:A1992HF63800031 PM 1311214 ER PT J AU SHARABI, Y ABRAHAM, VS SYKES, M SACHS, DH AF SHARABI, Y ABRAHAM, VS SYKES, M SACHS, DH TI MIXED ALLOGENEIC CHIMERAS PREPARED BY A NON-MYELOABLATIVE REGIMEN - REQUIREMENT FOR CHIMERISM TO MAINTAIN TOLERANCE SO BONE MARROW TRANSPLANTATION LA English DT Article ID BONE-MARROW; MONOCLONAL-ANTIBODIES; TRANSPLANTATION TOLERANCE; HOST DISEASE; CELLS; GRAFT; SURFACE; SPECIFICITY; IRRADIATION; ENGRAFTMENT AB We have recently described a non-myeloablative conditioning regimen permitting engraftment of allogeneic bone marrow in mice which involves administration of anti-CD4 (GK1.5) plus anti-CD8 (2.43) monoclonal antibodies in vivo, 3 Gy whole body irradiation, plus 7 Gy thymic irradiation. B10 (H-2b) mice prepared by this regimen and infused with unmanipulated B10.D2 (H-2d) bone marrow develop permanent mixed lymphohematopoietic chimerism and specific tolerance to donor skin grafts. We now demonstrate that mixed chimerism persists longer than 170 days in the lymphoid tissues including spleen, thymus and bone marrow of such animals, and that equivalent levels of donor chimerism are observed in both T and B cell compartments. In addition stable mixed chimeras were found to be unresponsive to host (B10) and donor (B10.D2) stimulator cells in mixed lymphocyte reaction and in cell mediated lympholysis assays, while responses to a third party (B10.BR, H-2k) were intact. Persistent chimerism was found to be necessary for the maintenance of skin graft tolerance in these animals, since in vivo depletion of donor cells by treatment with an anti-H-2d (34-2-12) monoclonal antibody resulted in the subsequent rejection of donor skin grafts. These studies demonstrate that mixed allogeneic chimeras produced using this regimen are specifically tolerant to donor in vitro and in vivo, and that persistence of donor chimerism is critical for the maintenance of tolerance. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. FU NCI NIH HHS [R01 CA5590]; PHS HHS [R01 A131158] NR 23 TC 124 Z9 124 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD MAR PY 1992 VL 9 IS 3 BP 191 EP 197 PG 7 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA HL770 UT WOS:A1992HL77000007 PM 1387333 ER PT J AU KORN, EL SIMON, R AF KORN, EL SIMON, R TI SELECTING DOSE-INTENSE DRUG-COMBINATIONS - METASTATIC BREAST-CANCER SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE BREAST CANCER; CHEMOTHERAPY; DOSE INTENSITY; MATHEMATICAL MODELING ID BONE-MARROW TRANSPLANTATION; REFRACTORY OVARIAN-CANCER; CALIFORNIA-ONCOLOGY-GROUP; SMALL-CELL-CARCINOMA; PHASE-I TRIAL; CYCLOPHOSPHAMIDE THERAPY; COLORECTAL-CARCINOMA; HYPERTONIC SALINE; SOLID TUMORS; AUTOLOGOUS MARROW AB A mathematical model previously described is applied to the problem of selecting drug combinations for metastatic breast cancer. The model accounts for the differing single-agent activities of the drugs as well as their differing profiles of toxicity. With no bone marrow protection, combinations with cisplatin offer a small improvement in total equivalent dose over therapy with the more active single-agents. Restricting consideration to the four most commonly used agents, single-agent doxorubicin has the greatest equivalent dose. With protection for leukopenia or willingness to accept a higher incidence of severe leukopenia, a combination with large doses of cyclophosphamide, doxorubicin, and fluorouracil, and a small dose of cisplatin has greatest equivalent dose. The doublets cyclophosphamide/fluorouracil or fluorouracil/cisplatin at higher doses are almost as good. With protection for leukopenia and thrombocytopenia, a cyclophosphamide/thiotepa combination at very high doses maximizes total equivalent dose. This approach can be used to identify regimens worthy of prospective evaluation. RP KORN, EL (reprint author), NCI,BIOMETR RES BRANCH,EPN 739,BETHESDA,MD 20892, USA. NR 46 TC 4 Z9 4 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PD MAR PY 1992 VL 20 IS 3 BP 155 EP 166 PG 12 WC Oncology SC Oncology GA HK073 UT WOS:A1992HK07300002 PM 1349245 ER PT J AU SCHUSTER, CR AF SCHUSTER, CR TI DRUG-ABUSE RESEARCH AND HIV AIDS - A NATIONAL PERSPECTIVE FROM THE UNITED-STATES SO BRITISH JOURNAL OF ADDICTION LA English DT Article AB The National Institute on Drug Abuse (NIDA), the lead Federal agency charged with research on reducing the demand for illicit drugs in the US, has actively pursued the associated challenge of reducing drugs-related HIV transmission. Drug abuse-related spread of the virus occurs not only through sharing contaminated needles but also sexually to partners and perinatally from infected mothers to their offspring. Through a national research and demonstration program, NIDA supports primary AIDS risk reduction activities focused on identifying effective drug abuse prevention and treatment strategies. AIDS is increasingly a disease found in women, children, minorities, and people who live in rural areas. NIDA's efforts are clearly responsive to the changing nature of this epidemic. Among the many promising initiatives currently underway are a medications development program to find new pharmacotherapies for treating drug addiction; an array of National AIDS Outreach Demonstration Projects implementing alternative control strategies for drug abusers not attracted to or successful in drug abuse treatment; establishment of several treatment research units for designing and conducting studies on treatment effectiveness; and a variety of programs aimed at identifying and potentially reducing the risks of prenatal drug use to both mother and child. Effective dissemination of our findings is particularly critical to the overall impact of our research efforts. Collaborative activities teaming NIDA with a multitude of organizations also addressing AIDS related issues are designed to provide a synergistic impact on this complex and multifaceted public health crisis. RP SCHUSTER, CR (reprint author), NATL INST DRUG ABUSE,5600 FISHERS LANE,ROOM 10-05,ROCKVILLE,MD 20857, USA. NR 0 TC 10 Z9 10 U1 0 U2 0 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0952-0481 J9 BRIT J ADDICT PD MAR PY 1992 VL 87 IS 3 BP 355 EP 361 PG 7 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA HH740 UT WOS:A1992HH74000003 PM 1559034 ER PT J AU GRALNICK, HR WILLIAMS, SB MCKEOWN, L SHAFER, B CONNAGHAN, GD HANSMANN, K VAIL, M MAGRUDER, L AF GRALNICK, HR WILLIAMS, SB MCKEOWN, L SHAFER, B CONNAGHAN, GD HANSMANN, K VAIL, M MAGRUDER, L TI ENDOGENOUS PLATELET FIBRINOGEN - ITS MODULATION AFTER SURFACE EXPRESSION IS RELATED TO SIZE-SELECTIVE ACCESS TO AND CONFORMATIONAL-CHANGES IN THE BOUND FIBRINOGEN SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article ID GLYCOPROTEIN-IIIA COMPLEX; OPEN CANALICULAR SYSTEM; ACTIVATED PLATELETS; MONOCLONAL-ANTIBODIES; VONWILLEBRAND-FACTOR; HUMAN MEGAKARYOCYTES; BLOOD-PLATELETS; RECEPTOR; BINDING; IIB AB Platelet stimulation results in the release of endogenous platelet fibrinogen which binds to the platelet surface. Previous studies have demonstrated that plasma fibrinogen bound to activated platelets becomes inaccessible to a variety of probes. We have studied endogenous platelet fibrinogen binding to activated platelets by employing an immunopurified polyclonal anti-fibrinogen antibody and F26, a monoclonal anti-fibrinogen antibody, which recognizes fibrinogen only when it is bound to a surface. Employing the Ig or F(ab')2 of the poly-or monoclonal antibody we found a marked decrease of fibrinogen accessibility 30-60 min after platelet activation. In contrast, platelet-bound fibrinogen remains accessible to the Fab fragment of F26 at a constant level for 30 min and increases at 60 min. The reduction of the polyclonal Fab fragment binding at 30 and 60 min is similar to the F26 Ig. These results indicate that the decreased accessibility of bound fibrinogen is related to two mechanisms; (1) that the access route to fibrinogen is size selective for the antibody probes and only small antibody probes, e.g. Fab fragments, can gain access to fibrinogen and (2) fibrinogen undergoes a conformational change(s) after binding which exposes at least one neo-epitope in the D domain of fibrinogen and which may decrease or mask the reactivity of other fibrinogen domains. Only the F26 Fab probe has full access to and identifies fibrinogen present on the platelet surface 60 min after stimulation. RP NIH, HEMATOL SERV, BLDG 10, ROOM 2C390, BETHESDA, MD 20892 USA. NR 46 TC 28 Z9 28 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0007-1048 EI 1365-2141 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD MAR PY 1992 VL 80 IS 3 BP 347 EP 357 DI 10.1111/j.1365-2141.1992.tb08144.x PG 11 WC Hematology SC Hematology GA HH946 UT WOS:A1992HH94600013 PM 1374628 ER PT J AU MCLAUGHLIN, JK CHEN, JQ DOSEMECI, M CHEN, RA REXING, SH WU, Z HEARL, FJ MCCAWLEY, MA BLOT, WJ AF MCLAUGHLIN, JK CHEN, JQ DOSEMECI, M CHEN, RA REXING, SH WU, Z HEARL, FJ MCCAWLEY, MA BLOT, WJ TI A NESTED CASE-CONTROL STUDY OF LUNG-CANCER AMONG SILICA EXPOSED WORKERS IN CHINA SO BRITISH JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article ID MORTALITY; MINERS AB In an attempt to assess whether silica induces lung cancer, a nested case-control study of 316 male lung cancer cases and 1352 controls was carried out among pottery workers and tungsten, copper-iron, and tin miners from five provinces in south central China. Exposure to dust and silica for each study subject was evaluated quantitatively by cumulative exposure measures based on historical industrial hygiene records. Measurements on confounders such as inorganic arsenic, polycyclic aromatic hydrocarbons (PAHs), and radon were also collected from the worksites. Information on cigarette smoking was obtained by interviews of the subjects or their next of kin. A significant trend of increasing risk of lung cancer with exposure to silica was found for tin miners, but not for miners working in tungsten or copper-iron mines. Concomitant and highly correlated exposures to arsenic and PAHs among tin miners were also found. Risk of lung cancer among pottery workers was related to exposure to silica, although the dose-response gradient was not significant. Risks of lung cancer were significantly increased among silicotic subjects in iron-copper and tin mines, but not in pottery factories or tungsten mines. The results of this study provide only limited support for an aetiological association between silica and lung cancer. C1 TONGJI MED UNIV,SCH PUBL HLTH,DEPT LABOR HLTH & OCCUPAT DIS,WUHAN,PEOPLES R CHINA. WESTAT CORP,ROCKVILLE,MD 20850. NIOSH,DIV RESP DIS STUDIES,MORGANTOWN,WV 26505. RP MCLAUGHLIN, JK (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892, USA. NR 25 TC 62 Z9 62 U1 2 U2 3 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-1072 J9 BRIT J IND MED PD MAR PY 1992 VL 49 IS 3 BP 167 EP 171 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HG582 UT WOS:A1992HG58200005 PM 1313281 ER PT J AU KAROUM, F EGAN, MF AF KAROUM, F EGAN, MF TI DOPAMINE RELEASE AND METABOLISM IN THE RAT FRONTAL-CORTEX, NUCLEUS-ACCUMBENS, AND STRIATUM - A COMPARISON OF ACUTE CLOZAPINE AND HALOPERIDOL SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE DOPAMINE RELEASE AND METABOLISM; NEUROLEPTICS; HALOPERIDOL; CLOZAPINE; CORTEX; NUCLEUS ACCUMBENS; STRIATUM ID ATYPICAL NEUROLEPTICS; INVIVO RELEASE; IMPULSE FLOW; BRAIN; NEURONS; 3-METHOXYTYRAMINE; DRUGS; AUTORECEPTORS; DIALYSIS; NORMETANEPHRINE AB 1 The effects of the typical and typical neuroleptic agents clozapine (CLZ) (2.5-20 mg kg-1, i.p.) and haloperidol (Hal) (0.05-1.0 mg kg-1), were compared on dopamine release and metabolism in the rat prefrontal cortex (PFC), nucleus accumbens (ACC) and striatum (ST). Dopamine release was estimated by measuring the steady-state concentration of 3-methoxytyramine (3-MT) and the level of 3-MT 10 min after pargyline (3-MT accumulation); dopamine metabolism was evaluated from the steady-state concentrations of its acidic metabolites. 2 Both drugs increased 3-MT accumulation in the PFC in a dose-dependent manner. In contrast to Hal, CLZ failed to increase 3-MT accumulation in the ACC or ST. The ST was the region most sensitive to Hal in terms of 3-MT accumulation and, by inference, dopamine release. 3 Both CLZ and Hal dose-dependently elevated the concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in all 3 brain regions studied. The ACC appears to be the region most sensitive to these drugs in terms of changes in the levels of HVA. 4 The result of the present investigations suggest measurements of 3-MT production in the 3 brain regions analysed might be a useful and simple pharmacological tool in the search for atypical neuroleptic drugs with a selectivity of action for the cortical systems. RP KAROUM, F (reprint author), NIMH,NEUROSCI RES CTR,INTRAMURAL RES PROGRAM,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032, USA. NR 67 TC 47 Z9 47 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD MAR PY 1992 VL 105 IS 3 BP 703 EP 707 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HG584 UT WOS:A1992HG58400036 PM 1628156 ER PT J AU BRODER, S KARP, JE AF BRODER, S KARP, JE TI THE EXPANDING CHALLENGE OF HIV-ASSOCIATED MALIGNANCIES SO CA-A CANCER JOURNAL FOR CLINICIANS LA English DT Editorial Material AB Dr. Samuel Broder, Director of the National Cancer Institute, and his colleague, Dr. Judith E. Karp, present an overview of the research strategies currently being employed to meet the challenge of the increasing numbers of cancers now recognized as being related to infection with the human immunodeficiency virus. RP BRODER, S (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU AMER CANCER SOC PI NEW YORK PA C/O JB LIPPINCOTT CO 1180 AVE OF THE AMERICAS 6TH FLOOR, NEW YORK, NY 10036 SN 0007-9235 J9 CA-CANCER J CLIN JI CA-Cancer J. Clin. PD MAR-APR PY 1992 VL 42 IS 2 BP 69 EP 73 DI 10.3322/canjclin.42.2.69 PG 5 WC Oncology SC Oncology GA HJ708 UT WOS:A1992HJ70800001 PM 1311619 ER PT J AU SKRTIC, D EANES, ED AF SKRTIC, D EANES, ED TI EFFECT OF DIFFERENT PHOSPHOLIPID-CHOLESTEROL MEMBRANE COMPOSITIONS ON LIPOSOME-MEDIATED FORMATION OF CALCIUM PHOSPHATES SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE CALCIUM PHOSPHATES; LIPOSOMES; ANIONIC, NEUTRAL PHOSPHOLIPDS; CHOLESTEROL; MATRIX VESICLES ID CONTAINING ANIONIC LIPOSOMES; AQUEOUS SUSPENSIONS; PRECIPITATION; TISSUES; LIPIDS; BONE AB The present report compares the effects of different membrane phospholipid (PL)-cholesterol compositions on the kinetics of liposome-mediated formation of calcium phosphates from metastable solutions (2.25 mM CaCl2; 1.5 mM KH2PO4) at 22-degrees-C, pH 7.4 and 240 mOsm. In most experiments, the liposomes were composed of 7:2:X mixtures of phosphatidylcholine (PC), neutral or acidic phospholipids, and cholesterol (Chol, X = 0, 10, 35, or 50 mol%). The neutral phospholipids (NPL) examined, in addition to PC, were phosphatidylethanolamine (PE) and sphingomyelin (Sph), and the acidic phospholipids (APL) examined were dicetylphosphate (DCP), dioleolylphosphatidylglycerol (DOPG), dioleolylphosphatidic acid (DOPA), phosphatidylserine (PS) and phosphatidylinositol (PI). The 7:2:X liposomes did not initiate mineralization in metastable external solutions per se or, with the exception of DOPA, show extensive Ca-PL binding. However, solution Ca2+ losses due to precipitation occurred when the liposomes were encapsulated with 50 mM KH2PO4 and made permeable to external Ca2+ with X-537A. The extent of these Ca2+ losses was sensitive to both the phospholipid and Chol makeup of the membrane. Moderate-to-extensive intraliposomal precipitation occurred in all 7PC:2APL and 7PC:2NPL liposomes containing 0 or 10 mol% Chol. In contrast, at 50 mol% Chol, mineralization inside all liposomes was negligible. The only significant discriminating effect on internal mineralization among the different phospholipids was observed at 35 mol% Chol, where mineral accumulations ranged from negligible to moderate. At 0 or 10 mol% Chol, extraliposomal precipitation was extensive in all but DOPA- and PS-containing liposomes. However, once intraliposomal yields declined at the higher Chol levels, external mineralization was either delayed or totally blocked in all liposome preparations. Other experiments showed that Sph substituted for PC in 7NPL:2DCP:1Chol liposomes totally blocked both intra- and extraliposomal precipitation. PE substituted in this manner, however, blocked only extraliposomal precipitation. The results of this study suggest that interference of the membrane transport processes controlling intraliposomal precipitation [15] by high (50 mol%) Chol levels is not significantly compromised by the specific APL or NPL incorporated in the membrane. Similarly, the data suggest that Chol does not directly affect the specific interactions of the different membrane APLs with the mineral phase. On the other hand, the substitution of other NPLs for PC can affect the role of APLs such as DCP in liposome-mediated mineralization. C1 NATL INST STAND & TECHNOL,NIDR,BONE RES BRANCH,RES ASSOCIATE PROGRAM,BLDG 224,ROOM A143,GAITHERSBURG,MD 20899. NR 24 TC 13 Z9 13 U1 1 U2 11 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD MAR PY 1992 VL 50 IS 3 BP 253 EP 260 DI 10.1007/BF00296290 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HD540 UT WOS:A1992HD54000009 PM 1617500 ER PT J AU BOIVIN, JF HUTCHISON, GB LUBIN, JH MAUCH, P AF BOIVIN, JF HUTCHISON, GB LUBIN, JH MAUCH, P TI CORONARY-ARTERY DISEASE MORTALITY IN PATIENTS TREATED FOR HODGKINS-DISEASE SO CANCER LA English DT Article ID CASE-COHORT DESIGN; BREAST-CANCER; POSTOPERATIVE RADIOTHERAPY; HEART-DISEASE; IRRADIATION; RADIATION AB The authors conducted a follow-up study of the association between mediastinal irradiation, chemotherapy, and mortality from coronary artery disease in 4665 patients treated for Hodgkin's disease. Study subjects were followed after the diagnosis of Hodgkin's disease until death or the closing date of the study. The average duration of follow-up was 7 years; 2415 patients died, and 124 cases of coronary artery disease were identified from death certificates, including 68 cases of acute myocardial infarction. The age-adjusted relative risks (RR) of death with any coronary artery disease after mediastinal irradiation and after chemotherapy were 1.87 (95% confidence interval [CI], 0.92 to 3.80) and 1.28 (CI, 0.77 to 2.15), respectively. A significantly increased risk of death in the subcategory myocardial infarction was observed after mediastinal irradiation (RR, 2.56; CI, 1.11 to 5.93) but not after chemotherapy (RR, 0.97; CI, 0.53 to 1.77). These results support the hypothesis that radiation therapy to the mediastinum increases the risk of coronary artery disease. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. NCI,BIOSTAT BRANCH,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DEPT RADIAT THERAPY,BOSTON,MA 02115. RP BOIVIN, JF (reprint author), MCGILL UNIV,DEPT EPIDEMIOL & BIOSTAT,1020 PINE AVE W,MONTREAL H3A 1A2,QUEBEC,CANADA. FU NCI NIH HHS [2R01CA-22849] NR 19 TC 188 Z9 200 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 1 PY 1992 VL 69 IS 5 BP 1241 EP 1247 PG 7 WC Oncology SC Oncology GA HF672 UT WOS:A1992HF67200027 PM 1739922 ER PT J AU POTTERN, LM GART, JJ NAM, JM DUNSTON, G WILSON, J GREENBERG, R SCHOENBERG, J SWANSON, GM LIFF, J SCHWARTZ, AG FRAUMENI, JF HOOVER, RN AF POTTERN, LM GART, JJ NAM, JM DUNSTON, G WILSON, J GREENBERG, R SCHOENBERG, J SWANSON, GM LIFF, J SCHWARTZ, AG FRAUMENI, JF HOOVER, RN TI HLA AND MULTIPLE-MYELOMA AMONG BLACK-AND-WHITE MEN - EVIDENCE OF A GENETIC ASSOCIATION SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID RISK AB To evaluate the possibility that genetic factors contribute to the excess rates of multiple myeloma among blacks, serological typing of human leukocyte antigens (HLA) was conducted for black and white male patients and controls who participated in a large population-based case-control interview study. Forty-six black cases, 88 black controls, 85 white cases, and 122 white controls were typed for the Class I antigens (HLA-A, -B, -C) and for the Class II antigens (HLA-DR, HLA-DQ). Black cases had significantly higher gene frequencies than black controls for Bw65, Cw2, and DRw14, while white cases had higher gene frequencies than white controls for A3 and Cw2 and blanks at the DR and DQ loci. Further analysis of the association between Cw2 and multiple myeloma revealed relative risks of 5.7 (95% confidence interval = 1.5-26.6) and 2.6 (95% confidence interval = 1.0-7.2) for blacks and whites, respectively. The frequency of Cw2 in black and white controls was similar. These findings suggest that the Cw2 allele enhances the risk of myeloma in blacks and whites but do not explain the higher incidence of this cancer among blacks. The study also suggests that undefined DQ antigens may play an etiological role, supporting the need for further research into the immunogenetic determinants of myeloma. C1 HOWARD UNIV,COLL MED,DEPT MICROBIOL,WASHINGTON,DC 20059. EMORY UNIV,SCH MED,SCH PUBL HLTH,ATLANTA,GA 30329. NEW JERSEY STATE DEPT HLTH,SPECIAL EPIDEMIOL PROGRAM,TRENTON,NJ 08625. MICHIGAN STATE UNIV,CTR CANC,E LANSING,MI 48824. MICHIGAN CANC FDN,DIV EPIDEMIOL,DETROIT,MI 48201. RP POTTERN, LM (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892, USA. NR 23 TC 31 Z9 31 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD MAR-APR PY 1992 VL 1 IS 3 BP 177 EP 182 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA HN952 UT WOS:A1992HN95200003 PM 1306102 ER PT J AU MELONI, AM STEPHENSON, CF LI, FP SANDBERG, AA AF MELONI, AM STEPHENSON, CF LI, FP SANDBERG, AA TI DEL(6Q) AS A POSSIBLE PRIMARY CHANGE IN MALIGNANT MESOTHELIOMA SO CANCER GENETICS AND CYTOGENETICS LA English DT Article ID CYTOGENETIC ANALYSIS; CHROMOSOMAL-ABNORMALITIES; PERITONEAL MESOTHELIOMA; PLEURAL MESOTHELIOMA; ASBESTOS-EXPOSURE; SURVIVAL AB Detailed cytogenetic and fluorescence in situ hybridization analysis of an untreated pleural malignant mesothelioma revealed two clonal cell populations, both with a single abnormality affecting chromosome 6. The majority of cells had a deletion together with an inversion of the long arm of chromosome 6, while a smaller population showed loss of this chromosome. The normal 6 was retained. Most reports show that mesotheliomas are characterized by complex karyotypes, involving numerous chromosomes. Abnormalities of chromosome 6 (particularly deletions of the long arm) are among the consistent changes. Our case apparently is the first report of a mesothelioma with a single change involving chromosome 6, which could be the primary cytogenetic change. C1 GENETRIX INC,CTR CANC,6401 E THOMAS RD,SCOTTSDALE,AZ 85251. NCI,BOSTON,MA. FU NCI NIH HHS [CP-71018] NR 34 TC 23 Z9 23 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0165-4608 J9 CANCER GENET CYTOGEN JI Cancer Genet. Cytogenet. PD MAR PY 1992 VL 59 IS 1 BP 57 EP 61 DI 10.1016/0165-4608(92)90159-6 PG 5 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA HM018 UT WOS:A1992HM01800012 PM 1555192 ER PT J AU SCHLOM, J EGGENSPERGER, D COLCHER, D MOLINOLO, A HOUCHENS, D MILLER, LS HINKLE, G SILER, K AF SCHLOM, J EGGENSPERGER, D COLCHER, D MOLINOLO, A HOUCHENS, D MILLER, LS HINKLE, G SILER, K TI THERAPEUTIC ADVANTAGE OF HIGH-AFFINITY ANTICARCINOMA RADIOIMMUNOCONJUGATES SO CANCER RESEARCH LA English DT Article ID MONOCLONAL-ANTIBODY B72.3; GAMMA-DETECTING PROBE; GLYCOPROTEIN TAG-72; OVARIAN-CANCER; CARCINOMA; ANTIGEN; TUMORS; RADIOIMMUNOTHERAPY; GENERATION; CELLS AB The effect of the relative affinity (K(a)) on the antitumor efficacy of monoclonal antibodies (MAbs) has been questioned. It has previously been shown in experimental models that the use of MAbs with higher relative K(a)s manifests itself in a higher percentage of injected dose of MAb bound to tumor. On the other hand, mathematical models have proposed that the use of higher affinity MAbs may be disadvantageous for antitumor effects, since higher K(a) MAbs would bind more antigen and prevent penetration of MAb through tumor. To test this hypothesis, three MAbs reacting to the human pancarcinoma antigen TAG-72 were used as radioimmunoconjugates for therapeutic efficacy versus the LS-174T human colon carcinoma xenograft. MAbs B72.3, CC49, and CC83 have all been shown by depletion studies to react to the same molecule and to all react with overlapping epitopes. While the relative K(a) of B72.3 is 2.5 x 10(9) M-1, the relative K(a)s of CC49 and CC83 are 16.2 and 27.7 x 10(9) M-1, respectively. Each MAb was radiolabeled with I-131, and each radioimmunoconjugate was assayed at five dose levels for therapeutic efficacy using the human xenograft model. The results of these studies demonstrate substantial therapeutic advantage of the higher affinity MAbs CC49 and CC83 versus B72.3 at every dose level. While 500-mu-Ci of B72.3 were required to reduce tumor growth in only a minority of tumor-bearing animals, the use of the same amount or less of the radioimmunoconjugates of CC49 or CC83 resulted in strong antitumor effects in 80 to 100% of tumor-bearing animals. Thus, stronger antitumor effects were seen using as little as 2.5- to 3-fold less of the higher K(a) immunoconjugates CC49 and CC83 as compared with B72.3. While we acknowledge the potential disadvantages of higher K(a) MAbs in some situations, at least the experimental studies and model system described here show that a distinct therapeutic advantage exists with the use of higher affinity immunoconjugates. C1 BATTELLE MEM INST,COLUMBUS,OH 43201. OHIO STATE UNIV,DIV NUCL MED,COLUMBUS,OH 43210. RP SCHLOM, J (reprint author), NCI,TUMOR IMMUNOL & BIOL LAB,BLDG 10,ROOM 8B07,BETHESDA,MD 20892, USA. NR 30 TC 126 Z9 126 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 1 PY 1992 VL 52 IS 5 BP 1067 EP 1072 PG 6 WC Oncology SC Oncology GA HF637 UT WOS:A1992HF63700002 PM 1310638 ER PT J AU FRUCHT, H GAZDAR, AF PARK, JA OIE, H JENSEN, RT AF FRUCHT, H GAZDAR, AF PARK, JA OIE, H JENSEN, RT TI CHARACTERIZATION OF FUNCTIONAL RECEPTORS FOR GASTROINTESTINAL HORMONES ON HUMAN COLON CANCER-CELLS SO CANCER RESEARCH LA English DT Article ID VASOACTIVE INTESTINAL PEPTIDE; HIGH-AFFINITY RECEPTORS; HUMAN GASTRIC-CARCINOMA; SWISS 3T3 CELLS; LUNG-CANCER; VIP RECEPTORS; LINE HGT-1; MOLECULAR-IDENTIFICATION; MUSCARINIC RECEPTORS; REGULATORY PEPTIDES AB Studies demonstrate that some colon cancers possess receptors for various gastrointestinal hormones or neurotransmitters, the occupation of which can affect growth. These results are limited because frequently only a small number of tumors are studied, only 1 or 2 receptors are sought, and the effect on cell function is not investigated. In the present study, 10 recently characterized human colon cancer cell lines were studied to determine whether they possess receptors for any of 12 different gastrointestinal hormones or neurotransmitters and to determine whether these receptors mediate changes in cellular function. Each of the cell lines exhibited receptors for at least one radioligand. Receptors for vasoactive intestinal peptide (VIP) and muscarinic cholinergic agents occurred on 60%, bombesin and gastrin on 30%, beta-adrenergic agents and gastrin-releasing peptide (GRP) on 20%, and somatostatin, opiates, neuromedin B, and substance P on 10%. Analysis of [H-3]N-methylscopolamine binding revealed a K(d) of 0.2 nM for N-methylscopolamine with a binding capacity of 2500 sites/cell. With the agonist carbamylcholine, the receptor exhibited 2 classes of binding sites: one of high affinity (K(d) 55-mu-M) representing 75% of the binding sites and one of low affinity (K(d) 0.3 mM) representing 25% of the binding sites. Analysis of I-125-[Tyr4]bombesin binding revealed a receptor of high affinity (K(d) 2.1-mu-M) with a binding capacity of 3300 sites/cell. Inhibition of binding by agonists revealed relative potencies of I-125-[Tyr4]bombesin > GRP >> neuromedin B, and two recently described antagonists were similar in potency to GRP. Analysis of I-125-VIP binding revealed a receptor having 2 classes of binding sites: one of high affinity (K(d) 3.6 nM) and one of low affinity (K(d) 1.7-mu-M) which represented the majority of the 5.5 x 10(6) binding sites/cell. The relative potencies of agonists were VIP > helodermin > peptide histidine methionine > secretin. Evaluation of biological activity mediated by the muscarinic cholinergic and bombesin receptors revealed an increase of intracellular calcium and of inositol triphosphate by specific receptor agonists. The presence or absence of receptors detected by binding correlated closely with the ability of selective receptor agonists to alter cell function. These results demonstrate the presence of several different receptors for gastrointestinal hormones or neurotransmitters, some described for the first time, on human colon cancer cell lines, including bombesin-related peptides, VIP, somatostatin, substance P, beta-adrenergic agents, calcitonin gene-related peptide, gastrin, muscarinic cholinergic agents, and opiates. These receptors are functional because occupation by selective agonists altered intracellular mediators. These results suggest that it will be important to extend these studies to evaluate growth effects. C1 NIDDKD,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892. NCI,USA,MED ONCOL BRANCH,BETHESDA,MD 20892. RI Park, Jae-Gahb/J-5494-2012 NR 60 TC 114 Z9 114 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 1 PY 1992 VL 52 IS 5 BP 1114 EP 1122 PG 9 WC Oncology SC Oncology GA HF637 UT WOS:A1992HF63700010 PM 1310640 ER PT J AU MITCHELL, RB MOSCHEL, RC DOLAN, ME AF MITCHELL, RB MOSCHEL, RC DOLAN, ME TI EFFECT OF O6-BENZYLGUANINE ON THE SENSITIVITY OF HUMAN TUMOR XENOGRAFTS TO 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA AND ON DNA INTERSTRAND CROSS-LINK FORMATION SO CANCER RESEARCH LA English DT Article ID MAMMALIAN O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE; ALKYLATING-AGENTS; O6-METHYLGUANINE-DNA METHYLTRANSFERASE; CYTO-TOXICITY; HUMAN-CELLS; HELA-CELLS; CHLOROETHYLNITROSOUREA; DEPLETION; INVIVO; INACTIVATION AB We have previously shown that O6-benzylguanine can be used to deplete cells of the DNA repair protein O6-alkylguanine-DNA alkyltransferase and to enhance the sensitivity of human glioma (SF767) and colon tumor (HT29) cells to the cytotoxic effects of alkylnitrosoureas. In the present study, the combination of O6-benzylguanine and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) was evaluated in vitro to determine the number of DNA interstrand cross-links formed and in vivo to compare the therapeutic index with that of BCNU alone. The number of DNA interstrand cross-links, as measured by alkaline elution, was increased in HT29 cells treated with 10-mu-M O6-benzylguanine for 2 h prior to BCNU exposure compared to cells treated with BCNU only. The number of single strand breaks was not increased by prior exposure to O6-benzylguanine. To evaluate the therapeutic index, HT29 and SF767 cells were grown as xenografts in nude mice and the tumor growth rate after treatment with BCNU alone was compared with the rate after treatment with O6-benzylguanine and BCNU. Treatment was administered i.p. when tumors reached 100-200 mm3. For animals bearing HT29 xenografts that were treated with 60 mg/kg O6-benzylguanine 1 h prior to 20 mg/kg BCNU, the average time for tumor volume to increase by 200% was 25 days, compared to 10 days for animals treated with 20 mg/kg BCNU alone. For animals bearing SF767 xenografts, the tumor growth of controls was not significantly different from that of animals treated with O6-benzylguanine alone or BCNU alone up to the maximally tolerated dose (50 mg/kg). For these 3 groups, the average time for tumors to reach 300 mm3 was 9-12 days. However, when animals were treated with 80 mg/kg O6-benzylguanine 1 h prior to receiving 20 mg/kg BCNU tumor size did not increase for at least 21 days. Our studies demonstrate that the therapeutic index of BCNU can be increased when given in combination with O6-benzylguanine. C1 UNIV CHICAGO,DEPT MED,HEMATOL ONCOL SECT,5841 S MARYLAND AVE,BOX MC2115,CHICAGO,IL 60637. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101, CA-47228]; NIDDK NIH HHS [5T32-DK-07134] NR 29 TC 141 Z9 141 U1 0 U2 5 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 1 PY 1992 VL 52 IS 5 BP 1171 EP 1175 PG 5 WC Oncology SC Oncology GA HF637 UT WOS:A1992HF63700018 PM 1737376 ER PT J AU GUADAGNI, F ROSELLI, M AMATO, T COSIMELLI, M PERRI, P CASALE, V CARLINI, M SANTORO, E CAVALIERE, R GREINER, JW SCHLOM, J AF GUADAGNI, F ROSELLI, M AMATO, T COSIMELLI, M PERRI, P CASALE, V CARLINI, M SANTORO, E CAVALIERE, R GREINER, JW SCHLOM, J TI CA-72-4 MEASUREMENT OF TUMOR-ASSOCIATED GLYCOPROTEIN-72 (TAG-72) AS A SERUM MARKER IN THE MANAGEMENT OF GASTRIC-CARCINOMA SO CANCER RESEARCH LA English DT Article ID MONOCLONAL-ANTIBODY B72.3; IMMUNORADIOMETRIC ASSAY; ANTIGEN TAG-72; CANCER; CA-19-9; RADIOIMMUNOASSAY; DIAGNOSIS; STOMACH; CEA AB The presence of three distinct serum markers of carcinoma, tumor-associated glycoprotein 72 (TAG-72; as measured by the CA 724 assay), CA 19-9, and carcinoembryonic antigen (CEA), was evaluated in 194 patients diagnosed with either malignant (n = 94) or benign (n = 100) gastric disease. Of the 94 patients diagnosed with gastric carcinoma, the percentage of patients whose serum samples were positive for TAG-72, CA 19-9, or CEA was 42.6, 31.9, and 20.2%, respectively. Furthermore, fewer false positive samples were observed for TAG-72 than either CA 19-9 or CEA. The analysis of serum TAG-72, CA 19-9, and CEA levels in patients diagnosed with early (stage I and II) versus advanced (stage III and IV) disease revealed a significantly higher level of TAG-72 and CA 19-9 in the serum of patients with advanced stage gastric carcinoma. The serum samples were also analyzed to determine whether any advantage might be gained by simultaneously measuring two or more of the tumor markers. The data clearly indicate that the measurement of TAG-72 with CA 19-9 significantly increased the percentage of gastric carcinoma patients with positive serum levels of either antigen. This advantage was achieved with no significant increase in the number of false positives. Twenty-one patients were followed postsurgically for up to 3 years to determine whether the appearance or reappearance of TAG-72, CA 19-9, or CEA accurately predicted disease recurrence. Positive serum TAG-72 levels correlated with disease recurrence in 7 of 10 patients, compared with 5 and 2 patients for CA 19-9 and CEA, respectively. The findings suggest that serum TAG-72 as measured by the CA 72-4 assay may be a useful marker for late stage gastric carcinoma and its measurement alone or in combination with CA 19-9 may have utility in the clinical management of gastric carcinoma. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BLDG 10,ROOM 8B07,BETHESDA,MD 20892. UNIV ROME 2,SCH MED,DEPT SURG 1,ROME,ITALY. UNIV ROME 2,SCH MED,DEPT DIGEST ENDOSCOPY,ROME,ITALY. UNIV ROME 2,SCH MED,REGINA ELENA CANC INST,ROME,ITALY. UNIV ROME 2,SCH MED,DEPT SURG 2,ROME,ITALY. UNIV ROME 2,SCH MED,DEPT SURG,ROME,ITALY. RI Guadagni, Fiorella/J-4432-2013 OI Guadagni, Fiorella/0000-0003-3652-0457 NR 32 TC 64 Z9 70 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 1 PY 1992 VL 52 IS 5 BP 1222 EP 1227 PG 6 WC Oncology SC Oncology GA HF637 UT WOS:A1992HF63700028 PM 1737383 ER PT J AU POVEY, AC WILSON, VL ZWEIER, JL KUPPUSAMY, P ONEILL, IK HARRIS, CC AF POVEY, AC WILSON, VL ZWEIER, JL KUPPUSAMY, P ONEILL, IK HARRIS, CC TI DETECTION BY P-32 POSTLABELING OF DNA ADDUCTS INDUCED BY FREE-RADICALS AND UNSATURATED ALDEHYDES FORMED DURING THE AEROBIC DECOMPOSITION OF FECAPENTAENE-12 SO CARCINOGENESIS LA English DT Article ID LARGE-BOWEL-CANCER; COLON CANCER; HUMAN FECES; BACTERIAL ORIGIN; EPITHELIAL-CELLS; FECAL MUTAGEN; CARCINOGEN; ETIOLOGY; RELEVANT; DAMAGE AB Fecapentaene-12 (fec-12), excreted in human faeces, is genotoxic to human cells and a known animal carcinogen. The mechanism of its genotoxicity is unknown but may involve direct alkylation and/or free-radical generation. The formation of reactive species during fec-12 aerobic degradation was thus investigated by electron paramagnetic resonance (EPR) and NMR spectroscopic techniques. Oxy- and alkyl-radicals were detected as the 5,5'-dimethyl-1-pyrroline-N-oxide spin-trap adducts at fec-12 concentrations of between 0.1 and 2.0 mM. Under anaerobic conditions no free-radical generation was observed. NMR spectroscopy indicated that fec-12 degraded at least initially into three unsaturated aldehydes. The co-formation of free-radicals and unsaturated aldehydes suggests that fec-12 decomposed aerobically via a process analogous to lipid peroxidation. As both types of species, thus formed, may subsequently interact with DNA to form adducts, fec-12-induced DNA damage was investigated by P-32-postlabelling techniques. Using procedures that detect alkyl-type adducts, a number of putative adducts were detected in fec-12-treated DNA; two of similar mobility were observed in fec-12-treated 2'-deoxyguanosine-3'-monophosphate. Adducts with similar mobility have been detected in acrolein-treated DNA. One adduct with similar mobility was also observed in DNA obtained from normal human fibroblasts treated with fec-12. Using a C-18 ODS column, these putative adducts were eluted in 60-85% methanol, whereas 8-hydroxydeoxyguanosine-3'-monophosphate (80HdGp) was eluted with 1% acetonitrile. Also unlike these putative adducts, the detection of 80HdGp required HPLC fractionation prior to P-32-postlabelling. The formation of adducts, possibly aldehyde-related, and free-radical damage suggests that fec-12 genotoxicity may be the result of several different mechanisms, the relative importance of each is as yet unknown. Hydroxyl radicals were also detected during the aerobic decomposition of deca-2,4,6,8-tetraenal, a possible degradation product of fec-12 and a less potent mutagen, suggesting that free-radical generation may have only a minor role in fec-12-induced genotoxicity. C1 NCI, HUMAN CARCINOGENESIS LAB, BETHESDA, MD 20892 USA. CHILDRENS HOSP, MOLEC GENET ONCOL LAB, DENVER, CO 80218 USA. JOHNS HOPKINS, MED INST, SCH MED, DIV CARDIOL, EPR LABS, BALTIMORE, MD 21224 USA. INT AGCY RES CANC, F-69372 LYONS, FRANCE. NR 38 TC 10 Z9 10 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD MAR PY 1992 VL 13 IS 3 BP 395 EP 401 DI 10.1093/carcin/13.3.395 PG 7 WC Oncology SC Oncology GA HJ824 UT WOS:A1992HJ82400014 PM 1547529 ER PT J AU LAKATTA, EG AF LAKATTA, EG TI FUNCTIONAL IMPLICATIONS OF SPONTANEOUS SARCOPLASMIC-RETICULUM CA2+ RELEASE IN THE HEART SO CARDIOVASCULAR RESEARCH LA English DT Review DE CARDIAC CELLS; CALCIUM; SARCOPLASMIC RETICULUM; SPONTANEOUS CA2+ OSCILLATIONS; DIASTOLIC FUNCTION; ARRHYTHMIAS ID CARDIAC PURKINJE-FIBERS; TRANSIENT INWARD CURRENT; INTRACELLULAR CALCIUM-CONCENTRATION; PIG VENTRICULAR MYOCYTES; FERRET PAPILLARY-MUSCLE; GUINEA-PIG; RAT-HEART; MAMMALIAN HEART; CA-2+ RELEASE; SELECTIVE MICROELECTRODES RP LAKATTA, EG (reprint author), NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 131 TC 132 Z9 133 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6363 J9 CARDIOVASC RES JI Cardiovasc. Res. PD MAR PY 1992 VL 26 IS 3 BP 193 EP 214 DI 10.1093/cvr/26.3.193 PG 22 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HH717 UT WOS:A1992HH71700001 PM 1423412 ER PT J AU HUANG, SK KLEIN, DC KORF, HW AF HUANG, SK KLEIN, DC KORF, HW TI IMMUNOCYTOCHEMICAL DEMONSTRATION OF ROD-OPSIN, S-ANTIGEN, AND NEURON-SPECIFIC PROTEINS IN THE HUMAN PINEAL-GLAND SO CELL AND TISSUE RESEARCH LA English DT Article DE PINEALOCYTES; ROD-OPSIN; RETINAL S-ANTIGEN; SYNAPTOPHYSIN; NEUROFILAMENTS; HUMAN ID RETINOID-BINDING PROTEIN; PARENCHYMAL TUMORS; ORGAN; IMMUNOREACTIVITY; LOCALIZATION; PINEOCYTOMA; ANTIBODY AB The aim of this study was to examine whether rod-opsin and S-antigen immunoreactions were present in the pineal organ of adult man and how these immunoreactions were correlated with neuronal markers, e.g., synaptophysin, and neurofilaments L, H and M. Three perfusion-fixed epithalamic regions including the pineal organ and five pineal glands obtained at routine autopsy were used. The specimens were taken from female or male patients, 25 to 85 years of age. All immunoreactions were performed using highly specific, well-characterized antibodies. Rod-opsin and S-antigen-immunoreactive pinealocytes occurred in all pineal organs investigated; however, the immunoreaction was restricted to small subpopulations of pinealocytes (rod-opsin immunoreaction: approximately 3%-5%; S-antigen immunoreaction: approximately 5%-10% of the total population). In contrast, immunoreactions for synaptophysin and neurofilaments M and H were present in numerous pinealocytes. Immunoreactivity for neurofilament L was not found. These data suggest that the cellular composition of the human pineal organ is heterogeneous. Moreover, the presence of rod-opsin and S-antigen immunoreactions in the human pineal organ indicates that it may be affected by autoimmune retinal diseases that are provoked by antibodies against these proteins, as is the case in rodents and non-human primates. C1 UNIV FRANKFURT,ZENTRUM MORPHOL,THEODOR STERN KAI 7,W-6000 FRANKFURT 1,GERMANY. UNIV GIESSEN,INST ANAT & ZYTOBIOL,W-6300 GIESSEN,GERMANY. NICHHD,DEV NEUROBIOL LAB,NEUROENDOCRINOL SECT,BETHESDA,MD 20892. NR 33 TC 40 Z9 40 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0302-766X J9 CELL TISSUE RES JI Cell Tissue Res. PD MAR PY 1992 VL 267 IS 3 BP 493 EP 498 DI 10.1007/BF00319371 PG 6 WC Cell Biology SC Cell Biology GA HE295 UT WOS:A1992HE29500010 PM 1533347 ER PT J AU GOBEL, V LIPKOWITZ, S KOZAK, CA KIRSCH, IR AF GOBEL, V LIPKOWITZ, S KOZAK, CA KIRSCH, IR TI NSCL-2 - A BASIC DOMAIN HELIX-LOOP-HELIX GENE EXPRESSED IN EARLY NEUROGENESIS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID DNA-BINDING MOTIF; PROTEINS; MYOD AB We have identified a new basic domain helix-loop-helix (bHLH) gene, NSCL-2, which was cloned because of its homology to the previously described putative hematopoietic transcription factor, SCL. NSCL-2 has been identified in both human and murine DNA. NSCL-2 complementary DNA clones were obtained from an 11.5-day murine embryo library. The coding region is 405 base pairs and encodes a predicted protein of 15.6 kilodaltons. There is 74% homology at the nucleotide level with the coding region of the murine SCL and 27% protein homology. Unlike the majority of previously described bHLH genes, the NSCL-2 coding region ends only six amino acids beyond the second amphipathic helix of the HLH domain. The NSCL-2 gene shows A markedly restricted pattern of expression predominantly confined to murine embryos at days 11-13 of development, although low level expression can be detected in murine embryos flanking this time point. Examination of 11- and 12-day mouse embryos by tissue in situ hybridization reveals expression of NSCL-2 in the developing nervous system, most likely in developing neurons. The NSCL-2 gene maps to murine chromosome 3. The temporally and tissue restricted pattern of expression of this gene and its identification as a member of a family of transcription factors relevant to growth and development in a wide variety of species suggest a role for NSCL-2 in the development of the eukaryotic nervous system. C1 NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20892. NCI,METAB BRANCH,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 18 TC 56 Z9 59 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD MAR PY 1992 VL 3 IS 3 BP 143 EP 148 PG 6 WC Cell Biology SC Cell Biology GA HH538 UT WOS:A1992HH53800001 PM 1633105 ER PT J AU BARNER, M MESSING, LT CULTRARO, CM BIRRER, MJ SEGAL, S AF BARNER, M MESSING, LT CULTRARO, CM BIRRER, MJ SEGAL, S TI REGIONS WITHIN THE C-MYC PROTEIN THAT ARE NECESSARY FOR TRANSFORMATION ARE ALSO REQUIRED FOR INHIBITION OF DIFFERENTIATION OF MURINE ERYTHROLEUKEMIA-CELLS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID LEUCINE ZIPPER; EMBRYO FIBROBLASTS; LUNG-CANCER; DNA-BINDING; N-MYC; GENE; EXPRESSION; RAS; ONCOGENES; TRANSLOCATION AB The c-, L-, and N-Myc nuclear phosphoproteins share several highly conserved regions that partially overlap putative functional domains of the c-Myc protein. All three myc oncogenes can cooperate with an activated ras gene to transform primary rat embryo cells (REC), and deregulated expression of c- and L-myc can block differentiation of murine erythroleukemia (MEL) cells. In the present study, we demonstrate that N-myc also can block MEL cell differentiation, and we identify regions within the c-Myc protein that are necessary for inhibition of MEL differentiation. C19 MEL cells were transfected with six human c-myc genes which were partially deleted in different areas of the coding region. Four of the genes lack sequences that overlap either the putative transcriptional activation domain, the helix-loop-helix motif, or the leucine zipper motif and were previously shown to have lost REC cotransforming activity (J. Stone, T. DeLange, G. Ramsay, E. Jakobovitz, J. M. Bishop, H. Varmus, and W. Lee, Mol. Cell. Biol., 7: 1697-1709, 1987). In this study, we demonstrate that they also fail to inhibit N,N'-hexamethylene-bisacetamide-induced differentiation of MEL cells. In contrast, two partially deleted c-myc genes, one lacking a short NH2-terminal region and the other lacking 118 amino acids at the center of the coding region, which were fully active in REC cotransformation, also exhibited full activity associated with the former and only partial activity with the latter in blocking MEL differentiation. We conclude that the mutated genes tested in this study behave similarly in inhibition of MEL cell differentiation and in REC cotransformation. C1 NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. NCI,BIOMARKERS & PREVENT RES BRANCH,BETHESDA,MD 20892. NR 42 TC 27 Z9 27 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD MAR PY 1992 VL 3 IS 3 BP 183 EP 190 PG 8 WC Cell Biology SC Cell Biology GA HH538 UT WOS:A1992HH53800006 PM 1633109 ER PT J AU BERAUD, E KOTAKE, S CASPI, RR ODDO, SM CHAN, CC GERY, I NUSSENBLATT, RB AF BERAUD, E KOTAKE, S CASPI, RR ODDO, SM CHAN, CC GERY, I NUSSENBLATT, RB TI CONTROL OF EXPERIMENTAL AUTOIMMUNE UVEORETINITIS BY LOW-DOSE T-CELL VACCINATION SO CELLULAR IMMUNOLOGY LA English DT Article ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; RETINOID-BINDING PROTEIN; MYELIN BASIC-PROTEIN; S-ANTIGEN; MULTIPLE-SCLEROSIS; LINE CELLS; ARTHRITIS; IMMUNODOMINANT; DISEASE; HYPERSENSITIVITY C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 36 TC 22 Z9 23 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD MAR PY 1992 VL 140 IS 1 BP 112 EP 122 DI 10.1016/0008-8749(92)90180-W PG 11 WC Cell Biology; Immunology SC Cell Biology; Immunology GA HF041 UT WOS:A1992HF04100009 PM 1739982 ER PT J AU KOTAKE, S SASAMOTO, Y KAWANO, Y SANUI, H WIGGERT, B CHADER, GJ GERY, I AF KOTAKE, S SASAMOTO, Y KAWANO, Y SANUI, H WIGGERT, B CHADER, GJ GERY, I TI THE EXISTENCE OF 2 COMPLETELY DISTINCT ANTIGENIC SITES WITHIN A DECAPEPTIDE SO CELLULAR IMMUNOLOGY LA English DT Article ID RETINOID-BINDING PROTEIN; AMINO-ACID-RESIDUES; T-CELL EPITOPES; PEPTIDE; UVEORETINITIS; DETERMINANT; RECOGNITION; IMMUNODOMINANCE; PINEALITIS; RECEPTOR C1 NEI,IMMUNOL LAB,BLDG 10,ROOM 10N208,BETHESDA,MD 20892. NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 25 TC 8 Z9 8 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 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD MAR PY 1992 VL 140 IS 1 BP 123 EP 129 DI 10.1016/0008-8749(92)90181-N PG 7 WC Cell Biology; Immunology SC Cell Biology; Immunology GA HF041 UT WOS:A1992HF04100010 PM 1371240 ER PT J AU TING, CC HARGROVE, ME AF TING, CC HARGROVE, ME TI IL-4 REGULATION OF A PROTEIN-KINASE-C INDEPENDENT PATHWAY FOR THE GENERATION OF ALPHA-CD3-INDUCED ACTIVATED KILLER-CELLS SO CELLULAR IMMUNOLOGY LA English DT Article ID STIMULATORY FACTOR-I; MONOCLONAL-ANTIBODY; CYTO-TOXICITY; LYMPHOCYTE-T; COSTIMULATORY SIGNAL; CYTOPLASMIC GRANULES; ANTI-CD3 ANTIBODY; GROWTH-FACTOR; TARGET-CELLS; PROLIFERATION RP TING, CC (reprint author), NCI,DIV CANC BIOL,ROOM 4B17,BLDG 10,BETHESDA,MD 20892, USA. NR 43 TC 14 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD MAR PY 1992 VL 140 IS 1 BP 130 EP 144 DI 10.1016/0008-8749(92)90182-O PG 15 WC Cell Biology; Immunology SC Cell Biology; Immunology GA HF041 UT WOS:A1992HF04100011 PM 1531452 ER PT J AU ANASTASSIOU, ED YAMADA, H BOUMPAS, DT TSOKOS, GC THYPHRONITIS, G BALOW, J MOND, JJ AF ANASTASSIOU, ED YAMADA, H BOUMPAS, DT TSOKOS, GC THYPHRONITIS, G BALOW, J MOND, JJ TI CHOLERA-TOXIN PROMOTES THE PROLIFERATION OF ANTI-MU ANTIBODY-PRESTIMULATED HUMAN B-CELLS SO CELLULAR IMMUNOLOGY LA English DT Article ID ADP-RIBOSYLATION; ADENYLATE-CYCLASE; IMMUNE-RESPONSE; LYMPHOCYTES-B; GROWTH-FACTOR; ACTIVATION; PROTEINS; SURFACE; CAMP; MEMBRANE C1 UNIFORMED SERV UNIV HLTH SCI,DEPT MED,A3060,4301 JONES BRIDGE RD,BETHESDA,MD 20814. NIDDKD,KIDNEY DIS SECT,BETHESDA,MD 20892. FU NIAID NIH HHS [AI24273, AI27465] NR 33 TC 8 Z9 8 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD MAR PY 1992 VL 140 IS 1 BP 237 EP 247 DI 10.1016/0008-8749(92)90190-Z PG 11 WC Cell Biology; Immunology SC Cell Biology; Immunology GA HF041 UT WOS:A1992HF04100019 PM 1310902 ER PT J AU ALBRO, PW KNECHT, KT SCHROEDER, JL CORBETT, JT MARBURY, D COLLINS, BJ CHARLES, J AF ALBRO, PW KNECHT, KT SCHROEDER, JL CORBETT, JT MARBURY, D COLLINS, BJ CHARLES, J TI ISOLATION AND CHARACTERIZATION OF THE INITIAL RADICAL ADDUCT FORMED FROM LINOLEIC-ACID AND ALPHA-(4-PYRIDYL 1-OXIDE)-N-TERT-BUTYLNITRONE IN THE PRESENCE OF SOYBEAN LIPOXYGENASE SO CHEMICO-BIOLOGICAL INTERACTIONS LA English DT Article DE SPIN TRAP; LIPOXYGENASE; LINOLEIC ACID; ALPHA-(4-PYRIDYL-1-OXIDE)-N-TERT-BUTYLNITRONE; HIGH PRESSURE LIQUID CHROMATOGRAPHY; ISOLATION AND CHARACTERIZATION; MASS SPECTRA; RADICAL ADDUCTS ID ELECTRON-SPIN RESONANCE; ANAEROBIC REACTION; OXIDATION; CHROMATOGRAPHY; MECHANISM; HYDROXYL AB The spin trapping agent alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (POBN) was used to trap the initial radical formed from [U-C-14]linoleic acid in the reaction with soybean lipoxygenase. By using low levels of enzyme and relatively short incubation times it was possible to avoid the formation of secondary oxidation products and polymers. The adduct was extracted after methyl esterification, and isolated by a combination of open column chromatography on silicic acid and high pressure liquid chromatography on Spherisorb S5 CN with non-aqueous solvents. The 1:1 POBN-linoleate adduct was characterized by UV, IR and ESR spectra of the appropriate HPLC column fraction, by the ratio of the UV absorption to C-14 content, and by mass spectrometry of the reduced (hydroxylamine) form. The results indicated that POBN trapped a linoleic acid carbon-centered radical such that POBN was attached to the fatty acid chain at C-13 or C-9 (two isomers), the linoleate double bonds having become conjugated in the process. The exact locations of the bridges in the two isomers were only tentatively determined. There was no evidence for the presence of oxygen-bridged adducts. The trapped linoleoyl radical adduct provides evidence for the production of a free radical as part of the enzymatic mechanism of soybean lipoxygenase. C1 NIEHS,CARCINOGENESIS & TOXICOL EVALUAT BRANCH,RES TRIANGLE PK,NC 27511. UNIV N CAROLINA,SCH PUBL HLTH,DEPT ENVIRONM SCI & ENGN,CHAPEL HILL,NC 27514. RP ALBRO, PW (reprint author), NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27511, USA. NR 23 TC 17 Z9 17 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0009-2797 J9 CHEM-BIOL INTERACT JI Chem.-Biol. Interact. PD MAR PY 1992 VL 82 IS 1 BP 73 EP 89 DI 10.1016/0009-2797(92)90015-D PG 17 WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology GA HK762 UT WOS:A1992HK76200006 PM 1312396 ER PT J AU ROM, WN TRAVIS, WD AF ROM, WN TRAVIS, WD TI LYMPHOCYTE-MACROPHAGE ALVEOLITIS IN NONSMOKING INDIVIDUALS OCCUPATIONALLY EXPOSED TO ASBESTOS SO CHEST LA English DT Article ID TUMOR NECROSIS FACTOR; BRONCHOALVEOLAR LAVAGE FLUID; ACTIVE PULMONARY SARCOIDOSIS; FIBROBLAST COLLAGEN-SYNTHESIS; RECOMBINANT INTERFERON-GAMMA; CELL-MEDIATED-IMMUNITY; PERIPHERAL-BLOOD; FIBRONECTIN PRODUCTION; SPONTANEOUS RELEASE; GRANITE WORKERS AB A disordered immunologic activity has been observed in humans and animal models of asbestosis and silicosis. To characterize the lung immunologic response following long-term occupational exposure to asbestos, bronchoalveolar lavage (BAL) was performed on 28 nonsmoking individuals. Increased BAL lymphocytes were observed in one third. Lung lymphocytes were predominantly of the CD4+ helper-inducer subtype with increased CD4+/CD8+ ratio and increased surface expression of DR antigen consistent with the activation phenotype. Histologic evaluation of lung tissue from two individuals with lymphocytic-macrophage alveolitis and asbestos exposure revealed an infiltration of alveolar walls with chronic inflammatory mononuclear cells (lymphocytes). Interferon gamma was spontaneously released by BAL cells from 19 (76 percent) of 25 of the individuals with asbestos exposure and only one of ten normal controls. The release of interferon gamma by BAL cells could be further stimulated with concanavalin A and suppressed by cyclosporine. Although asbestosis is characterized by a predominant alveolar macrophage alveolitis, there is a subgroup with lymphocytic alveolitis and activated lymphocytes participating in the inflammatory response, especially in those without respiratory impairment early in the course of the disease process. C1 NYU,BELLEVUE HOSP CTR,MED CTR,DEPT ENVIRONM MED,NEW YORK,NY 10016. NYU,BELLEVUE HOSP CTR,MED CTR,CHEST SERV,NEW YORK,NY 10016. NCI,DIV CANC BIOL & PREVENT,PATHOL LAB,BETHESDA,MD 20892. RP ROM, WN (reprint author), NYU,BELLEVUE HOSP CTR,MED CTR,DEPT MED,DIV PULM & CRIT CARE MED,NEW YORK,NY 10016, USA. NR 65 TC 25 Z9 26 U1 0 U2 3 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAR PY 1992 VL 101 IS 3 BP 779 EP 786 DI 10.1378/chest.101.3.779 PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA HG784 UT WOS:A1992HG78400037 PM 1541147 ER PT J AU BENNETT, WP HOLLSTEIN, MC HSU, IC SIDRANSKY, D LANE, DP VOGELSTEIN, B HARRIS, CC AF BENNETT, WP HOLLSTEIN, MC HSU, IC SIDRANSKY, D LANE, DP VOGELSTEIN, B HARRIS, CC TI MUTATIONAL SPECTRA AND IMMUNOHISTOCHEMICAL ANALYSES OF P53 IN HUMAN CANCERS SO CHEST LA English DT Article ID CELLULAR TUMOR-ANTIGEN; LUNG-CANCER; BREAST-CANCER; GENE; TRANSFORMATION; CARCINOMA; FORMS; ADENOCARCINOMA; HETEROZYGOSITY; CHROMOSOME-13 C1 NCI,DEC,LHC,BLDG 37,RM 2CO7,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. INT AGCY RES CANC,F-69372 LYONS,FRANCE. UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. UNIV DUNDEE,INST MED SCI,CANC RES CAMPAIGN LAB,DUNDEE DD1 4HN,SCOTLAND. RI Lane, David/C-4920-2008 NR 26 TC 18 Z9 20 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAR PY 1992 VL 101 IS 3 SU S BP S19 EP S20 DI 10.1378/chest.101.3_Supplement.19S PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA HP993 UT WOS:A1992HP99300010 PM 1541189 ER PT J AU NETTESHEIM, P FERRIOLA, P STEIGERWALT, R ROBERTSON, A RUNDHAUG, J AF NETTESHEIM, P FERRIOLA, P STEIGERWALT, R ROBERTSON, A RUNDHAUG, J TI THE ROLE OF GROWTH-FACTORS IN THE REGULATION OF PROLIFERATION OF TRACHEOBRONCHIAL EPITHELIUM SO CHEST LA English DT Article RP NETTESHEIM, P (reprint author), NIEHS,BLDG 101,RM D-235,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 5 TC 5 Z9 5 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAR PY 1992 VL 101 IS 3 SU S BP S23 EP S24 DI 10.1378/chest.101.3_Supplement.23S PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA HP993 UT WOS:A1992HP99300014 PM 1541193 ER PT J AU RANDELL, SH AF RANDELL, SH TI PROGENITOR-PROGENY RELATIONSHIPS IN AIRWAY EPITHELIUM SO CHEST LA English DT Article ID HAMSTER TRACHEAL EPITHELIUM; BASAL CELLS; FLOW-CYTOMETRY; RAT TRACHEA; DIFFERENTIATION; REPOPULATION; ADHESION; KINETICS; RABBITS; LUNGS RP RANDELL, SH (reprint author), NIEHS,PULM PATHOBIOL LAB,IPP MD D2-01,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 29 TC 17 Z9 17 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAR PY 1992 VL 101 IS 3 SU S BP S11 EP S16 PG 6 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA HP993 UT WOS:A1992HP99300006 PM 1541185 ER PT J AU CANNON, RO CAMICI, PG EPSTEIN, SE AF CANNON, RO CAMICI, PG EPSTEIN, SE TI PATHOPHYSIOLOGICAL DILEMMA OF SYNDROME-X SO CIRCULATION LA English DT Article DE CLINICAL PROGRESS SERIES; SYNDROME X; FLOW; ANGIOGRAPHY; ANGINA; ISCHEMIA ID NORMAL CORONARY ARTERIOGRAMS; POSITRON EMISSION TOMOGRAPHY; ISCHEMIC-HEART-DISEASE; STABLE ANGINA-PECTORIS; MYOCARDIAL BLOOD-FLOW; CHEST PAIN; FOLLOW-UP; MICROVASCULAR ANGINA; VASODILATOR RESERVE; ARTERY DISEASE C1 CNR,INST CLIN PHYSIOL,PISA,ITALY. UNIV PISA,IST PATOL MED,I-56100 PISA,ITALY. RP CANNON, RO (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B15,BETHESDA,MD 20892, USA. NR 71 TC 260 Z9 268 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1992 VL 85 IS 3 BP 883 EP 892 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HG541 UT WOS:A1992HG54100001 PM 1537124 ER PT J AU DILSIZIAN, V BONOW, RO AF DILSIZIAN, V BONOW, RO TI DIFFERENTIAL UPTAKE AND APPARENT TI-201 WASHOUT AFTER THALLIUM REINJECTION - OPTIONS REGARDING EARLY REDISTRIBUTION IMAGING BEFORE REINJECTION OR LATE REDISTRIBUTION IMAGING AFTER REINJECTION SO CIRCULATION LA English DT Article DE CORONARY ARTERY DISEASE; MYOCARDIAL ISCHEMIA; TI-201 SCINTIGRAPHY ID WALL-MOTION; PERSISTENT DEFECTS; TL-201 REINJECTION; METABOLIC-ACTIVITY; VIABLE MYOCARDIUM; TOMOGRAPHY; SPECT; REVASCULARIZATION; REVERSIBILITY; SCINTIGRAPHY AB Background. Because thallium reinjection enhances the identification of viable myocardium, many laboratories have adopted the routine practice of performing reinjection imaging instead of 3-4-hour redistribution imaging. This approach assumes that the stress-reinjection protocol provides the necessary information regarding both exercise-induced ischemia and myocardial viability. Because apparent "washout" of thallium may occur between redistribution and reinjection studies, we examined the limitations created by eliminating 3-4-hour redistribution images. Methods and Results. We studied 50 patients with chronic stable coronary artery disease by exercise thallium tomography, radionuclide angiography, and coronary arteriography. Immediately after the 3-4-hour redistribution images, 1 mCi thallium was injected at rest, and images were reacquired both 10 minutes and 24 hours after reinjection. The stress, redistribution, reinjection, and 24-hour images were then analyzed quantitatively, and the magnitude of change in regional thallium activity after reinjection was termed "differential uptake." Of the 127 abnormal myocardial regions on the stress images, 55 (43%) demonstrated either complete or partial reversibility on 3-4-hour redistribution images. After reinjection, 14 of these regions (25%) demonstrated apparent thallium washout due to low differential uptake of thallium, which was only 46 +/- 20% of that observed in normal regions. As a result, the relative thallium activity, which was 55 +/- 13% during stress (relative to normal regions) and increased significantly to 75 +/- 13% on 3-4-hour redistribution studies (p < 0.001), decreased to only 58 +/- 13% after thallium reinjection. At 24 hours, redistribution again developed in all 14 regions, resulting in a relative thallium activity of 71 +/- 16% (p < 0.03), which was similar to that achieved on 3-4-hour redistribution images. Twelve of the 14 regions (86%) exhibiting apparent washout after reinjection were supplied by a totally occluded coronary artery, of which eight (67%) had normal wall motion at rest. In contrast, only 41% of the regions with either improved or unchanged thallium uptake after reinjection were supplied by a totally occluded coronary artery (p < 0.05). Conclusions. These data indicate that regions with thallium defects that are reversible on 3-4-hour redistribution images may demonstrate apparent washout of thallium after reinjection due to low differential uptake. Although this occurs in only a small fraction of regions (8%) identified as abnormal on exercise images, these regions represent approximately 25% of regions showing redistribution. Such defects would appear irreversible if redistribution imaging is not performed before reinjection. However, these same myocardial regions also redistribute further after reinjection and are identified as reversible on 24-hour images. Thus, one of two imaging options, either stress-redistribution-reinjection imaging or stress-reinjection-24-hour imaging, may be used for a comprehensive assessment of myocardial ischemia and viability. C1 NIH,DEPT NUCL MED,BETHESDA,MD 20892. RP DILSIZIAN, V (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 20 TC 69 Z9 69 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1992 VL 85 IS 3 BP 1032 EP 1038 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HG541 UT WOS:A1992HG54100019 PM 1537101 ER PT J AU CANNON, RO DILSIZIAN, V OGARA, PT UDELSON, JE TUCKER, E PANZA, JA FANANAPAZIR, L MCINTOSH, CL WALLACE, RB BONOW, RO AF CANNON, RO DILSIZIAN, V OGARA, PT UDELSON, JE TUCKER, E PANZA, JA FANANAPAZIR, L MCINTOSH, CL WALLACE, RB BONOW, RO TI IMPACT OF SURGICAL RELIEF OF OUTFLOW OBSTRUCTION ON THALLIUM PERFUSION ABNORMALITIES IN HYPERTROPHIC CARDIOMYOPATHY SO CIRCULATION LA English DT Article DE HYPERTROPHIC CARDIOMYOPATHY; TI-201; SCINTIGRAPHY; MYOCARDIAL ISCHEMIA; LEFT VENTRICLE ID LEFT-VENTRICULAR HYPERTROPHY; EMISSION COMPUTED-TOMOGRAPHY; MITRAL-VALVE REPLACEMENT; SUB-AORTIC STENOSIS; TERM FOLLOW-UP; SUBAORTIC STENOSIS; MYOCARDIAL-METABOLISM; EXERCISE PERFORMANCE; SYMPTOMATIC STATUS; SEPTAL MYOTOMY AB Background. To assess the impact of surgical relief of left ventricular outflow obstruction on myocardial perfusion abnormalities in patients with obstructive hypertrophic cardiomyopathy, 20 symptomatic patients who underwent a septal myectomy or mitral valve replacement were studied with assessment of myocardial perfusion during exercise by Tl-201 emission computed tomography before and 6 months after surgery. Methods and Results. Before surgery, 15 patients had myocardial perfusion defects during exercise that completely normalized at rest, one patient had both reversible and fixed perfusion defects, two patients had fixed defects only, and two patients had normal exercise and rest thallium scans. After surgical relief of left ventricular outflow obstruction (basal gradient reduced from 62 +/- 40 to 7 +/- 12 mm Hg, p < 0.001; peak provokable gradient reduced from 131 +/- 27 to 49 +/- 36 mm Hg, p < 0.001), repeat exercise thallium studies showed complete normalization of perfusion defects in 11 patients, including the two patients with fixed defects alone before surgery, and improvement in the magnitude and distribution of perfusion defects in five additional patients. This was associated with a significant reduction in the number of patients with reversible regional defects (five patients compared with 13 patients before surgery, p = 0.026) and of patients with endocardial hypoperfusion (four patients compared with 12 patients before surgery, p = 0.024). Furthermore, increased lung uptake of thallium was noted in five patients after surgery, compared with 12 patients before surgery (p = 0.055). Only two patients with reversible perfusion defects before surgery had unchanged postoperative studies. However, four patients acquired new fixed defects as a consequence of surgery, and two of these four had the greatest severity and distribution of left ventricular hypertrophy by echocardiography. These four patients experienced a substantially greater decrease in ejection fraction (-26 +/- 15%) after surgery than the remaining patients (-3 +/- 14%, p < 0.01). Conclusions. Surgical relief of left ventricular outflow obstruction results in normalization or improvement of myocardial perfusion in the majority of patients with reversible and fixed perfusion defects by Tl-201 scintigraphy. However, surgery may result in myocardial injury and scarring, with consequent decreased left ventricular ejection fraction in some patients. C1 NHLBI,CARDIAC SURG BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV HOSP,DIV CARDIAC SURG,WASHINGTON,DC 20007. RP CANNON, RO (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B15,BETHESDA,MD 20892, USA. NR 32 TC 47 Z9 48 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1992 VL 85 IS 3 BP 1039 EP 1045 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HG541 UT WOS:A1992HG54100020 PM 1537102 ER PT J AU FLUGELMAN, MY JAKLITSCH, MT NEWMAN, KD CASSCELLS, W BRATTHAUER, GL DICHEK, DA AF FLUGELMAN, MY JAKLITSCH, MT NEWMAN, KD CASSCELLS, W BRATTHAUER, GL DICHEK, DA TI LOW-LEVEL INVIVO GENE-TRANSFER INTO THE ARTERIAL-WALL THROUGH A PERFORATED BALLOON CATHETER SO CIRCULATION LA English DT Article DE GENETICS; BETA-GALACTOSIDASE; CATHETERS; POLYMERASE CHAIN REACTION ID ENDOTHELIAL-CELLS; EXPRESSION INVIVO; RETROVIRAL VECTORS; HUMAN-SERUM; PROLIFERATION; MOUSE; IMPLANTATION; SEQUENCES; DELIVERY; RECEPTOR AB Background. Gene transfer into the arterial wall may provide a novel therapeutic strategy for the treatment of coronary artery restenosis. Previously described methods for gene transfer into the arterial wall require total vessel occlusion for 30 minutes. We sought to develop a protocol for gene transfer within a more clinically relevant time frame. Methods and Results. We used a perforated balloon (Wolinsky) catheter to inject retroviral vector-containing virions into rabbit aortas in vivo. The virions were injected within 1 minute. Aortas were removed 5-14 days after injection and analyzed for evidence of gene transfer. In initial studies, nine rabbits were injected with a vector expressing the beta-galactosidase gene, and nine rabbits were injected with either non-beta-galactosidase-containing vectors or with a vehicle control. Histochemical staining of aortic tissues revealed blue (positive) cells in eight of nine experimental rabbits and six of nine controls. Because of the lack of specificity of the beta-galactosidase detection system, we adopted a polymerase chain reaction-based protocol in which oligonucleotide primers were used to amplify specific vector-related sequences from aortic tissue extracts. The polymerase chain reaction protocol, calibrated with standards containing known numbers of transduced cells, revealed low amounts of vector-related sequences in six of 12 vector-injected rabbits and in one of 13 controls (p < 0.03). Comparison with standards indicated that fewer than 100 transduced cells were present in a 2-cm length of the injected aortic tissue. Conclusions. Although in vivo gene transfer through an infusion balloon catheter can be accomplished within 1 minute, the therapeutic use of this protocol is limited by the small number of cells that are transduced. C1 CHILDRENS NATL MED CTR,DEPT SURG,WASHINGTON,DC. ARMED FORCES INST PATHOL,DEPT CELLULAR PATHOL,WASHINGTON,DC 20306. NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 43 TC 156 Z9 157 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1992 VL 85 IS 3 BP 1110 EP 1117 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HG541 UT WOS:A1992HG54100029 PM 1537109 ER PT J AU LAROSA, JC CLEEMAN, JI AF LAROSA, JC CLEEMAN, JI TI CHOLESTEROL LOWERING AS A TREATMENT FOR ESTABLISHED CORONARY HEART-DISEASE SO CIRCULATION LA English DT Article ID MYOCARDIAL-INFARCTION; PRIMARY PREVENTION; SERUM-CHOLESTEROL; APOLIPOPROTEIN-B; ARTERY DISEASE; MEN; MORTALITY; TRIALS; ATHEROSCLEROSIS; REGRESSION C1 GEORGETOWN UNIV,MED CTR,LIPID RES CLIN,WASHINGTON,DC 20007. NHLBI,NATL CHOLESTEROL EDUC PROGRAM,BETHESDA,MD 20892. NR 32 TC 61 Z9 62 U1 1 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1992 VL 85 IS 3 BP 1229 EP 1235 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HG541 UT WOS:A1992HG54100048 PM 1346980 ER PT J AU SARTORI, A ROQUEBARREIRA, MC COE, J CAMPOSNETO, A AF SARTORI, A ROQUEBARREIRA, MC COE, J CAMPOSNETO, A TI IMMUNE-COMPLEX GLOMERULONEPHRITIS IN EXPERIMENTAL KALA-AZAR .2. DETECTION AND CHARACTERIZATION OF PARASITE ANTIGENS AND ANTIBODIES ELUTED FROM KIDNEYS OF LEISHMANIA-DONOVANI-INFECTED HAMSTERS SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article DE LEISHMANIA-DONOVANI; GLOMERULONEPHRITIS; EXPERIMENTAL KALA-AZAR; IMMUNE COMPLEXES ID AMERICAN VISCERAL LEISHMANIASIS; ACID-PHOSPHATASE; PROLIFERATIVE GLOMERULONEPHRITIS; POLYACRYLAMIDE GELS; RENAL-DISEASE; PROTEINS; IMMUNOSUPPRESSION; PURIFICATION; INVOLVEMENT; ACTIVATION AB In a previous report analysing kidney sections by immunofluorescence we showed that hamsters infected with L. donovani develop a glomerulonephritis (GN) associated with deposition of hamster immunoglobulins and parasite antigens in the glomeruli. In this study we characterize these immune components eluted from the kidneys. The eluted immunoglobulins showed specificity for L. donovani antigens and hamster immunoglobulins (rheumatoid factor-like activity). The four isotypes IgG1, IgG2, IgA and IgM were detected. Several L. donovani antigens were detected in the renal eluates by Western blot and immunoprecipitation using I-125-labelled eluates. Proteins with mol. wt of 134. 82, 52, 31, and 26 kD were detected by Western blot and proteins with 134, 110, 93, 89 and 48 kD were detected by immunoprecipitation. With the exception of the 134 kD protein which was recognized by both rabbit anti-promastigote and rabbit anti-amastigote sera all the others were recognized only by the anti-amastigote serum. The 134 kD protein was the only one isolated from the kidneys of infected hamster immunocomplexed with IgG and was the only one detected in a promastigote lysate using IgG from L. donovani-infected hamsters. C1 UNIV SAO PAULO,RIBEIRAO PRETO MED SCH,DEPT IMMUNOL,BR-14049 RIBEIRAO PRETO,BRAZIL. NIH,HAMILTON,MT. RI Roque-Barreira, Maria-Cristina/A-4552-2008 OI Roque-Barreira, Maria-Cristina/0000-0001-7425-0908 NR 57 TC 12 Z9 12 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD MAR PY 1992 VL 87 IS 3 BP 386 EP 392 PG 7 WC Immunology SC Immunology GA HG588 UT WOS:A1992HG58800010 PM 1544224 ER PT J AU EMANCIPATOR, K AF EMANCIPATOR, K TI LOW BIAS IN ASSAYED VALUES OF LIPOPROTEIN ANTIGENS LIPOPROTEIN(A) AND APOLIPOPROTEIN-A-I AND APOLIPOPROTEIN-B IN MIDDAY POSTPRANDIAL BLOOD SPECIMENS COMPARED WITH MORNING FASTING SPECIMENS SO CLINICAL CHEMISTRY LA English DT Article DE SAMPLE COLLECTION; VARIATION, SOURCE OF ID PLASMA AB Two-hour postprandial specimens have a -14% proportional bias for lipoprotein(a) [Lp(a)], a -0.035 g/L systematic bias for apolipoprotein (apo) A-I, and a -9% proportional bias for apo B, compared with values in 12-h fasting specimens. Although a physiological hemodilution appears to account for a portion of these biases, other major factors must be implicated for Lp(a) and apo B. Even after dilutional effects are controlled for, assayed values of Lp(a) are 11-13% lower, and assayed values of apo B are 8-9% lower, in postprandial specimens than in fasting specimens. Therefore, the time of collection of a blood sample relative to the last meal can significantly affect assayed values of lipoprotein antigens. Further studies are needed to determine whether these observations result from a physiological sequestering of lipoproteins in the postprandial state or from negative interferences affecting the assays of lipoprotein antigens. C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,BETHESDA,MD 20892. NR 6 TC 9 Z9 9 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD MAR PY 1992 VL 38 IS 3 BP 431 EP 433 PG 3 WC Medical Laboratory Technology SC Medical Laboratory Technology GA HJ870 UT WOS:A1992HJ87000023 PM 1532140 ER PT J AU WOLINSKY, SM DREW, JB MILMAN, G HOFF, R DRAGON, EA HUI, J OTTO, P GUPTA, P FARZADEGAN, H WHETSELL, AJ AF WOLINSKY, SM DREW, JB MILMAN, G HOFF, R DRAGON, EA HUI, J OTTO, P GUPTA, P FARZADEGAN, H WHETSELL, AJ TI NONRADIOISOTOPIC DETECTION OF NUCLEIC-ACIDS AMPLIFIED WITH PCR-BASED TECHNIQUES SO CLINICAL CHEMISTRY LA English DT Article; Proceedings Paper CT 1991 SAN DIEGO CONF ON NUCLEIC ACIDS : THE LEADING EDGE CY 1991 CL SAN DIEGO, CA SP AMER ASSOC CLIN CHEM, SAN DIEGO SECT, AMER ASSOC CLIN CHEM, MOLEC PATHOL DIV ID HUMAN IMMUNODEFICIENCY VIRUS; INFANTS C1 NIAID,BETHESDA,MD 20892. ROCHE DIAGNOST SYST,FAIR LAWN,NJ 07410. UNIV PITTSBURGH,PITTSBURGH,PA 15261. JOHNS HOPKINS UNIV,BALTIMORE,MD 21205. RP WOLINSKY, SM (reprint author), NORTHWESTERN UNIV,CHICAGO,IL 60611, USA. RI Wolinsky, Steven/B-2893-2012 NR 6 TC 6 Z9 6 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD MAR PY 1992 VL 38 IS 3 BP 459 EP 460 PG 2 WC Medical Laboratory Technology SC Medical Laboratory Technology GA HJ870 UT WOS:A1992HJ87000052 ER PT J AU EASTMAN, RC ARAKAKI, RF SHAWKER, T SCHOCK, R ROACH, P COMI, RJ GORDEN, P AF EASTMAN, RC ARAKAKI, RF SHAWKER, T SCHOCK, R ROACH, P COMI, RJ GORDEN, P TI A PROSPECTIVE EXAMINATION OF OCTREOTIDE-INDUCED GALLBLADDER CHANGES IN ACROMEGALY SO CLINICAL ENDOCRINOLOGY LA English DT Article ID LONG-TERM TREATMENT; SOMATOSTATIN ANALOG SMS-201-995; REQUIRING PROLONGED OBSERVATION; CHOLELITHIASIS; GALLBLADDER; PITUITARY; ASPIRIN; PATIENT; TUMORS; STONES AB OBJECTIVE We wished to determine the effects of octreotide acetate, a somatostatin analogue, on gall-bladder function during treatment of acromegaly. DESIGN We used a prospective, open label trial of somatostatin analogue. PATIENTS Seventeen patients with acromegaly took part. MEASUREMENTS Ultrasonographic evaluation of gall-bladder contents were performed pretreatment, after 1 month, and subsequently at intervals of 3-6 months. RESULTS Non-shadowing floating echogenic particles were observed in the gall-bladder in 12 of 17 patients after (mean +/- SEM) 2.5 +/- 0.6 months of treatment. During long-term treatment (mean 20.8 +/- 4.3, median 13, range 1-59 months), ultrasound evidence for cholelithiasis was observed in four patients after 20 +/- 4 months (range 4.2-43) months of octreotide therapy. No symptoms of biliary tract disease have been observed. Duration of acromegaly, average GH, average IGF-I, gender, age at entry, dose of analogue, and concurrent use of non-steroidal anti-inflammatory drugs did not affect the occurrence of sludge or gallstones. CONCLUSIONS Formation of non-shadowing, floating echogenic particles occurs commonly during the first 6 months of treatment with octreotide acetate. Cholelithiasis is a risk of long-term treatment. C1 NIH,CTR CLIN,DEPT NURSING,BETHESDA,MD 20892. NIDDKD,BETHESDA,MD. UNIV HAWAII,SCH MED,DEPT MED,HONOLULU,HI 96813. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DIV ENDOCRINOL,HANOVER,NH 03756. RP EASTMAN, RC (reprint author), NIH,DIABET BRANCH,BLDG 10,ROOM 85-243,BETHESDA,MD 20892, USA. NR 23 TC 18 Z9 18 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0300-0664 J9 CLIN ENDOCRINOL JI Clin. Endocrinol. PD MAR PY 1992 VL 36 IS 3 BP 265 EP 269 DI 10.1111/j.1365-2265.1992.tb01442.x PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HF551 UT WOS:A1992HF55100009 PM 1563079 ER PT J AU SPITZER, RE STITZEL, AE TSOKOS, GC AF SPITZER, RE STITZEL, AE TSOKOS, GC TI STUDY OF THE IDIOTYPIC RESPONSE TO AUTOANTIBODY TO THE ALTERNATIVE PATHWAY C3/C5 CONVERTASE IN NORMAL INDIVIDUALS, PATIENTS WITH MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS, AND EXPERIMENTAL-ANIMALS SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID C3-C5 CONVERTASE; NEPHRITIC FACTOR; INTERNAL IMAGE; C3 CONVERTASE; ANTIBODY; ANTIGEN; COMPLEMENT; VACCINE C1 NIH,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. RP SPITZER, RE (reprint author), SUNY HLTH SCI CTR,DEPT PEDIAT,SYRACUSE,NY 13210, USA. NR 20 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD MAR PY 1992 VL 62 IS 3 BP 291 EP 294 DI 10.1016/0090-1229(92)90105-W PG 4 WC Immunology; Pathology SC Immunology; Pathology GA HH787 UT WOS:A1992HH78700007 PM 1541054 ER PT J AU WALSH, TJ LEE, JW ROILIDES, E FRANCIS, P BACHER, J LYMAN, CA PIZZO, PA AF WALSH, TJ LEE, JW ROILIDES, E FRANCIS, P BACHER, J LYMAN, CA PIZZO, PA TI EXPERIMENTAL ANTIFUNGAL CHEMOTHERAPY IN GRANULOCYTOPENIC ANIMAL-MODELS OF DISSEMINATED CANDIDIASIS - APPROACHES TO UNDERSTANDING INVESTIGATIONAL ANTIFUNGAL COMPOUNDS FOR PATIENTS WITH NEOPLASTIC DISEASES SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID ENCAPSULATED AMPHOTERICIN-B; CEREBROSPINAL-FLUID; CILOFUNGIN LY121019; TISSUE PENETRATION; FUNGAL-INFECTIONS; CANCER-PATIENTS; FLUCONAZOLE PENETRATION; CRYPTOCOCCAL MENINGITIS; HEPATIC CANDIDIASIS; INVITRO ACTIVITY AB Disseminated candidiasis is the most common life-threatening invasive fungal infection in granulocytopenic patients. A review of recent approaches to pre-clinical laboratory investigation of promising antifungal compounds, which may have potential utility in granulocytopenic patients is presented. A particularly useful strategy is the study of persistently granulocytopenic rabbit models of acute, subacute, and chronic forms of disseminated candidiasis. When the antifungal triazoles (fluconazole, itraconazole, and SCH 39304 [SCH 42427]) were each evaluated for use as preventive, early treatment, or delayed treatment in the different models, the triazoles were consistently more active when used for preventive and early treatment than for delayed treatment. These triazoles were as active as amphotericin B plus flucytosine (AB + FC) when used for early treatment but were less active than AB + FC when used for delayed treatment. Several lipid formulations of amphotericin B demonstrate reduced nephrotoxicity at higher safely achievable dosages in comparison to those of deoxycholate amphotericin B in several models of disseminated candidiasis. When administered to follow non-linear saturable Michaelis-Menten-type plasma pharmacokinetics, the antifungal activity of the echinocandin compound cilofungin was significantly augmented. Thoughtfully designed and carefully conducted laboratory investigations in appropriate animal models of disseminated candidiasis can provide a scientific foundation and guide for development of clinical protocols investigating new approaches to prevention and treatment of invasive candidiasis in granulocytopenic patients. C1 NATL CTR RES RESOURCES,SURG BRANCH,BETHESDA,MD. RP WALSH, TJ (reprint author), NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892, USA. NR 59 TC 26 Z9 27 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAR PY 1992 VL 14 SU 1 BP S139 EP S147 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HF382 UT WOS:A1992HF38200021 PM 1562687 ER PT J AU OREN, DA JACOBSEN, FM WEHR, TA CAMERON, CL ROSENTHAL, NE AF OREN, DA JACOBSEN, FM WEHR, TA CAMERON, CL ROSENTHAL, NE TI PREDICTORS OF RESPONSE TO PHOTOTHERAPY IN SEASONAL AFFECTIVE-DISORDER SO COMPREHENSIVE PSYCHIATRY LA English DT Article ID LIGHT THERAPY RP OREN, DA (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,BLDG 10,ROOM 4S239,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 13 TC 42 Z9 42 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0010-440X J9 COMPR PSYCHIAT JI Compr. Psychiat. PD MAR-APR PY 1992 VL 33 IS 2 BP 111 EP 114 DI 10.1016/0010-440X(92)90006-C PG 4 WC Psychiatry SC Psychiatry GA HH791 UT WOS:A1992HH79100006 PM 1544295 ER PT J AU DANFORTH, DN AF DANFORTH, DN TI HORMONE RECEPTORS IN MALIGNANCY SO CRITICAL REVIEWS IN ONCOLOGY/HEMATOLOGY LA English DT Review ID EPIDERMAL GROWTH-FACTOR; HUMAN-BREAST-CANCER; HUMAN ANDROGEN RECEPTOR; RENAL-CELL CARCINOMA; HUMAN GLUCOCORTICOID RECEPTOR; CHRONIC LYMPHOCYTIC-LEUKEMIA; HUMAN PROGESTERONE-RECEPTOR; MESSENGER-RIBONUCLEIC-ACID; HUMAN ESTROGEN-RECEPTOR; MAMMARY-TUMOR VIRUS RP DANFORTH, DN (reprint author), NCI, SURG BRANCH, BLDG 10, RM 2B38, BETHESDA, MD 20892 USA. NR 574 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1040-8428 J9 CRIT REV ONCOL HEMAT JI Crit. Rev. Oncol./Hematol. PD MAR PY 1992 VL 12 IS 2 BP 91 EP 149 DI 10.1016/1040-8428(92)90086-6 PG 59 WC Oncology; Hematology SC Oncology; Hematology GA HM522 UT WOS:A1992HM52200002 PM 1317180 ER PT J AU NI, M YAMAKI, K KIKUCHI, T FERRICK, M SHINOHARA, T NUSSENBLATT, RB CHAN, CC AF NI, M YAMAKI, K KIKUCHI, T FERRICK, M SHINOHARA, T NUSSENBLATT, RB CHAN, CC TI DEVELOPMENTAL EXPRESSION OF S-ANTIGEN IN FETAL HUMAN AND RAT EYE SO CURRENT EYE RESEARCH LA English DT Article ID BETA-ADRENERGIC-RECEPTOR; ALPHA-TRANSDUCIN; 48-KDA PROTEIN; MESSENGER-RNAS; BOVINE RETINA; PINEAL-GLAND; ARRESTIN; DROSOPHILA; CDNA; IMMUNOREACTIVITY AB Developmental expression of S-antigen and its mRNA in human and rat fetal retina was studied by immunocytochemical and in situ hybridization techniques. Immunocytochemistry indicated that S-antigen was present after 4 months gestation in the fetal human retina. In the rat, S-antigen was detected in the retina only after birth. In situ hybridization studies indicated that the S-antigen mRNA was present at 13 weeks gestational age in the human and at 15 days in the rat embryo. S-antigen mRNA was expressed not only in the retina but also in ocular tissues of neural crest origin in the fetus. C1 NEI,IMMUNOL LAB,BLDG 10,RM 10N206,BETHESDA,MD 20892. NEI,RETINAL CELLS & MOLEC BIOL LAB,BETHESDA,MD 20892. OI Shinohara, Toshimichi/0000-0002-7197-9039 NR 35 TC 12 Z9 13 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD MAR PY 1992 VL 11 IS 3 BP 219 EP 229 DI 10.3109/02713689209001773 PG 11 WC Ophthalmology SC Ophthalmology GA HQ148 UT WOS:A1992HQ14800004 PM 1587145 ER PT J AU ROSARIO, MO PERKINS, SL OBRIEN, DA ALLEN, RL EDDY, EM AF ROSARIO, MO PERKINS, SL OBRIEN, DA ALLEN, RL EDDY, EM TI IDENTIFICATION OF THE GENE FOR THE DEVELOPMENTALLY EXPRESSED 70KDA HEAT-SHOCK PROTEIN (P70) OF MOUSE SPERMATOGENIC CELLS SO DEVELOPMENTAL BIOLOGY LA English DT Article ID MALE GERM LINE; HSP70 GENE; NUCLEOTIDE-SEQUENCE; MESSENGER-RNAS; MORPHOLOGICAL CHARACTERIZATION; CLONING; RECEPTOR; TESTIS; MEMBER; FAMILY C1 ENSYS INC,DEPT IMMUNOL,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,REPROD BIOL LAB,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT PEDIAT,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC 27599. RP ROSARIO, MO (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,GAMETE BIOL SECT,RES TRIANGLE PK,NC 27709, USA. NR 45 TC 89 Z9 91 U1 1 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD MAR PY 1992 VL 150 IS 1 BP 1 EP 11 DI 10.1016/0012-1606(92)90002-X PG 11 WC Developmental Biology SC Developmental Biology GA HF811 UT WOS:A1992HF81100001 PM 1537426 ER PT J AU BIBEN, M AF BIBEN, M TI ALLOMATERNAL VOCAL BEHAVIOR IN SQUIRREL-MONKEYS SO DEVELOPMENTAL PSYCHOBIOLOGY LA English DT Article ID SAIMIRI-SCIUREUS AB Three groups of squirrel monkeys, containing 1-3 infants (N = 7) and 4 adult females each, were observed weekly for the first 12 weeks of the infants' lives. Infants received approximately 100 vocalizations, mostly "caregiver" calls, per waking hour from their mothers and the other adult females with whom they were housed (allomothers). Mothers vocalized very little to their own infants during the first few weeks of life, when infants remain on the mother's back full-time. Instead, allomothers (who were often carrying their own dependent infants) vocalized copiously to others' very young infants. Infants responded vocally to these allomaternal caregiver calls as early as Day 1 but were less responsive to mothers. When infants began leaving the mothers' backs, mothers' rates of calling increased five-fold as they used caregiver calls to retrieve separated infants. Early vocalizing to infants involves them in their first social exchanges and is probably performed by allomothers rather than mothers because the infant rides dorsally in this genus. RP BIBEN, M (reprint author), NICHHD,COMPARAT ETHOL LAB,NIHAC,BLDG 112,RM 205,BETHESDA,MD 20892, USA. NR 29 TC 6 Z9 6 U1 1 U2 4 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0012-1630 J9 DEV PSYCHOBIOL JI Dev. Psychobiol. PD MAR PY 1992 VL 25 IS 2 BP 79 EP 92 DI 10.1002/dev.420250202 PG 14 WC Developmental Biology; Psychology SC Developmental Biology; Psychology GA HM537 UT WOS:A1992HM53700001 PM 1577205 ER PT J AU HEROLD, KC BLUESTONE, JA MONTAG, AG PARIHAR, A WIEGNER, A GRESS, RE HIRSCH, R AF HEROLD, KC BLUESTONE, JA MONTAG, AG PARIHAR, A WIEGNER, A GRESS, RE HIRSCH, R TI PREVENTION OF AUTOIMMUNE DIABETES WITH NONACTIVATING ANTI-CD3 MONOCLONAL-ANTIBODY SO DIABETES LA English DT Article ID TUMOR-NECROSIS-FACTOR; T-CELL FUNCTION; GAMMA-INTERFERON; RECENT-ONSET; IFN-GAMMA; INVIVO; MICE; STREPTOZOTOCIN; OKT3; IMMUNOSUPPRESSION AB Autoreactive T cells mediate diabetes in animal models of insulin-dependent diabetes mellitus (IDDM) and are believed to cause the disease in humans. Therefore, immunotherapies directed against T cells are of particular interest for the treatment of IDDM. One candidate for such immunotherapy is anti-CD3 monoclonal antibodies (MoAbs), but clinical side effects are common with anti-CD3 treatment due to the ability of these MoAbs to activate T cells in vivo. However, F(ab')2 fragments of anti-CD3 are nonactivating and immunosuppressive. We evaluated the effects of whole anti-CD3 MoAb and F(ab')2 fragments in the setting of experimental autoimmune diabetes. Treatment with whole MoAb or F(ab')2 fragments significantly reduced the hyperglycemia induced with multiple low dosages of streptozocin (MDSDM; 232 +/- 23 mg/dl, P < 0.01 and 235 +/- 16 mg/dl, P < 0.01 vs. 325 +/- 25 mg/dl, respectively) in male CD1 mice. Both whole MoAb and F(ab')2 fragments suppressed the development of insulitis (P < 0.001). Treatment with whole MoAb resulted in marked weight loss (10.4 +/- 1.5% of total body wt), and the mice appeared ill and listless, whereas, mice treated with F(ab')2 fragments gained weight (4.9 +/- 5.5% of total body wt) and appeared healthy. Treatment with whole MoAb caused activation of T cells in vivo as reflected by proliferation of freshly isolated spleen cells to recombinant interleukin-2. Depletion of T cells with whole MoAb was more pronounced than with F(ab')2 fragments, and T-cell receptor (TCR) reexpression on remaining cells occurred with F(ab')2 fragments within 48 h after F(ab')2 treatment. Despite the expression of this surface molecule, signaling by the TCR complex was blocked because T cells stimulated with anti-CD3 MoAb failed to produce lymphokines. We conclude that treatment with either whole anti-CD3 MoAb or F(ab')2 fragments suppresses the hyperglycemia and insulitis of MDSDM. The morbidity seen with whole MoAb does not occur with F(ab')2 fragments and is correlated with the failure of the latter to activate T cells in vivo. Nonactivating forms of anti-CD3 MoAbs may be a useful form of immunosuppressive treatment for incipient IDDM because they do not cause morbidity associated with activation of T cells, which occurs with whole MoAb. C1 UNIV CHICAGO,COMM IMMUNOL,CHICAGO,IL 60637. UNIV CHICAGO,BEN MAY INST,DEPT PATHOL,CHICAGO,IL 60637. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP HEROLD, KC (reprint author), UNIV CHICAGO,BEN MAY INST,DEPT MED,BOX 435,5841 S MARYLAND AVE,CHICAGO,IL 60637, USA. FU NIDDK NIH HHS [DK-01938] NR 29 TC 104 Z9 108 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD MAR PY 1992 VL 41 IS 3 BP 385 EP 391 DI 10.2337/diabetes.41.3.385 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HQ276 UT WOS:A1992HQ27600019 PM 1532369 ER PT J AU KIM, H KADOWAKI, H SAKURA, H ODAWARA, M MOMOMURA, K TAKAHASHI, Y MIYAZAKI, Y OHTANI, T AKANUMA, Y YAZAKI, Y KASUGA, M TAYLOR, SI KADOWAKI, T AF KIM, H KADOWAKI, H SAKURA, H ODAWARA, M MOMOMURA, K TAKAHASHI, Y MIYAZAKI, Y OHTANI, T AKANUMA, Y YAZAKI, Y KASUGA, M TAYLOR, SI KADOWAKI, T TI DETECTION OF MUTATIONS IN THE INSULIN-RECEPTOR GENE IN PATIENTS WITH INSULIN RESISTANCE BY ANALYSIS OF SINGLE-STRANDED CONFORMATIONAL POLYMORPHISMS SO DIABETOLOGIA LA English DT Article DE HYPERINSULINEMIA; TYROSINE KINASE ACTIVITY; TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS; OBESITY; SCREENING ID POLYMERASE CHAIN-REACTION; TYROSINE KINASE DOMAIN; ACANTHOSIS NIGRICANS; GEL-ELECTROPHORESIS; POINT MUTATIONS; MUTANT ALLELES; DNA; SEQUENCE; CLEAVAGE; AMPLIFICATION AB We analyzed single-stranded conformational polymorphisms to screen for mutations and polymorphisms in the insulin receptor gene in subjects with or without insulin resistance. Using this new technique, we demonstrated the existence of mutations in the insulin receptor gene which we had identified previously. In addition, a new mutation was found in exon 20 of the insulin receptor gene in a patient with moderate insulin resistance associated with morbid obesity, acanthosis nigricans, and polycystic ovary syndrome. The patient was heterozygous for a mutation substituting Leu (CTG) for Pro (CCG) at codon 1178. Pro1178 is a part of a characteristic sequence motif (D1150 F1151 G1152---A1177 P1178 E1179) common to many protein kinases. Analysis of single-stranded conformational polymorphisms was also used to estimate the frequency of a polymorphism at codon 1058. The two codons CAC (1058 His) and CAT (1058 His) both had a prevalence of 50 % in 30 Japanese subjects. These data demonstrate that analysis of single-stranded conformational polymorphisms is a simple and sensitive screening method for mutations and polymorphisms in the insulin receptor gene in subjects with or without insulin resistance. Identification of a mutation in the insulin receptor gene in a patient with a moderate degree of insulin resistance associated with morbid obesity suggests that insulin receptor mutations may exist in patients with Type 2 (non-insulin-dependent) diabetes mellitus associated with a moderate degree of insulin resistance. C1 UNIV TOKYO,FAC MED,DEPT INTERNAL MED 3,HONGO 7-3-1,BUNKYO KU,TOKYO 113,JAPAN. TOKYO WOMENS MED COLL,DEPT PEDIAT,TOKYO 162,JAPAN. KOBE UNIV,FAC MED,DEPT INTERNAL MED 2,KOBE 657,JAPAN. NIH,DIABET BRANCH,BETHESDA,MD 20892. MISATO KENWA HOSP,MISATO,JAPAN. ASAHI LIFE FDN,INST DIABET CARE & RES,TOKYO,JAPAN. NR 33 TC 55 Z9 57 U1 1 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD MAR PY 1992 VL 35 IS 3 BP 261 EP 266 DI 10.1007/BF00400927 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HF812 UT WOS:A1992HF81200011 PM 1563582 ER PT J AU ZIERDT, CH AF ZIERDT, CH TI LIGHT-MICROSCOPIC MORPHOLOGY, ULTRASTRUCTURE, CULTURE, AND RELATIONSHIP TO DISEASE OF THE NUTRITIONAL AND CELL-WALL-DEFICIENT ALPHA-HEMOLYTIC STREPTOCOCCI SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE LA English DT Article ID VARIANT STREPTOCOCCI; ENDOCARDITIS AB Alpha-Hemolytic streptococci, variously described as cell-wall deficient (C), L form (L), thiol dependent (O), satelliting (S), pyridoxal dependent (PY), and nutritionally deficient (N), or CLOSPYN, were isolated from patients with endocarditis, brain abscess, subauricular abscess, septicemia, acute and chronic urethritis, recurrent aphthous stomatitis, and fever of undetermined origin. With the aid of satelliting, most of the strains were adapted to grow on a human Mycoplasma growth agar consisting of brain-heart infusion agar fortified with 20% human blood, yeast extract, and arginine. Selected CLOSPYN strains required extensive subculture for only partial reversion to parentallike characteristics. Four of six strains biochemically tested were judged Streptococcus morbillorum. Two were unidentifiable. The CLOSPYN form was relatively inert biochemically, but glucose was converted mainly to lactic acid, with acetic acid also present. Guanine-cytosine values were 39%-43%. Cell wall material was present by transmission electron microscopy (TEM), but its synthesis was uneven on single cells and abnormally thickened on other cells. Closely spaced, incompleted septa occurred in cell chains, which resulted in unusually long chains of flattened cells resembling on TEM a stack of checkers. Mesosomes were frequent, greatly enlarged, convoluted, and elongated. They were often sectioned as circular and laminated, with 2-5 layers. Mesosomes were in close contact with nucleoid bodies, which, in turn, were closely apposed or integral with the cytoplasmic membranes in areas of cross-wall development. Chaotic morphology typifies the group. The inclusion of urinary tract infections is new in the gamut of diseases caused by CLOSPYN streptococci. RP ZIERDT, CH (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,MICROBIOL SERV,DEPT CLIN PATHOL,BETHESDA,MD 20892, USA. NR 25 TC 4 Z9 5 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0732-8893 J9 DIAGN MICR INFEC DIS JI Diagn. Microbiol. Infect. Dis. PD MAR-APR PY 1992 VL 15 IS 3 BP 185 EP 194 DI 10.1016/0732-8893(92)90112-7 PG 10 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA HM342 UT WOS:A1992HM34200001 PM 1582162 ER PT J AU LESOT, H FAUSSER, JL AKIYAMA, SK STAUB, A BLACK, D KUBLER, MD RUCH, JV AF LESOT, H FAUSSER, JL AKIYAMA, SK STAUB, A BLACK, D KUBLER, MD RUCH, JV TI THE CARBOXY-TERMINAL EXTENSION OF THE COLLAGEN BINDING DOMAIN OF FIBRONECTIN MEDIATES INTERACTION WITH A 165 KDA MEMBRANE-PROTEIN INVOLVED IN ODONTOBLAST DIFFERENTIATION SO DIFFERENTIATION LA English DT Article ID EPITHELIAL-MESENCHYMAL INTERACTIONS; DENTAL CYTODIFFERENTIATION INVITRO; AMINO-ACID SEQUENCE; EXTRACELLULAR-MATRIX; CELL ATTACHMENT; PLASMA FIBRONECTIN; TOOTH DEVELOPMENT; RAT INCISOR; POLYACRYLAMIDE GELS; SYNTHETIC PEPTIDES AB Terminal differentiation of the odontoblast is characterized by an elongation and a polarization of the cell. The change in the cell shape and the reorganization of the cytoplasm involve the microfilament system. An immunological approach has previously implicated a transmembrane interaction between fibronectin and vinculin in the control of odontoblast differentiation. A 165 kDa protein localized on the cell-surface of odontoblasts mediated this interaction. In order to define the nature of the interaction of the 165 kDa protein with fibronectin, peptides were prepared by proteolytic cleavage of fibronectin with alpha-chymotrypsin. The results indicate that the 165 kDa protein interacted with a 62 kDa peptide located towards the amino-terminal extremity of fibronectin, but not with a 47 kDa related fragment. Both these 62 kDa and 47 kDa peptides included the collagen-binding domain and were retarded on a heparin-Ultrogel column. Microsequences demonstrated that the 62 kDa and 47 kDa fragments had the same amino-terminal extremity and that the larger fragment was extended in the carboxy-terminal direction. This carboxy-terminal extension of the collagen binding domain of fibronectin is implicated in the interaction of this molecule with the 165 kDa protein. On the other hand, odontoblasts differentiated normally when tooth germs were cultured in the presence of GRGDS synthetic peptide, suggesting that RGD-dependent integrins were not involved in odontoblast differentiation. Staining of dental mesenchymal cells in primary culture and of differentiated odontoblasts in situ with antibodies directed against the beta-1-subunit of integrins confirmed previous observations and showed that although beta-1 integrins are involved in the attachment of cultured dental cells, they are not implicated in the process of odontoblast differentiation. C1 FAC MED STRASBOURG,INST CHIM BIOL,CNRS,GENET MOLEC EUCARYOTES LAB,INSERM,U184,F-67085 STRASBOURG,FRANCE. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. RP LESOT, H (reprint author), FAC MED STRASBOURG,INSERM,INST BIOL MED,CJF 88-08,11 RUE HUMANN,F-67085 STRASBOURG,FRANCE. NR 76 TC 39 Z9 42 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD MAR PY 1992 VL 49 IS 2 BP 109 EP 118 DI 10.1111/j.1432-0436.1992.tb00775.x PG 10 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA HN085 UT WOS:A1992HN08500007 PM 1597256 ER PT J AU DENIZOT, Y CHAUSSADE, S NATHAN, N COLOMBEL, JF BOSSANT, MJ CHEROUKI, N BENVENISTE, J COUTURIER, D AF DENIZOT, Y CHAUSSADE, S NATHAN, N COLOMBEL, JF BOSSANT, MJ CHEROUKI, N BENVENISTE, J COUTURIER, D TI PAF-ACETHER AND ACETYLHYDROLASE IN STOOL OF PATIENTS WITH CROHNS-DISEASE SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE ACETYLHYDROLASE; CROHNS DISEASE; PAF-ACETHER; STOOL ID PLATELET-ACTIVATING-FACTOR; ISCHEMIC BOWEL NECROSIS; COLONIC MUCOSA; PHOSPHOLIPASE-A2; BIOSYNTHESIS; PRECURSORS; STOMACH; COLITIS; RELEASE; ILEAL AB PAF-acether (PAF) is a phospholipid mediator with potent biological effects on the digestive tract. We report the presence of PAF in stool of patients with active Crohn's disease (39.1 +/- 13.5 ng/g of stool, mean +/- SEM, N = 19) and its absence in patients with irritable bowel syndrome with diarrhea and diarrhea with malabsorption. Fecal PAF acetylhydrolase activity was higher (P < 0.04) in patients with Crohn's disease as compared to patients with irritable bowel syndrome with diarrhea and diarrhea with malabsorption. We also report a solid-phase extraction of fecal PAF using silica minicolumns, which yielded results highly correlated with those obtained with a high-performance liquid chromatography method (r = 0.86, P < 0.001, N = 16). These findings may allow us to implicate PAF in the onset and perpetuation of digestive tract inflammatory symptoms observed during Crohn's disease. They would warrant to investigate the influence of various therapeutic agents, including PAF antagonists, on fecal PAF levels during inflammatory digestive ailments. C1 HOP COCHIN,SERV HEPATOGASTROENTEROL,27 RUE FAUBOURG ST JACQUES,F-75674 PARIS 14,FRANCE. INSERM,U200,F-92140 CLAMART,FRANCE. HOP HURIEZ,SERV HEPATOGASTROENTEROL,F-59037 LILLE,FRANCE. NIAAA,DICBR,CLIN STUDIES LAB,BETHESDA,MD 20892. RI Denizot, Yves Pierre/H-9769-2016 NR 26 TC 52 Z9 54 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD MAR PY 1992 VL 37 IS 3 BP 432 EP 437 DI 10.1007/BF01307739 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HF320 UT WOS:A1992HF32000018 PM 1735366 ER PT J AU CHEN, HW PLOUZEK, CA LIU, JL CHEN, CL CHOU, JY AF CHEN, HW PLOUZEK, CA LIU, JL CHEN, CL CHOU, JY TI CHARACTERIZATION OF A MAJOR MEMBER OF THE RAT PREGNANCY-SPECIFIC GLYCOPROTEIN FAMILY SO DNA AND CELL BIOLOGY LA English DT Article ID ANTIGEN GENE FAMILY; HUMAN CARCINOEMBRYONIC ANTIGEN; MEMBRANE ECTO-ATPASE; INSULIN-RECEPTOR; TYROSINE KINASE; SUBSTRATE-SPECIFICITY; ENDOGENOUS SUBSTRATE; IMMUNOGLOBULIN-LIKE; SYNTHETIC PEPTIDES; ADHESION MOLECULE AB The gene encoding the human pregnancy-specific glycoprotein (PSG) belongs to a gene subfamily, comprised of the carcinoembryonic antigen (CEA) and PSG subgroups, within the immunoglobulin superfamily. To study the functional roles of PSG during development in an animal model, we isolated and characterized a near full-length cDNA (rnCGM6) encoding a PSG-related protein from a rat placental cDNA library. rnCGM6 is 2,068 bp in length and contains an open reading frame that encodes a 475-amino-acid polypeptide with a predicted molecular mass of 53 kD. The 5' noncoding sequence is 173 nucleotides, and primer-extension experiments demonstrate that the transcriptional initiation site is located 22-24 nucleotides further upstream. The 3' noncoding sequence contains 470 nucleotides which is followed by a poly(A) tail. In contrast to human PSGs, which contain one immunoglobulin variable-like and two to three immunoglobulin constant-like protein domains, rnCGM6 contains three immunoglobulin variable-like domains and one immunoglobulin constant-like domain. rnCGM6 contains six potential N-linked glycosylation sites and, in its carboxyl-terminal domain, a tyrosine protein kinase phosphorylation site. The tyrosine phosphorylation site is conserved among all rat and human PSG members. rnCGM6 hybridized with a major 2.5-kb and two minor 3.0- and 3.5-kb mRNAs, all primarily expressed in the rat placenta. Ribonuclease protection analysis, using probes specific to the 5', middle, and 3' regions of rnCGM6, and the 5' region of a previously identified cDNA, rnCGM1, mainly yielded fully-protected fragments indicating relatively low sequence similarity among rat PSG-related proteins. Northern hybridization and ribonuclease protection assays also suggest that rnCGM6 may be the major PSG member in rat. C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892. UNIV FLORIDA,COLL VET MED,DEPT LARGE ANIM CLIN SCI,GAINESVILLE,FL 32610. NR 49 TC 13 Z9 13 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1044-5498 J9 DNA CELL BIOL JI DNA Cell Biol. PD MAR PY 1992 VL 11 IS 2 BP 139 EP 148 DI 10.1089/dna.1992.11.139 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA JG482 UT WOS:A1992JG48200005 PM 1547019 ER PT J AU MCCRAE, RR COSTA, PT AF MCCRAE, RR COSTA, PT TI DISCRIMINANT VALIDITY OF NEO-PIR FACET SCALES SO EDUCATIONAL AND PSYCHOLOGICAL MEASUREMENT LA English DT Article ID 5-FACTOR MODEL; PERSONALITY AB Two analyses were conducted to examine the discriminant validity of 30 facet scales from the Revised NEO Personality Inventory (NEO-PIR). To examine cross-observer validity of specific variance in the facet scales, partial correlations between self-reports and peer (N = 250) and spouse (N = 68) ratings on the facets were calculated, controlling for the five common factors. All 60 convergent partial correlations were positive, and 48 (80%) were significant. In the second analysis, Adjective Check List (Gough and Heilbrun, 1983) correlates of the facet scales were identified in a sample of 305 adults. Judges correctly matched scales to correlates in most cases, providing additional evidence for discriminant validity. RP MCCRAE, RR (reprint author), NIA,GERONTOL RES CTR,PERSONAL & COGNIT LAB,4940 EASTERN AVE,BETHESDA,MD 20892, USA. NR 14 TC 111 Z9 112 U1 21 U2 63 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0013-1644 J9 EDUC PSYCHOL MEAS JI Educ. Psychol. Meas. PD SPR PY 1992 VL 52 IS 1 BP 229 EP 237 DI 10.1177/001316449205200128 PG 9 WC Psychology, Educational; Mathematics, Interdisciplinary Applications; Psychology, Mathematical SC Psychology; Mathematics GA HH290 UT WOS:A1992HH29000028 ER PT J AU GARNER, MM CHRAMBACH, A AF GARNER, MM CHRAMBACH, A TI RESOLUTION OF CIRCULAR, NICKED CIRCULAR AND LINEAR DNA, 4.4 KB IN LENGTH, BY ELECTROPHORESIS IN POLYACRYLAMIDE SOLUTIONS SO ELECTROPHORESIS LA English DT Note ID GEL-ELECTROPHORESIS; DEPENDENCE; MOBILITY AB Circular DNA of more than 1,400 bp in size is known not to migrate into polyacrylamide gels. The migration of supercoiled plasmid pBR322 DNA (4,363 bp) into uncrosslinked polyacrylamide (M(w) 5 X 10(6)) solutions and its separation, on the basis of conformation, from its nicked form is demonstrated in this study. Migration of the supercoiled, nicked circular and linear forms of the plasmid DNA is retarded in proportion to the concentration of uncrosslinked polyacrylamide, the degree of retardation being highest for the nicked circular form. Decreasing the level of supercoiling of the covalently closed circular form by decreasing the concentration of the intercalating dye (ethidium homodimer) shows that the degree of retardation decreases in proportion to the superhelix density. RP GARNER, MM (reprint author), NICHHD,MACROMOLEC ANAL SECT,THEORET & PHYS BIOL LAB,BLDG 10,RM 6C101,BETHESDA,MD 20892, USA. NR 15 TC 19 Z9 20 U1 2 U2 16 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD MAR PY 1992 VL 13 IS 3 BP 176 EP 178 DI 10.1002/elps.1150130136 PG 3 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA HQ640 UT WOS:A1992HQ64000013 PM 1592050 ER PT J AU KONVALINKA, J HOREJSI, M ANDREANSKY, M NOVEK, P PICHOVA, I BLAHA, I FABRY, M SEDLACEK, J FOUNDLING, S STROP, P AF KONVALINKA, J HOREJSI, M ANDREANSKY, M NOVEK, P PICHOVA, I BLAHA, I FABRY, M SEDLACEK, J FOUNDLING, S STROP, P TI AN ENGINEERED RETROVIRAL PROTEINASE FROM MYELOBLASTOSIS ASSOCIATED VIRUS ACQUIRES PH-DEPENDENCE AND SUBSTRATE-SPECIFICITY OF THE HIV-1 PROTEINASE SO EMBO JOURNAL LA English DT Article DE HIV; MAV; PROTEINASE ACTIVITY AND SPECIFICITY; SITE-DIRECTED MUTAGENESIS ID VIRAL PROTEINASES; PROTEASE; RESOLUTION AB In an attempt to understand the structural reasons for differences in specificity and activity of proteinases from two retroviruses encoded by human immunodeficiency virus (HIV) and myeloblastosis associated virus (MAV), we mutated five key residues predicted to form part of the enzyme subsites S1, S2 and S3 in the substrate binding cleft of the wild-type MAV proteinase wMAV PR. These were changed to the residues occupying a similar or identical position in the HIV-1 enzyme. The resultant mutated MAV proteinase (mMAV PR) exhibits increased enzymatic activity, altered substrate specificity, a substantially changed pH activity profile and a higher pH stability close to that observed in the HIV-1 PR. This dramatic alteration of MAV PR activity achieved by site-directed mutagenesis suggests that we have identified the amino acid residues contributing substantially to the differences between MAV and HIV-1 proteinases. C1 CZECHOSLOVAK ACAD SCI,INST MOLEC GENET,PRAGUE 6,CZECHOSLOVAKIA. NCI,FREDERICK CANC RES DEV LABS,FREDERICK,MD 21702. RP KONVALINKA, J (reprint author), CZECHOSLOVAK ACAD SCI,INST ORGAN CHEM & BIOCHEM,FLEMINGOVO N2,PRAGUE 6,CZECHOSLOVAKIA. RI Konvalinka, Jan/G-7518-2014; Fabry, Milan/G-3602-2014; Pichova, Iva/G-7917-2014; Sedlacek, Juraj/G-3606-2014; OI Konvalinka, Jan/0000-0003-0695-9266 NR 14 TC 27 Z9 27 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD MAR PY 1992 VL 11 IS 3 BP 1141 EP 1144 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HH082 UT WOS:A1992HH08200039 PM 1547777 ER PT J AU BAGNATO, A MORETTI, C OHNISHI, J FRAJESE, G CATT, KJ AF BAGNATO, A MORETTI, C OHNISHI, J FRAJESE, G CATT, KJ TI EXPRESSION OF THE GROWTH HORMONE-RELEASING HORMONE GENE AND ITS PEPTIDE PRODUCT IN THE RAT OVARY SO ENDOCRINOLOGY LA English DT Article ID MESSENGER-RIBONUCLEIC-ACID; LOCALIZATION; PRECURSOR; RNA; PLACENTA; IDENTIFICATION; HYPOTHALAMUS; MOUSE AB GH-releasing hormone (GHRH) is a potent cAMP-mediated agonist in the rat ovary, where it binds to a common vasoactive intestinal peptide/GHRH receptor and enhances the actions of FSH on granulosa cell maturation. A GHRH-like peptide has been detected by immunocytochemistry in the human ovary and by RIA in follicular fluid, suggesting local synthesis of the peptide. In rat ovarian poly(A)+ RNA, Northern blot hybridization analysis with a P-32-labeled 48-nucleotide (nt) rat GHRH oligonucleotide probe revealed the presence of one major and two minor mRNA species. The major ovarian GHRH mRNA (1750 nt) was much larger than that present in hypothalamus and placenta (750 nt), but was similar to that observed in the rat testis. Two well defined higher mol wt forms of 3.2 and 3.6 kilobases were also present and probably represent unprocessed precursors of the 1750-nt mRNA. Further evidence of GHRH gene expression in the ovary and testis was provided by reverse transcription polymerase chain reaction of ovarian mRNA and restriction enzyme analysis of the amplified product. In addition, immunoreactive (ir) GHRH was detected in ovarian extracts and in the incubation medium of cultured rat granulosa cells. Ovaries from PMSG-treated female rats, aged 22-27 days, contained 400 +/- 25 pg/g ir-GHRH. The GHRH content of the hypothalamus of the same animals was 2.9 +/- 0.1 ng/g. Cultured rat granulosa cells released 20 +/- 0.1 pg ir-GHRH/4 x 10(5) cells.3 h into the incubation medium. The GHRH immunoreactivity detected in ovarian extracts coeluted on gel filtration chromatography with authentic rGHRH (5.2 kilodaltons). A larger form of ir-GHRH (approximately 16.5 kilodaltons) was also present. These data demonstrate that the rat ovary contains a 1750-nt transcript that could arise from the GHRH gene by tissue-specific initiation, alternative splicing, or transcript termination. The translation product of this mRNA is the same similar size as the rat hypothalamic neuropeptide and may promote follicular maturation by autocrine or paracrine modulation of the stimulatory action of FSH on granulosa cell function. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLDG 10,ROOM B1-L400,BETHESDA,MD 20892. UNIV ROME LA SAPIENZA,MED CLIN 5,I-00161 ROME,ITALY. RI Bagnato, Anna/G-9747-2016; OI Bagnato, Anna/0000-0002-7269-9522; MORETTI, COSTANZO/0000-0003-4006-2575 NR 32 TC 81 Z9 81 U1 0 U2 2 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 1992 VL 130 IS 3 BP 1097 EP 1102 DI 10.1210/en.130.3.1097 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HG161 UT WOS:A1992HG16100004 PM 1537276 ER PT J AU LOPEZ, FJ LIPOSITS, Z MERCHENTHALER, I AF LOPEZ, FJ LIPOSITS, Z MERCHENTHALER, I TI EVIDENCE FOR A NEGATIVE ULTRASHORT LOOP FEEDBACK REGULATING GALANIN RELEASE FROM THE ARCUATE NUCLEUS-MEDIAN EMINENCE FUNCTIONAL UNIT SO ENDOCRINOLOGY LA English DT Article ID CENTRAL NERVOUS-SYSTEM; VASOACTIVE INTESTINAL POLYPEPTIDE; GROWTH-HORMONE; PARAVENTRICULAR NUCLEUS; POSSIBLE INVOLVEMENT; HYPOTHALAMIC SLICES; FRAGMENTS INVITRO; RAT HYPOTHALAMUS; MESSENGER-RNA; BINDING-SITES AB Recent studies from our laboratory have demonstrated that galanin (GAL) is a member of the hypothalamic-hypophysiotropic hormone family. Most of the hypothalamic hormones regulate their own secretion rate by ultrashort loop feedback mechanisms. The purpose of these studies was to evaluate the possibility that hypothalamic GAL could regulate its own release through a similar mechanism. Galanin secretion from median eminence (ME) fragments incubated in vitro increased exponentially with time, whereas GAL release from arcuate nucleus-ME (AN-ME) fragments depicted a secretory profile consisting of an initial exponential rising phase, followed by a plateau phase in which GAL secretion was apparently abolished. Moreover, preexposure of AN-ME fragments to porcine GAL (pGAL) increased tissue responsiveness to K+-induced depolarization, suggesting that pGAL reduced the gain of the system. Thus, after pGAL removal, AN-ME fragments appear to be more sensitive to the depolarizing stimulus. In addition, blockade of GAL biological activity in vivo by administration of a sheep antirat GAL serum increased GAL release from AN-ME fragments in vitro, whereas this treatment did not affect GAL release from ME terminals. These results indicate that GAL neurons may diminish their own activity, establishing, therefore, a negative ultrashort loop feedback that controls the firing of the AN galaninergic network and maintains a balanced physiological status. By means of electron microscopy, we demonstrated that GAL-containing perikarya and proximal dendrites receive synapsing axons immunoreactive for the same peptide in the AN, which provides the anatomical basis for interactions between galaninergic neurons. In conclusion, our data support the notion that the galaninergic system, as other peptidergic neurotransmitters, is able to regulate its own release via a negative ultrashort loop feedback control mechanism that is operative at the level of the AN. C1 NIEHS,MOLEC & INTEGRAT NEUROSCI,REPROD SECT,RES TRIANGLE PK,NC 27709. NIEHS,MOLEC & INTEGRAT NEUROSCI,FUNCT MORPHOL SECT,RES TRIANGLE PK,NC 27709. NR 48 TC 19 Z9 19 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 1992 VL 130 IS 3 BP 1499 EP 1507 DI 10.1210/en.130.3.1499 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HG161 UT WOS:A1992HG16100055 PM 1371452 ER PT J AU CULLER, MD AF CULLER, MD TI INHIBIN SUPPRESSES LUTEINIZING-HORMONE (LH)-RELEASING HORMONE SELF-PRIMING - DIRECT ACTION ON FOLLICLE-STIMULATING-HORMONE SECRETION AND OPPOSITION OF ESTRADIOL-ENHANCED LH-SECRETION SO ENDOCRINOLOGY LA English DT Article ID GONADOTROPIN-RELEASING-HORMONE; INDUCED OVARIAN HYPERSTIMULATION; ANTERIOR-PITUITARY CELLS; PROTEIN KINASE-C; ENDOGENOUS INHIBIN; BOVINE INHIBIN; NONSTEROIDAL FACTOR; ESTROUS-CYCLE; FEMALE RATS; SURGE AB Previous studies have suggested that the ovary produces a factor that maintains the pituitary in a state of low LHRH responsiveness that must be overcome by the self-priming action of LHRH. To determine the role of inhibin in maintaining low LHRH responsiveness in pituitaries of diestrous female rats, endogenous inhibin was passively immunoneutralized in vivo, and the pituitaries were removed 18-20 h later and examined for LHRH responsiveness in vitro. Pituitaries from diestrous control rats produced the biphasic pattern of gonadotropin secretion that typifies LHRH self-priming: an initial low secretory response to LHRH (lag phase), followed by a protein synthesis-dependent transition to an enhanced rate of secretion with continued LHRH exposure (primed phase). Immunoneutralization of endogenous inhibin [antiserum (AS) treated] resulted in an increased rate of LH secretion during the lag phase, while no change was observed in the primed phase rate of LH secretion. FSH secretion from pituitaries of AS-treated rats was increased during the lag phase to a rate of secretion similar to that observed during the primed phase of FSH secretion from control pituitaries, and it was increased further during the primed phase of secretion. These results suggest that inhibin is at least partially responsible for the low secretion of LH observed during the lag phase response to LHRH exposure and is totally responsible for the lowered rate of FSH secretion during the lag phase. The observation that the enhanced rate of gonadotropin secretion observed with AS-treated pituitaries during the lag phase was resistant to inhibition of protein synthesis provides further evidence that a partial transition from the lag to the primed phase had already occurred. Pituitaries from ovariectomized rats were also examined in order to place the contribution of inhibin in perspective with the total ovarian influence on pituitary responsiveness to LHRH. Unexpectedly, LH secretion during the lag phase was similar to the low secretion rate of diestrous control pituitaries, and the higher primed rate of secretion failed to fully develop, suggesting that an additional ovarian factor was required to induce and maintain pituitary responsiveness to LHRH in terms of LH secretion. FSH secretion from the ovariectomized rats was similar to that observed from pituitaries of AS-treated rats, thus further supporting the concept that inhibin is fully responsible for the suppression of FSH secretion in response to LHRH. Plasma from the AS-treated rats revealed a 2-fold increase in estradiol levels compared with diestrous control rats. To determine the contribution of estradiol, pituitaries were examined from ovariectomized rats in which estradiol levels were maintained at both the level observed in diestrous controls and that in AS-treated rats. Estradiol replacement completely restored the LH secretion response to LHRH during both the lag and primed phases to the levels observed with pituitaries from AS-treated rats. FSH secretion was again similar to that observed with AS-treated pituitaries. These results demonstrate that estradiol is necessary to maintain pituitary responsiveness to LHRH in terms of LH secretion. The observation that normal diestrous day 2 levels of estradiol in the absence of inhibin (ovariectomized rats with diestrous day 2 level of estradiol maintenance) can induce the same degree of pituitary priming as immunoneutralization of endogenous inhibin in intact rats suggests that inhibin may have a direct action at the level of the pituitary to oppose the stimulatory action of estradiol on pituitary sensitivity to LHRH. In addition, inhibin appears to indirectly oppose the stimulatory action of estradiol on pituitary sensitivity to LHRH by maintaining lowered plasma levels of estradiol. The observation that AS treatment, but not ovariectomy or estradiol maintenance, induced an increased rate of FSH secretion in response to LHRH during the primed phase suggests the presence of an additional ovarian factor that enhances LHRH-induced FSH secretion and is normally opposed by inhibin. RP CULLER, MD (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,REPROD NEUROENDOCRINOL SECT,RES TRIANGLE PK,NC 27709, USA. NR 50 TC 15 Z9 15 U1 0 U2 2 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 1992 VL 130 IS 3 BP 1605 EP 1614 DI 10.1210/en.130.3.1605 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HG161 UT WOS:A1992HG16100069 PM 1537310 ER PT J AU CHEGINI, N FLANDERS, KC AF CHEGINI, N FLANDERS, KC TI PRESENCE OF TRANSFORMING GROWTH-FACTOR-BETA AND THEIR SELECTIVE CELLULAR-LOCALIZATION IN HUMAN OVARIAN TISSUE OF VARIOUS REPRODUCTIVE STAGES SO ENDOCRINOLOGY LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; RAT GRANULOSA-CELLS; THECAL-INTERSTITIAL-CELLS; ANDROGEN PRODUCTION; DIFFERENTIATION; INHIBIN; FACTOR-BETA-1; EXPRESSION; PHYSIOLOGY; PROTEINS AB Immunohistochemical studies were performed using specific polyclonal antibodies to transforming growth factor (TGF)-beta-1 and TGF-beta-2 to determine their presence and cellular localization in human ovarian tissues of various reproductive states. In the small ovarian follicles, the immunostaining for TGF-beta-1 was present in oocytes, follicle cells, and granulosa and theca cell layers. The level of immunostaining associated with granulosa and theca cell layers intensified as the size of the follicles increased. In the luteal tissue, both the small and large luteal cells immunostained for TGF-beta-1 and their intensities were similar to theca and granulosa cell layers, respectively. The patterns of immunostaining were similar in early (days 14-19), mid (days 22-25), and late (days 26-29) luteal phases; however, the intensity was highest at mid and decreased at late luteal phase. Corpus albicans showed a very weak immunostaining for TGF-beta-1, whereas ectopic pregnancy small luteal cells immunostained relatively intensely. The ovarian stromal, luteal tissue fibroblasts, and arterioles endothelial and smooth muscle cells were also immunostained for TGF-beta-1. The immunostaining of the ovarian tissues for TGF-beta-2 indicated that the theca cell layers were the exclusive cells in the follicles with intense immunostaining, which increased in the larger follicles. A low immunostaining was also observed in granulosa cell of the large follicles. In the luteal tissues, only small luteal cells showed intense immunostaining for TGF-beta-2, which was similar in intensity to that in the theca cells; however, the large luteal cells showed a low level of immunostaining at midluteal phase. The small luteal cells in corpus albicans and ectopic pregnancy luteal tissues retained their immunostaining for TGF-beta-2, but with lower intensity. Endothelial and smooth muscle cells of arterioles also immunostained for TGF-beta-2, but not ovarian stromal cells. Atretic follicles showed very low or no detectable immunostaining for TGF-beta-1 or TGF-beta-2. The results of present studies show that human ovarian tissue at all the reproductive states locally produces TGF-beta-1 and TGF-beta-2, and although TGF-beta-1 is present in most major ovarian cell types, TGF-beta-2 is only produced by theca cells in the follicles and small luteal cells in luteal tissues. C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. RP CHEGINI, N (reprint author), UNIV FLORIDA,DEPT OBSTET & GYNECOL,BOX 100294 JHMHC,GAINESVILLE,FL 32610, USA. NR 33 TC 90 Z9 91 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 1992 VL 130 IS 3 BP 1707 EP 1715 DI 10.1210/en.130.3.1707 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HG161 UT WOS:A1992HG16100080 PM 1537318 ER PT J AU MIGLIACCIO, S NEWBOLD, RR BULLOCK, BC MCLACHLAN, JA KORACH, KS AF MIGLIACCIO, S NEWBOLD, RR BULLOCK, BC MCLACHLAN, JA KORACH, KS TI DEVELOPMENTAL EXPOSURE TO ESTROGENS INDUCES PERSISTENT CHANGES IN SKELETAL TISSUE SO ENDOCRINOLOGY LA English DT Note ID DIETHYLSTILBESTROL; CELLS; MICE; 17-BETA-ESTRADIOL; ADENOCARCINOMA; RATS AB Short-term exposure to estrogens during development has been reported to cause irreversible changes including neoplasia in estrogen target tissues, i.e. reproductive tract and mammary gland. Moreover, it has been established that estrogens have a dramatic effect on bone turnover. The recent demonstration of a low level of estrogen receptor (ER) in bone cells strongly suggests that these estrogenic effects are direct. This report was designed to evaluate whether neonatal exposure to diethylstilbestrol (DES) induces irreversible changes in bone tissue as demonstrated in other specific target organs. We show that short-term exposure of newborn mice (day 1-5) to DES (2-mu-g/pup/day) induces permanent changes in skeletal tissue in adulthood; femurs of DES-treated animals were significantly shorter than age-matched control mice. Furthermore, a significant increment (1.5 fold) in the amount of bone in the femurs (representative of long bone) and vertebrae (representative of short bone) was observed in DES-exposed animals. These data provide further evidence that bone tissue is a specific estrogen target tissue. Finally, we postulate that physiological exposure to estrogens in childhood might be one of the key factors in determining the final peak bone density in adulthood. C1 NIEHS,REPROD & DEV TOXICOL LAB,DEV ENDOCRINOL & PHARMACOL SECT,RES TRIANGLE PK,NC 27709. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT COMPARAT MED,WINSTON SALEM,NC 27103. OI Migliaccio, Silvia/0000-0002-4563-6630; Korach, Kenneth/0000-0002-7765-418X NR 25 TC 26 Z9 26 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 1992 VL 130 IS 3 BP 1756 EP 1758 DI 10.1210/en.130.3.1756 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HG161 UT WOS:A1992HG16100090 PM 1537323 ER PT J AU SORLIE, PD ROGOT, E JOHNSON, NJ AF SORLIE, PD ROGOT, E JOHNSON, NJ TI VALIDITY OF DEMOGRAPHIC CHARACTERISTICS ON THE DEATH CERTIFICATE SO EPIDEMIOLOGY LA English DT Note DE DATA COLLECTION; DEATH CERTIFICATES; DEMOGRAPHY; MORTALITY; HISPANIC AMERICANS; ETHNIC GROUPS; NORTH AMERICAN INDIANS; RACE; GENDER AB In a sample of the United States population from the Census Bureau's Current Population Surveys, we compared demographic characteristics with those recorded on the death certificate for the 43,000 decedents in the sample followed from 1979 to 1985. Overall percentage agreements were: Sex 99.5, Race 99.4, Place of birth 99.4, Hispanic origin 98.7, and Veteran status 95.2. Relatively fewer American Indians and Asian/Pacific Islanders had death certificates that agreed with the baseline race (73.6% and 82.4%, respectively). The direction of disagreement suggests that current estimates of mortality rates for American Indians and Asian/Pacific Islanders are underestimated. RP SORLIE, PD (reprint author), NHLBI,FED BLDG,ROOM 3A10,BETHESDA,MD 20892, USA. NR 0 TC 96 Z9 96 U1 0 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD MAR PY 1992 VL 3 IS 2 BP 181 EP 184 DI 10.1097/00001648-199203000-00018 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HH938 UT WOS:A1992HH93800018 PM 1576225 ER PT J AU WEISS, SRB NIERENBERG, J LEWIS, R POST, RM AF WEISS, SRB NIERENBERG, J LEWIS, R POST, RM TI CORTICOTROPIN-RELEASING HORMONE - POTENTIATION OF COCAINE-KINDLED SEIZURES AND LETHALITY SO EPILEPSIA LA English DT Article DE NEUROLOGIC MODELS; KINDLING; CONVULSIONS; CRH; STRESS; COCAINE; CARBAMAZEPINE ID IMMUNOREACTIVE NEURONS; CARBAMAZEPINE; CRF; RAT; BRAIN; INCREASES; LIDOCAINE AB Carbamazepine (CBZ) blocks the development of local anesthetic seizures kindled by cocaine and lidocaine. Cocaine and lidocaine release corticotropin-releasing hormone (CRH) in hypothalamic cell cultures, and this effect is also blocked by CBZ. Because CRH administered intracerebroventricularly (i.c.v.) can produce seizures, its potential role in the development of cocaine seizures and in the anticonvulsant effects of CBZ was studied. CRH (at doses of 5, 10, and 100-mu-g) potentiated cocaine-kindled seizure development and lethality in a dose-related fashion. CRH also reversed the effects of CBZ on cocaine kindling and lethality, but only at the highest doses, which also affected cocaine kindling. Thus, a selective role for CRH in the anticonvulsant effects of CBZ was not demonstrated. The findings suggest a potentially important role for CRH in exacerbating cocaine-seizure evolution and its associated lethality and confirm the inhibition of cocaine kindling and lethality by CBZ. RP WEISS, SRB (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BLDG 10-3N212,BETHESDA,MD 20892, USA. NR 26 TC 17 Z9 17 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD MAR-APR PY 1992 VL 33 IS 2 BP 248 EP 254 DI 10.1111/j.1528-1157.1992.tb02313.x PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA HK729 UT WOS:A1992HK72900006 PM 1547754 ER PT J AU DEVINSKY, O EMOTO, S GOLDSTEIN, DS STULL, R PORTER, RJ THEODORE, WH NADI, NS AF DEVINSKY, O EMOTO, S GOLDSTEIN, DS STULL, R PORTER, RJ THEODORE, WH NADI, NS TI CEREBROSPINAL-FLUID AND SERUM LEVELS OF DOPA, CATECHOLS, AND MONOAMINE METABOLITES IN PATIENTS WITH EPILEPSY SO EPILEPSIA LA English DT Article DE EPILEPSY; SEIZURES; NEUROTRANSMITTERS; CATECHOLAMINES; SEROTONIN; CEREBROSPINAL FLUID ID PLASMA; SEIZURES; BRAIN AB We measured CSF and serum concentrations of monoamines and monoamine metabolites in normal control subjects and in patients with partial epilepsy between and less than 2 h after complex partial seizures (CPS) or secondarily generalized tonic-clonic seizures (SGTCs). After SGTCs, concentrations of norepinephrine in CSF were significantly higher (p < 0.05) than interictal concentrations, concentrations after PSs, and concentrations in control subjects. Serum epinephrine levels also were significantly higher after SGTCs than interictal and control subjects' levels. CSF HVA levels were significantly higher after PSs than interictal or control subjects' levels. CSF concentrations of norepinephrine and its intraneuronal metabolite, dihydroxyphenylglycol, were highly correlated, both interictally and following SGTCs, whereas correlations between serum and CSF levels of these catechols generally were not statistically significant. The results indicate that seizures are associated with release of catecholamines in the central nervous system. C1 NHLBI,HYPERTENS ENDOCRINE BRANCH,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,BETHESDA,MD 20892. NYU,SCH MED,DEPT NEUROL,NEW YORK,NY 10003. NINCDS,BIOMETRY BRANCH,BETHESDA,MD 20892. NR 30 TC 30 Z9 30 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD MAR-APR PY 1992 VL 33 IS 2 BP 263 EP 270 DI 10.1111/j.1528-1157.1992.tb02315.x PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA HK729 UT WOS:A1992HK72900008 PM 1547755 ER PT J AU TEO, KK YUSUF, S WITTES, J THEODOROPOULOS, S DHALLA, N AIKENHEAD, J YACOUB, M AF TEO, KK YUSUF, S WITTES, J THEODOROPOULOS, S DHALLA, N AIKENHEAD, J YACOUB, M TI PRESERVED LEFT-VENTRICULAR FUNCTION DURING SUPINE EXERCISE IN PATIENTS AFTER ORTHOTOPIC CARDIAC TRANSPLANTATION SO EUROPEAN HEART JOURNAL LA English DT Article DE CARDIAC TRANSPLANTATION; EXERCISE; VENTRICULAR FUNCTION; HEMODYNAMICS ID UPRIGHT BICYCLE EXERCISE; DENERVATED HEART; CONTRACTILITY; CYCLOSPORINE; RECIPIENTS; RECOVERY; VOLUMES C1 NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,CLIN TRIALS BRANCH,FED BLDG,BETHESDA,MD 20892. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BIOSTAT RES BRANCH,BETHESDA,MD 20892. HAREFIELD HOSP,HAREFIELD,MIDDX,ENGLAND. RI Dhalla, Naranjan/C-8279-2014 OI Dhalla, Naranjan/0000-0002-4894-4727 NR 31 TC 8 Z9 8 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0195-668X J9 EUR HEART J JI Eur. Heart J. PD MAR PY 1992 VL 13 IS 3 BP 321 EP 329 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HF957 UT WOS:A1992HF95700006 PM 1597218 ER PT J AU SLOAND, EM KLEIN, HG BANKS, SM VARELDZIS, B MERRITT, S PIERCE, P AF SLOAND, EM KLEIN, HG BANKS, SM VARELDZIS, B MERRITT, S PIERCE, P TI EPIDEMIOLOGY OF THROMBOCYTOPENIA IN HIV-INFECTION SO EUROPEAN JOURNAL OF HAEMATOLOGY LA English DT Article DE THROMBOCYTOPENIA; AIDS; HIV ID HUMAN-IMMUNODEFICIENCY-VIRUS; IMMUNE-DEFICIENCY; HOMOSEXUAL MEN; HEMATOLOGIC MANIFESTATIONS; PURPURA; AIDS; AZIDOTHYMIDINE; ZIDOVUDINE; ADDICTS; CELLS AB Thrombocytopenia is a known complication of human immunodeficiency virus Type-1 (HIV-1) infection, and more data need to be collected on its frequency, severity, and clinical sequelae. We determined the frequency of thrombocytopenia and its relationship to other HIV infection characteristics from a review of records of 1004 HIV-infected patients attending two outpatient clinics in Washington, D.C. The self-reported sources of HIV-1 exposure were male homosexual activity (68%), bisexual activity (10%), heterosexual activity (6%), and intravenous drug use (15%). Fifty-nine percent of the individuals were white, 37% were black and 94% were male. Fifteen percent had AIDS. Thrombocytopenia occurred more frequently in subjects with AIDS (21.2%) than in HIV-infected individuals who did not fit clinical criteria for AIDS (9.2%) (p < 0.001). Patients with few CD4-positive cells and an advanced stage of disease were more likely to have low platelet counts: 30% with an absolute CD4 cell count lower than 200/mm3 vs 8% with CD4 counts between 200 and 500 (p < 0.00001), and 18.5% with Stage IV disease compared to 7.6% in Stage II (p < 0.001) had platelet counts less than 150 000/mm3. Thrombocytopenia was more frequent in white males and older subjects. Although subjects infected by heterosexual exposure had a lower frequency of thrombocytopenia, intravenous drug users and homosexual men exhibited similar frequencies of thrombocytopenia. Of all subjects with platelet counts less than 50 000/mm3, 40% reported bleeding and 1 died of an intracranial hemorrhage. Thrombocytopenia occurs frequently in HIV-infected people, primarily in those with AIDS. low CD4 cell numbers, and advanced stages of diseases. C1 WHITMAN WALKER CLIN,WASHINGTON,DC. NIAID,BETHESDA,MD 20892. NIH,DEPT TRANSFUS MED,BETHESDA,MD 20892. GEORGETOWN UNIV HOSP,WASHINGTON,DC 20007. RP SLOAND, EM (reprint author), NHLBI,BLDG 31,ROOM 5A-52,BETHESDA,MD 20892, USA. NR 26 TC 69 Z9 69 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-4441 J9 EUR J HAEMATOL JI Eur. J. Haematol. PD MAR PY 1992 VL 48 IS 3 BP 168 EP 172 PG 5 WC Hematology SC Hematology GA HP962 UT WOS:A1992HP96200008 PM 1348479 ER PT J AU IZQUIERDO, M DOWNWARD, J OTANI, H LEONARD, WJ CANTRELL, DA AF IZQUIERDO, M DOWNWARD, J OTANI, H LEONARD, WJ CANTRELL, DA TI INTERLEUKIN (IL)-2 ACTIVATION OF P21RAS IN MURINE MYELOID CELLS TRANSFECTED WITH HUMAN IL-2 RECEPTOR BETA-CHAIN SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID PROTEIN KINASE-C; LYMPHOCYTES-T; STIMULATION; RAS; DEFICIENT; BINDING; GTPASE AB The T cell growth factor interleukin-2 (IL-2) induces p21ras activation in T lymphocytes. To determine whether the IL-2 receptor (IL-2R) can regulate p21ras when expressed in a non-T cell environment we have examined the ability of IL-2 to activate p21ras in 32D murine myeloid progenitor cells transduced with human IL-2R beta-chains. These cells are denoted beta-53 cells. 32D cells normally proliferate in response to IL-3 but the expression of the IL-2R beta-chain confers IL-2 responsiveness to the cells. Our data show that IL-3 is able to activate p21ras in the parental 32D cells and both IL-2 and IL-3 can stimulate p21ras in the IL-2R-expressing beta-53 clone of 32D. In T lymphocytes, activation of protein kinase C (PKC) with phorbol esters is sufficient to stimulate p21ras. However, in 32D and beta-53 cells activation of PKC with phorbol esters does not result in p21ras activation even though these cells express functional PKC. It appears, therefore, that a PKC-mediated pathway for p21ras regulation exists in T lymphocytes but not in 32D cells. The IL-2R can couple to p21ras independently of the concomitant presence of the PKC pathway for p21ras regulation. These data imply that multiple intracellular mechanisms may exist to regulate p21ras and that cells of different lineages may differ with regard to p21ras regulation. C1 IMPERIAL CANC RES FUND,SIGNAL TRANSDUCT LAB,LONDON WC2A 3PX,ENGLAND. NICHHD,CELL BIOL & METAB BRANCH,PULM & MOLEC IMMUNOL SECT,BETHESDA,MD 20892. NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. RP IZQUIERDO, M (reprint author), IMPERIAL CANC RES FUND,LYMPHOCYTE ACTIVAT LAB,POB 123,LINCOLNS INN FIELDS,LONDON WC2A 3PX,ENGLAND. RI Izquierdo , Manuel/I-4812-2013 OI Izquierdo , Manuel/0000-0002-7701-1002 NR 22 TC 29 Z9 29 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 MAR PY 1992 VL 22 IS 3 BP 817 EP 821 DI 10.1002/eji.1830220328 PG 5 WC Immunology SC Immunology GA HK529 UT WOS:A1992HK52900027 PM 1547824 ER PT J AU CAREY, MA SMITH, MW AF CAREY, MA SMITH, MW TI ENHANCEMENT OF VALIDITY THROUGH QUALITATIVE APPROACHES - INCORPORATING THE PATIENTS PERSPECTIVE SO EVALUATION & THE HEALTH PROFESSIONS LA English DT Article AB Validity of research in a medical environment is enhanced through incorporating the patient's perspective by using qualitative approaches. Our efforts to improve the validity of measures led us to examine the research process more broadly through mechanisms of patient participation: a protocol adviser, a participant advisory panel, and focus groups. In our research program of biopsychosocial HIV studies in the military population, feedback from patient participants provided the research staff with information important for refining standard measures, improving the research process, and interpreting the quantitative data analyses. C1 HENRY M JACKSON FDN ADVANCEMENT MIL MED,ROCKVILLE,MD. RP CAREY, MA (reprint author), NATL CTR NURSING RES,BETHESDA,MD, USA. NR 11 TC 9 Z9 9 U1 0 U2 0 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0163-2787 J9 EVAL HEALTH PROF JI Eval. Health Prof. PD MAR PY 1992 VL 15 IS 1 BP 107 EP 114 DI 10.1177/016327879201500107 PG 8 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA HD991 UT WOS:A1992HD99100007 PM 10117741 ER PT J AU KINSELLA, JL GRANT, DS WEEKS, BS KLEINMAN, HK AF KINSELLA, JL GRANT, DS WEEKS, BS KLEINMAN, HK TI PROTEIN-KINASE-C REGULATES ENDOTHELIAL-CELL TUBE FORMATION ON BASEMENT-MEMBRANE MATRIX, MATRIGEL SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID INDUCE ANGIOGENESIS INVITRO; CAPILLARY-LIKE STRUCTURES; PROMOTING PHORBOL ESTERS; EXTRACELLULAR-MATRIX; PHENOTYPIC MODULATION; DIFFERENTIATION; MORPHOGENESIS; ORGANIZATION; INHIBITORS; LAMININ C1 NIH, DEV BIOL LAB, BETHESDA, MD 20892 USA. RP KINSELLA, JL (reprint author), NIA, GERONTOL RES CTR, CARDIOVASC SCI LAB, BALTIMORE, MD 21224 USA. NR 25 TC 51 Z9 51 U1 1 U2 8 PU ELSEVIER INC PI SAN DIEGO PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD MAR PY 1992 VL 199 IS 1 BP 56 EP 62 DI 10.1016/0014-4827(92)90461-G PG 7 WC Oncology; Cell Biology SC Oncology; Cell Biology GA HE278 UT WOS:A1992HE27800007 PM 1370939 ER PT J AU CHOI, AMK FARGNOLI, J CARLSON, SG HOLBROOK, NJ AF CHOI, AMK FARGNOLI, J CARLSON, SG HOLBROOK, NJ TI CELL-GROWTH INHIBITION BY PROSTAGLANDIN-A(2) RESULTS IN ELEVATED EXPRESSION OF GADD153 MESSENGER-RNA SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID CYCLOPENTENONE PROSTAGLANDINS; CYCLE PROGRESSION; PROTEIN; INDUCTION; ARREST; INTERFERON; MECHANISM; SITE C1 JOHNS HOPKINS MED INST, DIV PULM & CRIT CARE, BALTIMORE, MD 21224 USA. RP NIA, GERONTOL RES CTR, MOLEC GENET LAB, 4940 EASTERN AVE, BALTIMORE, MD 21224 USA. NR 27 TC 44 Z9 44 U1 0 U2 0 PU ELSEVIER INC PI SAN DIEGO PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4827 EI 1090-2422 J9 EXP CELL RES JI Exp. Cell Res. PD MAR PY 1992 VL 199 IS 1 BP 85 EP 89 DI 10.1016/0014-4827(92)90464-J PG 5 WC Oncology; Cell Biology SC Oncology; Cell Biology GA HE278 UT WOS:A1992HE27800010 PM 1735464 ER PT J AU RINAUDO, JAS ZELENKA, PS AF RINAUDO, JAS ZELENKA, PS TI EXPRESSION OF C-FOS AND C-JUN MESSENGER-RNA IN THE DEVELOPING CHICKEN LENS - RELATIONSHIP TO CELL-PROLIFERATION, QUIESCENCE, AND DIFFERENTIATION SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID POLYMERASE CHAIN-REACTION; PROTOONCOGENE EXPRESSION; CRYSTALLIN SYNTHESIS; DELTA-CRYSTALLIN; GENE-EXPRESSION; PROTO-ONCOGENE; CULTURED-CELLS; ANTISENSE RNA; GROWTH-FACTOR; 3T3 CELLS C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 43 TC 43 Z9 43 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 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD MAR PY 1992 VL 199 IS 1 BP 147 EP 153 DI 10.1016/0014-4827(92)90472-K PG 7 WC Oncology; Cell Biology SC Oncology; Cell Biology GA HE278 UT WOS:A1992HE27800018 PM 1735454 ER PT J AU DASGUPTA, S HOHMAN, TC CARPER, D AF DASGUPTA, S HOHMAN, TC CARPER, D TI HYPERTONIC STRESS INDUCES ALPHA-B-CRYSTALLIN EXPRESSION SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE ALPHA-B-CRYSTALLIN; HYPERTONIC STRESS; INDUCTION; CELL CULTURE; PROTEIN; MESSENGER RNA ID NON-LENTICULAR TISSUES; LENS EPITHELIAL-CELLS; ALDOSE-REDUCTASE; OSMOTIC-STRESS; DIABETIC NEUROPATHY; GEL-ELECTROPHORESIS; EXTRACELLULAR NACL; ESCHERICHIA-COLI; MEDULLARY CELLS; MESSENGER-RNA C1 NEI,BLDG 6,ROOM 232,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. WYETH AYERST LABS CN 8000,PRINCETON,NJ 08540. NR 52 TC 189 Z9 191 U1 0 U2 1 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 MAR PY 1992 VL 54 IS 3 BP 461 EP 470 DI 10.1016/0014-4835(92)90058-Z PG 10 WC Ophthalmology SC Ophthalmology GA HK996 UT WOS:A1992HK99600015 PM 1381680 ER PT J AU BHATTACHARYA, S BHATTACHARYA, A DIAMOND, LS AF BHATTACHARYA, S BHATTACHARYA, A DIAMOND, LS TI ENTAMOEBA-HISTOLYTICA EXTRACHROMOSOMAL CIRCULAR RIBOSOMAL DNA - ANALYSIS OF CLONAL VARIATION IN A HYPERVARIABLE REGION SO EXPERIMENTAL PARASITOLOGY LA English DT Article DE ENTAMOEBA-HISTOLYTICA; RIBOSOMAL DNA, CLONAL VARIATION; EXTRACHROMOSOMAL DNA; HYPERVARIABLE REGION ID RNA GENES; POLYMORPHISM; DISEASE C1 JAWAHARLAL NEHRU UNIV,SCH LIFE SCI,NEW DELHI 110067,INDIA. JAWAHARLAL NEHRU UNIV,SCH ENVIRONM SCI,NEW DELHI 110067,INDIA. RP BHATTACHARYA, S (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA. NR 13 TC 22 Z9 22 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4894 J9 EXP PARASITOL JI Exp. Parasitol. PD MAR PY 1992 VL 74 IS 2 BP 200 EP 204 DI 10.1016/0014-4894(92)90047-E PG 5 WC Parasitology SC Parasitology GA HH292 UT WOS:A1992HH29200009 PM 1346767 ER PT J AU PAUL, SM PURDY, RH AF PAUL, SM PURDY, RH TI NEUROACTIVE STEROIDS SO FASEB JOURNAL LA English DT Review DE NEUROACTIVE STEROIDS; GABA-A RECEPTORS; ANESTHETIC STEROIDS AND BARBITURATES; NONGENOMIC ACTIONS; MEMBRANE RECEPTORS; RAPID MODULATION OF INHIBITORY AND EXCITATORY NEUROTRANSMITTERS; NEUROSTEROIDS ID GABAA RECEPTOR SUBUNIT; CHLORIDE-ION FLUX; BENZODIAZEPINE RECEPTORS; RAT-BRAIN; PREGNENOLONE-SULFATE; HORMONE METABOLITES; PHYSICAL SEPARATION; CENTRAL NEURONS; A RECEPTORS; GLIAL-CELLS AB Neuroactive steroids are natural or synthetic steroids that rapidly alter the excitability of neurons by binding to membrane-bound receptors such as those for inhibitory and (or) excitatory neurotransmitters. The best-studied neuroactive steroids are a series of sedative-hypnotic 3-alpha-hydroxy ring A-reduced pregnane steroids that include the major metabolites of progesterone and deoxycorticosterone, 3-alpha-hydroxy-5-alpha-pregnan-20-one (allopregnanolone) and 3-alpha,21-dihydroxy-5-alpha-pregnan-20-one (allotetrahydroDOC), respectively. These 3-alpha-hydroxysteroids do not interact with classical intracellular steroid receptors but bind stereoselectively and with high affinity to receptors for the major inhibitory neurotransmitter in brain, gamma-aminobutyric acid (GABA). Biochemical and electrophysiological studies have shown that these steroids markedly augment GABA-activated chloride ion currents in a manner similar (but not identical) to that of anesthetic barbiturates. Several steroids have also been observed to have convulsant or proconvulsant properties, including the synthetic amidine 3-alpha-hydroxy-16-imino-5-beta-17-azaandrostan-11-one (RU5135) and the natural sulfate esters of pregnenolone and dehydroepiandrosterone. Several of these have been shown to be bicuculline or picrotoxin-like GABA(A) receptor antagonists. Examples of steroids that alter neuronal excitability rapidly by augmenting or inhibiting excitatory amino acid receptor-mediated responses have also been reported. Recently, allopregnanolone and allotetrahydroDOC have also been measured in brain and plasma where their levels have been shown to fluctuate in response to stress and during the estrous and menstrual cycles of rats and humans, respectively. Although the major fraction of allopregnanolone in tissue, including brain, is of adrenal and/or ovarian origin, appreciable levels of allopregnanolone can still be measured in the brains of adrenalectomized and/or oophorectomized animals. Receptor-active neurosteroids may represent an important class of neuromodulators that can rapidly alter central nervous system excitability via novel nongenomic mechanisms. C1 SW FDN BIOMED RES,DEPT ORGAN CHEM,SAN ANTONIO,TX 78228. RP PAUL, SM (reprint author), NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BLDG 10,ROOM 4N224,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 97 TC 1247 Z9 1260 U1 9 U2 41 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1992 VL 6 IS 6 BP 2311 EP 2322 PG 12 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA HJ252 UT WOS:A1992HJ25200008 PM 1347506 ER PT J AU KURATA, Y DIWAN, BA WARD, JM AF KURATA, Y DIWAN, BA WARD, JM TI LACK OF RENAL TUMOR-INITIATING ACTIVITY OF A SINGLE DOSE OF POTASSIUM BROMATE, A GENOTOXIC RENAL CARCINOGEN IN MALE F344/NCR RATS SO FOOD AND CHEMICAL TOXICOLOGY LA English DT Note ID CHEMICAL CARCINOGENESIS; EPITHELIAL TUMORS; BARBITURIC-ACID; DNA-SYNTHESIS; CELL TUMORS; KIDNEY; SODIUM; GLUTATHIONE; PROMOTION; TUBULES AB The renal tumour-initiating activity of potassium bromate (KBrO3), a known genotoxic rat renal carcinogen, was investigated in male F344/NCr rats. 6-wk-old rats were given KBrO3 intragastrically as a single dose of 300 mg/kg body weight, which was confirmed by our preliminary toxicity study as a maximum tolerated single dose for this strain of rat. Starting 2 wk after KBrO3 treatment, groups of 39 rats received either a basal diet or a diet containing 4000 ppm barbital sodium (BBNa) as a promoting regimen and were killed at 30, 52, or 104 wk. Control rats received either dietary BBNa (4000 ppm) or the basal diet alone from wk 2 to 52 or 104 wk. Nephropathy was observed in all rats treated with KBrO3 followed by BBNa at 30 wk and in rats receiving BBNa alone, but not in rats exposed to KBrO3 alone. Dysplastic renal tubular cell foci (DTF), putative preneoplastic renal tubular cell lesions were found associated with nephropathy in rats exposed to KBrO3 followed by BBNa from 47 wk. The incidences and multiplicities of DTF and renal tubular cell tumours observed from 31 to 104 wk revealed no initiating effect of KBrO3 treatment. These results indicate that the KBrO3 dose of 300 mg/kg did not initiate renal carcinogenesis. C1 NCI,DIV CANC ETIOL,COMP CARCINOGENESIS LAB,TUMOUR PATHOL & PATHOGENESIS SECT,FREDERICK,MD 21702. PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74102] NR 35 TC 16 Z9 16 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0278-6915 J9 FOOD CHEM TOXICOL JI Food Chem. Toxicol. PD MAR PY 1992 VL 30 IS 3 BP 251 EP 259 DI 10.1016/0278-6915(92)90041-I PG 9 WC Food Science & Technology; Toxicology SC Food Science & Technology; Toxicology GA JB113 UT WOS:A1992JB11300012 PM 1618449 ER PT J AU PISEGNA, JR NORTON, JA SLIMAK, GG METZ, DC MATON, PN GARDNER, JD JENSEN, RT AF PISEGNA, JR NORTON, JA SLIMAK, GG METZ, DC MATON, PN GARDNER, JD JENSEN, RT TI EFFECTS OF CURATIVE GASTRINOMA RESECTION ON GASTRIC SECRETORY FUNCTION AND ANTISECRETORY DRUG REQUIREMENT IN THE ZOLLINGER-ELLISON SYNDROME SO GASTROENTEROLOGY LA English DT Article ID ACID-SECRETION; H2-RECEPTOR ANTAGONISTS; GASTROINTESTINAL HORMONES; EXPLORATORY LAPAROTOMY; HYPERSECRETORY STATES; LOCALIZE GASTRINOMAS; CELL-PROLIFERATION; ANTRECTOMIZED RATS; MANAGEMENT; OMEPRAZOLE C1 NIH,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892. NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 65 TC 71 Z9 71 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 MAR PY 1992 VL 102 IS 3 BP 767 EP 778 PG 12 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HF721 UT WOS:A1992HF72100003 PM 1537514 ER PT J AU WINTER, HS FOX, CH HENDREN, RB ISSELBACHER, KJ FOLKMAN, J LETVIN, NL AF WINTER, HS FOX, CH HENDREN, RB ISSELBACHER, KJ FOLKMAN, J LETVIN, NL TI USE OF AN ANIMAL-MODEL FOR THE STUDY OF THE ROLE OF HUMAN IMMUNODEFICIENCY VIRUS-1 IN THE HUMAN INTESTINE SO GASTROENTEROLOGY LA English DT Article ID MUCOSAL-T-CELLS; GASTROINTESTINAL MANIFESTATIONS; SYNDROME AIDS; AMPLIFICATION; ABNORMALITIES; ENTEROPATHY; LYMPHOCYTE; INFECTION; DISEASE C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,BOSTON,MA 02115. NIAID,BETHESDA,MD 20892. FU NIAID NIH HHS [AI27747] NR 34 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 MAR PY 1992 VL 102 IS 3 BP 834 EP 839 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HF721 UT WOS:A1992HF72100012 PM 1537521 ER PT J AU HAUN, RS MOSS, J AF HAUN, RS MOSS, J TI LIGATION-INDEPENDENT CLONING OF GLUTATHIONE-S-TRANSFERASE FUSION GENES FOR EXPRESSION IN ESCHERICHIA-COLI SO GENE LA English DT Article DE EXPRESSION VECTOR; POLYMERASE CHAIN REACTION; PLASMID; THROMBIN; GUANINE NUCLEOTIDE-BINDING (G) PROTEINS; ADP-RIBOSYLATION FACTOR ID SITE-DIRECTED MUTAGENESIS; POLYMERASE CHAIN-REACTION; STEP PURIFICATION; PCR PRODUCTS; THROMBIN; DNA; PROTEINS; MALTOSE AB A plasmid vector has been constructed that allows the ligation-independent cloning of cDNAs in any reading frame and directs their synthesis in Escherichia coli as glutathione S-transferase-linked fusion proteins. The cloning procedure does not require restriction enzyme digestion of the target sequence and does not introduce any additional sequences between the thrombin cleavage site and the foreign protein. Extended single-stranded tails complementary between the vector and insert, generated by the (3' --> 5') exonuclease activity of T4 DNA polymerase, obviate the need for in vitro ligation prior to bacterial transformation. This cloning procedure is rapid and highly efficient, and has been used successfully to construct a series of fusion proteins to investigate the sequence requirements for efficient thrombin cleavage. RP HAUN, RS (reprint author), NHLBI,CELLULAR METAB LAB,BLDG 10,RM 5N307,BETHESDA,MD 20892, USA. NR 18 TC 45 Z9 45 U1 0 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD MAR 1 PY 1992 VL 112 IS 1 BP 37 EP 43 DI 10.1016/0378-1119(92)90300-E PG 7 WC Genetics & Heredity SC Genetics & Heredity GA HL489 UT WOS:A1992HL48900006 PM 1339364 ER PT J AU JHAPPAN, C GALLAHAN, D STAHLE, C CHU, E SMITH, GH MERLINO, G CALLAHAN, R AF JHAPPAN, C GALLAHAN, D STAHLE, C CHU, E SMITH, GH MERLINO, G CALLAHAN, R TI EXPRESSION OF AN ACTIVATED NOTCH-RELATED INT-3 TRANSGENE INTERFERES WITH CELL-DIFFERENTIATION AND INDUCES NEOPLASTIC TRANSFORMATION IN MAMMARY AND SALIVARY-GLANDS SO GENES & DEVELOPMENT LA English DT Article DE CDC10; DUCTULAR HYPERPLASIA; MALE STERILITY; LACTATION DEFICIENCY; MMTV ID CYCLE CONTROL PROTEINS; YEAST HO GENE; TUMOR VIRUS; ONCOGENE PRODUCT; REL ONCOGENE; KAPPA-B; MICE; DROSOPHILA; HOMOLOGY; IDENTIFICATION AB Expression of the int-3 locus is activated in mouse mammary tumors as a consequence of insertional mutagenesis by the mouse mammary tumor virus (MMTV). Integration of the MMTV provirus into the int-3 locus promotes the transcription and translation of flanking cellular int-3 sequences sharing significant homology with the intracellular domain of the neurogenic Notch gene of Drosophila, and with the yeast cell cycle regulatory genes cdc10 and SWI6. To determine the in vivo consequences of activated int-3 expression, transgenic mice were generated harboring a genomic tumor DNA fragment consisting of the MMTV LTR and the flanking cellular int-3 sequences. All six int-3 founder transgenic mice and the progeny of one established line exhibited similar dramatic phenotypic abnormalities in tissues in which the transgene was expressed. Focal and often multiple poorly differentiated mammary and salivary adenocarcinomas appeared in the majority of transgenic mice between 2 and 7 months of age. Significantly, mammary glands were arrested in development and were lactation deficient in all female int-3 mice. The salivary glands, glands of the nasal mucosa and maxillary sinus, the extraorbital lacrimal glands, and the Harderian glands of juvenile and adult transgenic mice all contained proliferating immature ductule cells and were incompletely differentiated. In addition, all male int-3 transgenic mice were sterile, apparently the result of severe hyperplasia of the epididymis. These findings demonstrate in vivo that expression of the activated Notch-related int-3 gene causes deregulation of normal developmental controls and hyperproliferation of glandular epithelia. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,DIV CANC BIOL DIAG & CTR,TUMOR IMMUNOL,BETHESDA,MD 20892. NR 34 TC 287 Z9 293 U1 2 U2 5 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD MAR PY 1992 VL 6 IS 3 BP 345 EP 355 DI 10.1101/gad.6.3.345 PG 11 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA HM444 UT WOS:A1992HM44400002 PM 1372276 ER PT J AU ROTH, SY SHIMIZU, M JOHNSON, L GRUNSTEIN, M SIMPSON, RT AF ROTH, SY SHIMIZU, M JOHNSON, L GRUNSTEIN, M SIMPSON, RT TI STABLE NUCLEOSOME POSITIONING AND COMPLETE REPRESSION BY THE YEAST ALPHA-2 REPRESSOR ARE DISRUPTED BY AMINO-TERMINAL MUTATIONS IN HISTONE-H4 SO GENES & DEVELOPMENT LA English DT Article DE ALPHA-2; REPRESSION; NUCLEOSOME; HISTONE-H4; TRANSCRIPTION; CHROMATIN ID MATING-TYPE LOCUS; SACCHAROMYCES-CEREVISIAE; CELL-TYPE; DNA-BINDING; INVERTASE SYNTHESIS; GENE; PROTEIN; CHROMATIN; OPERATOR; TRANSCRIPTION AB Nucleosomes are positioned in the presence of the yeast repressor-alpha-2 in minichromosomes containing the alpha-2 operator and on the promoters of a-cell-specific genes regulated by alpha-2. To investigate the possibility that alpha-2 directs nucleosome position through an interaction with a component of the core particle, we analyzed chromatin structures adjacent to the operator in alpha-cells containing mutations in the amino-terminal region of histone H4. Deletion or point mutation of specific amino acids in histone H4 altered the location and/or stability of nucleosomes adjacent to the alpha-2 operator. These changes in chromatin structure were accompanied by partial derepression of a beta-galactosidase reporter construct under alpha-2 control, even though alpha-2 remained bound to its operator sequence. Our data suggest that complete repression by alpha-2 requires stable positioning of nucleosomes in promoter regions and this positioning involves the conserved amino-terminal region of histone H4. C1 UNIV CALIF LOS ANGELES,DEPT BIOL,INST MOLEC BIOL,LOS ANGELES,CA 90024. RP ROTH, SY (reprint author), NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892, USA. NR 56 TC 146 Z9 146 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD MAR PY 1992 VL 6 IS 3 BP 411 EP 425 DI 10.1101/gad.6.3.411 PG 15 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA HM444 UT WOS:A1992HM44400008 PM 1547940 ER PT J AU POLYMEROPOULOS, MH XIAO, H GLODEK, A GORSKI, M ADAMS, MD MORENO, RF FITZGERALD, MG VENTER, JC MERRIL, CR AF POLYMEROPOULOS, MH XIAO, H GLODEK, A GORSKI, M ADAMS, MD MORENO, RF FITZGERALD, MG VENTER, JC MERRIL, CR TI CHROMOSOMAL ASSIGNMENT OF 46-BRAIN-CDNAS SO GENOMICS LA English DT Article ID GENES; POLYMORPHISMS; EXPRESSION; REGION; RNA C1 NINCDS,RECEPTOR BIOCHEM & MOLEC BIOL SECT,BETHESDA,MD 20892. RP POLYMEROPOULOS, MH (reprint author), ST ELIZABETH HOSP,CTR NEUROSCI,NATL INST MENTAL HLTH,BIOCHEM GENET LAB,WASHINGTON,DC 20032, USA. NR 23 TC 66 Z9 66 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR PY 1992 VL 12 IS 3 BP 492 EP 496 DI 10.1016/0888-7543(92)90439-Y PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA HD434 UT WOS:A1992HD43400010 PM 1559700 ER PT J AU YAMAMOTO, JH OKAJIMA, O MOCHIZUKI, M SHINOHARA, T WIGGERT, B CHADER, GJ GERY, I NUSSENBLATT, RB AF YAMAMOTO, JH OKAJIMA, O MOCHIZUKI, M SHINOHARA, T WIGGERT, B CHADER, GJ GERY, I NUSSENBLATT, RB TI CELLULAR IMMUNE-RESPONSES TO RETINAL ANTIGENS IN RETINITIS-PIGMENTOSA SO GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY LA English DT Article ID BINDING PROTEIN IRBP; S-ANTIGEN; UVEITIS PATIENTS; IDENTIFICATION; PRIMATES; UVEORETINITIS; PROLIFERATION; STIMULATION; PINEALITIS; MODEL AB Patients with retinitis pigmentosa and a group of controls were tested for their cellular immune response toward two retinal proteins, S-antigen and interphotoreceptor retinoid-binding protein (IRBP), as well as their reaction against two synthetic peptides ("M" and "N") derived from the sequence of S-antigen and peptide "R14", derived from IRBP. Positive responses to the retinal antigens were found in larger proportions and with higher levels in the patient group than in the controls. The difference between the two groups was statistically significant in their response to S-antigen, but the patients reacted better than the controls against the other antigens as well. Of particular interest was the finding that several patients responded to both retinal proteins and/or to their peptides. These patients suffered from severe retinal changes and the data are thus interpreted as suggesting that the responses to the retinal antigens are secondary to these changes and to non-physiological release of retinal antigens. C1 KURUME UNIV,SCH MED,DEPT OPHTHALMOL,67 ASAHI MACHI,KURUME,FUKUOKA 830,JAPAN. UNIV TOKYO,DEPT OPHTHALMOL,TOKYO 113,JAPAN. NEI,BETHESDA,MD 20892. RI Yamamoto, Joyce/B-6192-2015; OI Shinohara, Toshimichi/0000-0002-7197-9039 NR 30 TC 8 Z9 9 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0721-832X J9 GRAEF ARCH CLIN EXP JI Graefes Arch. Clin. Exp. Ophthalmol. PD MAR PY 1992 VL 230 IS 2 BP 119 EP 123 DI 10.1007/BF00164648 PG 5 WC Ophthalmology SC Ophthalmology GA HJ970 UT WOS:A1992HJ97000005 PM 1577290 ER PT J AU ADASHI, EY RESNICK, CE HURWITZ, A RICCIARELLIE, E HERNANDEZ, ER ROBERTS, CT LEROITH, D ROSENFELD, R AF ADASHI, EY RESNICK, CE HURWITZ, A RICCIARELLIE, E HERNANDEZ, ER ROBERTS, CT LEROITH, D ROSENFELD, R TI THE INTRA-OVARIAN IGF SYSTEM SO GROWTH REGULATION LA English DT Review DE OVARY; INSULIN-LIKE GROWTH FACTORS; IGF ID GROWTH FACTOR-I; RAT GRANULOSA-CELLS; FOLLICLE-STIMULATING-HORMONE; MESSENGER-RIBONUCLEIC-ACID; FACTOR-BINDING PROTEIN; SOMATOMEDIN-C; GENE-EXPRESSION; INDUCED DIFFERENTIATION; PREOVULATORY FOLLICLES; SYNERGISTIC ACTIONS C1 NIDDK,BETHESDA,MD 20892. STANFORD UNIV,MED CTR,STANFORD,CA 94305. RP ADASHI, EY (reprint author), UNIV MARYLAND,SCH MED,DEPT OBSTET & GYNECOL,DIV REPROD ENDOCRINOL,BALTIMORE,MD 21201, USA. OI Roberts, Charles/0000-0003-1756-5772 FU NICHD NIH HHS [1-K04-HD-00697, HD-19998] NR 67 TC 67 Z9 67 U1 0 U2 1 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0956-523X J9 GROWTH REGULAT JI Growth Regul. PD MAR PY 1992 VL 2 IS 1 BP 10 EP 15 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL903 UT WOS:A1992HL90300002 PM 1486332 ER PT J AU PARSHAD, R PRICE, FM OSHIMURA, M BARRETT, JC SATOH, H WEISSMAN, BE STANBRIDGE, EJ SANFORD, KK AF PARSHAD, R PRICE, FM OSHIMURA, M BARRETT, JC SATOH, H WEISSMAN, BE STANBRIDGE, EJ SANFORD, KK TI COMPLEMENTATION OF A DNA-REPAIR DEFICIENCY IN 6 HUMAN TUMOR-CELL LINES BY CHROMOSOME-11 SO HUMAN GENETICS LA English DT Article ID DYSKERATOSIS CONGENITA FIBROBLASTS; ATAXIA TELANGIECTASIA CELLS; CHROMATID RADIOSENSITIVITY; SUPPRESSES TUMORIGENICITY; ABERRATION PRODUCTION; X-IRRADIATION; CYCLE PERIOD; LOCALIZATION; EXPRESSION; LYMPHOCYTES AB Human tumor cells, after x-irradiation during the G2 phase of the cell cycle, show an abnormally high frequency of persistent chromatid breaks and gaps resulting from deficient DNA repair. Addition of a single human chromosome 11 from normal fibroblasts by micro-cell fusion to cell lines from six different tumors resulted in efficient repair of the radiation-induced damage to the level in normal cells. For one of the cell lines, addition of the long arm of chromosome 11 was sufficient to restore repair efficiency. In four of the six tumor lines, restoration of efficient DNA repair by chromosome 11 was associated with tumor suppression in nude mice. These results suggest that chromosome 11 carries a DNA repair gene or genes that complement the repair deficiency of tumor cells and that this gene for at least one tumor is localized to the long arm. C1 NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,ROOM 2D15,BETHESDA,MD 20892. UNIV N CAROLINA,LINEBERGER CANC RES CTR,CHAPEL HILL,NC 27599. UNIV CALIF IRVINE,DEPT MICROBIOL & GENET,IRVINE,CA 92717. HOWARD UNIV,COLL MED,DEPT PATHOL,WASHINGTON,DC 20001. NIEHS,RES TRIANGLE PK,NC 27709. FU NCI NIH HHS [CA44470, CA19401] NR 51 TC 19 Z9 19 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 MAR PY 1992 VL 88 IS 5 BP 524 EP 528 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA HJ345 UT WOS:A1992HJ34500006 PM 1312990 ER PT J AU CARRINGTON, M MILLER, T WHITE, M GERRARD, B STEWART, C DEAN, M MANN, D AF CARRINGTON, M MILLER, T WHITE, M GERRARD, B STEWART, C DEAN, M MANN, D TI TYPING OF HLA-DQA1 AND DQB1 USING DNA SINGLE-STRAND CONFORMATION POLYMORPHISM SO HUMAN IMMUNOLOGY LA English DT Article ID POINT MUTATIONS; POLYMERASE AB The technique of single-strand conformation polymorphism (SSCP), which is capable of distinguishing DNA sequence variability, was adapted to the identification of the HLA-DQA1 and DQB1 alleles. Eight DQA1 alleles and 12 DQB1 alleles were distinguished by amplifying the second exon of the genes in the presence of radioactive deoxynucleotide, denaturing the products with heat, and separating the single strands by electrophoresis in nondenaturing gels. For DQA1, it was possible to distinguish the eight alleles with standard bis-acrylamide or with a Hydrolink gel matrix. Twelve DQB1 alleles were identified by a protocol employing a combination of oligohybridization and SSCP using products amplified by specific DQB1 primers. C1 NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. RP CARRINGTON, M (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 FU NCI NIH HHS [N01-CO-74102] NR 10 TC 66 Z9 66 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD MAR PY 1992 VL 33 IS 3 BP 208 EP 212 DI 10.1016/0198-8859(92)90073-V PG 5 WC Immunology SC Immunology GA HZ462 UT WOS:A1992HZ46200007 PM 1618658 ER PT J AU KLEE, MM AF KLEE, MM TI A CASE OF BAD ADVICE SO IEEE ENGINEERING IN MEDICINE AND BIOLOGY MAGAZINE LA English DT Article C1 MICHIGAN STATE UNIV,COLL ENGN,E LANSING,MI 48824. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 0739-5175 J9 IEEE ENG MED BIOL JI IEEE Eng. Med. Biol. Mag. PD MAR PY 1992 VL 11 IS 1 BP 78 EP 78 PG 1 WC Engineering, Biomedical; Medical Informatics SC Engineering; Medical Informatics GA HD899 UT WOS:A1992HD89900014 ER PT J AU UNSER, M ALDROUBI, A EDEN, M AF UNSER, M ALDROUBI, A EDEN, M TI ON THE ASYMPTOTIC CONVERGENCE OF B-SPLINE WAVELETS TO GABOR FUNCTIONS SO IEEE TRANSACTIONS ON INFORMATION THEORY LA English DT Letter DE WAVELET TRANSFORM; GABOR TRANSFORM; UNCERTAINTY PRINCIPLE; POLYNOMIAL SPLINE; BETA-SPLINES; TIME-FREQUENCY LOCALIZATION ID SIGNAL; DECOMPOSITION; LOCALIZATION; ONDELETTES AB A family of nonorthogonal polynomial spline wavelet transforms is considered. These transforms are fully reversible and can be implemented efficiently. The corresponding wavelet functions have a compact support. It is proven that these B-spline wavelets converge to Gabor functions (modulated Gaussian) pointwise and in all L(p)-norms with 1 less-than-or-equal-to p < + infinity as the order of the spline (n) tends to infinity. In fact, the approximation error for the cubic B-spline wavelet (n = 3) is already less than 3%; this function is also near optimal in terms of its time/frequency localization in the sense that its variance product is within 2% of the limit specified by the uncertainty principle. RP UNSER, M (reprint author), NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13,BETHESDA,MD 20892, USA. RI Unser, Michael/A-1550-2008; Aldroubi, Akram/J-7186-2012 NR 22 TC 155 Z9 179 U1 0 U2 7 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 0018-9448 J9 IEEE T INFORM THEORY JI IEEE Trans. Inf. Theory PD MAR PY 1992 VL 38 IS 2 BP 864 EP 871 DI 10.1109/18.119742 PN 2 PG 8 WC Computer Science, Information Systems; Engineering, Electrical & Electronic SC Computer Science; Engineering GA HG008 UT WOS:A1992HG00800022 ER PT J AU SCHIFFER, M KABAT, EA WU, TT AF SCHIFFER, M KABAT, EA WU, TT TI SUBGROUPS OF TCR ALPHA-CHAINS AND CORRELATION WITH T-CELL FUNCTION SO IMMUNOGENETICS LA English DT Article ID VARIABLE REGION GENES; RECEPTOR BETA-CHAINS; ANTIGEN-RECEPTOR; V-ALPHA; CHROMOSOME-14 INVERSION; ALLELIC EXCLUSION; MYELOMA PROTEINS; GERMLINE GENE; LYMPHOCYTES-T; LIGHT-CHAINS AB T-cell receptor (Tcr) alpha-chains are classified into four subgroups (I, II, III, and miscellaneous) based on the amino acid residues at positions 61 and 62. Subgroup I has Gly Phe at these positions, subgroup II has Arg Phe, subgroup III has Arg Leu, and subgroup miscellaneous has several other combinations. Variability plots for subgroups I, II, and III sequences show higher values around positions 93-103, 105, 108, 111, 113, and 115, suggesting that these positions may interact with the processed antigen molecules. Smaller peaks are present at various other regions which may bind the major histocompatibility complex class I or II molecules. The patterns of variability within one subgroup are similar for all species, for human alone, and for mouse alone. These subgroup patterns appear much less complicated than patterns for sequences in all subgroups taken together, implying that subgroups may be related to Tcr functions. Among 83 mouse chains, 15 are from cytotoxic cells and 40 from helper cells. Of the 15 from cytotoxic cells, 11, 2, 0, and 2 are in subgroups I, II, III, and miscellaneous; and of the 40 from helper cells, 9, 16, 12, and 3 are in subgroups I, II, III, and miscellaneous, respectively. Thus, a correlation between sequence and function of Tcr Tcr-alpha-chains seems possible. C1 COLUMBIA UNIV,DEPT MICROBIOL,NEW YORK,NY 10032. COLUMBIA UNIV,DEPT GENET & DEV,NEW YORK,NY 10032. COLUMBIA UNIV,DEPT NEUROL,NEW YORK,NY 10032. COLUMBIA UNIV,INST CANC RES,NEW YORK,NY 10032. NIH,OFF DIRECTOR,BETHESDA,MD 20892. NORTHWESTERN UNIV,DEPT APPL MATH,EVANSTON,IL 60201. NORTHWESTERN UNIV,DEPT BIOMED ENGN,EVANSTON,IL 60201. NORTHWESTERN UNIV,DEPT BIOCHEM,EVANSTON,IL 60201. NORTHWESTERN UNIV,DEPT MOLEC BIOL,EVANSTON,IL 60201. NORTHWESTERN UNIV,DEPT CELL BIOL,EVANSTON,IL 60201. RP SCHIFFER, M (reprint author), ARGONNE NATL LAB,DIV BIOL & MED RES,ARGONNE,IL 60439, USA. RI Wu, Tai/B-7638-2009 FU NIAID NIH HHS [5R01-AI25616-03, 2R01-AI19042-07A2, 5R01-AI127508-03] NR 81 TC 15 Z9 15 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD MAR PY 1992 VL 35 IS 4 BP 224 EP 234 DI 10.1007/BF00166827 PG 11 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA HJ373 UT WOS:A1992HJ37300002 PM 1531805 ER PT J AU MANOHAR, V BROWN, EM CHUSED, TM AF MANOHAR, V BROWN, EM CHUSED, TM TI MURINE SPLENIC NULL-CELL COMPARTMENT CONTAINS DISTINCT HEMATOPOIETIC SUBPOPULATIONS - ENLARGEMENT OF A MYELOID AND AN UNDIFFERENTIATED SUBSET WITH THE DEVELOPMENT OF SPLENOMEGALY IN NEW-ZEALAND BLACK MICE SO IMMUNOLOGY LA English DT Article ID HEMATOPOIETIC STEM-CELLS; MONOCLONAL-ANTIBODY; DIFFERENTIATION ANTIGENS; MOUSE MACROPHAGE; T-CELLS; B-CELLS; SURFACE; IDENTIFICATION; LYMPHOCYTES; RECEPTOR AB We have previously reported that non-T, non-B 'null' cells increase with age in New Zealand Black (NZB) mice resulting in splenomegaly. Using a panel of monoclonal antibodies recognizing lineage-specific cell surface antigens we demonstrate four distinct subsets within this null cell compartment: (1) undifferentiated; (2) T lineage with undetectable Thy-1.2; (3) myeloid/erythroid; and (4) a pre-B/plasma cell type. All four subsets also occur in non-autoimmune mice. The frequency of these populations are similar in the young mice of all the strains examined, although the total number of null cells is higher in NZB. The elevation of null cells in young NZB mice is controlled by a single dominant gene in the genetic cross with New Zealand White (NZW) mice and does not appear closely related to the subsequent development of autoimmune disease. The proportion of myeloid/erythroid null cells increases with age in NZB as splenomegaly develops. C1 US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL,CELL BIOL LAB,BETHESDA,MD 20014. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 32 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD MAR PY 1992 VL 75 IS 3 BP 448 EP 455 PG 8 WC Immunology SC Immunology GA HH312 UT WOS:A1992HH31200009 PM 1572692 ER PT J AU FISHELSON, Z SHLANGER, S BOMSTEIN, Y EVANS, CH AF FISHELSON, Z SHLANGER, S BOMSTEIN, Y EVANS, CH TI THE HUMAN LYMPHOKINE LEUKOREGULIN INDUCES CELL RESISTANCE TO COMPLEMENT-MEDIATED LYSIS SO IMMUNOLOGY LETTERS LA English DT Article DE RESISTANCE TO LYSIS; HUMAN; LYMPHOKINE; LEUKOREGULIN ID PROTEIN KINASE-C; CYTO-TOXIC FACTORS; NUCLEATED CELLS; NATURAL-KILLER; PLASMA-MEMBRANE; POLYMORPHONUCLEAR LEUKOCYTES; HUMAN-NEUTROPHILS; TARGET-CELLS; K562 CELLS; LYMPHOCYTES AB Leukoregulin (LR) is a lymphokine secreted by human natural killer (NK) cells. Its effect on the susceptibility of K562 human erythroleukemic cells to lysis by antibody and complement was examined. As reported here, treatment of K562 cells with LR for 60 min at 37-degrees-C confers on them resistance to complement damage. The LR-induced state of complement resistance is transient and the cells recover within 4-6 h unless a second dose of LR is added. The protective action of LR was observed using both conventional Cr-51-release and trypan blue inclusion assays. The protein synthesis inhibitors puromycin and cycloheximide and the protein kinase inhibitors tamoxifen, polymyxin B and W-7, could each block this action of LR. Fewer membrane attack complexes were found, following complement activation, on LR-treated than control cells. These results suggest that LR increases the capacity of K562 cells to down-regulate complement activation or repair the complement damage, possibly by inducing synthesis of defense proteins and/or activation of protective protein kinases. C1 NCI,BIOL LAB,BETHESDA,MD 20892. RP FISHELSON, Z (reprint author), WEIZMANN INST SCI,DEPT CHEM IMMUNOL,POB 26,IL-76100 REHOVOT,ISRAEL. NR 51 TC 3 Z9 3 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-2478 J9 IMMUNOL LETT JI Immunol. Lett. PD MAR PY 1992 VL 32 IS 1 BP 35 EP 42 DI 10.1016/0165-2478(92)90196-U PG 8 WC Immunology SC Immunology GA HL681 UT WOS:A1992HL68100007 PM 1500082 ER PT J AU SHIMIZU, Y NEWMAN, W TANAKA, Y SHAW, S AF SHIMIZU, Y NEWMAN, W TANAKA, Y SHAW, S TI LYMPHOCYTE INTERACTIONS WITH ENDOTHELIAL-CELLS SO IMMUNOLOGY TODAY LA English DT Review ID LEUKOCYTE ADHESION MOLECULE-1; T-CELL; HOMOTYPIC ADHESION; HELPER-INDUCER; SURFACE; EXPRESSION; RECEPTOR; RECOGNITION; MECHANISMS; MIGRATION AB Adhesion of lymphocytes to endothelium is vital to lymphocyte migration into lymphoid tissue and into inflammatory sites. In this review, Yoji Shimizu and colleagues identify the molecules that mediate lymphocyte-endothelial cell adhesion, describe the underlying principles of lymphocyte migration, and discuss a model of the sequence of events that allow a lymphocyte to successfully attach to endothelium and migrate into the surrounding tissue. C1 OTSUKA AMER PHARMACEUT INC,DEPT ENDOTHELIAL CELL BIOL,ROCKVILLE,MD 20850. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP SHIMIZU, Y (reprint author), UNIV MICHIGAN,SCH MED,DEPT MICROBIOL & IMMUNOL,ANN ARBOR,MI 48109, USA. OI Shimizu, Yoji/0000-0001-9760-0288 FU NIAID NIH HHS [AI31126] NR 83 TC 712 Z9 719 U1 1 U2 5 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD MAR PY 1992 VL 13 IS 3 BP 106 EP 112 DI 10.1016/0167-5699(92)90151-V PG 7 WC Immunology SC Immunology GA HH079 UT WOS:A1992HH07900007 PM 1622542 ER PT J AU COLE, MF HSU, SD SHERIDAN, MJ STILES, HM AF COLE, MF HSU, SD SHERIDAN, MJ STILES, HM TI NATURAL TRANSMISSION OF STREPTOCOCCUS-SOBRINUS IN RATS - SALIVA AND SERUM ANTIBODY-RESPONSES TO COLONIZATION SO INFECTION AND IMMUNITY LA English DT Article ID PRIMARY ORAL INFECTION; EARLY ESTABLISHMENT; IMMUNE-RESPONSE; IGA ANTIBODY; MUTANS; INFANTS; ANTIGENS; MOUTHS; HUMANS; GLUCOSYLTRANSFERASE AB One hundred and twenty weanling rats fed diet NIH 2000 that were free of Streptococcus sobrinus and other mutans streptococci were employed in this study. Sixty rats were inoculated orally with S. sobrinus 6715. Each infected rat (donor) was paired and housed with an uninfected recipient. Saliva and serum samples were collected from 24 (12 donor and 12 recipient) rats at the baseline (day 0) and from groups of 12 recipients sacrificed on days 10, 24, 38, and 52, and the level of infection with S. sobrinus was monitored. Salivary immunoglobulin A (IgA) and IgG and serum IgM and IgG antibodies reactive with whole cells (WC), glucosyltransferase (GTF), and the serotype carbohydrate (g) of S. sobrinus were measured by an indirect enzyme-linked immunosorbent assay. Although the rats were free of S. sobrinus and other mutans streptococci at baseline, they exhibited salivary IgA and serum IgM antibodies reactive with S. sobrinus WC, GTF, and g and serum IgG antibodies reactive with WC and GTF. Infection of recipients with S. sorbinus did not induce salivary antibodies reactive with WC, GTF, or g. In contrast, increases in serum IgM and IgG antibodies reactive with WC and serum IgM antibodies reactive with g were observed. C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. NIH,DIV RES GRANTS,BETHESDA,MD 20892. RP COLE, MF (reprint author), GEORGETOWN UNIV,SCH MED,DEPT MICROBIOL,WASHINGTON,DC 20007, USA. NR 44 TC 8 Z9 8 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 MAR PY 1992 VL 60 IS 3 BP 778 EP 783 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HH195 UT WOS:A1992HH19500010 PM 1531814 ER PT J AU DORWARD, DW HUGUENEL, ED DAVIS, G GARON, CF AF DORWARD, DW HUGUENEL, ED DAVIS, G GARON, CF TI INTERACTIONS BETWEEN EXTRACELLULAR BORRELIA-BURGDORFERI PROTEINS AND NON-BORRELIA-DIRECTED IMMUNOGLOBULIN-M ANTIBODIES SO INFECTION AND IMMUNITY LA English DT Article ID LYME-DISEASE; NEISSERIA-GONORRHOEAE; BINDING; AGENT AB Previous work showed that outer surface protein A (OspA) and OspB of Borrelia burgdorferi may occur within an extracellular multiprotein complex, which was resolved by electrophoresis as an 83-kDa major extracellular protein band. To characterize the 83-kDa band, we sequenced the N terminus of the predominant peptide in the band and examined the interaction between the associated proteins. Peptide sequence and amino acid composition comparisons showed identity with the heavy chain of immunoglobulin M (IgM). Reduction sensitivity experiments and the recognition of the band by antibodies specific for rabbit mu-chain indicated that the multiprotein complex contained pentameric IgM. Immunoelectron microscopy showed that anti-mu-chain antibodies and monoclonal antibodies to OspA and OspB bound to extracellular amorphous material surrounding cells. Furthermore, the Osps coprecipitated with either nonspecific polyclonal rabbit IgM antibodies or with murine monoclonal anti-human serum albumin IgM antibodies, using insoluble anti-mu-chain antibody conjugates. Although the apparent 83-kDa complex was stable under conditions of chelation and concentrated salts, it was disrupted by treatment with neuraminidase. These results indicate that extracellular B. burgdorferi proteins, including OspA and OspB, interact with IgM. The association is apparently not a classic antibody-antigen interaction but may result from other mechanisms. C1 MILES RES CTR,W HAVEN,CT 06516. RP DORWARD, DW (reprint author), NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840, USA. NR 25 TC 21 Z9 22 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 MAR PY 1992 VL 60 IS 3 BP 838 EP 844 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HH195 UT WOS:A1992HH19500019 PM 1541558 ER PT J AU VARMA, A EDMAN, JC KWONCHUNG, KJ AF VARMA, A EDMAN, JC KWONCHUNG, KJ TI MOLECULAR AND GENETIC-ANALYSIS OF URA5 TRANSFORMANTS OF CRYPTOCOCCUS-NEOFORMANS SO INFECTION AND IMMUNITY LA English DT Article ID NEUROSPORA-CRASSA; SCHIZOSACCHAROMYCES-POMBE; ASCOBOLUS-IMMERSUS; DUPLICATED DNA; SEQUENCES; REARRANGEMENT; INACTIVATION; INTEGRATION; REPLICATION; PLASMIDS AB Cryptococcus neoformans var. neoformans ura5 mutants were transformed with linearized or circular plasmids containing the C. neoformans orotidine monophosphate pyrophosphorylase gene. Following electroporation, randomly isolated transformants were analyzed for the mitotic and meiotic stability of uracil prototrophy. All stable transformants tested showed nonspecific ectopic integration. Uracil prototrophy in these transformants was stable through meiosis. Some of the stable transformants showed integration of both URA5 and vector sequences, while others lacked any vector sequences. Unstable transformants exhibited the presence of an autonomously replicating plasmid which had undergone significant sequence rearrangement. The autonomously replicating plasmid in the transformants was observed to be the same size or smaller than the transforming plasmid, was maintained in a linear form, and had acquired a genomic sequence(s) with homology to a sequence(s) on all the chromosomes. The conservation of a 300-bp sequence at the 5' end of the URA5 gene was observed in all the rearranged plasmids. These results suggest mechanisms of plasmid maintenance in C. neoformans that are different from those reported for other yeasts. The ura5 mutant was significantly less virulent than the wild type. The transformants did not recover virulence regardless of prototrophic stability. C1 UNIV CALIF SAN FRANCISCO,HORMONE RES INST,SAN FRANCISCO,CA 94143. RP VARMA, A (reprint author), NIAID,CLIN INVEST LAB,CLIN MYCOL SECT,BETHESDA,MD 20892, USA. NR 29 TC 75 Z9 77 U1 1 U2 4 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 MAR PY 1992 VL 60 IS 3 BP 1101 EP 1108 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HH195 UT WOS:A1992HH19500056 PM 1541525 ER PT J AU HUGHES, CV ANDERSEN, RN KOLENBRANDER, PE AF HUGHES, CV ANDERSEN, RN KOLENBRANDER, PE TI CHARACTERIZATION OF VEILLONELLA-ATYPICA PK1910 ADHESIN-MEDIATED COAGGREGATION WITH ORAL STREPTOCOCCUS SPP SO INFECTION AND IMMUNITY LA English DT Article ID BACTEROIDES-LOESCHEII PK1295; FIMBRIA-ASSOCIATED ADHESINS; ACTINOMYCES-NAESLUNDII; POLYACRYLAMIDE GELS; GNOTOBIOTIC-RATS; DENTAL PLAQUE; PROTEINS; MUTANS; ALCALESCENS; SANGUIS AB The gram-negative human oral bacterium Veillonella atypica PK1910 exhibits both lactose-inhibitable and lactose-noninhibitable coaggregations with certain human oral streptococci. A mild sonication procedure was used to obtain a veillonella surface protein preparation against which antisera were prepared. To characterize the lactose-inhibitable coaggregation, coaggregation-defective (COG-) mutants unable to exhibit this kind of coaggregation (class 1 mutants) were used to absorb the antisera. Only the lactose-inhibitable coaggregations were blocked by these absorbed antisera. The absorbed antiserum also reacted with a 45-kDa protein found in the parent and in class 2 COG- mutants that exhibited lactose-inhibitable coaggregation. This protein was not detected in surface protein preparations of class 1 COG- mutants. Two affinity protocols, involving agarose-lactose beads and the streptococcal coaggregation partner cells, were used to bind surface proteins from V. atypica PK1910. In each protocol, the 45-kDa protein was eluted by a solution containing 100 mM lactose. Antiserum was prepared against agarose-lactose beads with bound 45-kDa protein. When absorbed with class 1 COG- mutants, the antiserum blocked lactose-inhibitable coaggregation and reacted with the 45-kDa protein in immunoblots. When the same antiserum was absorbed with class 2 COG- mutant cells, it lost both properties, suggesting that the 45-kDa protein is an adhesin that mediates coaggregation with streptococci. The proposed adhesin does not seem to be the structural subunit of veillonella fimbriae, since no differences in fimbriae were observed by electron microscopy of the parent and all three classes of mutants. C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. RI Hughes, Christopher/E-1438-2014 NR 40 TC 21 Z9 22 U1 0 U2 3 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 MAR PY 1992 VL 60 IS 3 BP 1178 EP 1186 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HH195 UT WOS:A1992HH19500066 PM 1541534 ER PT J AU LEWIS, LL AF LEWIS, LL TI CONGENITAL-SYPHILIS - SEROLOGIC DIAGNOSIS IN THE YOUNG INFANT SO INFECTIOUS DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID TREPONEMA-PALLIDUM ANTIGENS; CEREBROSPINAL-FLUID; IMMUNOGLOBULIN-M; RHEUMATOID-FACTOR; FETAL IGM; ANTIBODIES; NEUROSYPHILIS C1 NCI,INFECT DIS SECT,PEDIAT BRANCH,BETHESDA,MD 20892. NR 44 TC 9 Z9 10 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0891-5520 J9 INFECT DIS CLIN N AM JI Infect. Dis. Clin. North Am. PD MAR PY 1992 VL 6 IS 1 BP 31 EP 39 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JT666 UT WOS:A1992JT66600004 PM 1578121 ER PT J AU STEIN, PH SINGER, A AF STEIN, PH SINGER, A TI SIMILAR CO-STIMULATION REQUIREMENTS OF CD4+ AND CD8+ PRIMARY T-HELPER CELLS - ROLE OF IL-1 AND IL-6 IN INDUCING IL-2 SECRETION AND SUBSEQUENT PROLIFERATION SO INTERNATIONAL IMMUNOLOGY LA English DT Article ID LYMPHOCYTES-T; CLASS-I; DENDRITIC CELLS; DISTINCT ROLES; INTERLEUKIN-1; LYMPHOKINE; RESPONSES; ACTIVATION; EXPRESSION; RECEPTORS AB Primary murine CD4+ and CD8+ T helper (Th) cells provide help for various immune responses by secreting lymphokines which activate effector cells. The purpose of the present study was to investigate the co-stimulatory signals that, together with T cell receptor (TCR) cross-linking, induce phenotypically distinct primary Th cells to secrete IL-2 and proliferate. We isolated highly purified populations of primary CD4+ or CD8+ T cells and stimulated them in vitro with plate-bound anti-CD3 mAb. TCR cross-linking by anti-CD3 mAb induced both IL-2 receptor expression and responsiveness to exogenous IL-2, but was not sufficient to induce either IL-2 secretion or T cell proliferation. Rather, for both CD4+ and CD8+ primary Th cells, IL-2 secretion and proliferation required both TCR cross-linking and antigen presenting cell (APC)-derived co-stimulatory signals. Based on G-10 adherence and sensitivity to gamma-irradiation, the APC populations able to induce primary CD4+ Th cells and primary CD8+ Th cells to secrete IL-2 were indistinguishable. In addition, we found that either IL-1 or IL-6 could replace the requirement for APC-derived co-stimulatory signals for IL-2 secretion and proliferation by both primary CD4+ Th cells and primary CD8+ Th cells. Thus, the present study has examined and compared the co-stimulatory requirements of rigorously purified subsets of IL-2-secreting primary CD4+ and primary CD8+ T cells. We conclude that the co-stimulatory requirements for IL-2 secretion by primary CD4+ and CD8+ Th cells share many similarities, and that they differ significantly from the reported co-stimulatory requirements of antigen-primed IL-2-secreting CD4+ Th cell clones. C1 NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B-17,BETHESDA,MD 20892. NR 44 TC 37 Z9 37 U1 0 U2 0 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 MAR PY 1992 VL 4 IS 3 BP 327 EP 335 DI 10.1093/intimm/4.3.327 PG 9 WC Immunology SC Immunology GA HK131 UT WOS:A1992HK13100004 PM 1533149 ER PT J AU TAMISLEMONDA, CS BORNSTEIN, MH CYPHERS, L TODA, S OGINO, M AF TAMISLEMONDA, CS BORNSTEIN, MH CYPHERS, L TODA, S OGINO, M TI LANGUAGE AND PLAY AT ONE YEAR - A COMPARISON OF TODDLERS AND MOTHERS IN THE UNITED-STATES AND JAPAN SO INTERNATIONAL JOURNAL OF BEHAVIORAL DEVELOPMENT LA English DT Article ID NATURALISTIC EXCHANGES; 3-MONTH-OLD INFANTS; MATERNAL SPEECH; BEHAVIOR; ATTENTION; COMPETENCE; PSYCHOLOGY; CULTURE AB The present study compared American and Japanese toddlers and their mothers on dimensions of language and play when the toddlers were 13 months of age. In both cultures and in both domains, individual variation in toddlers was associated with individual variation in mothers. In general, the frequency and variance of language and play activities were similar in the two groups. However, two notable cultural differences emerged. American toddlers were more advanced in both their productive and receptive vocabularies, and this cultural difference was matched by the tendency for American mothers to label and describe properties, objects, and events in the environment more frequently. In contrast, Japanese toddlers were more advanced on symbolic play, and their advanced play was matched by more advanced play in Japanese mothers, particularly for "other-directed" acts of pretence. These findings suggest that during this early period of symbolic development, as expressed through language and play, American and Japanese dyads emphasise different modes of representation and do so in ways that accord with traditional cultural concerns. C1 SOPHIA UNIV,TOKYO 102,JAPAN. NICHHD,CHILD & FAMILY RES SECT,BETHESDA,MD 20892. RP TAMISLEMONDA, CS (reprint author), NYU,INFANCY STUDIES PROGRAM,239 GREENE ST,5TH FLOOR,NEW YORK,NY 10003, USA. NR 68 TC 40 Z9 40 U1 1 U2 5 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE, EAST SUSSEX, ENGLAND BN3 2FA SN 0165-0254 J9 INT J BEHAV DEV JI Int. J. Behav. Dev. PD MAR PY 1992 VL 15 IS 1 BP 19 EP 42 PG 24 WC Psychology, Developmental SC Psychology GA HK184 UT WOS:A1992HK18400002 ER PT J AU MCNIECE, IK BERTONCELLO, I KELLER, JR RUSCETTI, FW HARTLEY, CA ZSEBO, KM AF MCNIECE, IK BERTONCELLO, I KELLER, JR RUSCETTI, FW HARTLEY, CA ZSEBO, KM TI TRANSFORMING GROWTH-FACTOR-BETA INHIBITS THE ACTION OF STEM-CELL FACTOR ON MOUSE AND HUMAN HEMATOPOIETIC PROGENITORS SO INTERNATIONAL JOURNAL OF CELL CLONING LA English DT Article DE STEM CELLS; SCF; TGF-BETA; INHIBITORS; HEMATOPOIESIS ID PURIFICATION; EXPRESSION; CLONING; IDENTIFICATION; BONE; GENE; RAT AB In agar culture of post 5-fluorouracil mouse bone marrow cells (FUBM), recombinant rat stem cell factor (rrSCF) synergises with granulocyte colony-stimulating factor (G-CSF), interleukin-3 (IL-3) or interleukin-6 (IL-6) to stimulate primitive progenitor cells (HPP-CFCs). The addition of recombinant human transforming growth factor beta (rhTGF-beta) to cultures of FUBM containing rrSCF plus rhG-CSF, rrSCF plus recombinant murine (rm)IL-3, or rrSCF plus rhIL-6 resulted in 100% inhibition of colony formation. Highly enriched populations of primitive bone marrow cells were obtained by isolating lineage negative (Lin-), Sca-1-positive (Sca-1+) cells from normal mouse bone marrow. RhTGF-beta inhibited 90% of colony formation stimulated by rrSCF plus rmIL-3 in agar culture of the Sca-1+ cells. RhTGF-beta also inhibited colony formation in agar culture of post FU human bone marrow cells. The synergistic increase in colony formation obtained with recombinant human SCF (rhSCF) plus rhGM-CSF and rhSCF plus rhIL-3 was inhibited by rhTGF-beta (approx. 60% and 87% inhibition, respectively). RhTGF-beta also totally inhibited the erythroid colony formation stimulated by rhSCF plus recombinant human erythropoietin (rhEpo). These data demonstrate that TGF-beta inhibits SCF-stimulated colony formation of mouse and human BM. This inhibition on progenitor cells appears to be a direct action of TGF-beta and is consistent with the target cells of SCF being more primitive progenitors than the CFCs stimulated by the CSFs alone. C1 PETER MACCALLUM CANC INST,MELBOURNE,VIC,AUSTRALIA. FREDERICK CANC RES FACIL,FREDERICK,MD 21701. RP MCNIECE, IK (reprint author), AMGEN INC,AMGEN CTR,THOUSAND OAKS,CA 91320, USA. RI Bertoncello, Ivan/B-9235-2008 NR 27 TC 41 Z9 42 U1 0 U2 0 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 0737-1454 J9 INT J CELL CLONING PD MAR PY 1992 VL 10 IS 2 BP 80 EP 86 PG 7 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA HJ631 UT WOS:A1992HJ63100003 PM 1372030 ER PT J AU DU, DL VOLPE, DA GRIESHABER, CK MURPHY, MJ AF DU, DL VOLPE, DA GRIESHABER, CK MURPHY, MJ TI COMPARISON OF THE INVITRO TOXICITY OF 2',3'-DIDEOXYNUCLEOSIDES TO MURINE HEMATOPOIETIC PROGENITOR CELLS SO INTERNATIONAL JOURNAL OF CELL CLONING LA English DT Article DE HEMATOPOIETIC PROGENITORS; MURINE; DDI; DDA; DDC; 5-F-DDC; INVITRO ID CFU-E; 2',3'-DIDEOXYCYTIDINE; PRECURSOR; ANALOGS; DRUGS; ASSAY AB Four nucleoside analogues, 2',3'-dideoxyinosine (ddI), 2',3'-dideoxyadenosine (ddA), 2',3'-dideoxycytosine (ddC) and 5-fluoro-2',3'-dideoxycytosine (5-F-ddC), were evaluated for their potential in vitro myelotoxic effects on normal murine hematopoietic progenitor cells. Myeloid granulocyte-macrophage colony-forming units (CFU-gm), erythroid burst-forming units (BFU-e) and colony-forming units (CFU-e) and megakaryocytic (CFU-meg) progenitors were exposed to the agents for 1 h prior to culture in Petri dish assays or continuously throughout the entire culture period. At 10-mu-M, both ddA and ddI were moderately toxic (2-36% colony inhibition) to murine CFU-gm, BFU-e, CFU-e and CFU-meg following either 1 h or continuous exposure. Colony inhibition for the progenitors ranged from 2-31% at 10-mu-M for 1 h ddC or 5-F-ddC exposure. Continuous exposure to ddC was highly myelotoxic to murine hematopoietic progenitors with 100-mu-M suppressing colony formation 82-89%. At the same concentration and exposure time, 5-F-ddC inhibited colony formation 56-67%. Our results demonstrate that 1 h and continuous exposures to ddA and ddI were similarly myelotoxic to murine hematopoietic cells regardless of exposure time. In contrast, continuous ddC or 5-F-ddC exposure was more toxic to murine progenitors than 1 h exposure to these agents. C1 HIPPLE CANC RES CTR,4100 S KETTERING BLVD,DAYTON,OH 45439. NCI,BETHESDA,MD 20892. FU NCI NIH HHS [CM-77831] NR 17 TC 3 Z9 3 U1 0 U2 0 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 0737-1454 J9 INT J CELL CLONING PD MAR PY 1992 VL 10 IS 2 BP 87 EP 93 PG 7 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA HJ631 UT WOS:A1992HJ63100004 PM 1545153 ER PT J AU ZHANG, Y SAMULSKI, TV JOINES, WT MATTIELLO, J LEVIN, RL LEBIHAN, D AF ZHANG, Y SAMULSKI, TV JOINES, WT MATTIELLO, J LEVIN, RL LEBIHAN, D TI ON THE ACCURACY OF NONINVASIVE THERMOMETRY USING MOLECULAR-DIFFUSION MAGNETIC-RESONANCE-IMAGING SO INTERNATIONAL JOURNAL OF HYPERTHERMIA LA English DT Article DE HYPERTHERMIA; TEMPERATURE; DIFFUSION; MAGNETIC RESONANCE ID INTRAVOXEL INCOHERENT MOTIONS; STATE FREE PRECESSION; HYPERTHERMIA AB Temperature measurement using magnetic resonance imaging (MRI) of water self-diffusion is investigated. Diffusion images and derived temperatures are obtained in polyacrylamide gel phantom. The temperatures measured from MRI are compared with those from temperature probes to verify their accuracy. In general, the difference between temperatures determined from MRI diffusion images over 0.3 cm3 regions of interest and from temperature probes were 0.2-degrees-C. It is concluded that current MRI technology allows noninvasive temperature tomography that is comparable with invasive thermometry with respect to temperature accuracy. has spatial and time resolutions that would be useful in hyperthermic oncology. C1 DUKE UNIV,MED CTR,DEPT RADIAT ONCOL,DURHAM,NC 27710. NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,BETHESDA,MD 20892. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. RP ZHANG, Y (reprint author), DUKE UNIV,DEPT ELECT ENGN,DURHAM,NC 27706, USA. FU NCI NIH HHS [2 POL CA42745-04] NR 21 TC 55 Z9 54 U1 0 U2 2 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0265-6736 J9 INT J HYPERTHER JI Int. J. Hyperthermia PD MAR-APR PY 1992 VL 8 IS 2 BP 263 EP 274 DI 10.3109/02656739209021781 PG 12 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HG365 UT WOS:A1992HG36500011 PM 1573315 ER PT J AU CHAN, PC HUFF, J HASEMAN, JK QUEST, JA HALL, W AF CHAN, PC HUFF, J HASEMAN, JK QUEST, JA HALL, W TI LIVER CARCINOGENESIS BY METHYL CARBAMATE IN F344 RATS AND NOT IN B6C3F1 MICE SO JAPANESE JOURNAL OF CANCER RESEARCH LA English DT Article DE METHYL CARBAMATE; HEPATOCARCINOGENESIS; RATS ID CELL MUTAGENESIS ASSAY; CHEMICALS; MOUSE AB Short-term and long-term carcinogenicity of methyl carbamate (MCB) was evaluated in F344 rats and B6C3F1 mice. In experiments lasting 6, 12, and 18 months, MCB was given in water by gavage to groups of 10 male and 10 female rats at 0 or 400 mg/kg body weight, 5 days per week, and to similar groups of mice at 0 or 1,000 mg/kg. At 6 months, MCB induced atypical mitoses, cytologic alterations, cytomegaly, pigmentation, necrosis, and neoplastic nodules of the liver in rats. At 12 and 18 months, carcinomas of the liver were induced by MCB in 80-90% of male rats and in 60-80% of female rats. None was observed in control rats or in mice. In the 2-year studies, MCB was given to groups of 50 male and 50 female rats at 0, 100, or 200 mg/kg and to similar groups of mice at 0, 500, or 1,000 mg/kg, 5 days/week. Chronic focal inflammation, cytologic alteration, hyperplasia, and neoplastic nodules and carcinomas (200 mg/kg groups only) of the liver were induced by MCB in rats. Liver tumor incidence data for combined experiments in rats were: males - 5% in controls, 0% in 100 mg/kg group, 14% in 200 mg/kg group, and 77% in 400 mg/kg group; females - 0% in controls, 0% in 100 mg/kg group, 12% in 200 mg/kg group, and 63% in 400 mg/kg group. MCB was not shown to be carcinogenic in mice. C1 MICROBIOL ASSOCIATES INC,BETHESDA,MD 20816. RP CHAN, PC (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 41 TC 5 Z9 5 U1 0 U2 0 PU JAPANESE CANCER ASSOCIATION PI TOKYO PA EDITORIAL OFFICE 7TH FLOOR, JOHKOH BLDG 2-23-11, KOISHIKAWA, TOKYO 112, JAPAN SN 0910-5050 J9 JPN J CANCER RES JI Jpn. J. Cancer Res. PD MAR PY 1992 VL 83 IS 3 BP 258 EP 263 PG 6 WC Oncology SC Oncology GA HL413 UT WOS:A1992HL41300008 PM 1582888 ER PT J AU ITO, A ICHIHARA, M HISANAGA, N ONO, Y KAYUKAWA, Y OHTA, T OKADA, T OZAKI, N AF ITO, A ICHIHARA, M HISANAGA, N ONO, Y KAYUKAWA, Y OHTA, T OKADA, T OZAKI, N TI PREVALENCE OF SEASONAL MOOD CHANGES IN LOW LATITUDE AREA - SEASONAL PATTERN ASSESSMENT QUESTIONNAIRE SCORE OF QUEZON CITY WORKERS SO JAPANESE JOURNAL OF PSYCHIATRY AND NEUROLOGY LA English DT Article; Proceedings Paper CT 6TH WORKSHOP FOR THE CLINICAL RESEARCH ON CHRONOBIOLOGY CY OCT 16-17, 1991 CL NAGOYA, JAPAN C1 NAGOYA UNIV,SCH MED,DEPT HYG,NAGOYA,AICHI 464,JAPAN. NAGOYA UNIV,SCH MED,DEPT PSYCHIAT,NAGOYA,AICHI 464,JAPAN. NIMH,ENVIRONM STUDIES SECT,BETHESDA,MD 20892. RP ITO, A (reprint author), FUJITA HLTH UNIV,SCH MED,DEPT PSYCHIAT,NAGOYA,JAPAN. RI Ozaki, Norio/M-8908-2014 OI Ozaki, Norio/0000-0002-7360-4898 NR 2 TC 14 Z9 14 U1 0 U2 0 PU FOLIA PUBL SOC PI TOKYO PA ACADEMIC SOCIETIES BLDG 2-4-16 YAYOI, BUNKYO-KU, TOKYO 113, JAPAN SN 0912-2036 J9 JPN J PSYCHIAT NEUR PD MAR PY 1992 VL 46 IS 1 BP 249 EP 249 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA HU987 UT WOS:A1992HU98700040 PM 1635329 ER PT J AU OH, SK CRUIKSHANK, WW RAINA, J BLANCHARD, GC ADLER, WH WALKER, J KORNFELD, H AF OH, SK CRUIKSHANK, WW RAINA, J BLANCHARD, GC ADLER, WH WALKER, J KORNFELD, H TI IDENTIFICATION OF HIV-1 ENVELOPE GLYCOPROTEIN IN THE SERUM OF AIDS AND ARC PATIENTS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV-1; ARC; ELISA; GP160/120; CD4; IMMUNE COMPLEXES; DIAGNOSIS ID HUMAN-IMMUNODEFICIENCY-VIRUS; GP120; ANTIGEN; ANTIBODIES; PURIFICATION; ACTIVATION; INFECTION; PROTEINS AB Binding of the human immunodeficiency virus type 1 (HIV-1) external envelope glycoprotein (gp120) has been reported to alter the function and surface antigen expression of lymphocytes and monocytes in vitro. To determine whether these in vitro findings could be relevant in vivo, we searched for the presence of this antigen in the serum of patients with AIDS and the AIDS-related complex (ARC). Using an antigen capture enzyme-linked immunosorbent assay (ELISA) with polyclonal anti-gp120 antibody, we detected envelope antigens (gp160/120) in serum of 22 of 32 AIDS patients. In contrast, an ELISA using solid-phase recombinant CD4 to capture gp160/120 failed to detect any positives. A modification of the anti-gp120-based ELISA identified gp160/120-IgG immune complexes in all of 11 AIDS patients tested and in 4 ARC patients who were negative for gp160/120 antigen. We conclude that gp160/120, predominantly in the form of immune complexes, can be identified as circulating antigen in patients with AIDS. The potential pathogenic consequences of this antigenemia, its relation to soluble CD4 therapy, and its application as a clinical marker of disease merit further study. C1 AMER BIOTECHNOL INC,CAMBRIDGE,MA. VET ADM MED CTR JAMAICA PLAIN,BOSTON,MA 02130. BOSTON UNIV,SCH MED,DEPT MICROBIOL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,CTR PULM,BOSTON,MA 02118. NIA,CLIN IMMUNOL SECT,BETHESDA,MD 20892. FU NHLBI NIH HHS [1 RO1 HL 44846-01] NR 24 TC 173 Z9 175 U1 2 U2 8 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 MAR PY 1992 VL 5 IS 3 BP 251 EP 256 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HF287 UT WOS:A1992HF28700005 PM 1740750 ER PT J AU BLOMBERG, J ROBERTGUROFF, M BLATTNER, WA PIPKORN, R AF BLOMBERG, J ROBERTGUROFF, M BLATTNER, WA PIPKORN, R TI TYPE-SPECIFIC AND GROUP-SPECIFIC CONTINUOUS ANTIGENIC DETERMINANTS OF HTLV - USE OF SYNTHETIC PEPTIDES FOR SEROTYPING OF HTLV-I AND HTLV-II INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HTLV-I; HTLV-II; STLV-I; SYNTHETIC PEPTIDE; SEROTYPING ID T-CELL LEUKEMIA; VIRUS TYPE-I; HUMAN IMMUNODEFICIENCY VIRUS; TROPICAL SPASTIC PARAPARESIS; C-TERMINAL REGION; P19 CORE PROTEIN; MONOCLONAL-ANTIBODIES; IMMUNODOMINANT EPITOPE; CROSS-REACTIVITY; STLV-I AB The human T lymphotropic viruses (HTLV-I and -II) are relatively common in subpopulations of certain countries, notably intravenous drug abusers in North America. Infections with these malignancy-associated human retroviruses are hard to discriminate with currently available commercial serological tests. We studied the distribution of antigenicity and the degree of cross-reactivity of epitopes in gag and env of the two viruses. Sequences in the carboxyl terminus of the matrix protein (MA) and the middle of the outer glycoprotein (SU) reacted in a type-specific fashion, while sequences from the capsid protein (CA), the carboxyl terminus of SU, and conserved portions of the transmembrane protein (TM) mainly reacted in a group-specific fashion, correlating with the degree of sequence dissimilarity between the two viruses. The serological discrimination obtained with the peptides was evaluated in a panel of 25 sera where infection with HTLV-I or -II had been typed by competition in a p24 enzyme-linked immunosorbent assay (ELISA) or by the polymerase chain reaction (PCR). After processing peptide results in a computer program, a typing result concordant with earlier results was obtained in 21 of 25 sera. Of the remaining five sera, four were labeled "too weak for typing" and one "HTLV of uncertain type" by the program. They did not react sufficiently strongly or clearly with the peptides to allow classification. A combination of synthetic peptides may become useful for serotyping HTLV infection and become an alterative to Western blots for confirmation of HTLV positivity. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. NOVABIOCHEM GMBH,SANDHAUSEN,GERMANY. RP BLOMBERG, J (reprint author), UNIV LUND,DEPT MED MICROBIOL,VIROL SECT,SOLVEGATAN 23,S-22362 LUND,SWEDEN. NR 44 TC 10 Z9 10 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 MAR PY 1992 VL 5 IS 3 BP 294 EP 302 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HF287 UT WOS:A1992HF28700011 PM 1371319 ER PT J AU PEDEN, KWC AF PEDEN, KWC TI INSTABILITY OF HIV SEQUENCES IN HIGH COPY NUMBER PLASMIDS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Note DE HIV; PLASMIDS ID RETROVIRUS; CLONING AB Plasmid proviral molecular clones of the LAI isolate of HIV-1 and the ROD isolate of HIV-2 were originally prepared in moderate copy number plasmids derived from pBR322, which contains the colE1 origin of replication. In these plasmid vectors, the HIV sequences are stable to continuous passage in bacteria. However, when the colE1 origin was replaced by the mutant origin from pUC18, pGEM, or pBluescript plasmids, which replicates to much higher copy numbers in bacteria, then deletions of HIV sequences occurred even in RecA defective strains. Deletions occurred in two different media, at room temperature and 37-degrees-C, and with or without plasmid amplification in the presence of chloramphenicol. These results raise a cautionary note when cloning immunodeficiency viral sequences into plasmid vectors containing a high copy number origin of replication. RP PEDEN, KWC (reprint author), NIAID,MOLEC MICROBIOL LAB,BLDG 4,ROOM 310,BETHESDA,MD 20892, USA. NR 8 TC 19 Z9 20 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 MAR PY 1992 VL 5 IS 3 BP 313 EP 315 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HF287 UT WOS:A1992HF28700014 PM 1740758 ER PT J AU CONE, EJ DICKERSON, S PAUL, BD MITCHELL, JM AF CONE, EJ DICKERSON, S PAUL, BD MITCHELL, JM TI FORENSIC DRUG-TESTING FOR OPIATES .4. ANALYTICAL SENSITIVITY, SPECIFICITY, AND ACCURACY OF COMMERCIAL URINE OPIATE IMMUNOASSAYS SO JOURNAL OF ANALYTICAL TOXICOLOGY LA English DT Article ID GAS-CHROMATOGRAPHY; ABUSE C1 USN,DRUG SCREENING LAB,NAVA AIR STN,NORFOLK,VA 23511. USN,DRUG SCREENING LAB,NAVAL AIR STN,JACKSONVILLE,FL 32212. RP CONE, EJ (reprint author), NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 9 TC 33 Z9 34 U1 0 U2 5 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 MAR-APR PY 1992 VL 16 IS 2 BP 72 EP 78 PG 7 WC Chemistry, Analytical; Toxicology SC Chemistry; Toxicology GA HK153 UT WOS:A1992HK15300002 PM 1501467 ER PT J AU TAKIFF, HE BAKER, T COPELAND, T CHEN, SM COURT, DL AF TAKIFF, HE BAKER, T COPELAND, T CHEN, SM COURT, DL TI LOCATING ESSENTIAL ESCHERICHIA-COLI GENES BY USING MINI-TN10 TRANSPOSONS - THE PDXJ OPERON SO JOURNAL OF BACTERIOLOGY LA English DT Article ID RNC OPERON; RNASE-III; TRANSCRIPTION; PROTEIN; K-12; EXPRESSION; TN10; ERA; TERMINATION; SEQUENCES AB The mini-Tn10 transposon (DELTA-16-DELTA-17Tn10) confers tetracycline resistance. When inserted between a gene and its promoter, it blocks transcription and prevents expression of that gene. Tetracycline in the medium induces divergent transcription of the tetA and tetR genes within the transposon, and this transcription extends beyond the transposon in both directions into the bacterial genes. If the mini-Tn10 inserts between an essential bacterial gene and its promoter, the insertion mutation can cause conditional growth which is dependent on the presence of tetracycline. Two essential genes in adjacent operons of Escherichia coli have been detected by screening for tetracycline dependence among tetracycline-resistant insertion mutants. These essential genes are the era gene in the rnc operon and the dpj gene in the adjacent pdxJ operon. The pdxJ operon has not been described previously. It consists of two genes, pdxJ and dpj. Whereas the dpj gene is essential for E. coli growth in all media tested, pdxJ is not essential. The pdxJ gene encodes a protein required in the biosynthesis of pyridoxine (vitamin B-6). C1 NCI,FREDERICK CANC RES & DEV CTR,CHROMOSOME BIOL LAB,MOLEC CONTROL & GENET SECT,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,MOLEC VIROL & CARCINOGENESIS LAB,PROT STRUCT GRP,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 34 TC 80 Z9 83 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 MAR PY 1992 VL 174 IS 5 BP 1544 EP 1553 PG 10 WC Microbiology SC Microbiology GA HF279 UT WOS:A1992HF27900014 PM 1537799 ER PT J AU SCHAAPER, RM CORNACCHIO, R AF SCHAAPER, RM CORNACCHIO, R TI AN ESCHERICHIA-COLI DNAE MUTATION WITH SUPPRESSOR ACTIVITY TOWARD MUTATOR MUTD5 SO JOURNAL OF BACTERIOLOGY LA English DT Article ID POLYMERASE-III HOLOENZYME; MISMATCH REPAIR; REPLICATION ERRORS; EPSILON-SUBUNIT; GENE; EXONUCLEASE; FIDELITY; PRODUCT; IDENTIFICATION; MUTAGENESIS AB The Escherichia coli mutator mutD5 is a conditional mutator whose strength is moderate when the strain is growing in minimal medium but very strong when it is growing in rich medium. The primary defect of this strain resides in the dnaQ gene, which encodes the epsilon (exonucleolytic proofreading) subunit of the DNA polymerase III holoenzyme. In one of our mutD5 strains we discovered a mutation that suppressed the mutability of mutD5. Interestingly, the level of suppression was strong in minimal medium but weak in rich medium. The mutation was localized to the dnaE gene, which encodes the alpha (polymerase) subunit of the DNA polymerase III holoenzyme. This mutation, termed dnaE910, also conferred improved growth of the mutD5 strain and caused increased temperature sensitivity in both wild-type and dnaQ49 backgrounds. The reduction in mutator strength by dnaE910 was also observed when this allele was placed in a mutL, a mutT, or a dnaQ49 background. The results suggest that dnaE910 encodes an antimutator DNA polymerase whose effect might be mediated by improved insertion fidelity or by increased proofreading via its effect on the exonuclease activity. RP SCHAAPER, RM (reprint author), NIEHS,MOLEC GENET LAB,POB 12233,111 TW ALEXANDER DR,RES TRIANGLE PK,NC 27709, USA. NR 38 TC 32 Z9 32 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD MAR PY 1992 VL 174 IS 6 BP 1974 EP 1982 PG 9 WC Microbiology SC Microbiology GA HJ502 UT WOS:A1992HJ50200035 PM 1548237 ER PT J AU BARON, J WEISBERG, RA AF BARON, J WEISBERG, RA TI MUTATIONS OF THE PHAGE-LAMBDA NUTL REGION THAT PREVENT THE ACTION OF NUN, A SITE-SPECIFIC TRANSCRIPTION TERMINATION FACTOR SO JOURNAL OF BACTERIOLOGY LA English DT Article ID BACTERIOPHAGE-LAMBDA; N-PROTEIN; ANTITERMINATION; SEQUENCE; GENE; RECOGNITION; REPLICATION; EXPRESSION; SYSTEM AB Phage HK022 encodes a protein, Nun, that promotes transcription termination within the p(L) and p(R) operons of its relative, phage-lambda. The lambda-sequences required for termination had previously been shown to overlap the nut sites, which are essential for transcription antitermination during normal lambda-growth. To further specify the Nun target and to determine its relation to the nut sites, we constructed deletion and base substitution mutations of the lambda-nutL region and measured Nun-dependent reduction of the expression of a downstream reporter gene. The shortest construct that retained full Nun responsiveness was a 42-bp segment that included both boxA and boxB, sequences that have been implicated in lambda-antitermination. Deletion of boxA reduced Nun termination, and deletion of both sequences eliminated Nun termination. Base substitutions in boxA and the proximal portion of boxB impaired Nun termination, while base substitutions between boxA and boxB, in the distal portion of boxB, and immediately downstream from boxB had no appreciable effect. The termination defect of all of the base substitution mutations was relieved by increasing the level of Nun protein; in contrast, the deletions and a multiple-base substitution did not regain full Nun responsiveness at elevated Nun concentrations. We also asked if these mutant nut regions retained their ability to interact with N, the lambda-encoded antitermination protein. A qualitative assay showed that mutations within boxA or boxB reduced interaction, while mutations outside boxA and boxB did not. These data show that (i) the recognition sites for N and Nun overlap to a very considerable extent but are probably not identical and (ii) a high concentration of Nun promotes its interaction with mutant nut sites, a behavior also reported to be characteristic of N. C1 NICHHD,MOLEC GENET LAB,MOLEC GENET SECT,BLDG 6B,ROOM 413,BETHESDA,MD 20892. NR 26 TC 27 Z9 27 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD MAR PY 1992 VL 174 IS 6 BP 1983 EP 1989 PG 7 WC Microbiology SC Microbiology GA HJ502 UT WOS:A1992HJ50200036 PM 1532174 ER PT J AU URRUTIA, R KACHAR, B AF URRUTIA, R KACHAR, B TI AN IMPROVED METHOD FOR THE PURIFICATION OF KINESIN FROM BOVINE ADRENAL-MEDULLA SO JOURNAL OF BIOCHEMICAL AND BIOPHYSICAL METHODS LA English DT Article DE KINESIN; ADRENAL MEDULLA; ORGANELLE MOTILITY; PROTEIN PURIFICATION ID ACANTHAMOEBA-CASTELLANII; MONOCLONAL-ANTIBODY; CULTURED-CELLS; BRAIN KINESIN; MICROTUBULES; PROTEIN; LOCALIZATION; TRANSPORT; GLYCEROL; BINDING AB A method has been developed for the purification of bovine adrenal kinesin combining ion exchange chromatography on phosphocellulose and Mono-Q (FPLC), affinity binding to microtubules in the presence of tripolyphosphate and gel filtration on Superose 6 (FPLC). From 100 g of tissue this procedure yields 200-mu-g of a remarkably pure kinesin as assayed by SDS-PAGE and electron microscopy of rotary shadowed specimens. The enzyme has a Ca++ ATPase of 0.4-mu-mol/min per mg and a Mg++ ATPase of 0.03-mu-mol/min per mg in the absence of microtubules. The addition of microtubules (5-mu-M) activates the Mg++ ATPase activity by almost 70-fold to a value of 1.9-mu-mol/min per mg. This purification procedure results in a fairly large amount of a remarkably pure adrenal kinesin with high specific activity which is an important improvement over the method previously available. RP URRUTIA, R (reprint author), NIDOCD,CELLULAR BIOL LAB,BLDG 10,ROOM 5D-50,BETHESDA,MD 20892, USA. NR 23 TC 8 Z9 8 U1 0 U2 0 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 MAR PY 1992 VL 24 IS 1-2 BP 63 EP 70 DI 10.1016/0165-022X(92)90047-E PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HK067 UT WOS:A1992HK06700006 PM 1560182 ER PT J AU GOSSELIN, S MARTIN, BM MURRAY, GJ VISWANATHA, T AF GOSSELIN, S MARTIN, BM MURRAY, GJ VISWANATHA, T TI FLAVOBACTERIUM-MENINGOSEPTICUM PEPTIDE - N-GLYCOSIDASE - INFLUENCE OF IONIC-STRENGTH ON ENZYMATIC-ACTIVITY SO JOURNAL OF BIOCHEMICAL AND BIOPHYSICAL METHODS LA English DT Article DE PEPTIDE; N-GLYCOSIDASE; GLYCOPROTEIN; DEGLYCOSYLATION; IONIC STRENGTH ID ACETYLGLUCOSAMINIDASE-F; HIGH-MANNOSE; PEPTIDE-N-4-(N-ACETYL-BETA-D-GLUCOSAMINYL)ASPARAGINE AMIDASE; OLIGOSACCHARIDES; GLYCOPROTEINS; CLEAVAGE; DEGLYCOSYLATION; GLYCOPEPTIDES; CLONING; ALMOND AB Flavobacterium meningosepticum peptide: N-glycosidase-mediated deglycosylation of N-linked glycan strands of glycoproteins has been found to be strongly influenced by the ionic strength of the assay medium. By use of a modification of a previously published assay procedure for quantitative analysis of glycan release we have been able to improve reproducibility and thus to compare the extent of deglycosylation achieved under a variety of conditions of ionic strength. We have observed that enzyme activity is adversely affected by high ionic strength buffers such as those recommended for deglycosylation of various glycoproteins and recommend the use of low ionic strength buffers for routine use. C1 UNIV WATERLOO,GUELPH WATERLOO CTR GRAD WORK CHEM,WATERLOO N2L 3G1,ONTARIO,CANADA. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NINCDS,MOLEC GENET LAB,BETHESDA,MD 20892. NR 26 TC 2 Z9 2 U1 0 U2 0 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 MAR PY 1992 VL 24 IS 1-2 BP 71 EP 79 DI 10.1016/0165-022X(92)90048-F PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HK067 UT WOS:A1992HK06700007 PM 1560183 ER PT J AU ABRAMS, SA ESTEBAN, NV VIEIRA, NE SIDBURY, JB SPECKER, BL YERGEY, AL AF ABRAMS, SA ESTEBAN, NV VIEIRA, NE SIDBURY, JB SPECKER, BL YERGEY, AL TI DEVELOPMENTAL-CHANGES IN CALCIUM KINETICS IN CHILDREN ASSESSED USING STABLE ISOTOPES SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID BIRTH-WEIGHT INFANTS; ABSORPTION TESTS; HUMAN-MILK; METABOLISM; BONE; TRACERS AB Total exchangeable calcium pool size (TEP) and bone calcium accretion rate (V(o)+) were measured using stable isotopes in healthy children and young adults. Ca-42 or Ca-46 was given intravenously to 10 children aged 10 months to 14 years and 3 women aged 23-33 years. Calcium kinetic parameters were determined using a two- or three-exponential curve of the resultant serum and urine tracer excesses. These data were compared with previously reported (radiotracer) kinetic studies of 21 children and 5 adults without known bone disease. Current results are comparable to those previously obtained, and the data from all studies were analyzed together. Total V(o)+ was significantly greater in children aged 3-16 years than in adults (2.8 +/- 1.6 versus 0.7 +/- 0.2 g/day, p < 0.01). Both TEP and V(o)+ were significantly correlated to age independently of variations in body weight (p < 0.01 for each). The ratio k(o)+ = V(o)+/TEP was greater in children than adults (0.36 +/- 0.15 versus 0.12 +/- 0.03 day-1, p < 0.001). These data demonstrate increased bone flow of calcium associated with increases in exchangeable calcium pools in children compared to adults. V(o)+ and TEP may be maximum in early adolescence, associated with peak rates of net calcium accretion. The use of stable isotopes permits the safe evaluation of calcium kinetics in patients of all ages. C1 NICHHD,BETHESDA,MD 20892. CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC 20010. UNIV CINCINNATI,COLL MED,CINCINNATI,OH 45221. OI Specker, Bonny/0000-0003-4759-9957; Abrams, Steven/0000-0003-4972-9233 NR 47 TC 53 Z9 53 U1 0 U2 3 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD MAR PY 1992 VL 7 IS 3 BP 287 EP 293 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HJ344 UT WOS:A1992HJ34400006 PM 1585830 ER PT J AU KLAUSNER, RD DONALDSON, JG LIPPINCOTTSCHWARTZ, J AF KLAUSNER, RD DONALDSON, JG LIPPINCOTTSCHWARTZ, J TI BREFELDIN-A - INSIGHTS INTO THE CONTROL OF MEMBRANE TRAFFIC AND ORGANELLE STRUCTURE SO JOURNAL OF CELL BIOLOGY LA English DT Review ID TRANS-GOLGI NETWORK; ADP-RIBOSYLATION FACTOR; ENDOPLASMIC-RETICULUM; PROTEIN-TRANSPORT; INTRACELLULAR-TRANSPORT; IMMUNOELECTRON MICROSCOPY; SECRETORY PROTEINS; RAT HEPATOCYTES; CELLS; RECEPTOR RP KLAUSNER, RD (reprint author), NICHHD,CELL BIOL & METAB,BETHESDA,MD 20892, USA. NR 89 TC 1527 Z9 1535 U1 5 U2 49 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD MAR PY 1992 VL 116 IS 5 BP 1071 EP 1080 DI 10.1083/jcb.116.5.1071 PG 10 WC Cell Biology SC Cell Biology GA HF641 UT WOS:A1992HF64100001 PM 1740466 ER PT J AU STOCK, JL CODERRE, JA BURKE, EM DANNER, DB CHIPMAN, SD SHAPIRO, JR AF STOCK, JL CODERRE, JA BURKE, EM DANNER, DB CHIPMAN, SD SHAPIRO, JR TI IDENTIFICATION OF ESTROGEN-RECEPTOR MESSENGER-RNA AND THE ESTROGEN MODULATION OF PARATHYROID HORMONE-STIMULATED CYCLIC-AMP ACCUMULATION IN OPOSSUM KIDNEY-CELLS SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID DEPENDENT PHOSPHATE-TRANSPORT; PROTEIN KINASE-A; OK CELLS; NA+/PHOSPHATE COTRANSPORT; ADENYLATE-CYCLASE; RAT-KIDNEY; LINE; ESTRADIOL; EXPRESSION; INHIBITION AB The opossum kidney (OK) cell was used as a model to test the hypothesis that estrogen directly affects proximal renal tubular epithelial cells. To demonstrate the expression of estrogen receptor in OK cells, we developed an approach using reverse transcription and the polymerase chain reaction. Analysis of the DNA amplified with nested primers revealed the predicted size fragment and restriction enzyme digestion products. To demonstrate the functional effects of estrogen, OK cells at confluence were preincubated in serum-free medium for 7-10 days with or without 17-beta-estradiol. Bovine PTH(1-34) (bPTH(1-34)) then stimulated a dose-dependent intracellular accumulation of cAMP that was maximal after 1 min and then gradually declined. Cyclic AMP in the medium slowly increased over 60 min. Preincubation with 17-beta-estradiol did not affect cell proliferation as measured by total protein content but caused an inhibition of bPTH(1-34)-stimulated intracellular cAMP accumulation that was maximal at 10(-11) M 17-beta-estradiol (71 +/- 3% control, p < .001). bPTH(1-34) also increased cAMP release into the medium, an effect maximal using 10(-10) M 17-beta-estradiol (118 +/- 3% control, p < .001). Preincubation with the inactive isomer 17-alpha-estradiol caused no changes in cAMP accumulation or release. Coincubation with the antiestrogen tamoxifen blocked the effects of 17-beta-estradiol. Sodium-dependent phosphate transport was: (1) inhibited by 2-h incubations with 10(-8) or 10(-10) M bPTH(1-34) and not affected by preincubation with 17-beta-estradiol, and (2) not inhibited by a 20-min incubation with 10(-8) M bPTH(1-34) unless cells were preincubated with 10(-8) M 17-beta-estradiol, suggesting that any possible effects of estrogen on phosphate transport are not directly mediated by changes in cAMP. These studies demonstrate the presence of estrogen receptor mRNA in OK cells as well as direct and specific effects of physiologic concentrations of estrogen on cAMP accumulation in these cells. This system may be a good model for further study of estrogen and PTH effects on the kidney. C1 NIA,GERONTOL RES CTR,MOLEC GENET LAB,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DIV GERIATR MED & GERONTOL,BONE METAB RES LAB,BALTIMORE,MD 21224. MED CTR CENT MASSACHUSETTS MEM,DEPT MED,WORCESTER,MA 01605. UNIV MASSACHUSETTS,SCH MED,DEPT MED,WORCESTER,MA 01605. RP STOCK, JL (reprint author), MED CTR CENT MASSACHUSETTS MEM,ENDOCRINOL RES LAB,119 BELMONT ST,WORCESTER,MA 01605, USA. FU NIAMS NIH HHS [AR-39870] NR 42 TC 26 Z9 27 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD MAR PY 1992 VL 150 IS 3 BP 517 EP 525 DI 10.1002/jcp.1041500312 PG 9 WC Cell Biology; Physiology SC Cell Biology; Physiology GA HF671 UT WOS:A1992HF67100011 PM 1311330 ER PT J AU THOMPSON, EW PAIK, SM BRUNNER, N SOMMERS, CL ZUGMAIER, G CLARKE, R SHIMA, TB TORRI, J DONAHUE, S LIPPMAN, ME MARTIN, GR DICKSON, RB AF THOMPSON, EW PAIK, SM BRUNNER, N SOMMERS, CL ZUGMAIER, G CLARKE, R SHIMA, TB TORRI, J DONAHUE, S LIPPMAN, ME MARTIN, GR DICKSON, RB TI ASSOCIATION OF INCREASED BASEMENT-MEMBRANE INVASIVENESS WITH ABSENCE OF ESTROGEN-RECEPTOR AND EXPRESSION OF VIMENTIN IN HUMAN BREAST-CANCER CELL-LINES SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID EPITHELIAL-CELLS; CARCINOMA-CELLS; NUDE-MICE; INDEPENDENT GROWTH; MELANOMA-CELLS; TUMOR-CELLS; METASTASIS; INVASION; INVIVO; DEGRADATION AB Lack of estrogen receptor (ER) and presence of vimentin (VIM) associate with poor prognosis in human breast cancer. We have explored the relationships between ER, VIM, and invasiveness in human breast cancer cell lines. In the matrigel outgrowth assay, ER+/VIM- (MCF-7, T47D, ZR-75-1), and ER-/VIM- (MDA-MB-468, SK-Br-3) cell lines were uninvasive, while ER-/VIM+ (BT549, MDA-MB-231, MDA-MB-435, MDA-MB-436, Hs578T) lines formed invasive, penetrating colonies. Similarly, ER-/VIM+ cell lines were significantly more invasive than either the ER+/VIM- or ER-/VIM- cell lines in the Boyden chamber chemoinvasion assay. Invasive activity in nude mice was only seen with ER-/VIM+ cell lines MDA-MB-231, MDA-MB-435 and MDA-MB-436. Hs578T cells (ER-/VIM+) showed hematogenous dissemination to the lungs in one of five mice, but lacked local invasion. The ER-/VIM+ MCF-7ADR subline was significantly more active than the MCF-7 cells in vitro, but resembled the wild-type MCF-7 parent in in vivo activity. Data from these cell lines suggest that human breast cancer progression results first in the loss of ER, and subsequently in VIM acquisition, the latter being associated with increased metastatic potential through enhanced invasiveness. The MCF-7ADR data provide evidence that this transition can occur in human breast cancer cells. Vimentin expression may provide useful insights into mechanisms of invasion and/or breast cancer cell progression. C1 NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. RP THOMPSON, EW (reprint author), GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007, USA. RI Clarke, Robert/A-6485-2008; Thompson, Erik/A-1425-2009 OI Clarke, Robert/0000-0002-9278-0854; Thompson, Erik/0000-0002-9723-4924 FU NCI NIH HHS [UO1 CA51908-01] NR 56 TC 446 Z9 460 U1 3 U2 20 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD MAR PY 1992 VL 150 IS 3 BP 534 EP 544 DI 10.1002/jcp.1041500314 PG 11 WC Cell Biology; Physiology SC Cell Biology; Physiology GA HF671 UT WOS:A1992HF67100013 PM 1537883 ER PT J AU HODES, L AF HODES, L TI LIMITS OF CLASSIFICATION .2. COMMENT ON LAWSON AND JURS SO JOURNAL OF CHEMICAL INFORMATION AND COMPUTER SCIENCES LA English DT Article AB Lawson and Jurs 1,2 have two recent papers on clustering using data on a diverse set of 143 published acrylates. From our work 3 on clustering large diverse sets of compounds, we have found that a diverse set of compounds will generally have a dual nature-some clustered and some scattered compounds. Are the five published 2 clusters a good classification of that set of compounds? A further analysis throws more insight into the interrelations among the acrylates. RP HODES, L (reprint author), NCI,BETHESDA,MD 20892, USA. NR 6 TC 3 Z9 3 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0095-2338 J9 J CHEM INF COMP SCI JI J. Chem. Inf. Comput. Sci. PD MAR-APR PY 1992 VL 32 IS 2 BP 157 EP 166 DI 10.1021/ci00006a007 PG 10 WC Chemistry, Multidisciplinary; Computer Science, Information Systems; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA HL096 UT WOS:A1992HL09600007 ER PT J AU BATISTA, MC CARTLEDGE, TP ZELLMER, AW NIEMAN, LK MERRIAM, GR LORIAUX, DL AF BATISTA, MC CARTLEDGE, TP ZELLMER, AW NIEMAN, LK MERRIAM, GR LORIAUX, DL TI EVIDENCE FOR A CRITICAL ROLE OF PROGESTERONE IN THE REGULATION OF THE MIDCYCLE GONADOTROPIN SURGE AND OVULATION SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID MID-FOLLICULAR PHASE; LUTEINIZING-HORMONE; MENSTRUAL-CYCLE; ANTIPROGESTERONE RU-486; POSTMENOPAUSAL WOMEN; GRANULOSA-CELLS; ESTRADIOL; SECRETION; RELEASE; DEHYDROGENASE AB Serum concentrations of progesterone begin to rise just before the midcycle gonadotropin surge that leads to ovulation. To examine the role of progesterone in the regulation of these events, we evaluated the effects of a low dose (1 mg/day, orally) of the antiprogesterone RU 486 on the timing of the gonadotropin surge and ovulation in normally cycling women. The drug or a placebo was given for 5 or 15 days, starting when the dominant follicle reached 14-16 mm. RU 486 consistently delayed the timing of the midcycle gonadotropin surge and the subsequent collapse of the dominant follicle, despite rising estradiol concentrations and normal follicular development. Unexpectedly, RU 486 also delayed the emergence of the periovulatory progesterone rise. The addition of progesterone (5-10 mg/day, im, for 2 days) to a 5-day course of RU 486 after the emergence of a mature follicle readily induced LH and FSH surges and completely reversed the effects of RU 486 at midcycle. Our results suggest that RU 486 delays the midcycle gonadotropin surge and ovulation by suppressing or antagonizing an ovarian progestational signal. Progesterone may, thus, represent the ultimate ovarian signal to the estrogen-primed hypothalamic-pituitary unit to trigger the gonadotropin surge that leads to ovulation. C1 NIH, WARREN GRANT MAGNUSON CLIN CTR,DEPT NURSING, BLDG 10,ROOM 10N262, BETHESDA, MD 20892 USA. NICHHD, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. NR 33 TC 86 Z9 86 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD MAR PY 1992 VL 74 IS 3 BP 565 EP 570 DI 10.1210/jc.74.3.565 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HG332 UT WOS:A1992HG33200020 PM 1740491 ER PT J AU SALIVE, ME CORNONIHUNTLEY, J PHILLIPS, CL GURALNIK, JM COHEN, HJ OSTFELD, AM WALLACE, RB AF SALIVE, ME CORNONIHUNTLEY, J PHILLIPS, CL GURALNIK, JM COHEN, HJ OSTFELD, AM WALLACE, RB TI SERUM-ALBUMIN IN OLDER PERSONS - RELATIONSHIP WITH AGE AND HEALTH-STATUS SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE ALBUMIN; AGING; ANEMIA; DISABILITY; CIGARETTE SMOKING ID DISEASE; SMOKING; VALUES AB We analyzed data from 4115 persons aged 71 years and older who had blood drawn at a home visit in three communities to examine the cross-sectional distribution of serum albumin and correlates of hypoalbuminemia. Mean albumin was lower among older persons, from 41.6 g/l in men aged 71-74 years to 38.5 g/l in men 90 years or older, and from 41.1 g/l to 38.9 g/l in women of the same ages, respectively. Hypoalbuminemia (albumin < 35 g/l) was observed in 3.1 % of subjects. Hypoalbuminemia and lower serum albumin were independently associated with anemia, recent diagnosis of cancer, two or more limitations in activities of daily living, residence in a nursing home, heavy cigarette smoking (> 1 pack/day), and older age. A 10-year age increment was associated with 0.8 g/l lower serum albumin and odds ratio of 1.56 (95% CI 1.14, 2.13) for hypoalbuminemia after adjusting for demographic factors and health status. Characteristics associated with serum albumin may confound the reported relationship between serum albumin and mortality. C1 DUKE UNIV,CTR AGING & HUMAN DEV,DURHAM,NC 27706. YALE UNIV,SCH MED,DEPT EPIDEMIOL,NEW HAVEN,CT 06510. UNIV IOWA,DEPT PREVENT MED & ENVIRONM HLTH,IOWA CITY,IA 52240. RP SALIVE, ME (reprint author), NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,7201 WISCONSIN AVE,GATEWAY BLDG,BETHESDA,MD 20892, USA. NR 22 TC 90 Z9 90 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD MAR PY 1992 VL 45 IS 3 BP 213 EP 221 DI 10.1016/0895-4356(92)90081-W PG 9 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA HR885 UT WOS:A1992HR88500003 PM 1569418 ER PT J AU WAHL, SM AF WAHL, SM TI TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) IN INFLAMMATION - A CAUSE AND A CURE SO JOURNAL OF CLINICAL IMMUNOLOGY LA English DT Review ID NECROSIS-FACTOR-ALPHA; HEMATOPOIETIC PROGENITOR CELLS; FIBRONECTIN MESSENGER-RNAS; HUMAN DERMAL FIBROBLASTS; CYTOKINE PRODUCTION; GENE-EXPRESSION; HUMAN-PLATELETS; KILLER-CELLS; MACROPHAGE PRODUCTION; FACTOR-BETA-1 GENE RP WAHL, SM (reprint author), NIDR, CELLULAR IMMUNOL SECT, BETHESDA, MD 20892 USA. NR 161 TC 405 Z9 414 U1 3 U2 9 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0271-9142 J9 J CLIN IMMUNOL JI J. Clin. Immunol. PD MAR PY 1992 VL 12 IS 2 BP 61 EP 74 DI 10.1007/BF00918135 PG 14 WC Immunology SC Immunology GA HH975 UT WOS:A1992HH97500001 PM 1313827 ER PT J AU VALLARI, DS JETT, BW ALTER, HJ MIMMS, LT HOLZMAN, R SHIH, JWK AF VALLARI, DS JETT, BW ALTER, HJ MIMMS, LT HOLZMAN, R SHIH, JWK TI SEROLOGICAL MARKERS OF POSTTRANSFUSION HEPATITIS-C VIRAL-INFECTION SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID NON-B-HEPATITIS; NON-A; VIRUS; ANTIBODIES; CDNA AB Serological markers for hepatitis C virus (HCV) infection were measured in serial samples from 14 posttransfusion chronic non-A, non-B hepatitis patients by a semiquantitative dot blot immunoassay. The assay detected antibodies to HCV by use of recombinant proteins that represent putative HCV capsid (core), nonstructural protein 3 (NS3) (33c), and NS4 (c100) epitopes. Seroconversion to anti-HCV antibodies (anti-HCV) was detected in all patients. The average time to active antibody production detected by any of the recombinant proteins was 13.8 (range, 3.6 to 22.0) weeks posttransfusion or 4.6 (range, -4.5 to 13.4) weeks after the first biochemical marker of illness. Anti-HCV were detected earliest by the core antigen in most cases; however, the patterns of anti-HCV responses varied significantly among individuals. Overall, the addition of the core and NS3 antigens to the assay enabled the detection of the antibody response 4 to 5 weeks earlier than did the addition of the c100 antigen, the sole antigen used in current screening tests in the United States. Passively transferred antibodies were detected by at least one antigen in early posttransfusion samples from 12 patients and decayed below detectable levels for all antigens in only 2 patients. Antibodies to all three gene products were evident in the last sample from all five patients monitored for > 3 years from transfusion indicating the persistence of antibodies in patients with chronic illness. Our data show that the period following the onset of hepatitis during which anti-HCV are not detected by current screening assays can be greatly shortened by the detection of anti-HCV responses by a combination of core, NS3, and c100 antigens. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892. RP VALLARI, DS (reprint author), ABBOTT LABS,HEPATITIS RES & DEV,ABBOTT PK,IL 60064, USA. NR 18 TC 68 Z9 68 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 MAR PY 1992 VL 30 IS 3 BP 552 EP 556 PG 5 WC Microbiology SC Microbiology GA HE087 UT WOS:A1992HE08700004 PM 1372618 ER PT J AU MARCONI, RT LUBKE, L HAUGLUM, W GARON, CF AF MARCONI, RT LUBKE, L HAUGLUM, W GARON, CF TI SPECIES-SPECIFIC IDENTIFICATION OF AND DISTINCTION BETWEEN BORRELIA-BURGDORFERI GENOMIC GROUPS BY USING 16S RIBOSOMAL-RNA-DIRECTED OLIGONUCLEOTIDE PROBES SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID RIBOSOMAL-RNA; LYME-DISEASE; INVITRO CULTIVATION; TICKS; SPIROCHETE; DNA; HETEROGENEITY; HYBRIDIZATION; COMPLEMENTARY; ANTIGEN AB Examination of a number of previously published aligned Borrelia 16S rRNA sequences revealed the presence of regions which could serve as oligonucleotide probe targets for both species-specific identification of Borrelia burgdorferi and distinction between genomic groups. Total cellular RNA isolated from Borrelia cultures was used in slot blot analysis. Radiolabeled oligonucleotides designed to hybridize to specific 16S rRNA targets were used as probes. These probes allowed for both species-specific identification and genomic group typing of B. burgdorferi. RP MARCONI, RT (reprint author), NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840, USA. NR 33 TC 60 Z9 60 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 MAR PY 1992 VL 30 IS 3 BP 628 EP 632 PG 5 WC Microbiology SC Microbiology GA HE087 UT WOS:A1992HE08700020 PM 1372620 ER PT J AU CLEMENTS, ML SUBBARAO, EK FRIES, LF KARRON, RA LONDON, WT MURPHY, BR AF CLEMENTS, ML SUBBARAO, EK FRIES, LF KARRON, RA LONDON, WT MURPHY, BR TI USE OF SINGLE-GENE REASSORTANT VIRUSES TO STUDY THE ROLE OF AVIAN INFLUENZA-A VIRUS GENES IN ATTENUATION OF WILD-TYPE HUMAN INFLUENZA-A VIRUS FOR SQUIRREL-MONKEYS AND ADULT HUMAN VOLUNTEERS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID TEMPERATURE-SENSITIVE MUTANTS; INTERTYPIC RECOMBINANT; LIVE; H3N2; VACCINES; PROTEIN; NEUROVIRULENCE; CONSTELLATION; NUCLEOPROTEIN; RESTRICTION AB The transfer of six internal RNA segments from the avian influenza A/Mallard/New York/6750/78 (H2N2) virus reproducibly attenuates human influenza A viruses for squirrel monkeys and adult humans. To identify the avian influenza A virus genes that specify the attenuation and host range restriction of avian-human (ah) influenza A reassortant viruses (referred to as ah reassortants), we isolated six single-gene reassortant viruses (SGRs), each having a single internal RNA segment of the influenza A/Mallard/New York/6750/78 virus and seven RNA segments from the human influenza A/Los Angeles/2/87 (H3N2) wild-type virus. To assess the level of attenuation, we compared each SGR with the A/Los Angeles/2/87 wild-type virus and a 6-2 gene ah reassortant (having six internal RNA segments from the avian influenza A virus parent and two genes encoding the hemagglutinin and neuraminidase glycoproteins from the wild-type human influenza A virus) for the ability to replicate in seronegative squirrel monkeys and adult human volunteers. In monkeys and humans, replication of the 6-2 gene ah reassortant was highly restricted. In humans, the NS, M, PB2, and PB1 SGRs each replicated significantly less efficiently (P < 0.05) than the wild-type human influenza A virus parent, suggesting that each of these genes contributes to the attenuation phenotype. In monkeys, only the NP, PB2, and possibly the M genes contributed to the attenuation phenotype. These discordant observations, particularly with regard to the NP SGR, indicate that not all genetic determinants of attenuation of influenza A viruses for humans can be identified during studies of SGRs conducted with monkeys. The PB2 and M SGRs that were attenuated in humans each exhibited a new phenotype that was not observed for either parental virus. Thus, it was not possible to determine whether the avian influenza virus PB2 or M gene itself or a specific constellation of avian and human influenza A virus genes specified restriction of virus replication in humans. C1 GEORGETOWN UNIV,RETROVIRAL PATHOGENESIS SECT,MOLEC VIROL & IMMUNOL SECT,ROCKVILLE,MD 20852. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT INT HLTH,DIV VACCINE SCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. NIAID,INFECT DIS LAB,RESP VIRUS SECT,BETHESDA,MD 20892. RP CLEMENTS, ML (reprint author), JOHNS HOPKINS UNIV,CTR IMMUNIZAT RES,SCH HYG & PUBL HLTH,BALTIMORE,MD 21205, USA. FU NIAID NIH HHS [N01 AI 62515] NR 34 TC 71 Z9 73 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 MAR PY 1992 VL 30 IS 3 BP 655 EP 662 PG 8 WC Microbiology SC Microbiology GA HE087 UT WOS:A1992HE08700024 PM 1551982 ER PT J AU SCHWAN, TG SCHRUMPF, ME GAGE, KL GILMORE, RD AF SCHWAN, TG SCHRUMPF, ME GAGE, KL GILMORE, RD TI ANALYSIS OF LEPTOSPIRA SPP, LEPTONEMA-ILLINI, AND RICKETTSIA-RICKETTSII FOR THE 39-KILODALTON ANTIGEN (P39) OF BORRELIA-BURGDORFERI SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID LINKED IMMUNOSORBENT ASSAYS; MICE PEROMYSCUS-LEUCOPUS; LYME-DISEASE; CROSS-REACTIVITY; ANTIBODY; TESTS; SERA AB Five serovars of Leptospira interrogans, Leptospira biflexa, Leptonema illini, and Rickettsia rickettsii were examined and found not to contain the 39-kDa antigen (P39) of Borrelia burgdorferi, the Lyme disease spirochete. The specificity of this antigen and its reactivity with human Lyme disease sera should exclude the possibility of false-positive serum samples from patients having had either leptospirosis or Rocky Mountain spotted fever, as well as tick-borne relapsing fever and syphilis, as reported previously (W.J. Simpson, M. E. Schrumpf, and T. G. Schwan, J. Clin. Microbiol. 28:1329-1337, 1990). C1 NIAID,ROCKY MT LABS,INTRACELLULAR PARASITES LAB,HAMILTON,MT 59840. RP SCHWAN, TG (reprint author), NIAID,VECTORS & PATHOGENS LAB,ARTHROPOD BORNE DIS SECT,HAMILTON,MT 59840, USA. NR 18 TC 11 Z9 11 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD MAR PY 1992 VL 30 IS 3 BP 735 EP 738 PG 4 WC Microbiology SC Microbiology GA HE087 UT WOS:A1992HE08700042 PM 1551994 ER PT J AU CHESON, BD AF CHESON, BD TI THE PURINE ANALOGS - A THERAPEUTIC BEAUTY CONTEST SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID CHRONIC LYMPHOCYTIC-LEUKEMIA; HAIRY-CELL LEUKEMIA; PHASE-II TRIAL; FLUDARABINE PHOSPHATE; PENTOSTATIN; 2'-DEOXYCOFORMYCIN; CANCER; 2-CHLORODEOXYADENOSINE; DEOXYCOFORMYCIN; MONOPHOSPHATE RP CHESON, BD (reprint author), NCI,BETHESDA,MD 20892, USA. NR 39 TC 30 Z9 30 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAR PY 1992 VL 10 IS 3 BP 352 EP 355 PG 4 WC Oncology SC Oncology GA HF656 UT WOS:A1992HF65600002 PM 1346799 ER PT J AU SHEA, TC MASON, JR STORNIOLO, AM NEWTON, B BRESLIN, M MULLEN, M WARD, DM MILLER, L CHRISTIAN, M TAETLE, R AF SHEA, TC MASON, JR STORNIOLO, AM NEWTON, B BRESLIN, M MULLEN, M WARD, DM MILLER, L CHRISTIAN, M TAETLE, R TI SEQUENTIAL CYCLES OF HIGH-DOSE CARBOPLATIN ADMINISTERED WITH RECOMBINANT HUMAN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR AND REPEATED INFUSIONS OF AUTOLOGOUS PERIPHERAL-BLOOD PROGENITOR CELLS - A NOVEL AND EFFECTIVE METHOD FOR DELIVERING MULTIPLE COURSES OF DOSE-INTENSIVE THERAPY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID BONE-MARROW TRANSPLANTATION; NON-HODGKINS-LYMPHOMA; REFRACTORY OVARIAN-CANCER; BREAST-CANCER; PHASE-I; COMBINATION CHEMOTHERAPY; AUTO-TRANSPLANTATION; HUMAN INTERLEUKIN-3; STEM-CELLS; DISEASE C1 UNIV CALIF SAN DIEGO,DEPT MED,DIV HEMATOL,SAN DIEGO,CA 92103. UNIV CALIF SAN DIEGO,DEPT MED,DIV NEPHROL,SAN DIEGO,CA 92103. UNIV ARIZONA,ARIZONA CANC CTR,DEPT MED,TUCSON,AZ 85721. UNIV ARIZONA,ARIZONA CANC CTR,DEPT PATHOL,TUCSON,AZ 85721. NCI,CANC THERAPY & EVALUAT PROGRAM,BETHESDA,MD 20892. RP SHEA, TC (reprint author), UNIV N CAROLINA,CH,CB 7305,3009 OLD CLIN BLDG,CHAPEL HILL,NC 27599, USA. FU NCI NIH HHS [CA 00290]; NCRR NIH HHS [M01 RR000827] NR 42 TC 137 Z9 137 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAR PY 1992 VL 10 IS 3 BP 464 EP 473 PG 10 WC Oncology SC Oncology GA HF656 UT WOS:A1992HF65600019 PM 1740685 ER PT J AU DECARLI, C MAISOG, J MURPHY, DGM TEICHBERG, D RAPOPORT, SI HORWITZ, B AF DECARLI, C MAISOG, J MURPHY, DGM TEICHBERG, D RAPOPORT, SI HORWITZ, B TI METHOD FOR QUANTIFICATION OF BRAIN, VENTRICULAR, AND SUBARACHNOID CSF VOLUMES FROM MR IMAGES SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE MAGNETIC RESONANCE IMAGING, TECHNIQUES; AGING; BRAIN, VOLUME ID TEMPORAL-LOBE; CEREBROSPINAL-FLUID; HIPPOCAMPAL-FORMATION; WHITE MATTER; GRAY-MATTER; TOMOGRAPHY; SCHIZOPHRENIA; VALIDATION; DEMENTIA; AGE AB We describe a simple, rapid, and semiautomated method of MR analysis based on mathematical modeling of MR pixel intensity histograms. The method is shown to be accurate and reliable for regional analysis of brain, central, and subarachnoid CSF volumes. Application of the method t to five young and six older subjects revealed significant age-related changes in regional brain volumes whereas no difference was found for traced central CSF volumes or subarachnoid CSF volumes. We conclude that this is a simple method that can be applied to further studies of quantification of brain structure in healthy aging and brain disease. RP DECARLI, C (reprint author), NIA,NEUROSCI LAB,BLDG 10,ROOM 6 C 414,BETHESDA,MD 20892, USA. RI DeCarli, Charles/B-5541-2009 NR 28 TC 218 Z9 218 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD MAR-APR PY 1992 VL 16 IS 2 BP 274 EP 284 DI 10.1097/00004728-199203000-00018 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HK062 UT WOS:A1992HK06200018 PM 1545026 ER PT J AU SCOTT, BM DENNISTON, RW MAGRUDER, KM AF SCOTT, BM DENNISTON, RW MAGRUDER, KM TI ALCOHOL ADVERTISING IN THE AFRICAN-AMERICAN COMMUNITY SO JOURNAL OF DRUG ISSUES LA English DT Article ID ADVERTISEMENTS; CONSUMPTION AB Beverage alcohol is the most widely used, enjoyed, and abused addictive substance in the United States. Alcohol related problems - which range from alcoholism, cirrhosis, trauma, and criminal behavior to birth defects, cancer, and other long-term health problems - result in an estimated 100,000 deaths and cost the American society more than $135 billion each year. Alcohol abuse is the leading health and safety problem in the African-American community, making its health and social consequences especially severe. Given this backdrop, there are compelling reasons to be concerned when alcohol producers target African Americans with special advertising and promotions. It is important to examine the marketing and advertising practices of alcohol producers as they relate to African-American communities and their potential impact on alcohol-related behaviors. C1 NIMH,DIV APPL & SERV RES,SERV RES BRANCH,ROCKVILLE,MD 20857. RP SCOTT, BM (reprint author), OFF SUBST ABUSE PREVENT,DIV COMMUN PROGRAMS,5600 FISHERS LANE,ROCKWALL 2,ROCKVILLE,MD 20857, USA. NR 33 TC 10 Z9 10 U1 0 U2 1 PU J DRUG ISSUES INC PI TALLAHASSEE PA PO BOX 4021, TALLAHASSEE, FL 32315 SN 0022-0426 J9 J DRUG ISSUES JI J. Drug Issues PD SPR PY 1992 VL 22 IS 2 BP 455 EP 469 PG 15 WC Substance Abuse SC Substance Abuse GA JA530 UT WOS:A1992JA53000019 ER PT J AU BENDELAC, A MATZINGER, P SEDER, RA PAUL, WE SCHWARTZ, RH AF BENDELAC, A MATZINGER, P SEDER, RA PAUL, WE SCHWARTZ, RH TI ACTIVATION EVENTS DURING THYMIC SELECTION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID PERIPHERAL T-CELLS; MINOR HISTOCOMPATIBILITY ANTIGENS; MONOCLONAL-ANTIBODIES; MOUSE THYMUS; INTERFERON-GAMMA; LYMPHOCYTES-T; STEM-CELLS; IL-4; DIFFERENTIATION; PRECURSORS AB During their differentiation in the mouse thymus, CD4+8- cells undergo several of the sequential changes observed upon normal activation of mature, peripheral CD4+ lymphocytes. Expression of CD69, an early activation marker, is first observed on a minority of cells at the T cell receptor (TCR)lo/med double-positive stage, is maximal (50-90%) on heat-stable antigen (HSA)hi TCR(hi) double-positive, HSA(hi) TCR(med) CD4+8lo, and HSA(hi) TCR(hi) CD4+8- cells, and is downmodulated at the mature HSA(lo) CD4+8- stage. In contrast, CD44, a late activation marker, is selectively expressed at the HSA(lo) stage. The set of lymphokines that CD4+8-thymocytes can produce upon stimulation also characteristically expands from mainly interleukin 2 (IL-2) at the HSA(hi) stage, to IL-2 and very large amounts of IL-4, IL-5, IL-10, and interferon-gamma IFN-gamma) at the HSA(lo) stage. 1 in 30 HSA(lo) CD4+8- adult thymocytes secrete IL-4 upon stimulation through their TCR. This frequency is 25% of the frequency of IL-2 producers, about 100-fold above that of peripheral (mainly resting) CD4+ T cells. With time after their generation in organ culture, CD4+8- thymocytes lose their capacity to secrete IL-4, IL-5, and IFN-gamma, but not IL-2. Similarly, the frequency of IL-4, but not of IL-2, producers progressively decreases after emigration to the periphery as judged by direct comparison between thymic and splenic CD4+ cells in newborns, or by following the fate of intrathymically labeled CD4+8-cells in adults after their migration to the spleen. This sequence suggests that thymic selection results from an activation process rather than a simple rescue from death at the double-positive stage, and shows that the functional changes induced after intrathymic activation, although transient, are still evident after export to the periphery. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. RP BENDELAC, A (reprint author), NIAID,CELLULAR & MOLEC IMMUNOL LAB,BLDG 4,RM 111,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 58 TC 345 Z9 348 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 MAR 1 PY 1992 VL 175 IS 3 BP 731 EP 742 DI 10.1084/jem.175.3.731 PG 12 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HF640 UT WOS:A1992HF64000012 PM 1740662 ER PT J AU HUNT, HD MUNITZ, TI PEASE, LR AF HUNT, HD MUNITZ, TI PEASE, LR TI ALLOREACTIVE CYTOTOXIC LYMPHOCYTES-T RECOGNIZE EPITOPES DETERMINED BY BOTH THE ALPHA-HELICES AND BETA-SHEETS OF THE CLASS-I PEPTIDE BINDING-SITE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; AMINO-ACID SUBSTITUTIONS; MOUSE MHC ANTIGENS; CELL RECOGNITION; MONOCLONAL-ANTIBODIES; HLA-A2; MOLECULE; GENES; ALLORECOGNITION; GLYCOPROTEINS AB A chimeric class I glycoprotein was created to investigate the functional contribution of the alpha-helices and the beta-pleated sheets in forming the antigen recognition site (ARS) of antigen-presenting molecules. This novel molecule was generated by replacing the DNA sequences encoding the alpha-helices of the L(d) gene with the corresponding sequences from the K(b) gene. Serologic analysis of transfected L cells that expressed the chimeric molecule (K(alpha)(b)L(beta)d) revealed that the engineered class I glycoprotein retains two conformational epitopes associated with the alpha-helices of K(b), as defined by monoclonal antibodies K10.56 and 28-13-3. These results demonstrate that the alpha-helices of K(b) can associate with the beta-pleated sheets of Ld to form a stable structure, which is expressed on the cell surface. To address the role of the alpha-helices of the ARS in determining T cell crossreactivity, alloreactive cytotoxic T lymphocytes (CTL) were used to analyze L cells expressing K(alpha)(b)L(beta)d. CTL raised against K(b) or L(d) as alloantigens showed little, if any, ability to lyse L cells expressing K(alpha)(b)L(beta)d). Thus, alloreactive CTL did not recognize structures determined by the alpha-helices alone or by the beta-sheets of the ARS alone. However. bulk and cloned alloreactive CTL that were generated against the mutant K(b) glycoprotein K(bm8) reacted strongly with K(alpha)(b)L(beta)d. In addition to the K(b) alpha-helices, the K(bm8) ARS shares a single polymorphic amino acid at position 24 with K(alpha)(b)L(beta)d. Amino acid 24 is located on the beta-2 strand that forms part of the floor of the ARS and has been identified as a component of pocket B in the HLA class I ARS. The substitution of Glu to Ser at this position was shown previously to be the central determinant of the K(bm8) mutant alloantigenicity. The functional significance of this position in determining crossreactivity between bm8 and K(alpha)(b)L(beta)d identifies pocket B as a strong anchor for allogenic self-peptides. These findings demonstrate that determinants recognized by CTL on class I alloantigens are formed by interactions involving both the a helices and beta-sheets of the ARS. These interactions are best explained by the influence of the alpha-helices and beta-sheets on the peptide-binding properties of these antigen-presenting molecules. C1 MAYO CLIN & MAYO FDN,DEPT IMMUNOL,ROCHESTER,MN 55905. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. FU NCI NIH HHS [CA-09127]; NIAID NIH HHS [AI-00706, AI-22420] NR 32 TC 13 Z9 13 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD MAR 1 PY 1992 VL 175 IS 3 BP 821 EP 829 DI 10.1084/jem.175.3.821 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HF640 UT WOS:A1992HF64000020 PM 1371305 ER PT J AU GLAS, R STURMHOFEL, K HAMMERLING, GJ KARRE, K LJUNGGREN, HG AF GLAS, R STURMHOFEL, K HAMMERLING, GJ KARRE, K LJUNGGREN, HG TI RESTORATION OF A TUMORIGENIC PHENOTYPE BY BETA-2-MICROGLOBULIN TRANSFECTION TO EL-4 MUTANT-CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID H-2-DEFICIENT LYMPHOMA VARIANTS; NATURAL-KILLER-CELLS; CLASS-I GENE; MICE; RECOGNITION; RESISTANCE; MOLECULES; REJECTION; TRANSGENE; ANTIGENS AB It has frequently been suggested that loss of beta-2-microglobulin (beta-2m) in tumor cells may lead to malignant progression due to escape from immunological recognition. Here, we directly tested the role Of beta-2m expression in tumorigenicity. A beta-2m loss mutant (C4.4-25-), selected from the murine lymphoma EL-4, showed a marked reduction in tumorigenicity as compared with EL-4 in normal C57Bl/6 (B6) mice. The reduced tumorigenicity was directly related to beta-2m expression. Transfection of an intact murine beta-2m gene markedly increased the tumorigenic potential. The reduced tumorigenicity of C4.4-25- compared with beta-2m transfected cells was observed also in athymic B6 nu/nu mice, but was abolished in B6 mice depleted of natural killer (NK) 1.1-positive cells. These results show that restoration of beta-2m expression can promote tumorigenicity and demonstrate for the first time that induction of major histocompatibility complex class I expression by transfection can lead to escape from NK cells in vivo. C1 KAROLINSKA INST,DEPT TUMOR BIOL,BOX 60400,S-10401 STOCKHOLM 60,SWEDEN. NIAID,BRL,BETHESDA,MD 20892. GERMAN CANC RES CTR,INST IMMUNOL & GENET,W-6900 HEIDELBERG 1,GERMANY. FU NCI NIH HHS [1 R01 CA-44882-01, 5 R01 CA-25250-06] NR 17 TC 67 Z9 67 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 MAR 1 PY 1992 VL 175 IS 3 BP 843 EP 846 DI 10.1084/jem.175.3.843 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HF640 UT WOS:A1992HF64000022 PM 1740666 ER PT J AU HIRUMA, K NAKAMURA, H HENKART, PA GRESS, RE AF HIRUMA, K NAKAMURA, H HENKART, PA GRESS, RE TI CLONAL DELETION OF POSTTHYMIC T-CELLS - VETO CELLS KILL PRECURSOR CYTOTOXIC LYMPHOCYTES-T SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TRANSGENIC MICE; BONE-MARROW; NEGATIVE SELECTION; ANTIGEN RECEPTOR; SELF-TOLERANCE; ANERGY; ELIMINATION; INHIBITION; INDUCTION; RESPONSES AB Veto cell-mediated suppression of cytotoxic T lymphocyte (CTL) responses has been proposed as one mechanism by which self-tolerance is maintained in mature T cell populations. We have previously reported that murine bone marrow cells cultured in the presence of high-dose interleukin 2 (IL-2) (activated bone marrow cells [ABM]) mediate strong veto suppressor function. To examine mechanisms by which ABM may suppress precursor CTL (p-CTL) responses, we used p-CTL generated from spleen cells of transgenic mice expressing a T cell receptor specific for H-2 L(d). It was demonstrated that the cytotoxic response by these p-CTL after stimulation with irradiated H-2d/k spleen cells was suppressed by DBA/2 (H-2d) ABM, but not by B10.BR (H-2k) ABM or dml (D(d), L(d) mutant) ABM. Flow cytometry analysis with propidium iodide staining revealed that these p-CTL were specifically deleted by incubation with H-2d ABM, but not with H-2k ABM. These data indicate that ABM veto cells kill p-CTL with specificity for antigens expressed on the surface of the ABM, and that the mechanism for veto cell activity of ABM is clonal deletion of p-CTL. C1 NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B17,BETHESDA,MD 20892. CHIBA UNIV,SCH MED,DEPT INTERNAL MED 2,CHIBA 280,JAPAN. NR 28 TC 64 Z9 65 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 MAR 1 PY 1992 VL 175 IS 3 BP 863 EP 868 DI 10.1084/jem.175.3.863 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HF640 UT WOS:A1992HF64000025 PM 1371306 ER PT J AU HEALY, BP AF HEALY, BP TI BIOMEDICAL-RESEARCH - VULNERABLE INVESTIGATOR, ENDANGERED ENTERPRISE SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article; Proceedings Paper CT SYMP ON EDUCATION AND PROFESSIONAL ACCOUNTABILITY : INTERNAL MEDICINE IN THE 21ST CENTURY, IN HONOR OF JOHN A BENSON JR CY JUN 12, 1991 CL PHILADELPHIA, PA SP AMER BOARD INTERNAL MED RP HEALY, BP (reprint author), NIH,BLDG 1,ROOM 126,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD MAR-APR PY 1992 VL 7 IS 2 BP 228 EP 232 DI 10.1007/BF02598021 PG 5 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA HJ343 UT WOS:A1992HJ34300019 PM 1487773 ER PT J AU MARCONI, RT GARON, CF AF MARCONI, RT GARON, CF TI IDENTIFICATION OF A 3RD GENOMIC GROUP OF BORRELIA-BURGDORFERI THROUGH SIGNATURE NUCLEOTIDE ANALYSIS AND 16S RIBOSOMAL-RNA SEQUENCE DETERMINATION SO JOURNAL OF GENERAL MICROBIOLOGY LA English DT Article ID RIBOSOMAL-RNA; OLIGONUCLEOTIDE PROBES; LYME-DISEASE; COMPLEMENTARY AB As part of a continuing effort to assess genetic variation among isolates of Borrelia burgdorferi we have determined the 16S rRNA signature nucleotide makeup of two tick isolates from the USSR. Signature nucleotides were identified via reverse transcriptase primer extension sequencing of select regions of the 16S rRNA molecule. In addition, the near complete 16S rRNA sequence of one of the isolates, R-IP3, was determined and utilized in a phylogenetic assessment. The sequence was aligned with the 16S rRNA sequences of other B. burgdorferi isolates as well as with other Borrelia species. Distance matrix analyses were performed and a phylogenetic tree was constructed. These analyses demonstrate that these isolates belong to a third previously unidentified genomic group of B. burgdorferi. RP MARCONI, RT (reprint author), NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840, USA. NR 20 TC 56 Z9 58 U1 0 U2 0 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1287 J9 J GEN MICROBIOL JI J. Gen. Microbiol. PD MAR PY 1992 VL 138 BP 533 EP 536 PN 3 PG 4 WC Microbiology SC Microbiology GA HH673 UT WOS:A1992HH67300016 PM 1593264 ER PT J AU KIKUCHI, GE ROBERTS, K SHEVACH, EM COLIGAN, JE AF KIKUCHI, GE ROBERTS, K SHEVACH, EM COLIGAN, JE TI GENE-TRANSFER DEMONSTRATES THAT THE V-GAMMA-1.1C-GAMMA-4V-DELTA-6C-DELTA T-CELL RECEPTOR IS ESSENTIAL FOR AUTOREACTIVITY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID GAMMA-DELTA-LYMPHOCYTES; MONOCLONAL-ANTIBODY; ANTIGEN; EXPRESSION; ACTIVATION; IDENTIFICATION; SUBSET; RECOGNITION; THYMOCYTES; HYBRIDOMA AB Murine T cell lines and hybridomas derived from the epidermis that express the V-gamma-1.1C-gamma-4V-delta-6C-delta TCR and may, therefore, recognize an autoantigen, secrete cytokines spontaneously in culture. In addition, activation of these cells requires engagement of the vitronectin receptor (VNR) by extracellular matrix proteins. To further evaluate the role of the TCR, the VNR, and the putative autoantigen in the activation of this T cell subset, we cloned complete cDNA encoding the V-gamma-1.1C-gamma-4 and V-delta-6C-delta TCR and transfected the cDNA constructs into a TCR- murine hybridoma and into a TCR- variant of the human Jurkat line. The murine transfectant spontaneously produced IL-2 in culture and IL-2 production could be inhibited by anti-CD3, anticlonotypic mAb to the transfected TCR, and anti-VNR mAb, as well as by RGDS. These results demonstrate that transfection of the gamma-delta-TCR confers to recipient T cells the phenotype of constitutive activation, as well as dependence on engagement of the VNR as an accessory molecule. In contrast, the Jurkat gamma-delta-transfectant failed to produce cytokines spontaneously, although the transfected TCR was capable of signal transduction after stimulation by anti-TCR mAb. Surprisingly, neither the murine transfectant nor the human transfectant could be induced to respond to autoantigen bearing cells in coculture assays. One interpretation of these results is that coexpression on the surface of the same cell of the V-gamma-1.1 V-delta-6 TCR, the VNR, and a putative autoantigen are necessary for T cell activation in this system. C1 NIAID,BIOL RESOURCES BRANCH,BLDG 4,ROOM 413,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 34 TC 26 Z9 26 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 MAR 1 PY 1992 VL 148 IS 5 BP 1302 EP 1307 PG 6 WC Immunology SC Immunology GA HF266 UT WOS:A1992HF26600003 PM 1371523 ER PT J AU MARTIN, R UTZ, U COLIGAN, JE RICHERT, JR FLERLAGE, M ROBINSON, E STONE, R BIDDISON, WE MCFARLIN, DE MCFARLAND, HF AF MARTIN, R UTZ, U COLIGAN, JE RICHERT, JR FLERLAGE, M ROBINSON, E STONE, R BIDDISON, WE MCFARLIN, DE MCFARLAND, HF TI DIVERSITY IN FINE SPECIFICITY AND T-CELL RECEPTOR USAGE OF THE HUMAN CD4+ CYTOTOXIC T-CELL RESPONSE SPECIFIC FOR THE IMMUNODOMINANT MYELIN BASIC-PROTEIN PEPTIDE-87-106 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS PATIENTS; HLA CLASS-II; LIMITED HETEROGENEITY; HEALTHY-INDIVIDUALS; V-ALPHA; RECOGNITION; EPITOPES; RESTRICTION AB Multiple sclerosis (MS), a human demyelinating disease, is thought to be caused by an autoimmunologic process, and myelin basic protein (MBP) is considered a likely autoantigen. Studies of T cell lines (TCL) responding to different parts of the MBP molecule have indicated that amino acids 87 through 106 contain an immunodominant epitope of MBP. We have demonstrated previously that amino acids 89 through 99 represent the core of this 87-106 peptide epitope. Importantly, this epitope is not only encephalitogenic in SJL/J mice and Lewis rats but also has been shown to be recognized by human cytotoxic TCL in the context of four HLA-DR molecules that are associated with MS in different geographic areas. If the immune response to MBP peptide 87-106 was homogeneous with respect to epitope specificity and TCR usage, specific immunotherapies targeting the interaction of peptide, MHC, and TCR might be possible. In this study, the fine specificity of 29 CD4+ cytotoxic, long term, and limiting dilution TCL that had been generated against whole MBP and were derived from four MS patients and two healthy relatives was dissected using truncated and alanine-substituted peptides for the 87-106 peptide. In addition, the TCR-alpha and beta-chain usage of 15 CD4+ TCL was determined. Using truncated peptides, the presence of several nested immunogenic epitopes within amino acids 87 to 106 was demonstrated. TCL with identical restriction elements and similar responses to truncated peptides could be differentiated further using alanine-substituted peptides. Finally, heterogeneity of TCR usage was shown not only for those lines that differed in their peptide specificity but also for some that showed identical responses and were restricted by the same HLA-DR antigen. In conclusion, the CD4+ cytotoxic T cell response to the immunodominant MBP peptide 87-106 demonstrates a high degree of heterogeneity at the level of fine specificity and TCR usage. These findings indicate that specific immunotherapies aimed at TCR in MS will probably be more complicated than previously anticipated. C1 NINCDS,NEUROIMMUNOL BRANCH,BLDG 10,RM 5B-16,BETHESDA,MD 20892. NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT NEUROL,WASHINGTON,DC 20007. NR 40 TC 152 Z9 152 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 MAR 1 PY 1992 VL 148 IS 5 BP 1359 EP 1366 PG 8 WC Immunology SC Immunology GA HF266 UT WOS:A1992HF26600011 PM 1371525 ER PT J AU OSMAN, N KOZAK, CA MCKENZIE, IFC HOGARTH, PM AF OSMAN, N KOZAK, CA MCKENZIE, IFC HOGARTH, PM TI STRUCTURE AND MAPPING OF THE GENE ENCODING MOUSE HIGH-AFFINITY FC-GAMMA-RI AND CHROMOSOMAL LOCATION OF THE HUMAN FC-GAMMA-RI GENE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MOLECULAR-CLONING; RECEPTOR; IGG; EXPRESSION; SEQUENCES; MURINE; SUBUNIT; LY-17; LOCUS AB We describe the isolation and characterization of the gene encoding the mouse high affinity Fc receptor Fc-gamma-RI. Using a mouse cDNA Fc-gamma-RI probe four unique overlapping genomic clones were isolated and were found to encode the entire 9 kb of the mouse Fc-gamma-RI gene. Sequence analysis of the gene showed that six exons account for the entire Fc-gamma-RI cDNA sequences including the 5'- and 3'-untranslated sequences. The first and second exons encode the signal peptide; exons 3, 4, and 5 encode the extracellular Ig binding domains; and exon 6 encodes the transmembrane domain, the cytoplasmic region, and the entire 3'-untranslated sequence. This exon pattern is similar to Fc-gamma-RIII and Fc-epsilon-RI but differs from the related Fc-gamma-RII gene which contains 10 exons and encodes the b1 and b2 Fc-gamma-RII. Southern blot analysis had shown that the mouse Fc-gamma-RI gene is a single copy gene with no RFLP in inbred strains of mice, but analysis of an intersubspecies backcross of mice showed that unlike other mouse FcR genes which are on mouse chromosome 1 the locus encoding Fc-gamma-RI, termed Fcg1, is located on chromosome 3. Interestingly, the Fcg1 locus is located near the end of a region with known linkage homology to human chromosome 1. Analysis of human x rodent somatic cell hybrid cell lines indicates that the human FCG1 locus encoding the human Fc-gamma-RI maps to chromosome I and therefore possibly linked to other FcR genes on this chromosome. These results suggest that the linkage relationships among these genes in the human genome are not preserved in the mouse. C1 AUSTIN HOSP,AUSTIN RES INST,KRONHEIMER BLDG,BURGUNDY ST,HEIDELBERG,VIC 3084,AUSTRALIA. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 30 TC 26 Z9 27 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 MAR 1 PY 1992 VL 148 IS 5 BP 1570 EP 1575 PG 6 WC Immunology SC Immunology GA HF266 UT WOS:A1992HF26600040 PM 1531670 ER PT J AU BAYLOR, NW FU, T YAN, YD RUSCETTI, FW AF BAYLOR, NW FU, T YAN, YD RUSCETTI, FW TI INHIBITION OF HUMAN T-CELL LEUKEMIA-VIRUS BY THE PLANT FLAVONOID BAICALIN (7-GLUCURONIC ACID, 5,6-DIHYDROXYFLAVONE) SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID INVITRO INFECTIVITY; LYMPHOMA; RETROVIRUS; REPLICATION; PATIENT; BETA AB The ability of baicalin (7-glucuronic acid, 5,6-dihydroxyflavone), a flavonoid compound purified from the Chinese medicinal herb, Scutellaria baicalensis georgi, to inhibit human T cell leukemia virus type I (HTLV-1) was examined. Baicalin produced concentration-dependent inhibition of HTLV-I replication in productively infected T and B cells. Moreover, baicalin treatment selectively reduced the detectable levels of HTLV-I p19 gag protein in infected cells by > 70% at concentrations that produced insignificant effects on total cellular protein and DNA synthesis with no loss in cell viability. Resistance to HTLV-I infection and virus-mediated transformation was noted in uninfected peripheral blood lymphocytes pretreated with baicalin before cocultivation with lethally irradiated chronically infected cells. Baicalin inhibited reverse transcriptase activity in HTLV-I-infected cells as well as the activity of purified reverse transcriptase from Moloney murine leukemia virus and Rous-associated virus type 2. These results suggest that baicalin may be a potential therapeutic agent against HTLV-I-associated T cell diseases. C1 DYNCORP,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. JI LIN ARMY,AIRFORCE MED SCH,DEPT PHARM,JI LIN,PEOPLES R CHINA. FU NCI NIH HHS [CO-74102] NR 25 TC 39 Z9 46 U1 1 U2 4 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 MAR PY 1992 VL 165 IS 3 BP 433 EP 437 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HE466 UT WOS:A1992HE46600004 PM 1371535 ER PT J AU QUINN, TC GROSECLOSE, SL SPENCE, M PROVOST, V HOOK, EW AF QUINN, TC GROSECLOSE, SL SPENCE, M PROVOST, V HOOK, EW TI EVOLUTION OF THE HUMAN-IMMUNODEFICIENCY-VIRUS EPIDEMIC AMONG PATIENTS ATTENDING SEXUALLY-TRANSMITTED DISEASE CLINICS - A DECADE OF EXPERIENCE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID UNITED-STATES; HIV INFECTION; BISEXUAL MEN; REDUCTION; RISK AB Since human immunodeficiency virus (HIV) is predominantly sexually transmitted, serologic surveys for HIV infection in sexually transmitted disease (STD) clinics provide sentinel observations regarding HIV epidemiology. Over the past decade, 17,207 systematically collected sera from patients attending Baltimore STD clinics were analyzed. From 1979 through 1989, HIV seroprevalence rose from 0.23% to 5.35%, increasing significantly in both men and women (P < .001). Due to a marked increase in HIV infection among women during the mid-1980s, the male-to-female ratio of HIV infection declined from 16:1 in 1979-1982 to 1.0 in 1988-1989. HIV seroprevalence increased significantly (P < .001) in all age groups, with the greatest increase among teenagers, rising from 0.18% in 1979-1983 to 2.1% in 1987-1989 (P < .001). Although HIV seroprevalence was higher among whites than blacks during the early 1980s, it increased in blacks subsequently (P < .001), eventually resulting in a greater rate among black than white clinic patients (P < .01). These data reflect the evolution of the HIV epidemic in US inner cities. HIV prevalence has increased > 20-fold, with recent increases being most marked among women, teenagers, and blacks. Additional resources will undoubtedly be required to support further intensive behavioral and educational programs targeted at adolescents and inner-city minorities. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,BALTIMORE,MD 21205. CITY HLTH DEPT,BALTIMORE,MD. HAHNEMANN UNIV,MED CTR,DEPT OBSTET & GYNECOL,PHILADELPHIA,PA 19102. NR 16 TC 29 Z9 29 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 MAR PY 1992 VL 165 IS 3 BP 541 EP 544 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HE466 UT WOS:A1992HE46600020 PM 1538158 ER PT J AU HAUBRICH, RH TAKEDA, A KOFF, W SMITH, G ENNIS, FA AF HAUBRICH, RH TAKEDA, A KOFF, W SMITH, G ENNIS, FA TI STUDIES OF ANTIBODY-DEPENDENT ENHANCEMENT OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) TYPE-1 INFECTION MEDIATED BY FC-RECEPTORS USING SERA FROM RECIPIENTS OF A RECOMBINANT GP160 EXPERIMENTAL HIV-1 VACCINE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID PROTECTION; MACAQUES; CELLS; AIDS; CD4 AB Subneutralizing concentrations of sera from human immunodeficiency virus (HIV)-1-infected patients augment HIV infection mediated by Fc receptor uptake by human monocytes and the monocytic cell line U937. Antibody-dependent enhancement (ADE) and neutralization activity were studied in the sera of HIV-1 antibody-negative volunteers who had been immunized with three 40-mu-g doses of a recombinant gp160 (rgp160) candidate HIV vaccine. Volunteers were vaccinated with rgp160 or a hepatitis B vaccine as a control on days 0, 30, and 180. Sera were obtained before and after three doses of vaccine and were tested for ADE and neutralization activity. Serum samples collected before vaccination showed neither neutralization nor ADE activity. Thirteen sera from volunteers who received gp160 and four from placebo recipients failed to show ADE. Three sera showed low levels of neutralization of strain III(B) of HIV. Vaccination with this dose of rgp160 produced neutralizing antibodies in some subjects but did not induce detectable enhancing antibodies. C1 UNIV MASSACHUSETTS,MED CTR,DIV INFECT DIS & IMMUNOL,55 LAKE AVE N,WORCESTER,MA 01655. NIAID,AIDS VACCINE EVALUAT GRP,BETHESDA,MD 20892. MICROGENESYS INC,MERIDEN,CT. FU NIAID NIH HHS [AI-07272, AI-24750, AI-26458] NR 14 TC 21 Z9 21 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 MAR PY 1992 VL 165 IS 3 BP 545 EP 548 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HE466 UT WOS:A1992HE46600021 PM 1538159 ER PT J AU HAWKINS, RE RICKMAN, LS VERMUND, SH CARL, M AF HAWKINS, RE RICKMAN, LS VERMUND, SH CARL, M TI ASSOCIATION OF MYCOPLASMA AND HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION - DETECTION OF AMPLIFIED MYCOPLASMA-FERMENTANS DNA IN BLOOD SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID GENITAL MYCOPLASMAS; URETHRITIS; MEN AB A cross-sectional study was undertaken to determine the prevalence of Mycoplasma fermentans infection in patients with human immunodeficiency virus (HIV) infection using polymerase chain reaction methodology. Targeted M. fermentans DNA sequences could be amplified from the DNA extracted from the blood of 6 (11%) of 55 HIV-seropositive patients but from none of 26 HIV-seronegative subjects at low risk for HIV infection (P = .17). There was no correlation between M. fermentans infection and HIV clinical stage. There was a nonsignificant trend toward an association between M. fermentans infection and a history of syphilis. Infection with M. fermentans may occur more commonly in HIV-infected patients; however, a role as a copathogen or opportunistic infection was not established in this study. C1 NATL NAVAL MED CTR, DEPT INTERNAL MED, DIV INFECT DIS, BETHESDA, MD 20814 USA. USN, INST MED RES, DEPT INFECT DIS, ACCELERATED PROD DEV PROGRAM, BETHESDA, MD 20814 USA. NIAID, DIV AIDS, EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA. UNIV CALIF SAN DIEGO, DIV INFECT DIS, LA JOLLA, CA 92093 USA. OI Vermund, Sten/0000-0001-7289-8698 NR 15 TC 53 Z9 55 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 MAR PY 1992 VL 165 IS 3 BP 581 EP 585 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HE466 UT WOS:A1992HE46600030 PM 1538164 ER PT J AU ROSENTHAL, DS GRIFFITHS, CEM YUSPA, SH ROOP, DR VOORHEES, JJ AF ROSENTHAL, DS GRIFFITHS, CEM YUSPA, SH ROOP, DR VOORHEES, JJ TI ACUTE OR CHRONIC TOPICAL RETINOIC ACID TREATMENT OF HUMAN SKIN INVIVO ALTERS THE EXPRESSION OF EPIDERMAL TRANSGLUTAMINASE, LORICRIN, INVOLUCRIN, FILAGGRIN, AND KERATIN-6 AND KERATIN-13 BUT NOT KERATIN-1, KERATIN-10, AND KERATIN-14 SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID SQUAMOUS-CELL CARCINOMAS; CULTURED HUMAN KERATINOCYTES; TERMINAL DIFFERENTIATION; VITAMIN-A; SYNTHETIC RETINOIDS; EPITHELIA; PROLIFERATION; GROWTH; ANTIBODIES; INVITRO AB Histologic and immunocytochemical analyses were performed on cutaneous biopsies from 10 patients treated with retinoic acid under occlusion for 4 d compared to biopsies from 19 patients treated nightly for 16 weeks. Acute application of RA caused epidermal thickening (9 of 10 samples), stratum granulosum thickening (7 of 10), parakeratosis (4 of 10), a marked increase in the number of cell layers expressing epidermal transglutaminase (7 of 10), and focal expression of two non-epidermal keratins, K6 (8 of 10) and K13 (2 of 10), changes also observed with chronic treatment. Involucrin, filaggrin, and loricrin were also altered in samples from both acute and chronic treatment. An increased number of cell layers expressed both involucrin and filaggrin from both the acute (7 of 10) and chronic (14 of 19) treatment groups. In the acute group, loricrin expression was significantly reduced or absent in some regions of the epidermis (5 of 10), whereas most chronic samples showed an increased number of cell layers expressing loricrin (12 of 19). The pattern of expression of three major epidermal differentiation products, keratins K1, K10, and K14, was not significantly altered in any of the acute or chronic samples, although there was a slight reduction in the detection of K10 in two of the acute samples. Thus, acute topical RA treatment under occlusion caused substantial changes in the epidermis, and reproduced most, but not all of the effects of chronic treatment. C1 UNIV MICHIGAN,MED CTR,DEPT DERMATOL,ANN ARBOR,MI 48109. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. BAYLOR COLL MED,DEPT CELL BIOL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT DERMATOL,HOUSTON,TX 77030. RI Griffiths, Christopher/P-5448-2014 OI Griffiths, Christopher/0000-0001-5371-4427 FU NICHD NIH HHS [HD25479] NR 53 TC 115 Z9 115 U1 0 U2 6 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD MAR PY 1992 VL 98 IS 3 BP 343 EP 350 DI 10.1111/1523-1747.ep12499802 PG 8 WC Dermatology SC Dermatology GA HJ638 UT WOS:A1992HJ63800014 PM 1372028 ER PT J AU MICHEL, S BERNERD, F JETTEN, AM FLOYD, EE SHROOT, B REICHERT, U AF MICHEL, S BERNERD, F JETTEN, AM FLOYD, EE SHROOT, B REICHERT, U TI EXPRESSION OF KERATINOCYTE TRANSGLUTAMINE MESSENGER-RNA REVEALED BY INSITU HYBRIDIZATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID HUMAN EPIDERMAL-CELLS; CROSS-LINKED ENVELOPE; RETINOIC ACID; TERMINAL DIFFERENTIATION; CORNIFIED ENVELOPE; SKIN; PROTEIN AB Plasma membrane-bound transglutaminase (TGm) catalyzes the formation of cornified envelopes (CE) in terminally differentiating keratinocytes. The recent cloning of cDNA encoding rabbit TGm allows detailed studies of its gene expression and regulation. In the present paper, we describe the localization of TGm mRNA in rabbit tissues, as well as in normal and psoriatic human skin, as assessed by in situ hybridization. Furthermore, we correlate TGm mRNA localization with the distribution of the TGm protein detected by immunohistochemistry with a specific monoclonal antibody. In rabbit epidermis, TGm mRNA was expressed in supra-basal cells. The TGm protein was detected in the upper stratum spinosum and stratum granulosum. In rabbit esophagus, TGm mRNA and protein were already expressed to a high level in the first suprabasal cell layer, and their expression decreased in the more differentiated cells. In normal human skin, a small amount of TGm mRNA, restricted to the stratum granulosum, was found, whereas psoriatic skin samples contained high amounts of TGm mRNA in the suprabasal layers with a decreasing gradient into the rete ridges, i.e., the involutions of the epidermis into the dermal compartment. The TGm protein was absent from the rete ridges and confined to several cell layers expressing high levels of mRNA. There was virtually no difference between uninvolved psoriatic and normal epidermis. C1 NIEHS,PULM PATHOBIOL LAB,CELL BIOL SECT,RES TRIANGLE PK,NC 27709. RP MICHEL, S (reprint author), CTR INT RECH DERMATOL GALDERMA,SOPHIA ANTIPOLIS,F-06565 VALBONNE,FRANCE. NR 22 TC 47 Z9 47 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD MAR PY 1992 VL 98 IS 3 BP 364 EP 368 DI 10.1111/1523-1747.ep12499806 PG 5 WC Dermatology SC Dermatology GA HJ638 UT WOS:A1992HJ63800017 PM 1347556 ER PT J AU UITTO, J BAUER, EA MOSHELL, AN AF UITTO, J BAUER, EA MOSHELL, AN TI SYMPOSIUM ON EPIDERMOLYSIS-BULLOSA - MOLECULAR-BIOLOGY AND PATHOLOGY OF THE CUTANEOUS BASEMENT-MEMBRANE ZONE - JEFFERSON-MEDICAL-COLLEGE, PHILADELPHIA, PENNSYLVANIA, OCTOBER 4 AND 5, 1991 SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Editorial Material ID VII COLLAGEN; SIMPLEX; LINKAGE C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT BIOCHEM,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT MOLEC BIOL,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON INST MOLEC MED,MOLEC DERMATOL SECT,PHILADELPHIA,PA 19107. STANFORD UNIV,MED CTR,SCH MED,DEPT DERMATOL,STANFORD,CA 94305. NIAMSD,SKIN DIS BRANCH,BETHESDA,MD. RP UITTO, J (reprint author), THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT DERMATOL,233 S 10TH ST,450-BLSB,PHILADELPHIA,PA 19107, USA. FU NIAMS NIH HHS [1R13AR40984-01] NR 32 TC 21 Z9 21 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD MAR PY 1992 VL 98 IS 3 BP 391 EP 395 DI 10.1111/1523-1747.ep12499822 PG 5 WC Dermatology SC Dermatology GA HJ638 UT WOS:A1992HJ63800025 PM 1545149 ER PT J AU PARROTT, CL ALSAYED, N REBOURCET, R SANTAMARINAFOJO, S AF PARROTT, CL ALSAYED, N REBOURCET, R SANTAMARINAFOJO, S TI APOC-IIPARIS2 - A PREMATURE TERMINATION MUTATION IN THE SIGNAL PEPTIDE OF APOC-II RESULTING IN THE FAMILIAL CHYLOMICRONEMIA SYNDROME SO JOURNAL OF LIPID RESEARCH LA English DT Article DE APOC-II DEFICIENCY; CHEMICAL CLEAVAGE; MISMATCH ANALYSIS; POLYMERASE CHAIN REACTION; PREMATURE STOP CODON ID APOLIPOPROTEIN-C-II; PLASMA APOLIPOPROTEINS; LIPOPROTEIN LIPASE; ACID-SEQUENCE; A-I; DEFICIENCY; GENE; PATIENT; DNA; HYPERTRIGLYCERIDEMIA AB The chemical mismatch method has been utilized to screen for mutations in the apoC-II gene of a patient with familial chylomicronemia and apoC-II deficiency. Cleavage of heteroduplexes formed between normal and patient DNA strands with hydroxylamine and osmium tetroxide readily localized a mutation near base 2660 of the mutant apoC-II. Sequence analysis of PCR amplified patient DNA in the mismatched region localized by this method identified the substitution of a thymidine (T) for a cytosine (C) at base 2668 in exon 2 of the patient's gene within a CpG dinucleotide. The C to T transition in the apoC-II(Paris2) gene leads to the introduction of a premature termination codon (TGA) at a position corresponding to amino acid-19 of the signal peptide of apoC-II and the formation of a new Nla III restriction enzyme site absent in the normal apoC-II gene. Consistent with the history of consanguinity in this kindred, amplification of DNA isolated from the proband's parents by the polymerase chain reaction and digestion with Nla III established that the proband is a true homozygote for this genetic defect. Analysis of the patient's plasma by two-dimensional gel electrophoresis and immunoblotting failed to detect any plasma apoC-II. Thus, we have identified a novel mutation in the apoC-II gene of a patient with apoC-II deficiency from a Paris kindred presenting with severe hypertriglyceridemia and chylomicronemia. A single base substitution (C to T) occurring within a CpG dinucleotide present in the second exon of the apoC-II gene leads to the introduction of a premature stop codon in the signal peptide of the mutant gene, resulting in the inability to synthesize the mature apolipoprotein. The use of the chemical cleavage mismatch method to screen for mutations in the apoC-II(Paris2) gene facilitated the identification of the underlying genetic defect leading to the chylomicronemia syndrome in this kindred. C1 NIH,MOLEC DIS BRANCH,BETHESDA,MD 20892. HOP ENFANTS MALAD,PARIS,FRANCE. HOP PITIE,F-75651 PARIS 13,FRANCE. NR 27 TC 19 Z9 20 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 MAR PY 1992 VL 33 IS 3 BP 361 EP 367 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK057 UT WOS:A1992HK05700007 PM 1569385 ER PT J AU LONDON, RE PERLMAN, ME DAVIS, DG AF LONDON, RE PERLMAN, ME DAVIS, DG TI RELAXATION-MATRIX ANALYSIS OF THE TRANSFERRED NUCLEAR OVERHAUSER EFFECT FOR FINITE EXCHANGE-RATES SO JOURNAL OF MAGNETIC RESONANCE LA English DT Article ID ESCHERICHIA-COLI; MAGNETIC-RESONANCE; NMR-SPECTROSCOPY; CROSS-RELAXATION; RECEPTOR PROTEIN; CONFORMATIONS; BINDING; NOE; SYSTEMS RP LONDON, RE (reprint author), NIEHS,MOLEC BIOPHYS LAB MD 1705,RES TRIANGLE PK,NC 27709, USA. NR 25 TC 107 Z9 107 U1 1 U2 10 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-2364 J9 J MAGN RESON JI J. Magn. Reson. PD MAR PY 1992 VL 97 IS 1 BP 79 EP 98 DI 10.1016/0022-2364(92)90238-3 PG 20 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA HK096 UT WOS:A1992HK09600006 ER PT J AU SAKAI, RK MILLER, LH AF SAKAI, RK MILLER, LH TI EFFECTS OF HEAT-SHOCK ON THE SURVIVAL OF TRANSGENIC ANOPHELES-GAMBIAE (DIPTERA, CULICIDADE) UNDER ANTIBIOTIC SELECTION SO JOURNAL OF MEDICAL ENTOMOLOGY LA English DT Note DE INSECTA; ANOPHELES-GAMBIAE; HEAT SHOCK; TRANSFORMATION ID INTEGRATION; DNA AB A gene for neomycin resistance linked to a Drosophila hsp 70 heat shock promoter was introduced into the germ line of Anopheles gambiae Giles. Effects of heat shock at 37 and 41-degrees-C on the subsequent survival of the transgenic mosquito subjected to selection by the antibiotic G418 were studied. Heat shock did not enhance the survival of untransformed mosquitoes but greatly increased the survival of the transgenic mosquitoes. Survival after heat shock at 41-degrees-C was greater than after heat shock at 37-degrees-C. RP SAKAI, RK (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA. NR 7 TC 11 Z9 11 U1 0 U2 3 PU ENTOMOL SOC AMER PI LANHAM PA 9301 ANNAPOLIS RD, LANHAM, MD 20706 SN 0022-2585 J9 J MED ENTOMOL JI J. Med. Entomol. PD MAR PY 1992 VL 29 IS 2 BP 374 EP 375 PG 2 WC Entomology; Veterinary Sciences SC Entomology; Veterinary Sciences GA HG772 UT WOS:A1992HG77200045 PM 1495063 ER PT J AU BRODWICK, MS CURRAN, M EDWARDS, C AF BRODWICK, MS CURRAN, M EDWARDS, C TI EFFECTS OF OSMOTIC-STRESS ON MAST-CELL VESICLES OF THE BEIGE MOUSE SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE VESICLE; GEL MATRIX; TONICITY; BULK MODULUS; CAPACITANCE; FUSION ID ADRENAL CHROMAFFIN GRANULES; PHOSPHOLIPID-VESICLES; MEMBRANE; FUSION; EXOCYTOSIS; HISTAMINE AB The large size of the vesicles of beige mouse peritoneal mast cells (4-mu-m in diameter) facilitated the direct observation of the individual osmotic behavior of vesicles. The vesicle diameter increased as much as 73% when intact cells were perfused with a 10 mM pH buffer solution; the swelling of the vesicle membranes exceeded that of the insoluble vesicle gel matrix, which resulted in the formation of a clear space between the optically dense gel matrix and the vesicle membrane. Hypertonic solutions shrank intact vesicles of lysed cells in a nonideal manner, suggesting a limit to the compressibility of the gel matrix. The nonideality at high osmotic strengths can be adequately explained as the consequence of an excluded volume and/or a three-dimensional gel-matrix spring. The observed osmotic activity of the vesicles implies that the great majority of the histamine known to be present is reversibly bound to the gel matrix. This binding allows vesicles to store a large quantity of transmitter without doing osmotic work. The large size of the vesicles also facilitated the measurement of the kinetics of release as a collection of individual fusion events. Capacitance measurements in beige mast cells revealed little difference in the kinetics of release in hypotonic, isotonic, and hypertonic solutions, thus eliminating certain classes of models based on the osmotic theory of exocytosis for mast cells. C1 NIH,BETHESDA,MD 20817. RP BRODWICK, MS (reprint author), UNIV TEXAS,MED BRANCH,DEPT PHYSIOL & BIOPHYS,GALVESTON,TX 77550, USA. NR 45 TC 20 Z9 20 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD MAR PY 1992 VL 126 IS 2 BP 159 EP 169 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA HL563 UT WOS:A1992HL56300007 PM 1593615 ER PT J AU MERTZ, LM BAUM, BJ AMBUDKAR, IS AF MERTZ, LM BAUM, BJ AMBUDKAR, IS TI MEMBRANE-POTENTIAL MODULATES DIVALENT-CATION ENTRY IN RAT PAROTID ACINI SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE CA2+ ENTRY; MEMBRANE POTENTIAL; INTRACELLULAR CALCIUM MOBILIZATION; FLUID SECRETION; EXOCRINE GLAND ID CYTOSOLIC FREE CALCIUM; ENDOTHELIAL-CELLS; INTRACELLULAR CALCIUM; NA+/H+ EXCHANGE; PLASMA-MEMBRANE; CA-2+ POOL; TRANSPORT; ACTIVATION; INFLUX; I AB This study examines the effect of membrane potential on divalent cation entry in dispersed parotid acini following stimulation by the muscarinic agonist, carbachol, and during refill of the agonist-sensitive internal Ca2+ pool. Depolarizing conditions (addition of gramicidin to cells in Na+-containing medium or incubation of cells in medium with elevated [K+]) prevent carbachol-stimulated hyperpolarization of acini and also inhibit carbachol activation of Ca2+ and Mn2+ entry into these cells. Conditions promoting hyperpolarization (cells in medium with Na+ or with N-methyl-D-glucamine instead of Na+) enhance carbachol stimulation of divalent cation entry. Intracellular Ca2+ release (initial increase in [Ca2+]i) does not appear to be affected by these manipulations. Mn2+ entry into resting and internal Ca2+ pool-depleted cells (10-min carbachol stimulation in a Ca2+-free medium) is similarly affected by membrane potential modualtions, and refill of the internal pool by Ca2+ is inhibited by depolarization. The inhibitory effects of depolarization on divalent cation entry can be overcome by increasing extracellular [Ca2+] or [Mn2+]. These data demonstrate that the modulation of Ca2+ entry into parotid acini by membrane potential is most likely due to effects on the electrochemical gradient (E(m) - E(Ca)) for Ca2+ entry. C1 NIDR,CLIN INVESTIGAT & PATIENT CARE BRANCH,BETHESDA,MD 20892. NR 30 TC 26 Z9 27 U1 0 U2 0 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 MAR PY 1992 VL 126 IS 2 BP 183 EP 193 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA HL563 UT WOS:A1992HL56300009 PM 1593617 ER PT J AU VIKICTOPIC, D MINTAS, M RAOS, N AF VIKICTOPIC, D MINTAS, M RAOS, N TI C-13 NMR-SPECTRA OF SOME SYMMETRICALLY 2,2'-DISUBSTITUTED STILBENES - CONJUGATIONAL AND CONFORMATIONAL EFFECTS SO JOURNAL OF MOLECULAR STRUCTURE LA English DT Article AB In the C-13 NMR spectra of symmetrically 2,2'-disubstituted cis-stilbenes the decrease of alpha-effects and increase of gamma-effects at ortho-carbons with respect to trans-isomers were observed. However the most significant differences in substituent effects between trans- and cis-isomers were found for gamma-effects, at unsubstituted ortho-C-6 and C-4 atoms. The one bond C-H splitting of olefinic carbons is greater in cis- than trans-stilbenes. The differences in substituent effects and apparent coupling constants are assumed to originate mainly from the different conjugational interactions in cis- and trans-stilbenes. The conformational and configurational differences of these molecules were substantiated by molecular mechanics calculations. C1 UNIV ZAGREB,FAC TECHNOL,DEPT ORGAN CHEM,YU-41000 ZAGREB,YUGOSLAVIA. INST MED RES & OCCUPAT HLTH,YU-41000 ZAGREB,YUGOSLAVIA. RP VIKICTOPIC, D (reprint author), NIH,ANALYT CHEM LAB,BETHESDA,MD 20892, USA. NR 13 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-2860 J9 J MOL STRUCT JI J. Mol. Struct. PD MAR PY 1992 VL 267 BP 405 EP 410 DI 10.1016/0022-2860(92)87064-3 PG 6 WC Chemistry, Physical SC Chemistry GA HQ222 UT WOS:A1992HQ22200064 ER PT J AU MYSLOBODSKY, MS GOLDBERG, T JOHNSON, F HICKS, L WEINBERGER, DR AF MYSLOBODSKY, MS GOLDBERG, T JOHNSON, F HICKS, L WEINBERGER, DR TI LIPREADING IN PATIENTS WITH SCHIZOPHRENIA SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID PERCEPTION; SYSTEMS AB This study was designed to explore whether schizophrenic patients who are able to maintain their gaze with adequate persistence could competently lip-read. Four lipreading tests, designed to assess recognition of syllables, words, and overlearned sentences, were administered to 15 schizophrenic and 15 normal subjects matched for age, sex, and educational level. The patients proved to be competent lip-readers susceptible to the blend illusion and were inferior only in lipreading of overlearned sentences. The latter difficulty may tentatively be attributed to the inadequacy of the patient's premorbid social network for establishing contextual cues that aid in the recognition of overlearned sentences. C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,CLIN BRAIN DISORDER BRANCH,WASHINGTON,DC 20032. HOWARD UNIV,DEPT PSYCHOL,WASHINGTON,DC 20059. NR 21 TC 16 Z9 17 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD MAR PY 1992 VL 180 IS 3 BP 168 EP 171 DI 10.1097/00005053-199203000-00004 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA HJ014 UT WOS:A1992HJ01400004 PM 1588334 ER PT J AU MURPHY, VA RAPOPORT, SI AF MURPHY, VA RAPOPORT, SI TI BRAIN TRANSFER-COEFFICIENTS FOR GA-67 - COMPARISON TO FE-55 AND EFFECT OF CALCIUM DEFICIENCY SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE GALLIUM; ALUMINUM; IRON; BLOOD-BRAIN BARRIER; CALCIUM DEFICIENCY; CEREBROSPINAL FLUID ID ALZHEIMERS-DISEASE; ALUMINUM; BINDING; PLASMA; SERUM; RAT; TRANSPORT; CONSTANTS; RECEPTOR; BARRIER AB The transfer coefficients (K(in)) for the uptake of gallium-67 (Ga-67) into brain and CSF were determined in unanesthetized male Fischer -344 rats fed either a normal or a low-Ca diet. K(in) for Ga-67 was also compared with transfer coefficients for the uptake of iron-55 (Fe-55) and I-125-albumin in control animals. The value of CSF Ga-67 K(in) was 3 x 10(-7) ml.g-1.s-1 and was 50% larger in low-Ca animals. Brain regional K(in) values for Ga-67 were 3-9 x 10(-7) ml.g-1.s-1 with no differences in K(in) between normal and low-Ca rats. CSF K(in) values for Fe-55 were 40% and those for albumin were 15% of K(in) for Ga-67. For brain, K(in) values for Fe-55 were 15-40% smaller than for Ga-67, but for albumin the K(in) values were 85% less than for Ga-67. Ga-67 was found to be 99% bound to plasma proteins, whereas Fe-55 was 99.9% bound. The results indicate that metals that are primarily bound to transferrin enter the CSF and brain very slowly. Uptake of both metals was faster than albumin, which may indicate that metal bound to small chelates contributes significantly to brain uptake. In addition, Ca deficiency does not enhance entry of Ga into the brain. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 30 TC 7 Z9 7 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 MAR PY 1992 VL 58 IS 3 BP 898 EP 902 DI 10.1111/j.1471-4159.1992.tb09341.x PG 5 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HE275 UT WOS:A1992HE27500015 PM 1737998 ER PT J AU DYKSTRA, KH HSIAO, JK MORRISON, PF BUNGAY, PM MEFFORD, IN SCULLY, MM DEDRICK, RL AF DYKSTRA, KH HSIAO, JK MORRISON, PF BUNGAY, PM MEFFORD, IN SCULLY, MM DEDRICK, RL TI QUANTITATIVE EXAMINATION OF TISSUE CONCENTRATION PROFILES ASSOCIATED WITH MICRODIALYSIS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE MICRODIALYSIS; MATHEMATICAL MODELING; DIFFUSION; QUANTITATIVE AUTORADIOGRAPHY; BLOOD-BRAIN BARRIER; EDEMA ID BRAIN; INVITRO; PROBES; INVIVO; SPACE AB Spatial solute concentration profiles resulting from in vivo microdialysis were measured in rat caudate-putamen by quantitative autoradiography. Radiolabeled sucrose was included in the dialysate, and the tissue concentration profile measured after infusions of 14 min and 61.5 min in an acute preparation. In addition, the changes in sucrose extraction fraction over time were followed in vivo and in a simple in vitro system consisting of 0.5 % agarose. These experimental results were then compared with mathematical simulations of microdialysis in vitro and in vivo. Simulations of in vitro microdialysis agreed well with experimental results. In vivo, the autoradiograms of the tissue concentration profiles showed clear evidence of substantial differences between 14 and 61.5 min, even though the change in extraction fraction was relatively small over that period. Comparison with simulated results showed that the model substantially underpredicted the observed extraction fraction and overall amount of sucrose in the tissue. A sensitivity analysis of the various model parameters suggested a tissue extracellular volume fraction of approximately 40% following probe implantation. We conclude that the injury from probe insertion initially causes disruption of the blood-brain barrier in the vicinity of the probe, and this disruption leads to an influx of water and plasma constituents, causing a vasogenic edema. C1 NIH,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892. RP DYKSTRA, KH (reprint author), NIH,NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13,RM 3W13,BETHESDA,MD 20892, USA. NR 19 TC 130 Z9 130 U1 0 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD MAR PY 1992 VL 58 IS 3 BP 931 EP 940 DI 10.1111/j.1471-4159.1992.tb09346.x PG 10 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HE275 UT WOS:A1992HE27500020 PM 1738000 ER PT J AU HABER, R GOLDMAN, D AF HABER, R GOLDMAN, D TI EXPRESSION OF SIZE-SELECTED RNA ENCODING BRAIN-SEROTONIN TRANSPORTER IN XENOPUS-LAEVIS OOCYTES SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE XENOPUS-LAEVIS OOCYTES; SEROTONIN TRANSPORTER; SIZE-SELECTED RNA ID RAT-BRAIN; IMIPRAMINE; CITALOPRAM; SITES AB The mRNA that encodes a serotonin transporter was expressed using the Xenopus laevis oocyte expression system. Poly(A)+ RNA isolated from mouse brainstem was injected into Xenopus laevis oocytes, and the ability of oocytes to take up serotonin was measured 3 days postinjection. RNA-dependent serotonin uptake was sensitive to citalopram, a specific inhibitor of serotonin uptake, whereas background levels of serotonin uptake were not citalopram sensitive. Two RNA size fractions, 4.0 and 4.5 kb, were most efficient in stimulating uptake. Injection into Xenopus laevis oocytes of the 4.5-kb size fraction of mouse brainstem RNA resulted in threefold more serotonin uptake than did injection of unfractionated poly(A)+ RNA. RP HABER, R (reprint author), NATL INST ALCOHOL ABUSE & ALCOHOLISM,NEUROGENET LAB,BLDG 10,ROOM 3C215,BETHESDA,MD 20892, USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 18 TC 2 Z9 2 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 MAR PY 1992 VL 58 IS 3 BP 1165 EP 1167 DI 10.1111/j.1471-4159.1992.tb09376.x PG 3 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HE275 UT WOS:A1992HE27500050 PM 1371147 ER PT J AU SEI, Y MAKINO, M VITKOVIC, L CHATTOPADHYAY, SK HARTLEY, JW ARORA, PK AF SEI, Y MAKINO, M VITKOVIC, L CHATTOPADHYAY, SK HARTLEY, JW ARORA, PK TI CENTRAL-NERVOUS-SYSTEM INFECTION IN A MURINE RETROVIRUS-INDUCED IMMUNODEFICIENCY SYNDROME SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE ANIMAL MODEL; ASTROCYTE; CENTRAL NERVOUS SYSTEM; MICROGLIA; ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS), MURINE; LEUKEMIA VIRUS, MURINE ID LEUKEMIA-VIRUS; SPASTIC PARAPARESIS; C57BL/6 MICE; DISEASE; INDUCTION; CELLS; PATHOGENESIS; GROWTH; BRAINS; GENE AB Astrocyte-enriched primary glial cultures (AGC) from C57BL/6 mice were found to be highly susceptible to infection with the replication competent components of LP-BM5, consisting of the ecotropic and mink cell focus-inducing (MCF) helper murine leukemia viruses (MuLVs). The presence in infected AGC of defective LP-BM5 MuLV genome, a critical component for induction of the disease referred to as murine AIDS, was confirmed by Southern blot hybridization using a probe reactive with the p12 gag sequence of the 4.9 kb defective genome. Electron microscopic studies demonstrated C-type retrovirus particles in both astrocytes and microglial cells. In vivo studies demonstrated that the ecotropic MuLVs and the defective genome could be detected within AGC obtained form either 14-day-old mice following intraperitoneal inoculation or 7-day-old mice following intracranial inoculation. These findings suggest that: (1) the central nervous system (CNS) infection is present at an early stage in murine AIDS, (2) both astrocytes and microglial cells are possible CNS targets in which helper MuLVs replicate, and (3) these cells can harbor the defective genome that is a critical component for disease induction. C1 NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP SEI, Y (reprint author), NIDDK,NEUROSCI LAB,BLDG 8,ROOM 111,BETHESDA,MD 20892, USA. NR 33 TC 19 Z9 19 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD MAR PY 1992 VL 37 IS 1-2 BP 131 EP 140 DI 10.1016/0165-5728(92)90164-G PG 10 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA HG729 UT WOS:A1992HG72900015 PM 1548376 ER PT J AU YU, C LIN, PX FITZGERALD, S NELSON, P AF YU, C LIN, PX FITZGERALD, S NELSON, P TI HETEROGENEOUS CALCIUM CURRENTS AND TRANSMITTER RELEASE IN CULTURED MOUSE SPINAL-CORD AND DORSAL-ROOT GANGLION NEURONS SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID SYNTHETIC OMEGA-CONOTOXIN; CHICK SENSORY NEURONS; NERVE-TERMINALS; CA-CHANNEL; NEUROTRANSMITTER RELEASE; SYNAPTIC TRANSMISSION; HIPPOCAMPAL-NEURONS; SYMPATHETIC NEURONS; PERIPHERAL NEURONS; CILIARY GANGLION AB 1. Calcium currents and transmitter release were studied in cocultures of fetal mouse neurons from the ventral half of the spinal cord (VH neurons) and from dorsal root ganglion (DRG neurons). The effects of BayK 8644 and omega-conotoxin on calcium currents and transmitter release were compared. 2. The presence of low voltage-activated (LVA) calcium current in both VH and DRG neurons is variable. Some cells exhibit only high voltage-activated (HVA) currents, whereas others show both HVA and LVA currents. 3. BayK 8644 did not affect LVA currents but strongly augmented both steady and transient components of the HVA calcium conductance. 4. Omega-Conotoxin GVIA reduces both transient and steady components of the HVA but does not abolish either component even after 3 h of application. 5. Calcium currents that were resistant to omega-contoxin were augmented by BayK 8644. 6. Synaptic transmission between pairs of spinal cord neurons from the ventral half of the spinal cord (VH-VH connections) or between dorsal root ganglion neurons and VH neurons (DRG-VH connections) were studied with two-cell recording and stimulation techniques. 7. In approximately 70% of VH-VH connections and 50% of DRG-VH connections, BayK 8644 or its active optical isomer failed to affect transmitter output. Substantial augmentation of the remainder of the connections could be reliably produced by the dihydropyridines. Raised calcium in the extracellular medium produced augmentation of synaptic connections in all cases. BayK 8644 produced substantial, consistent augmentation of voltage-sensitive calcium channels in both VH and DRG neurons. 8. The toxin, omega-conotoxin, produced no consistent effect on excitatory or inhibitory postsynaptic potentials (EPSPs or IPSPs) elicited in VH neurons by stimulation of nearby VH neurons. VH EPSPs elicited by stimulation of nearby DRG neurons were reduced to approximately 50% of control values after 10 min of omega-conotoxin perfusion. Spontaneous and evoked synaptic activity could be recorded in VH neurons as long as 2 h after cultures were incubated in 0.5-mu-M omega-conotoxin. omega-Conotoxin produced a modest reduction in HVA currents in both VH and DRG neurons. 9. BayK 8644 did not produce consistent augmentation of transmission at the frog neuromuscular junction. omega-Conotoxin produced total blockade of transmission in this preparation. 10. We conclude that neither sustained nor inactivating high-threshold voltage-sensitive (HVA) calcium channels sensitive to BayK 8644 or omega-conotoxin such as those measured in the neuronal cell bodies are responsible for action-potential-evoked transmitter release from the majority of VH neurons. These channels may be involved in transmitter release in approximately 30% of these neurons. 11. Our results are consistent with the interpretation that transmitter release from DRG neurons is mediated by HVA calcium currents similar to those measured in the DRG cell body. 12. Calcium channel properties and disposition vary between different neurons and may be under a variety of regulatory influences within the same neuronal type. C1 NICHHD,DEV NEUROBIOL LAB,BLDG 36,RM 2A-21,BETHESDA,MD 20892. NR 48 TC 25 Z9 26 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD MAR PY 1992 VL 67 IS 3 BP 561 EP 575 PG 15 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA HK016 UT WOS:A1992HK01600006 PM 1374458 ER PT J AU MARTIN, PR RIO, D ADINOFF, B JOHNSON, JL BISSERBE, JC RAWLINGS, RR ROHRBAUGH, JW STAPLETON, JM ECKARDT, MJ AF MARTIN, PR RIO, D ADINOFF, B JOHNSON, JL BISSERBE, JC RAWLINGS, RR ROHRBAUGH, JW STAPLETON, JM ECKARDT, MJ TI REGIONAL CEREBRAL GLUCOSE-UTILIZATION IN CHRONIC ORGANIC MENTAL-DISORDERS ASSOCIATED WITH ALCOHOLISM SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; WERNICKE-KORSAKOFF SYNDROME; ALZHEIMERS-DISEASE; BRAIN-LESIONS; MEMORY; DEMENTIA; CEREBELLAR; ATROPHY; sarafotoxin > ET-3. Both ET-mediated stimulation of IP formation and [Ca2+]i increase were largely inhibited in the absence of external Ca2+ but unaffected by the depletion of external Na+ and the presence of dihydropyridine derivatives or verapamil. Inorganic Ca2+ channel blockers Cd2+, La3+, and Mn2+ at 1 mM inhibited both responses induced by ET. Cross-desensitization and nonadditivity were observed for both events among ET-related peptides tested, but not between ET and ATP. Pretreatment of cells with pertussis toxin (PTX) attenuated the PI response to ET, but had no effect on ET-elicited [Ca2+]i increase. ET-induced Ca2+ mobilization (measured in Ca2+-free medium) was only transient and was inhibited by 8-(N,N-diethylamino)octyl-3,4,5-trimethoxy-benzoate. Moreover, the intracellular Ca2+ pools mobilized by ET and ATP appeared to overlap, as indicated by their partial heterologous desensitization. Pretreatment with phorbol dibutyrate (PDBu) for 10 min reduced the PI response and Ca2+ mobilization but potentiated the [Ca2+]i increase induced by ET. In cells pretreated with PDBu for 24 hr, both responses to ET were attenuated. Our results suggest that, in C6 glioma, ET induces PI hydrolysis and causes Ca2+ influx. The former response is mediated by a PTX-sensitive G-protein, leading to intracellular Ca2+ mobilization, while the latter response results in further increase in [Ca2+]i. C1 NIMH,BIOL PSYCHIAT BRANCH,CHIEF UNIT MOLEC NEUROBIOL,BLDG 10,ROOM 3N212,BETHESDA,MD 20892. NATL TAIWAN UNIV,COLL MED,DEPT PHARMACOL,TAIPEI,TAIWAN. WALTER REED ARMY MED CTR,DEPT CLIN PHYSIOL,DIV MED,WASHINGTON,DC 20307. OI Lin, Wan Wan/0000-0002-3207-734X NR 49 TC 47 Z9 47 U1 0 U2 0 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 MAR PY 1992 VL 12 IS 3 BP 1077 EP 1085 PG 9 WC Neurosciences SC Neurosciences & Neurology GA HJ353 UT WOS:A1992HJ35300036 PM 1312133 ER PT J AU CUNNINGHAM, ET WADA, E CARTER, DB TRACEY, DE BATTEY, JF DESOUZA, EB AF CUNNINGHAM, ET WADA, E CARTER, DB TRACEY, DE BATTEY, JF DESOUZA, EB TI INSITU HISTOCHEMICAL-LOCALIZATION OF TYPE-I INTERLEUKIN-1 RECEPTOR MESSENGER-RNA IN THE CENTRAL-NERVOUS-SYSTEM, PITUITARY, AND ADRENAL-GLAND OF THE MOUSE SO JOURNAL OF NEUROSCIENCE LA English DT Article ID CORTICOTROPIN-RELEASING-FACTOR; CELL-LINE ATT-20; RAT-BRAIN; GROWTH-FACTOR; ELECTRICAL-STIMULATION; ALZHEIMER-DISEASE; GASTRIC-MOTILITY; ACID-SECRETION; ACTH-SECRETION; RAPHE NEURONS AB The cytokine interleukin-1 (IL-1) has a number of biologic activities, including pronounced effects on the nervous and neuroendocrine systems. In this study, in situ histochemical techniques were used to investigate the distribution of cells expressing type I IL-1 receptor mRNA in the CNS, pituitary, and adrenal gland of the mouse. Hybridization of S-35-labeled antisense cRNA probes derived from a murine T-cell IL-1 receptor cDNA revealed a distinct regional distribution of the type I IL-1 receptor, both in brain and in the pituitary gland. In the brain, an intense signal was observed over the granule cell layer of the dentate gyrus, over the entire midline raphe system, over the choroid plexus, and over endothelial cells of postcapillary venules throughout the neuraxis. A weak to moderate signal was observed over the pyramidal cell layer of the hilus and CA3 region of the hippocampus, over the anterodorsal thalamic nucleus, over Purkinje cells of the cerebellar cortex, and in scattered clusters over the external-most layer of the median eminence. In the pituitary gland, a dense and homogeneously distributed signal was observed over the entire anterior lobe. No autoradiographic signal above background was observed over the posterior and intermediate lobes of the pituitary, or over the adrenal gland. This study therefore provides evidence for discrete receptor substrates subserving the central effects of IL-1, thus supporting the notion that IL-1 acts as a neurotransmitter/neuromodulator in brain. It also supports studies suggesting that IL-1-mediated activation of the hypothalamic-pituitary-adrenal axis occurs primarily at the level of the brain and/or pituitary gland. C1 DUPONT MERCK PHARMACEUT CO,EXPTL STN,E400-4352,WILMINGTON,DE 19880. NIDA,NEUROBIOL LAB,BALTIMORE,MD 21224. NINCDS,NEUROCHEM LAB,BETHESDA,MD 20892. UPJOHN CO,MOLEC BIOL,KALAMAZOO,MI 49001. UPJOHN CO,HYPERSENSIT DIS RES,KALAMAZOO,MI 49001. NR 107 TC 262 Z9 265 U1 0 U2 1 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 MAR PY 1992 VL 12 IS 3 BP 1101 EP 1114 PG 14 WC Neurosciences SC Neurosciences & Neurology GA HJ353 UT WOS:A1992HJ35300039 PM 1532025 ER PT J AU SARIS, SC SPIESS, P LIEBERMAN, DM LIN, S WALBRIDGE, S OLDFIELD, EH AF SARIS, SC SPIESS, P LIEBERMAN, DM LIN, S WALBRIDGE, S OLDFIELD, EH TI TREATMENT OF MURINE PRIMARY BRAIN-TUMORS WITH SYSTEMIC INTERLEUKIN-2 AND TUMOR-INFILTRATING LYMPHOCYTES SO JOURNAL OF NEUROSURGERY LA English DT Article DE BRAIN NEOPLASM; IMMUNOTHERAPY; TUMOR-INFILTRATING LYMPHOCYTE; GLIOMA; INTERLEUKIN-2; LIVER; MOUSE ID ADOPTIVE IMMUNOTHERAPY; METASTATIC MELANOMA; CELLS; INVITRO; GLIOMA AB Methods have recently been described for the isolation and expansion of lymphocytes that have trafficked into animal and human tumors. These CD8-positive tumor-infiltrating lymphocytes (TIL's) have exceptional trafficking ability to, and efficacy against, tumor targets in extracranial sites. Prior to Phase I clinical trials for patients with gliomas, adoptive immunotherapy with TIL's was studied in a mouse model of primary brain tumors to determine if intracerebral tumors have a similar response. Glioma 261 (GL261) tumors were grown in the subcutaneous space of C57BL/6 mice. After enzymatic digestion, the cells were incubated in vitro with interleukin-2 (IL-2) until a confluent population of T lymphocytes was present. The in vitro efficacy of these TIL's was tested against fresh GL261 targets with a chromium release assay; the in vivo efficacy was tested against GL261 tumors in the liver and against irradiated and nonirradiated GL261 tumors in the brain. Mice received one of the following: intraperitoneal saline; intraperitoneal IL-2 (7500 to 50,000 U three times daily for 5 days); IL-2 plus intravenous TIL's (1 to 3 x 10(7) cells); 10 Gy cranial irradiation; irradiation plus IL-2; or irradiation plus IL-2 plus TIL's. The TIL preparation killed 77% of tumor targets in 4 hours at an effector:target ratio of 100:1. In animals with GL261 tumors in the liver, at 2 weeks there were 93 +/- 37, 128 +/- 45, and 21 +/- 14 fiver metastases in the control, IL-2, and IL-2 plus TIL groups, respectively. However, in animals with GL261 tumors in the brain, no treatment group had an increased survival rate compared to the control group. It is concluded that, although TIL and IL-2 immunotherapy can be used effectively to treat brain tumors in vitro and at sites outside the central nervous system, it is ineffective against the same type of tumor in the brain. Different methods of delivery or different combinations of these immunomodulators may be more effective; however, based on these findings, treatment of patients with IL-2 and TIL cannot be recommended until efficacy has been demonstrated in an animal model. C1 NINCDS,SURG NEUROL BRANCH,CLIN NEUROSURG SECT,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NCI,SURG ONCOL BRANCH,BETHESDA,MD 20892. TUFTS UNIV,NEW ENGLAND MED CTR,DEPT NEUROSURG,BOSTON,MA 02111. NR 17 TC 48 Z9 48 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD MAR PY 1992 VL 76 IS 3 BP 513 EP 519 DI 10.3171/jns.1992.76.3.0513 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA HF274 UT WOS:A1992HF27400019 PM 1738033 ER PT J AU PATTERSON, BH ZECH, LA AF PATTERSON, BH ZECH, LA TI DEVELOPMENT OF A MODEL FOR SELENITE METABOLISM IN HUMANS SO JOURNAL OF NUTRITION LA English DT Article; Proceedings Paper CT SYMP AT THE 75TH ANNUAL MEETING OF THE FEDERATION OF AMERICAN SOC FOR EXPERIMENTAL BIOLOGY CY APR 23, 1991 CL ATLANTA, GA SP FEDERAT AMER SOC EXPTL BIOL DE KINETICS; COMPARTMENTAL MODELING; SELENIUM; PHARMACOKINETICS ID GLUTATHIONE-PEROXIDASE; RAT AB The process of building a kinetic model for the metabolism of selenite in humans is described. Plasma, urine and fecal data from a selenium pharmacokinetics study are compared with an a priori model hypothesized before the study was conducted. The reasons for the rejection of the model are given. The iterative process of observing the fit of the model, modifying the model and testing the modification is illustrated by using as examples an intermediate model and a current working model. Several specific problems encountered in trying to fit the a priori and the intermediate model are described along with the approaches taken to resolve them. Finally, some uses of the current model are given, including checking an assumption underlying the pharmacokinetics study, making predictions about the effect of supplementation on plasma levels and developing research leads. C1 NCI,DIV CANC BIOL & DIAG,MATH BIOL LAB,BETHESDA,MD 20892. RP PATTERSON, BH (reprint author), NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,EXECUT PLAZA N,BETHESDA,MD 20892, USA. NR 6 TC 20 Z9 20 U1 0 U2 3 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD MAR PY 1992 VL 122 IS 3 SU S BP 709 EP 714 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HG411 UT WOS:A1992HG41100024 PM 1542037 ER PT J AU CHEN, JQ MCLAUGHLIN, JK ZHANG, JY STONE, BJ LUO, JM CHEN, RA DOSEMECI, M REXING, SH WU, Z HEARL, FJ MCCAWLEY, MA BLOT, WJ AF CHEN, JQ MCLAUGHLIN, JK ZHANG, JY STONE, BJ LUO, JM CHEN, RA DOSEMECI, M REXING, SH WU, Z HEARL, FJ MCCAWLEY, MA BLOT, WJ TI MORTALITY AMONG DUST-EXPOSED CHINESE MINE AND POTTERY WORKERS SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE LA English DT Article ID LUNG-CANCER; STOMACH-CANCER; SILICOSIS; COHORT; RISK; MEN AB A cohort study of approximately 68,000 persons employed during 1972 to 1974 at metal mines and pottery factories in south central China was conducted to evaluate mortality from cancer and other diseases among workers exposed to different levels of silica and other dusts. A follow-up of subjects through December 31, 1989 revealed 6,192 deaths, a number close to that expected based on Chinese national mortality rates. There was, however, a nearly 6-fold increase in deaths from pulmonary heart disease (standard mortality ratio, 581; 95% confidence interval 538 to 626), and a 48% excess of mortality from nonmaligant respiratory diseases (standard mortality ratio, 148; 95% confidence interval, 139 to 158), primarily because of a more than 30-fold excess of pneumoconiosis. Pulmonary heart disease and noncancerous respiratory disease rates rose in proportion to dust exposure. Cancer mortality overall was not increased among the miners or pottery workers. There was no increased risk of lung cancer, except among tin miners, and trends in risk of this cancer with increasing level of dust exposure were not significant. Risks of lung cancer were 22% higher among workers with than without silicosis. The findings indicate that respiratory disease continues to be an occupational hazard among Chinese miners and pottery workers, but that cancer risks are not as yet strongly associated with work in these dusty trades. C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. TONGJI MED UNIV,SCH PUBL HLTH,DEPT LABOR HLTH & OCCUPAT & OCCUPAT,WUHAN,PEOPLES R CHINA. WESTAT CORP,ROCKVILLE,MD. NIOSH,DIV RESP DIS STUDIES,MORGANTOWN,WV 26505. NR 20 TC 55 Z9 64 U1 0 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1076-2752 J9 J OCCUP ENVIRON MED JI J. Occup. Environ. Med. PD MAR PY 1992 VL 34 IS 3 BP 311 EP 316 DI 10.1097/00043764-199203000-00017 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HH544 UT WOS:A1992HH54400012 PM 1312152 ER PT J AU RILEY, C LONDON, JP BURMEISTER, JA AF RILEY, C LONDON, JP BURMEISTER, JA TI PERIODONTAL HEALTH IN 200 HIV-POSITIVE PATIENTS SO JOURNAL OF ORAL PATHOLOGY & MEDICINE LA English DT Article DE AIDS; ANUG; HIV; NUP; PERIODONTITIS ID INFECTION; CLASSIFICATION; MANIFESTATIONS; DIAGNOSIS; LESIONS AB Two hundred HIV-positive subjects were surveyed to determine their periodontal health status. Particular attention was given to the occurrence of a severe and rapidly progressing form of periodontal disease designated "HIV-associated periodontitis", which has been reported as being unique to AIDS patients. Among the subjects comprising the cohort, 85 subjects had good gingival health, 59 subjects exhibited gingivitis, 49 cases of adult periodontitis were observed, 5 subjects presented with advance adult periodontitis, and 2 cases of necrotizing ulcerative periodontitis (NUP) were found within the group. The periodontitis of the patients in this survey did not have unique or pathognomonic characteristics which could set their periodontal disease apart from the periodontal disease seen in HIV negative population. C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,SCH DENT,DEPT PERIODONT,RICHMOND,VA 23298. RP RILEY, C (reprint author), NIDR,MICROBIAL ECOL LAB,BLDG 10-1N103E,BETHESDA,MD 20892, USA. FU NIDCR NIH HHS [5F35-DE05587-02] NR 19 TC 44 Z9 46 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0904-2512 J9 J ORAL PATHOL MED JI J. Oral Pathol. Med. PD MAR PY 1992 VL 21 IS 3 BP 124 EP 127 DI 10.1111/j.1600-0714.1992.tb00995.x PG 4 WC Dentistry, Oral Surgery & Medicine; Pathology SC Dentistry, Oral Surgery & Medicine; Pathology GA HP837 UT WOS:A1992HP83700007 PM 1583595 ER PT J AU KOHN, WG GROSSMAN, E FOX, PC ARMANDO, I GOLDSTEIN, DS BAUM, BJ AF KOHN, WG GROSSMAN, E FOX, PC ARMANDO, I GOLDSTEIN, DS BAUM, BJ TI EFFECT OF IONIZING-RADIATION ON SYMPATHETIC-NERVE FUNCTION IN RAT PAROTID-GLANDS SO JOURNAL OF ORAL PATHOLOGY & MEDICINE LA English DT Article DE DOPAMINE; IONIZING RADIATION; NOREPINEPHRINE; PAROTID GLAND; SALIVA SECRETION; SYMPATHETIC INNERVATION ID X-IRRADIATION; ACINAR CELLS; SALIVARY; EXPRESSION; SECRETION; INJURY AB Ionizing radiation (IR) irreversibly damages salivary glands. The pathologic mechanism is unknown. Previously we reported that parotid serous acinar cells may not be the primary site of damage by IR. The purpose of this study was to determine if IR alters sympathetic nerve function in rat parotid glands. Male adult rats received a single dose of radiation (20 Gy) to the head and neck. Three days after IR, parotid saliva secretion induced by norepinephrine (NE) was completely blocked. Catecholamine uptake and metabolism were studied by injecting [H-3] dopamine ([H-3]DA) into irradiated rats, as a bolus. After 60 min, animals were sacrificed and the parotid gland, submandibular gland, and left ventricle removed. Tissue contents of [H-3]DA and [H-3]NE, identified by HPLC, were unaffected by IR. The results indicate that IR abolishes acinar responsiveness to NE without affecting parotid sympathetic nerve function. C1 NINCDS,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. RP KOHN, WG (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,9000 ROCKVILLE PIKE,BLDG 10,BETHESDA,MD 20892, USA. NR 24 TC 11 Z9 12 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0904-2512 J9 J ORAL PATHOL MED JI J. Oral Pathol. Med. PD MAR PY 1992 VL 21 IS 3 BP 134 EP 137 DI 10.1111/j.1600-0714.1992.tb00997.x PG 4 WC Dentistry, Oral Surgery & Medicine; Pathology SC Dentistry, Oral Surgery & Medicine; Pathology GA HP837 UT WOS:A1992HP83700009 PM 1583597 ER PT J AU BUTLER, KM DESMET, MD HUSSON, RN MUELLER, B MANJUNATH, K MONTRELLA, K LOVATO, G JAROSINSKI, P NUSSENBLATT, RB PIZZO, PA AF BUTLER, KM DESMET, MD HUSSON, RN MUELLER, B MANJUNATH, K MONTRELLA, K LOVATO, G JAROSINSKI, P NUSSENBLATT, RB PIZZO, PA TI TREATMENT OF AGGRESSIVE CYTOMEGALOVIRUS RETINITIS WITH GANCICLOVIR IN COMBINATION WITH FOSCARNET IN A CHILD INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS SO JOURNAL OF PEDIATRICS LA English DT Article ID IMMUNE-DEFICIENCY-SYNDROME; IMMUNOCOMPROMISED PATIENTS; AIDS; ZIDOVUDINE; EFFICACY; TOXICITY; THERAPY; INVITRO; DISEASE AB Ganciclovir and foscarnet are both effective for cytomegalovirus retinitis in patients with acquired immunodeficiency syndrome, but the benefits of either agent given alone are limited. A child infected with human immunodeficiency virus who had cytomegalovirus retinitis that progressed despite treatment with either agent alone received the combination of ganciclovir and foscarnet. This treatment resulted in a sustained clinical response. C1 NEI, IMMUNOL LAB, BETHESDA, MD 20892 USA. CLIN CTR ALBANY, DEPT PHARM, ALBANY, NY USA. ALBANY MED CTR, ALBANY, NY USA. RP BUTLER, KM (reprint author), NCI, PEDIAT BRANCH, CLIN ONCOL PROGRAM, BLDG 10, ROOM 13N240, BETHESDA, MD 20892 USA. OI de Smet, Marc/0000-0002-9217-5603 NR 17 TC 27 Z9 28 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD MAR PY 1992 VL 120 IS 3 BP 483 EP 486 DI 10.1016/S0022-3476(05)80926-6 PG 4 WC Pediatrics SC Pediatrics GA HG940 UT WOS:A1992HG94000030 PM 1311378 ER PT J AU MELLMAN, TA LEVERICH, GS HAUSER, P KRAMLINGER, K POST, RM UHDE, TW AF MELLMAN, TA LEVERICH, GS HAUSER, P KRAMLINGER, K POST, RM UHDE, TW TI AXIS-II PATHOLOGY IN PANIC AND AFFECTIVE-DISORDERS - RELATIONSHIP TO DIAGNOSIS, COURSE OF ILLNESS, AND TREATMENT RESPONSE SO JOURNAL OF PERSONALITY DISORDERS LA English DT Article ID DSM-III; PERSONALITY-DISORDER; MAJOR DEPRESSION AB Axis II criteria were assessed in 46 patients with panic or affective disorders (primarily bipolar type) by structured interviews utilizing the SID-P. Additional assessments were made of life course of illness, hospital course, and treatment response. The number of personality disorders did not differ between affective and panic patients and cluster III predominated in both groups. Affective patients, however, had a greater and more heterogenous loading for Axis II disorder "traits" and "features." There was a strong association of personality disorder with an early onset of illness in affective but not panic disorder patients. There was also a tendency for panic patients with personality disorders to demonstrate increased residual subsyndromal depressive symptoms following acute treatment. C1 NIMH,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS SECT,BLDG 10,BETHESDA,MD 20892. UNIV MIAMI,SCH MED,DEPT PSYCHIAT,ANXIETY DISORDERS PROGRAM,MIAMI,FL 33136. NIMH,BIOL PSYCHIAT BRANCH,PSYCHOBIOL SECT,BETHESDA,MD 20892. NR 14 TC 20 Z9 20 U1 0 U2 0 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0885-579X J9 J PERS DISORD JI J. Pers. Disord. PD SPR PY 1992 VL 6 IS 1 BP 53 EP 63 PG 11 WC Psychiatry SC Psychiatry GA HR830 UT WOS:A1992HR83000006 ER PT J AU GRANT, KA SNELL, LD ROGAWSKI, MA THURKAUF, A TABAKOFF, B AF GRANT, KA SNELL, LD ROGAWSKI, MA THURKAUF, A TABAKOFF, B TI COMPARISON OF THE EFFECTS OF THE UNCOMPETITIVE N-METHYL-D-ASPARTATE ANTAGONIST (+/-)-5-AMINOCARBONYL-10,11-DIHYDRO-5H-DIBENZO[A,D]CYCLOHEPTEN-5,10-IMIN E (ADCI) WITH ITS STRUCTURAL ANALOGS DIZOCILPINE (MK-801) AND CARBAMAZEPINE ON ETHANOL WITHDRAWAL SEIZURES SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID NMDA RECEPTOR; ALCOHOL-WITHDRAWAL; BINDING; 1-PHENYLCYCLOHEXYLAMINE; PHENCYCLIDINE; NEURONS; BLOCK; MICE AB The ability of [(+/-)-5-aminocarbonyl-10,11-dihydro-5H-di-benzo-[a,d]cyclohepten-5,10-imine (ADCI) and its structural analogs dizocilpine (MK-801) and carbamazepine to block ethanol withdrawal seizures was tested in mice made physically dependent upon ethanol. Three injections of either ADCI (ranging from 1.0-10.0 mg/kg), dizocilpine (ranging from 0.1-1.0 mg/kg) or carbamazepine (ranging from 17-50 mg/kg) were administered during the first 7 hr of ethanol withdrawal. The severity of ethanol withdrawal seizures was rated during the first 11 hr of withdrawal and again at 24 hr after withdrawal of ethanol. ADCI and dizocilpine suppressed the severity and occurrence of the withdrawal seizures in a dose-dependent fashion, whereas carbamazepine was ineffective in blocking the withdrawal seizures. The relative potencies of dizocilpine, ADCl and carbamazepine in suppressing ethanol withdrawal seizures corresponded with the relative potencies of the compounds in displacing [H-3]dizocilpine from mouse cortical membrane preparations. These findings are consistent with the suggestion that blockade of N-methyl-D-aspartate-mediated neurotransmission is an effective treatment for decreasing ethanol withdrawal seizures. ADCI also blocked the occurrence of withdrawal-associated whole body tremors, whereas dizocilpine and carbamazepine were ineffective in blocking the tremors. The doses of ADCI, dizocilpine and carbamazepine that resulted in motor incoordination on an accelerating rotarod task were determined in groups of naive mice. Dizocilpine in doses as low as 0.3 mg/kg produced a decreased ability to remain on the rotarod, whereas ADCI up to 30 mg/kg did not affect rotarod performance. The high efficacy and low motor toxicity of ADCI indicates that this compound may be therapeutically useful for treating ethanol withdrawal seizures and other aspects of the ethanol withdrawal syndrome. C1 NIAAA,RECEPTOR MECHANISMS LAB,ROCKVILLE,MD 20852. NIAAA,PHARMACOL & PHYSIOL STUDIES LAB,ROCKVILLE,MD 20852. NINCDS,NEURONAL EXCITABIL SECT,BETHESDA,MD 20892. UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80262. NEUROGEN CORP,BRANFORD,CT. RI Rogawski, Michael/B-6353-2009 OI Rogawski, Michael/0000-0002-3296-8193 NR 25 TC 78 Z9 78 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD MAR PY 1992 VL 260 IS 3 BP 1017 EP 1022 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HJ019 UT WOS:A1992HJ01900011 PM 1545374 ER PT J AU CLINE, EJ SCHEFFEL, U BOJA, JW CARROLL, FI KATZ, JL KUHAR, MJ AF CLINE, EJ SCHEFFEL, U BOJA, JW CARROLL, FI KATZ, JL KUHAR, MJ TI BEHAVIORAL-EFFECTS OF NOVEL COCAINE ANALOGS - A COMPARISON WITH INVIVO RECEPTOR-BINDING POTENCY SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID DOPAMINE UPTAKE SITES; H-3 COCAINE; RAT STRIATUM; NONHUMAN-PRIMATES; NUCLEUS ACCUMBENS; SQUIRREL-MONKEYS; LIGAND-BINDING; DRUGS; INHIBITION; NOREPINEPHRINE AB Several novel cocaine analogs, previously shown to be very potent in in vitro binding studies, have been examined for their stimulatory effects on locomotor activity and for their ability to displace [H-3]WIN 35,428 binding in vivo in mice. These compounds, like WIN 35,428, lack an ester link between the phenyl group and the tropane ring and have para-substitutions on the phenyl ring. They were much more potent than (-)-cocaine in producing increases in locomotor activity. In addition, they were more potent than (-)-cocaine in inhibiting [H-3]WIN 35,428 binding in vivo in mouse striatum. Thus, these compounds demonstrate similar high potency in behavioral tests and in receptor binding assays, both in vivo and in vitro. Results support the hypothesis of a relationship between binding at the dopamine transporter and the behavioral effects of cocaine-like drugs. Further, assuming that maximal occupancy occurs with total displacement of [H-3]WIN 35,428 binding in vivo, the data suggest that maximal locomotor effects occur with near total occupancy of transporter binding sites. C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,POB 5180,4940 EASTERN AVE,LEXINGTON,KY 40583. NIDA,ADDICT RES CTR,PRECLIN PHARMACOL BRANCH,LEXINGTON,KY 40583. JOHNS HOPKINS MED INST,DEPT RADIOL,DIV NUCL MED,BALTIMORE,MD 21205. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. OI Katz, Jonathan/0000-0002-1068-1159 FU NIDA NIH HHS [DA05477] NR 45 TC 84 Z9 84 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 MAR PY 1992 VL 260 IS 3 BP 1174 EP 1179 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HJ019 UT WOS:A1992HJ01900033 PM 1545384 ER PT J AU MELLO, NK LUKAS, SE KAMIEN, JB MENDELSON, JH DRIEZE, J CONE, EJ AF MELLO, NK LUKAS, SE KAMIEN, JB MENDELSON, JH DRIEZE, J CONE, EJ TI THE EFFECTS OF CHRONIC BUPRENORPHINE TREATMENT ON COCAINE AND FOOD SELF-ADMINISTRATION BY RHESUS-MONKEYS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID DOPAMINE ANTAGONIST; SQUIRREL-MONKEYS; FOLLICULAR PHASE; OPERANT ANALYSIS; MENSTRUAL-CYCLE; NALTREXONE; DIPRENORPHINE; PITUITARY; ABUSE; ACQUISITION AB The goal of this study was to determine if buprenorphine continues to reduce cocaine self-administration over long periods of treatment, or if tolerance develops to this effect. The effects of 30 to 120 days of buprenorphine treatment (0.32 mg/kg/day) on cocaine and food self-administration were examined in six rhesus monkeys. Saline control treatment was studied for 15 days before and after buprenorphine treatment. Intravenous cocaine (0.05 or 0.10 mg/kg) and food (1 g banana pellet) self-administration were maintained on a FR 4 (VR 16:S) schedule of reinforcement. Cocaine self-administration decreased significantly (P < .0001) and remained 60 to 97% below saline treatment baseline levels (52 +/- 2 injections/day) throughout 120 days of buprenorphine treatment (P < .01). After substitution of saline for buprenorphine, cocaine self-administration resumed and averaged between 21 (+/- 3.6) and 56 (+/- 6.5) injections per day over 20 days. Buprenorphine plasma levels averaged 18 (+/- 2.84) ng/ml (range 10.9-30 ng/ml) during buprenorphine treatment. Buprenorphine plasma levels usually decreased by 50% or more within 27 hr after the last buprenorphine dose. Low levels of buprenorphine (0.10-0.19 ng/ml) were measured for 30 to 74 days after abrupt termination of daily buprenorphine treatment. Food self-administration was initially reduced (P < .01-.05), but tolerance to buprenorphine's suppression of food-maintained responding developed over 30 to 70 days of treatment. Food self-administration returned to and significantly exceeded (P < .05-.01) saline treatment base-line levels, whereas cocaine self-administration remained significantly suppressed. We conclude that daily buprenorphine administration selectively reduced cocaine self-administration, and this effect persisted for as long as 120 days. These data confirm and extend our previous reports that 15 days of buprenorphine treatment (0.237-0.70 mg/kg/day) selectively reduced cocaine self-administration by rhesus monkeys. C1 NIDA,ADDICT RES CTR,CHEM & METAB LAB,LEXINGTON,KY 40583. RP MELLO, NK (reprint author), HARVARD UNIV,MCLEAN HOSP,SCH MED,ALCOHOL & DRUG ABUSE RES CTR,115 MILL ST,BELMONT,MA 02178, USA. FU NIDA NIH HHS [DA 00101, DA 02519, DA 04059] NR 52 TC 71 Z9 71 U1 1 U2 6 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 MAR PY 1992 VL 260 IS 3 BP 1185 EP 1193 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HJ019 UT WOS:A1992HJ01900035 PM 1545386 ER PT J AU ROBERTS, MW FOLIO, J MOFFA, JP GUCKES, AD AF ROBERTS, MW FOLIO, J MOFFA, JP GUCKES, AD TI CLINICAL-EVALUATION OF A COMPOSITE RESIN SYSTEM WITH A DENTIN BONDING AGENT FOR RESTORATION OF PERMANENT POSTERIOR TEETH - A 3-YEAR STUDY SO JOURNAL OF PROSTHETIC DENTISTRY LA English DT Article AB This study evaluated the clinical performance of a visible light-cured small particle bimodally filled hybrid condensable composite resin system that included a dentin bonding agent compared with an amalgam alloy in class II restorations of permanent teeth. A total of 108 restorations were placed in 34 patients. Fifty-three composite resin and 55 amalgam restorations were inserted. Each restoration was evaluated immediately after placement and then on an annual basis for a 3-year period using the Public Health Service (PHS) criteria. In addition, the Moffa-Lugassy scale was used to measure the loss of material on the occlusal surface of these materials. One hundred percent of the resin and amalgam restorations were evaluated, measured, and reasons for replacement were recorded over the 3-year period. There was no significant difference (p > 0.05) in the clinical performance of the composite resin and the amalgam when evaluated by the PHS criteria. Analyses of wear at each of the three annual recall periods did not reveal any significant difference (p > 0.05) between the two restorative materials when measured by the Moffa-Lugassy scale. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT RESTORAT DENT,SAN FRANCISCO,CA 94143. RP ROBERTS, MW (reprint author), UNIV N CAROLINA,SCH DENT,CB 7450,DEPT PEDIAT DENT,CHAPEL HILL,NC 27599, USA. FU NIDCR NIH HHS [2Y01-DE-4001-04] NR 8 TC 13 Z9 14 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-3913 J9 J PROSTHET DENT JI J. Prosthet. Dent. PD MAR PY 1992 VL 67 IS 3 BP 301 EP 306 DI 10.1016/0022-3913(92)90234-2 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HF661 UT WOS:A1992HF66100004 PM 1507089 ER PT J AU SELWITZ, RH COLLEY, BJ ROZIER, RG AF SELWITZ, RH COLLEY, BJ ROZIER, RG TI FACTORS ASSOCIATED WITH PARENTAL ACCEPTANCE OF DENTAL SEALANTS SO JOURNAL OF PUBLIC HEALTH DENTISTRY LA English DT Article DE PIT AND FISSURE SEALANTS; PREVENTIVE DENTISTRY; ORAL HEALTH ATTITUDES, BELIEFS, AND KNOWLEDGE ID KNOWLEDGE; PATTERNS; USAGE; CARE AB Whereas a number of surveys have documented oral disease preventive behaviors and associated factors, little is known about public knowledge and beliefs about dental sealants. In this study, factors associated with the presence of sealants were studied in first and second graders residing in Columbia, SC. From a sample of 1, 119 children, 88 were found clinically to have sealants; 508 did not have, but needed them. Parents of the sealant children (n = 87) and of a random sample of the no-sealant children (n = 289) were interviewed by telephone to obtain information regarding (1) factors related to parents' inclination to obtain sealants for their children, (2) ability of the family to obtain oral disease preventive services, and (3) the influence of others in the family's decision-making efforts. Analysis of 16 factors thought to be related to sealant presence revealed that parents were more likely to obtain dental sealants for their children if dentists or their staffs recommended them, if the parents were knowledgeable about dental sealants, if the parents were more highly educated, and if the parents had dental insurance coverage. Parents were less likely to obtain dental sealants for their children if they heard about them from mass media. The latter finding is unexpected and may have been influenced by conflicting or negative opinion expresses by some dental practitioners through mass media or other channels of communication. The results of this study suggest that efforts to enhance the utilization of dental sealants should include strategies to (1) encourage dentists to promote them with their parents and the public, (2) educate potential consumers about the benefits of dental sealants, and (3) promote greater insurance coverage for oral health care, including sealants. C1 S CAROLINA DEPT HLTH & ENVIRONM CONTROL,OFF VITAL RECORDS & PUBL HLTH STAT,COLUMBIA,SC 29201. UNIV N CAROLINA,SCH PUBL HLTH,CHAPEL HILL,NC 27514. RP SELWITZ, RH (reprint author), NIDR,EPIDEMIOL & ORAL DIS PREVENT PROGRAM,WESTWOOD BLDG,ROOM 538,5333 WESTBARD AVE,BETHESDA,MD 20816, USA. NR 38 TC 12 Z9 12 U1 0 U2 0 PU AAPHD NATIONAL OFFICE PI RICHMOND PA J PUBLIC HEALTH DENT 10619 JOUSTING LANE, RICHMOND, VA 23235 SN 0022-4006 J9 J PUBLIC HEALTH DENT JI J. Public Health Dent. PD SPR PY 1992 VL 52 IS 3 BP 137 EP 145 DI 10.1111/j.1752-7325.1992.tb02259.x PG 9 WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health GA HT844 UT WOS:A1992HT84400002 PM 1593521 ER PT J AU STOJILKOVIC, SS TORSELLO, A IIDA, T ROJAS, E CATT, KJ AF STOJILKOVIC, SS TORSELLO, A IIDA, T ROJAS, E CATT, KJ TI CALCIUM SIGNALING AND SECRETORY RESPONSES IN AGONIST-STIMULATED PITUITARY GONADOTROPHS SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article; Proceedings Paper CT 10TH INTERNATIONAL SYMP OF THE JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY : RECENT ADVANCES IN STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY CY MAY 26-29, 1991 CL PARIS, FRANCE SP J STEROID BIOCHEM & MOLEC BIOL ID RAT ANTERIOR-PITUITARY; PROTEIN KINASE-C; PROLACTIN SECRETION; HORMONE; CELLS; MOBILIZATION; CHANNELS; DESENSITIZATION; INHIBITION; CURRENTS AB In cultured pituitary gonadotrophs, gonadotropin-releasing hormone (GnRH) caused dose-dependent and biphasic increases in cytoplasmic calcium concentration ([Ca2+]i) and LH release. Both extra- and intracellular calcium pools participate in GnRH-induced elevation of [Ca2+]i and LH secretion. The spike phase of the [Ca2+]i response represents the primary signal derived predominantly from the rapid mobilization of intracellular Ca2+. In contrast, the prolonged phase of the Ca2+ signal depends exclusively on Ca2+ entry from the extracellular pool. The influx of Ca2+ occurs partially through dihydropyridine-sensitive calcium channels. Both [Ca2+]i and LH responses to increasing concentrations of GnRH occur over very similar time scales, suggesting that increasing degrees of receptor occupancy are transduced into amplitude-modulated Ca2+ responses, which in turn activate exocytosis in a linear manner. However, several lines of evidence indicated the complexity over the relationship between Ca2+ signaling and LH exocytosis. In contrast to [Ca2+]i measurements in cell suspension, single cell Ca2+ measurements revealed the existence of a more complicated pattern of Ca2+ response to GnRH, with a biphasic response to high agonist doses and prominent oscillatory responses to lower GnRH concentrations, with a log-linear correlation between GnRH dose and the frequency of Ca2+ spiking. In addition, analysis of the magnitudes of the [Ca2+]i and LH responses of gonadotrophs to a wide range of GnRH concentrations in the presence and absence of extracellular Ca2+, and to K+ and phorbol ester stimulation, showed non-linearity between these parameters with amplification of [Ca2+]i-mediated exocytosis. Studies on cell depleted of protein kinase C under conditions that did not change the LH pool suggested the participation of protein kinase C in this amplification, especially during the plateau phase of the secretory response to GnRH. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. NR 40 TC 35 Z9 35 U1 0 U2 1 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 MAR PY 1992 VL 41 IS 3-8 BP 453 EP 467 DI 10.1016/0960-0760(92)90371-O PG 15 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA HN847 UT WOS:A1992HN84700028 PM 1373299 ER PT J AU HIGUCHI, S MURAMATSU, T SHIGEMORI, K SAITO, M KONO, H DUFOUR, MC HARFORD, TC AF HIGUCHI, S MURAMATSU, T SHIGEMORI, K SAITO, M KONO, H DUFOUR, MC HARFORD, TC TI THE RELATIONSHIP BETWEEN LOW KM ALDEHYDE DEHYDROGENASE PHENOTYPE AND DRINKING BEHAVIOR IN JAPANESE SO JOURNAL OF STUDIES ON ALCOHOL LA English DT Article ID ALCOHOL SENSITIVITY; ETHNIC-DIFFERENCES; HAIR ROOTS; DEFICIENCY; ISOZYME; ALLELE AB The relationship between the low Km aldehyde dehydrogenase (ALDH2) phenotype determined by the isoelectric focusing of hair root lysates, facial flushing and alcohol drinking patterns in Japanese (N = 282) was examined. Men who had inactive ALDH2 drank significantly less alcohol than those with active ALDH2. Although the effect was less noticeable, a similar relationship was detected in women. Two types of flushing responses were determined: one due to the inactive ALDH2, the other unrelated to this variant form of the isozyme. A striking difference between these flushing types, in terms of the inhibitory influence over drinking patterns, was noted. Nearly 86% of the subjects who reported always flushing in the face were shown to have inactive ALDH2, whereas, infrequent flushing and absence of flushing were associated with active ALDH2. Thus, facial flushing may be used as an indicator of ALDH2 phenotype. C1 NIAAA,DIV BIOMETRY & EPIDEMIOL,ROCKVILLE,MD 20852. RP HIGUCHI, S (reprint author), KURIHAMA NATL HOSP,NATL INST ALCOHOLISM,2769 NOBI,YOKOSUKA,KANAGAWA 239,JAPAN. NR 31 TC 72 Z9 78 U1 0 U2 1 PU ALCOHOL RES DOCUMENTATION INC CENT ALCOHOL STUD RUTGERS UNIV PI PISCATAWAY PA PO BOX 969, PISCATAWAY, NJ 08855-0969 SN 0096-882X J9 J STUD ALCOHOL JI J. Stud. Alcohol PD MAR PY 1992 VL 53 IS 2 BP 170 EP 175 PG 6 WC Substance Abuse; Psychology SC Substance Abuse; Psychology GA HF156 UT WOS:A1992HF15600008 PM 1560668 ER PT J AU PANZA, JA QUYYUMI, AA DIODATI, JG CALLAHAN, TS BONOW, RO EPSTEIN, SE AF PANZA, JA QUYYUMI, AA DIODATI, JG CALLAHAN, TS BONOW, RO EPSTEIN, SE TI LONG-TERM VARIATION IN MYOCARDIAL-ISCHEMIA DURING DAILY LIFE IN PATIENTS WITH STABLE CORONARY-ARTERY DISEASE - ITS RELATION TO CHANGES IN THE ISCHEMIC THRESHOLD SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID MILDLY SYMPTOMATIC PATIENTS; LEFT-VENTRICULAR FUNCTION; CIRCADIAN VARIATION; ANGINA-PECTORIS; HEART-DISEASE; EXERCISE; ANGIOPLASTY; RISK; ATHEROSCLEROSIS; ARTERIOGRAPHY AB Long-term variation in the frequency of myocardial ischemia during daily activity in patients with coronary artery disease who do not experience symptomatic changes has not been documented. Because at one point in time, the magnitude of such ischemia is strongly related to the ischemic threshold measured during exercise testing, this study was undertaken to determine whether patients with stable coronary artery disease show long-term variations in the frequency and duration of myocardial ischemia and to establish whether such variability is related to parallel changes in the ischemic threshold during exercise testing. Forty consecutive patients (mean age 61 +/- 8 years) who showed a stable clinical course over greater-than-or-equal-to 12 months were studied with a repeat exercise treadmill test and ambulatory electrocardiographic (ECG) monitoring after withdrawal of antianginal medications. The ischemic threshold was determined as the exercise time at 1 mm of ST segment depression. The mean interval to both follow-up evaluations was 15 +/- 3 months. Among the 23 patients with myocardial ischemia on ambulatory ECG monitoring at initial evaluation, the number and duration of ischemic episodes at follow-up were increased in 5 patients (mean increase 3.6 +/- 2 episodes and 123 +/- 98 min), unchanged in 1 patient and decreased in 17 patients (mean decrease 2.6 +/- 2 episodes and 98 +/- 72 min). Of the 17 patients without ischemic episodes at initial evaluation, 3 had evidence of ischemia on follow-up ambulatory ECG monitoring. During follow-up exercise testing, the exercise ischemic threshold decreased significantly (from 12.5 +/- 6 to 8 +/- 4 min; p < 0.001) in those patients in whom the frequency (and duration) of myocardial ischemia on ambulatory monitoring increased. Conversely, the ischemic threshold significantly increased (from 8 +/- 5 to 10.2 +/- 5 min; p < 0.001) in those patients in whom the number (and duration) of ischemic episodes decreased during follow-up. The variations in the frequency of myocardial ischemia during follow-up ambulatory monitoring signficantly correlated with the changes in exercise ischemic threshold (r = -0.62; p < 0.001). These findings indicate that patients with coronary artery disease may show long-term variations in myocardial ischemia during daily activity, even without simultaneous symptomatic changes. The occurrence and magnitude of this variation are closely related to parallel changes in the exercise ischemic threshold. These findings may have important implications for the understanding of the mechanisms and prevalence of ischemia during daily activity and the longitudinal evaluation of patients with stable coronary artery disease. RP PANZA, JA (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 36 TC 10 Z9 10 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1992 VL 19 IS 3 BP 500 EP 506 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HF970 UT WOS:A1992HF97000004 PM 1538000 ER PT J AU BONOW, RO AF BONOW, RO TI DETERMINANTS OF EXERCISE CAPACITY IN HYPERTROPHIC CARDIOMYOPATHY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Editorial Material ID LEFT-VENTRICULAR HYPERTROPHY; PATHO-PHYSIOLOGY; DOPPLER ECHOCARDIOGRAPHY; CLINICAL MANIFESTATIONS; PRESSURE-GRADIENT; VERAPAMIL; INTERRELATIONS; ABNORMALITIES; MECHANISMS; RELAXATION RP BONOW, RO (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 24 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1992 VL 19 IS 3 BP 513 EP 515 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HF970 UT WOS:A1992HF97000006 PM 1538002 ER PT J AU MARON, BJ AF MARON, BJ TI NEW OBSERVATIONS ON THE INTERRELATION OF DYNAMIC SUBAORTIC OBSTRUCTION AND EXERCISE IN HYPERTROPHIC CARDIOMYOPATHY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Editorial Material ID SUB-AORTIC STENOSIS RP MARON, BJ (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B15,BETHESDA,MD 20892, USA. NR 18 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1992 VL 19 IS 3 BP 534 EP 535 PG 2 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HF970 UT WOS:A1992HF97000010 PM 1538005 ER PT J AU KAYE, JA DECARLI, C LUXENBERG, JS RAPOPORT, SI AF KAYE, JA DECARLI, C LUXENBERG, JS RAPOPORT, SI TI THE SIGNIFICANCE OF AGE-RELATED ENLARGEMENT OF THE CEREBRAL-VENTRICLES IN HEALTHY-MEN AND WOMEN MEASURED BY QUANTITATIVE COMPUTED X-RAY TOMOGRAPHY SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID ALZHEIMER TYPE; SEX-DIFFERENCES; BRAIN ATROPHY; DEMENTIA; VOLUME AB Objective: (1) To establish the range of cerebral atrophy across the adult age spectrum in optimally healthy, rigorously evaluated individuals. (2) To determine, across the age spectrum, the relation of gender and cerebral atrophy (as measured by ventricular enlargement) to cognitive function. Design: Cross-sectional comparison by age and gender. Setting: Ambulatory research unit. Participants: Sixty-four healthy men (mean age +/- SD = 49 +/- 18 yr) and 43 healthy women (51 +/- 18 yr) volunteers enrolled in a longitudinal study of healthy aging. The population was selected for optimal health; all were rigorously screened to exclude medical and psychiatric illness. Main Outcome Measures: Brain atrophy by CT scan and cognitive function by standardized neuropsychological testing. Results: After correction for inter-subject variability in cranial volume, women had smaller lateral, but not third, ventricles. For both genders, there were significant differences with age in ventricular volume. After an approximately constant 20% increase in ventricular volume per decade in both genders, a precipitous increase in volume was found beginning in the fifth decade in men and in the sixth decade in women. In men and women, there was a significant negative correlation between ventricular volume and the sum of performance scale scores on the Wechsler Adult Intelligence Scale (WPSS) but not in the sum of the verbal scale scores (WVSS). However, after controlling for age, ventricular volume no longer significantly contributed to the relation between age and WPSS. Conclusions: In unequivocally healthy individuals, gender plays an important role in age-associated central cerebral atrophy as measured by progressive ventricular enlargement. Increase in ventricle volume independent of age, does not explain normal age-related declines seen in WPSS scores. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. RI DeCarli, Charles/B-5541-2009; OI Kaye, Jeffrey/0000-0002-9971-3478 NR 23 TC 67 Z9 67 U1 1 U2 2 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 MAR PY 1992 VL 40 IS 3 BP 225 EP 231 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA HG945 UT WOS:A1992HG94500006 PM 1538040 ER PT J AU WHITNEY, RA AF WHITNEY, RA TI RESEARCH-AND-DEVELOPMENT TO ENHANCE LABORATORY-ANIMAL WELFARE SO JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION LA English DT Article; Proceedings Paper CT ANIMAL WELFARE FORUM : THE VETERINARIANS ROLE IN THE WELFARE OF WILDLIFE CY NOV 07, 1991 CL CHICAGO, IL SP AMER VET MED ASSOC C1 NIH,OFF ANIM CARE & USE,BETHESDA,MD 20892. RP WHITNEY, RA (reprint author), NIH,NATL CTR RES RESOURCES,BETHESDA,MD 20892, USA. NR 9 TC 2 Z9 2 U1 0 U2 2 PU AMER VETERINARY MEDICAL ASSOC PI SCHAUMBURG PA 1931 N MEACHAM RD SUITE 100, SCHAUMBURG, IL 60173-4360 SN 0003-1488 J9 J AM VET MED ASSOC JI J. Am. Vet. Med. Assoc. PD MAR 1 PY 1992 VL 200 IS 5 BP 663 EP 666 PG 4 WC Veterinary Sciences SC Veterinary Sciences GA HF684 UT WOS:A1992HF68400018 PM 1568907 ER PT J AU LUNDGREN, R HEIM, S MANDAHL, N ANDERSON, H MITELMAN, F SANDBERG, AA LINEHAN, WM AF LUNDGREN, R HEIM, S MANDAHL, N ANDERSON, H MITELMAN, F SANDBERG, AA LINEHAN, WM TI CHROMOSOME-ABNORMALITIES ARE ASSOCIATED WITH UNFAVORABLE OUTCOME IN PROSTATIC-CANCER PATIENTS SO JOURNAL OF UROLOGY LA English DT Article DE PROSTATIC NEOPLASMS; CYTOGENETICS; CHROMOSOME ABERRATIONS ID PROGNOSTIC FACTORS; CLINICAL-SIGNIFICANCE; CYTOGENETIC ANALYSIS; CARCINOMA; KARYOTYPE; LEUKEMIA; GRADE; GENE AB Potential clinico-cytogenetic correlations were assessed in 57 patients with prostatic cancer in whom cytogenetic analysis of the primary tumor had been successful. Clonal karyotypic abnormalities were found in 15 tumors, 18 had normal karyotypes with nonclonal structural abnormalities and 24 had normal karyotypes only. The study began in January 1987 and all patients were monitored regularly until death or through September 1990 (median followup from diagnosis 2.6 years and from surgery 1.3 years). Survival curves were estimated by the Kaplan-Meier method, and the log rank test was used in univariate analyses of possible prognostic factors. The patients with clonal karyotypic abnormalities had shorter survival times (1.3 years) than those with normal karyotypes (greater than 3 years). The difference in survival after surgery was statistically significant (p < 0.05) when all causes of death and when death from prostatic cancer alone were considered. The Cox proportional hazards regression model was used to evaluate the additional prognostic information of chromosomal changes in excess of that attributable to other well known prognostic factors, such as tumor stage and differentiation, acid and alkaline phosphatases, and performance status. In this analysis there also was a tendency for patients with clonal chromosome aberrations to have an unfavorable outcome but the association was not significant (p = 0.13), possibly due to the rather small number of patients and short followup. Thus, our study suggests that the presence of clonal karyotypic changes in the tumor cells is associated with an unfavorable outcome in prostatic cancer patients. C1 CANC CTR,SCOTTSDALE,AZ. NCI,SURG BRANCH,UROL ONCOL SECT,BETHESDA,MD 20892. UNIV LUND HOSP,SO SWEDISH REG TUMOUR REGISTRY,DEPT CLIN GENET,S-22185 LUND,SWEDEN. ODENSE UNIV,DEPT MED GENET,DK-5230 ODENSE,DENMARK. RP LUNDGREN, R (reprint author), UNIV LUND HOSP,DEPT UROL,S-22185 LUND,SWEDEN. NR 30 TC 30 Z9 30 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 MAR PY 1992 VL 147 IS 3 BP 784 EP 788 PN 2 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA HF976 UT WOS:A1992HF97600002 PM 1538480 ER PT J AU LINEHAN, WM AF LINEHAN, WM TI MOLECULAR-GENETICS OF TUMOR SUPPRESSOR GENES IN PROSTATE CARCINOMA - THE CHALLENGE AND THE PROMISE AHEAD SO JOURNAL OF UROLOGY LA English DT Editorial Material ID RENAL-CELL CARCINOMA; RETINOBLASTOMA GENE; WILMS TUMOR; LUNG-CANCER; SHORT ARM; MUTATION; CHROMOSOME-3; EXPRESSION; TUMORIGENICITY; ABNORMALITIES RP LINEHAN, WM (reprint author), NCI,SURG BRANCH,UROL ONCOL SECT,BETHESDA,MD 20892, USA. NR 34 TC 8 Z9 8 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 MAR PY 1992 VL 147 IS 3 BP 808 EP 809 PN 2 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA HF976 UT WOS:A1992HF97600007 PM 1538482 ER PT J AU LINDHOLM, PF REID, RL BRADY, JN AF LINDHOLM, PF REID, RL BRADY, JN TI EXTRACELLULAR TAX1 PROTEIN STIMULATES TUMOR NECROSIS FACTOR-BETA AND IMMUNOGLOBULIN-KAPPA LIGHT CHAIN EXPRESSION IN LYMPHOID-CELLS SO JOURNAL OF VIROLOGY LA English DT Article ID VIRUS TYPE-I; B TRANSCRIPTION FACTOR; ENHANCER-BINDING-PROTEIN; RECEPTOR-ALPHA-GENE; HTLV-I; 65-KD SUBUNIT; T-CELLS; ACTIVATION; LEUKEMIA; INTERLEUKIN-2 AB The human T-cell leukemia virus type I tax1 gene product is responsible for the increased expression of several cytokine and cellular genes that contain NF-kappa-B regulatory sequences. Our laboratory has previously demonstrated that purified, extracellular Tax1 protein induced the nuclear accumulation of NF-kappa-B binding activity in lymphoid cells. Since HTLV-I infection causes increased levels of lymphotoxin tumor necrosis factor-beta [TNF-beta] and immunoglobulin secretion, we have studied the interaction of NF-kappa-B proteins from Tax1-stimulated cells with the TNF-beta and immunoglobulin kappa (Ig-kappa) light chain genes. Tax1 induction of NF-kappa-B occurred in the presence of cycloheximide, and Tax1 stimulation did not result in increased levels of NF-kappa-B or c-rel RNA. These results indicate that new synthesis of NF-kappa-B proteins was not required for induction of NF-kappa-B-binding activity. With use of the Ig-kappa NF-kappa-B-binding site as a probe, two distinct NF-kappa-B gel shift complexes were induced by the Tax1 protein. A slower-migrating complex, C1, was inhibited by the addition of purified I-kappa-B. In contrast, the faster-migrating C2 complex was not inhibited by I-kappa-B, but C2 was increased by detergent treatment of cytoplasmic extracts, suggesting that its binding activity was also regulated by an inhibitor. The Tax1-stimulated proteins that interacted with the NF-kappa-B-binding sites in the Ig-kappa and TNF-beta promoters were distinct. A 75-kDa protein preferentially associated with the Ig-kappa NF-kappa-B-binding site. In contrast, a 59-kDa protein associated with the TNF-beta NF-kappa-B-binding site. Tax1 stimulation led to increased levels of TNF-beta and Ig-kappa mRNA, as measured by reverse transcription and polymerase chain reaction analysis. These results represent the first experimental evidence that extracellular Tax1 can regulate the expression of endogenous cellular genes. C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NCI,CTR MED,BETHESDA,MD 20892. NR 52 TC 85 Z9 85 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1992 VL 66 IS 3 BP 1294 EP 1302 PG 9 WC Virology SC Virology GA HD265 UT WOS:A1992HD26500002 PM 1738191 ER PT J AU TREMBLAY, PJ KOZAK, CA JOLICOEUR, P AF TREMBLAY, PJ KOZAK, CA JOLICOEUR, P TI IDENTIFICATION OF A NOVEL GENE, VIN-1, IN MURINE LEUKEMIA VIRUS-INDUCED T-CELL LEUKEMIAS BY PROVIRUS INSERTIONAL MUTAGENESIS SO JOURNAL OF VIROLOGY LA English DT Article ID INTEGRATION SITE; C57BL-KA MICE; RAT THYMOMAS; C-MYC; MOUSE; DNA; LYMPHOMAS; COMMON; HYBRIDIZATION; CHROMOSOME AB The BL/VL3 radiation leukemia virus is a nondefective retrovirus which induces clonal or oligoclonal T-cell leukemia in mice. To study the role of provirus insertional mutagenesis in the development of these neoplasias, we searched for common provirus integration sites in BL/VL3 radiation leukemia virus-induced tumors. Using cellular sequences flanking a provirus cloned from one of these thymomas, we found that the viral genome was integrated into a common region, designated Vin-1, in a low percentage (5%) of these tumors. The proviruses found in this locus were integrated in the same orientation, close to a CpG-rich island, at proximity of a transcriptional unit encoding a 6-kb RNA. Vin-1 RNA was detected in several organs of the adult mouse. Vin-1 RNA levels were high in tumors having a provirus inserted within the Vin-1 region but were also high in some other tumors whose Vin-1 region was not found to be rearranged. Vin-1 was found to be well conserved among mammalian species and was mapped to mouse chromosome 6, between raf and K-ras-2. Vin-1 appears to be a novel gene which may be involved in tumor development. C1 INST RECH CLIN MONTREAL,MOLEC BIOL LAB,MONTREAL H2W 1R7,QUEBEC,CANADA. UNIV MONTREAL,DEPT MICROBIOL & IMMUNOL,MONTREAL H3C 3J7,QUEBEC,CANADA. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 36 TC 35 Z9 35 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1992 VL 66 IS 3 BP 1344 EP 1353 PG 10 WC Virology SC Virology GA HD265 UT WOS:A1992HD26500008 PM 1738193 ER PT J AU DROPULIC, B LIN, NH MARTIN, MA JEANG, KT AF DROPULIC, B LIN, NH MARTIN, MA JEANG, KT TI FUNCTIONAL-CHARACTERIZATION OF A U5 RIBOZYME - INTRACELLULAR SUPPRESSION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 EXPRESSION SO JOURNAL OF VIROLOGY LA English DT Article ID PACKAGING CELL-LINE; SELF-CLEAVAGE; REVERSE-TRANSCRIPTASE; ANTISENSE OLIGODEOXYNUCLEOTIDES; MESSENGER-RNA; GENE-TRANSFER; DNA; REPLICATION; INHIBITION; INFECTIVITY AB We have designed a ribozyme that cleaves human immunodeficiency virus type 1 (HIV-1) RNA in U5 (at nucleotide +115). This ribozyme was tested in vitro and was found to give efficient and specific digestion of RNA containing the HIV-1 U5 sequence. When the U5 ribozyme was placed into the HIV-1 genome, virus replication was suppressed in tissue culture. Introduction of this ribozyme into cells by using an amphotropic retrovirus vector significantly reduced expression of U5-containing RNA in cells chronically infected with HIV-1. Naive T cells were cocultivated with packaging cells that produce defective amphotropic retroviruses containing the U5 ribozyme. These lymphocytes were found to be partially protected from HIV-1 infection. C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RI Jeang, Kuan-Teh/A-2424-2008 FU NIAID NIH HHS [K08 AI081545] NR 37 TC 120 Z9 121 U1 2 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1992 VL 66 IS 3 BP 1432 EP 1441 PG 10 WC Virology SC Virology GA HD265 UT WOS:A1992HD26500019 PM 1738200 ER PT J AU CAHOUR, A FALGOUT, B LAI, CJ AF CAHOUR, A FALGOUT, B LAI, CJ TI CLEAVAGE OF THE DENGUE VIRUS POLYPROTEIN AT THE NS3/NS4A AND NS4B/NS5 JUNCTIONS IS MEDIATED BY VIRAL PROTEASE NS2B-NS3, WHEREAS NS4A/NS4B MAY BE PROCESSED BY A CELLULAR PROTEASE SO JOURNAL OF VIROLOGY LA English DT Article ID YELLOW-FEVER VIRUS; BORNE ENCEPHALITIS-VIRUS; AMINO-ACID SEQUENCES; COMPLETE NUCLEOTIDE-SEQUENCE; NON-STRUCTURAL PROTEINS; GUINEA-C-STRAIN; NONSTRUCTURAL PROTEINS; TERMINAL SEQUENCES; FLAVIVIRUS KUNJIN; VACCINIA VIRUS AB The cleavage mechanism utilized for processing of the NS3-NS4A-NS4B-NS5 domain of the dengue virus polyprotein was studied by using the vaccinia virus expression system. Recombinant vaccinia viruses vNS2B-NS3-NS4A-NS4B-NS5, vNS3-NS4A-NS4B-NS5, vNS4A-NS4B-NS5, and vNS4B-NS5 were constructed. These recombinants were used to infect cells, and the labeled lysates were analyzed by immunoprecipitation. Recombinant vNS2B-NS3-NS4A-NS4B-NS5 expressed the authentic NS3 and NS5 proteins, but the other recombinants produced uncleaved polyproteins. These findings indicate that NS2B is required for processing of the downstream nonstructural proteins, including the NS3/NS4A and NS4B/NS5 junctions, both of which contain a dibasic amino acid sequence preceding the cleavage site. The flavivirus NS4A/NS4B cleavage site follows a long hydrophobic sequence. The polyprotein NS4A-NS4B-NS5 was cleaved at the NS4A/NS4B junction in the absence of other dengue virus functions. One interpretation for this finding is that NS4A/NS4B cleavage is mediated by a host protease, presumably a signal peptidase. Although vNS3-NS4A-NS4B-NS5 expressed only the polyprotein, earlier results demonstrated that cleavage at the NS4A/NS4B junction occurred when an analogous recombinant, vNS3-NS4A-84% NS4B, was expressed. Thus, it appears that uncleaved NS3 plus NS5 inhibit NS4A/NS4B cleavage presumably because the putative signal sequence is not accessible for recognition by the responsible protease. Finally, recombinants that expressed an uncleaved NS4B-NS5 polyprotein, such as vNS4A-NS4B-NS5 or vNS4B-NS5, produced NS5 when complemented with vNS2B-30% NS3 or with vNS2B plus v30% NS3. These results indicate that cleavage at the NS4B/NS5 junction can be mediated by NS2B and NS3 in trans. C1 NIAID,INFECT DIS LAB,MOLEC VIRAL BIOL SECT,BETHESDA,MD 20892. NR 52 TC 94 Z9 96 U1 2 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1992 VL 66 IS 3 BP 1535 EP 1542 PG 8 WC Virology SC Virology GA HD265 UT WOS:A1992HD26500031 PM 1531368 ER PT J AU GENG, YQ CHANDRAN, B JOSEPHS, SF WOOD, C AF GENG, YQ CHANDRAN, B JOSEPHS, SF WOOD, C TI IDENTIFICATION AND CHARACTERIZATION OF A HUMAN HERPESVIRUS-6 GENE SEGMENT THAT TRANSACTIVATES THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PROMOTER SO JOURNAL OF VIROLOGY LA English DT Article ID LONG TERMINAL REPEAT; CHLORAMPHENICOL ACETYLTRANSFERASE; CD4+ LYMPHOCYTES; X-PROTEIN; T-CELLS; EXPRESSION; HIV-1; REPLICATION; INFECTION; TRANSCRIPTION AB Human herpesvirus 6 (HHV-6) is a lymphotropic herpesvirus, and in vitro, HHV-6 can productively infect many of the same cell types as can human immunodeficiency virus (HIV). Coinfection by both viruses in vitro can lead to both activation of the HIV promoter and acceleration of cytopathic effects. We have previously demonstrated that a large, 22.25-kb cloned HHV-6 fragment, pZVB70, can trans activate HIV promoter expression in vitro. In this study, we show that the pZVB70 fragment can trans activate the HIV promoter in human T-cell lines as well as in the monkey kidney cell line CV-1. The pZVB70 insert was digested with various restriction enzymes, and individual fragments were transfected into cells to test for their ability to trans activate the HIV promoter. By this method, we have identified a 1.8-kb subfragment, B701, that is involved in trans activation. Sequence analyses show that B701 potentially encodes a 143-amino-acid protein. This protein shares no homology with other herpesvirus proteins, such as ICP0 and ICP4, that have been shown to trans activate the HIV promoter. However, it shows weak sequence homology with the gene products encoded by the cytomegalovirus early US22 gene family, suggesting that the putative B701 protein may be an HHV-6 early regulatory protein. The 143-amino-acid coding sequence of B701 was cloned by polymerase chain reaction, and transfection of this construct into cells activated HIV promoter expression. The target site on the HIV promoter for the putative B701 protein is mapped to the NF-kappa-B binding site. Our results suggest that the putative B701 protein may function by directly binding to the NF-kappa-B site or may involve cellular factors, such as NF-kappa-B, either directly or indirectly. C1 UNIV KANSAS,DEPT MICROBIOL,LAWRENCE,KS 66045. UNIV KANSAS,MED CTR,DEPT MICROBIOL MOLEC GENET & IMMUNOL,KANSAS CITY,KS 66103. NCI,BETHESDA,MD 20892. FU NIAID NIH HHS [AI24224, AI30355] NR 35 TC 56 Z9 60 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1992 VL 66 IS 3 BP 1564 EP 1570 PG 7 WC Virology SC Virology GA HD265 UT WOS:A1992HD26500034 PM 1310766 ER PT J AU CIMINALE, V PAVLAKIS, GN DERSE, D CUNNINGHAM, CP FELBER, BK AF CIMINALE, V PAVLAKIS, GN DERSE, D CUNNINGHAM, CP FELBER, BK TI COMPLEX SPLICING IN THE HUMAN T-CELL LEUKEMIA-VIRUS (HTLV) FAMILY OF RETROVIRUSES - NOVEL MESSENGER-RNAS AND PROTEINS PRODUCED BY HTLV TYPE-I SO JOURNAL OF VIROLOGY LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; LONG TERMINAL REPEATS; TRANSCRIPTIONAL ACTIVATION; RESPONSE ELEMENTS; GENE-EXPRESSION; REV PROTEIN; GENOME; DNA; P27X-III; P40X AB Novel cytoplasmic mRNA species produced by human T-cell leukemia virus type I (HTLV-I) were cloned by using the polymerase chain reaction technique. Five novel 3' splice sites located in the X region and upstream of the env gene were identified. Splicing to the 3' splice sites in the X region generates mRNAs that express two previously unidentified viral proteins, named Rof and Tof. Tof accumulates in the nucleoli of transfected cells. The other viruses of the HTLV family, such as HTLV-II and bovine leukemia virus, also have a complex splicing pattern and are capable of producing additional proteins encoded in the X region. These results suggest that HTLV-I and other members of the HTLV family produce novel proteins, which may contribute to the biological properties of these viruses. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS PATHOGENESIS GRP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS SECT,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 48 TC 191 Z9 192 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1992 VL 66 IS 3 BP 1737 EP 1745 PG 9 WC Virology SC Virology GA HD265 UT WOS:A1992HD26500054 PM 1310774 ER PT J AU CARBONE, M HAUSER, J CARTY, MP RUNDELL, K DIXON, K LEVINE, AS AF CARBONE, M HAUSER, J CARTY, MP RUNDELL, K DIXON, K LEVINE, AS TI SIMIAN VIRUS-40 (SV40) SMALL T-ANTIGEN INHIBITS SV40 DNA-REPLICATION INVITRO SO JOURNAL OF VIROLOGY LA English DT Note ID LARGE TUMOR-ANTIGEN; PROTEIN PHOSPHATASE-2A; DELETION MUTANTS; INFECTED-CELLS; TRANSFORMATION; PHOSPHORYLATION; ASSOCIATION AB We describe a biochemical function of simian virus 40 small t antigen, the inhibition of simian virus 40 large T antigen-mediated viral DNA replication in an in vitro replication system. Our results suggest that in this system, small t antigen prevents protein phosphatase 2A-mediated activation of large T antigen. C1 NORTHWESTERN UNIV,DEPT MICROBIOL & IMMUNOL,CHICAGO,IL 60611. RP CARBONE, M (reprint author), NICHHD,VIRUSES & CELLULAR BIOL SECT,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA21327] NR 30 TC 13 Z9 13 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1992 VL 66 IS 3 BP 1804 EP 1808 PG 5 WC Virology SC Virology GA HD265 UT WOS:A1992HD26500067 PM 1310784 ER PT J AU ROBERTS, AB MCCUNE, BK SPORN, MB AF ROBERTS, AB MCCUNE, BK SPORN, MB TI TGF-BETA - REGULATION OF EXTRACELLULAR-MATRIX SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT FOREFRONTS IN NEPHROLOGY SYMP ON MESANGIAL CELL AND EXTRACELLULAR MATRIX CY JUN 09-12, 1991 CL KLOSTER BANZ, GERMANY SP INT SOC NEPHROL ID GROWTH-FACTOR-BETA; PROTEOGLYCAN; CELLS RP ROBERTS, AB (reprint author), NCI,CHEMOPREVENT LAB,BLDG 41,ROOM C629,BETHESDA,MD 20892, USA. NR 23 TC 409 Z9 422 U1 0 U2 3 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD MAR PY 1992 VL 41 IS 3 BP 557 EP 559 DI 10.1038/ki.1992.81 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA HG070 UT WOS:A1992HG07000009 PM 1573828 ER PT J AU BROERS, JLV JENSEN, SM TRAVIS, WD PASS, H WHITSETT, JA SINGH, G KATYAL, SL GAZDAR, AF MINNA, JD LINNOILA, RI AF BROERS, JLV JENSEN, SM TRAVIS, WD PASS, H WHITSETT, JA SINGH, G KATYAL, SL GAZDAR, AF MINNA, JD LINNOILA, RI TI EXPRESSION OF SURFACTANT ASSOCIATED PROTEIN-A AND CLARA CELL 10 KILODALTON MESSENGER-RNA IN NEOPLASTIC AND NONNEOPLASTIC HUMAN LUNG-TISSUE AS DETECTED BY INSITU HYBRIDIZATION SO LABORATORY INVESTIGATION LA English DT Article DE HUMAN LUNG CANCER; MESSENGER RNA DETECTION; PERIPHERAL AIRWAYS; DIFFERENTIATION ID PULMONARY SURFACTANT; MONOCLONAL-ANTIBODIES; SECRETORY PROTEINS; EPITHELIAL-CELLS; LOCALIZATION; APOPROTEINS; CARCINOMAS; CANCER; RAT; DIFFERENTIATION AB Two markers for the progenitor cells of peripheral airways and their tumors are the 10 kilodalton (kd) Clara cell protein and the major surfactant associated protein-A (SP-A). We used the RNA-RNA in situ hybridization technique to study expression of the genes encoding these proteins at the cellular level in 19 pairs of non-neoplastic and neoplastic tissues from resected human lungs. Our results show that in non-neoplastic lung tissue, the Clara 10 kd protein gene was expressed in nonciliated cells of both bronchial and bronchiolar epithelium, indicating that, in contrast to previous assumptions, cells with Clara cell-like differentiation in humans may not be restricted to bronchiolar cells. The incidence of Clara 10 kd protein gene expression, as detected in lung carcinomas (1 out of 19 cases positive) was less than expected based on previous ultrastructural reports. The SP-A gene was strongly expressed in normal alveolar type II cells in non-neoplastic lung and, at higher levels, in hyperplastic cells. In addition, SP-A mRNA expression was observed in scattered bronchial and bronchiolar epithelial cells in 40% of the airways examined. Five out of 17 lung tumors, all of which were adenocarcinomas, were positive for SP-A expression, albeit generally less intense than type II cells. This expression was seen in carcinomas with papillolepidic as well as solid and glandular growth patterns. Our findings provide new insights into the peripheral airway cell differentiation. C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. USN,NCI,ONCOL BRANCH,BETHESDA,MD 20814. UNIV CINCINNATI,COLL MED,DEPT PEDIAT,CINCINNATI,OH 45221. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA 15261. VET AFFAIRS MED CTR,DEPT PATHOL,PITTSBURGH,PA. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. FU NHLBI NIH HHS [R01 HL108907] NR 46 TC 107 Z9 109 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD MAR PY 1992 VL 66 IS 3 BP 337 EP 346 PG 10 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HJ326 UT WOS:A1992HJ32600009 PM 1311398 ER PT J AU WEWER, UM ENGVALL, E PAULSSON, M YAMADA, Y ALBRECHTSEN, R AF WEWER, UM ENGVALL, E PAULSSON, M YAMADA, Y ALBRECHTSEN, R TI LAMININ A-SUBUNITS, B1-SUBUNITS, B2-SUBUNITS, S-SUBUNITS AND M-SUBUNITS IN THE POSTNATAL RAT-LIVER DEVELOPMENT AND AFTER PARTIAL-HEPATECTOMY SO LABORATORY INVESTIGATION LA English DT Article DE BASEMENT MEMBRANE; EXTRACELLULAR MATRIX ID BASEMENT-MEMBRANE PROTEINS; HEPATIC EXTRACELLULAR-MATRIX; MESSENGER-RNA; NEUROMUSCULAR-JUNCTION; INSITU HYBRIDIZATION; MULTIDOMAIN PROTEIN; CELL-LINE; CHAIN; FIBRONECTIN; EXPRESSION AB The expression of laminin subunits (A, B1, B2, S and M) in the perisinusoidal space of the rat liver was studied in early postnatal life, in the adult, and after partial hepatectomy. In the perisinusoidal space of the normal adult rat, laminin was detected with polyclonal antibodies only in small streaks of basement membranes extending from the portobiliary tract and to a lesser degree from the central vein. Occasionally, droplets of laminin immunoreactivity were also found along the intervening portions of the perisinusoidal spaces. All morphologically identifiable basement membranes of the rat liver (biliary ducts and blood vessels) irrespective of the age of animals exhibited B1, B2 and S immunoreactivity. Laminin A was restricted to the larger blood vessels and could not be detected in the biliary ducts. In the adult rat, immunoreactivity for the A-like M subunit was absent except for some negligible immunostaining of the blood vessels. In the neonatal rat strong linear laminin immunoreactivity was present in the perisinusoidal spaces throughout the entire lobule. Structurally, this laminin is not organized into a basement membrane as defined by electron microscopy. The perisinusoidal laminin was reactive with antibodies to B1, B2, S and M but the A subunit was absent. Sequential immunohistochemical studies of progressively older animals revealed that B1, B2, S and M immunoreactivity was weak in the perisinusoidal spaces before birth but during the postnatal life distinct linear immunoreactivities appeared. Most intense immunoreactivity was present at 1 to 2 weeks after birth. The perisinusoidal laminin gradually disappeared in growing animals and by 6 to 8 weeks basically no laminin could be detected in this location. By Northern blot analysis increased levels of B1 and B2 were detected in neonatal rats as compared to adult rats. S-laminin mRNA could readily be demonstrated in neonatal rat livers by Northern blot analysis, whereas A and M could not. Expression of S and M-laminin transcripts was demonstrated by polymerase chain reaction, but we were unable to obtain a laminin A product. After partial hepatectomy a transient laminin immunoreactivity, comparable to that in the neonatal rats, was detected in the perisinusoidal spaces. Laminin was most prominent 3 days after resection and reacted with antibodies to B1, B2, S and M. No A subunit could be detected in this extracellular matrix. Our results show that neonatal and post-hepatectomy rat liver cell growth and differentiation are associated with transient accumulation of laminin in the perisinusoidal spaces. This laminin appears to be in the form of two variants: M-B1-B2 and M-S-B2. C1 LA JOLLA CANC RES FDN,LA JOLLA,CA 92037. UNIV BERN,ME MUELLER INST BIOMECH,CH-3010 BERN,SWITZERLAND. NIDR,BETHESDA,MD 20892. RP WEWER, UM (reprint author), UNIV COPENHAGEN,INST PATHOL ANAT,FREDERIK VS VEJ 11,DK-2100 COPENHAGEN,DENMARK. FU NCI NIH HHS [CA 28896]; NIDDK NIH HHS [DK 30051] NR 62 TC 59 Z9 60 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD MAR PY 1992 VL 66 IS 3 BP 378 EP 389 PG 12 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HJ326 UT WOS:A1992HJ32600013 PM 1538591 ER PT J AU EPPS, RP MANLEY, MW AF EPPS, RP MANLEY, MW TI THE CLINICIAN ROLE IN PREVENTING SMOKING INITIATION SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID SMOKELESS TOBACCO; ADOLESCENTS; CIGARETTES; CHILDREN RP EPPS, RP (reprint author), NCI,DIV CANC PREVENT & CONTROL,CANC CONTROL SCI PROGRAM,BETHESDA,MD 20892, USA. NR 28 TC 14 Z9 14 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAR PY 1992 VL 76 IS 2 BP 439 EP 449 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA HJ313 UT WOS:A1992HJ31300009 PM 1548970 ER PT J AU MANLEY, MW EPPS, RP GLYNN, TJ AF MANLEY, MW EPPS, RP GLYNN, TJ TI THE CLINICIAN ROLE IN PROMOTING SMOKING CESSATION AMONG CLINIC PATIENTS SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID NICOTINE CHEWING-GUM; GENERAL-PRACTITIONERS ADVICE; CONTROLLED TRIAL; PHYSICIANS; HEALTH; MODEL; QUIT; CARE RP MANLEY, MW (reprint author), NCI,DIV CANC PREVENT & CONTROL,CANC CONTROL SCI PROGRAM,BETHESDA,MD 20892, USA. NR 30 TC 41 Z9 42 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAR PY 1992 VL 76 IS 2 BP 477 EP 494 PG 18 WC Medicine, General & Internal SC General & Internal Medicine GA HJ313 UT WOS:A1992HJ31300011 PM 1548972 ER PT J AU RODRIGUEZ, O COLLIER, E ARAKAKI, R GORDEN, P AF RODRIGUEZ, O COLLIER, E ARAKAKI, R GORDEN, P TI CHARACTERIZATION OF PURIFIED AUTOANTIBODIES TO THE INSULIN-RECEPTOR FROM 6 PATIENTS WITH TYPE-B INSULIN RESISTANCE SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID KINASE-ACTIVITY; MONOCLONAL-ANTIBODIES; GLUCOSE-TRANSPORT; BINDING; HYPOGLYCEMIA; IMMUNOGLOBULINS; PHOSPHORYLATION; PURIFICATION; DISORDERS; CELLS C1 NIDDKD,DIABET BRANCH,BLDG 10,ROOM 8-S-243,BETHESDA,MD 20892. NR 29 TC 16 Z9 16 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD MAR PY 1992 VL 41 IS 3 BP 325 EP 331 DI 10.1016/0026-0495(92)90279-J PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HG988 UT WOS:A1992HG98800017 PM 1542272 ER PT J AU HACKETT, KJ WHITCOMB, RF TULLY, JG LLOYD, JE ANDERSON, JJ CLARK, TB HENEGAR, RB ROSE, DL CLARK, EA VAUGHN, JL AF HACKETT, KJ WHITCOMB, RF TULLY, JG LLOYD, JE ANDERSON, JJ CLARK, TB HENEGAR, RB ROSE, DL CLARK, EA VAUGHN, JL TI LAMPYRIDAE (COLEOPTERA) - A PLETHORA OF MOLLICUTE ASSOCIATIONS SO MICROBIAL ECOLOGY LA English DT Article ID REQUIRING MOLLICUTES; SP-NOV; SPIROPLASMAS; ECOLOGY; MYCOPLASMAS; FIREFLIES; CLASSIFICATION; ACHOLEPLASMAS; MOSQUITOS; INSECTS AB Beetles (Coleoptera) harbor many species of Acholeplasma and Spiroplasma (division Tenericutes, class Mollicutes). Mollicutes were isolated from guts and/or hemocoels of firefly beetles (Lampyridae) from the United States (Maryland and West Virginia), Ecuador, and Tobago. Firefly beetles were frequent hosts for the group XIV spiroplasma, isolated from Ellychnia corrusca, and the group XIX spiroplasma, isolated from Photuris spp. The most unusual feature of the firefly-mollicute association is the carriage of four Mycoplasma species. Recent phylogenetic studies indicate that these species are members of a clade that includes a vertebrate pathogen, Mycoplasma mycoides. The high rate of occurrence of Mycoplasma species (which are, otherwise, infrequent in insects) in lampyrid beetles suggests that the association is significant. The unusual light-producing physiology of lampyrids (which is dependent on large pools of energy) and the production of large amounts of cardenolides from cholesterol (a critical growth factor for many mollicutes) may favor colonization by mollicutes. C1 NIAID,FREDERICK CANC RES FACIL,MOLEC MICROBIOL LAB,MYCOPLASMA SECT,FREDERICK,MD 21701. UNIV MARYLAND,DEPT ENTOMOL,COLLEGE PK,MD 20742. UNIV FLORIDA,DEPT ENTOMOL & NEMATOL,GAINESVILLE,FL 32611. RP HACKETT, KJ (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,INST PLANT PROTECT,INSECT BIOCONTROL LAB,BLDG 011A,ROOM 214,BELTSVILLE,MD 20705, USA. NR 45 TC 18 Z9 18 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0095-3628 J9 MICROBIAL ECOL JI Microb. Ecol. PD MAR-APR PY 1992 VL 23 IS 2 BP 181 EP 193 DI 10.1007/BF00172639 PG 13 WC Ecology; Marine & Freshwater Biology; Microbiology SC Environmental Sciences & Ecology; Marine & Freshwater Biology; Microbiology GA HV718 UT WOS:A1992HV71800007 PM 24192863 ER PT J AU GOPING, G YEDGAR, S POLLARD, HB KUIJPERS, GAJ AF GOPING, G YEDGAR, S POLLARD, HB KUIJPERS, GAJ TI FLAT EMBEDDING AND IMMUNOLABELING OF SW-1116 COLON-CARCINOMA CELLS IN LR WHITE - AN IMPROVED TECHNIQUE IN LIGHT AND ELECTRON-MICROSCOPY SO MICROSCOPY RESEARCH AND TECHNIQUE LA English DT Article DE MUCIN; IMMUNOFLUORESCENCE; IMMUNOELECTRON MICROSCOPY; MONOCLONAL ANTIBODY 19-9; MATRIGEL; PAS STAIN ID LOCALIZATION AB Human SW 1116 colon carcinoma cells were grown on matrix-covered coverslips and flat embedded in specially prepared gelatin capsules in the hydrophylic resin LR White. Dehydration and polymerization were carried out so as to maximize preservation of antigenicity. Sections were cut perpendicular to the substratum. To visualize mucin, semithin sections of SW 1116 cells were stained with periodic acid Schiff (PAS) reagent for light microscopy, and ultrathin sections were labelled with a monoclonal mucin antibody (Mab 19-9) and immunogold for electron microscopy. Immunofluorescence was carried out on whole cultured cells using Mab 19-9. The morphological preservation of SW 1116 cells embedded in LR White was comparable to that of Epon-embedded cells. Mucin was localized on the microvillar surface of the apical plasma membrane and occasionally in intercellular spaces between adjacent cells. Mucin was also present in vesicles in the apical and lateral part, and to a lesser extent in the basal part of the cells. We conclude that this new technology significantly improves the morphological preservation of cells and tissues in LR White, while also serving to sustain the antigenicity of cellular antigens. C1 HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT BIOCHEM,IL-91010 JERUSALEM,ISRAEL. RP GOPING, G (reprint author), NIDDK,CELL BIOL & GENET LAB,BLDG 8,ROOM 421,BETHESDA,MD 20892, USA. NR 13 TC 15 Z9 15 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1059-910X J9 MICROSC RES TECHNIQ JI Microsc. Res. Tech. PD MAR 1 PY 1992 VL 21 IS 1 BP 1 EP 9 DI 10.1002/jemt.1070210102 PG 9 WC Anatomy & Morphology; Biology; Microscopy SC Anatomy & Morphology; Life Sciences & Biomedicine - Other Topics; Microscopy GA HJ850 UT WOS:A1992HJ85000001 PM 1591409 ER PT J AU KLOTZ, FW ORLANDI, PA REUTER, G COHEN, SJ HAYNES, JD SCHAUER, R HOWARD, RJ PALESE, P MILLER, LH AF KLOTZ, FW ORLANDI, PA REUTER, G COHEN, SJ HAYNES, JD SCHAUER, R HOWARD, RJ PALESE, P MILLER, LH TI BINDING OF PLASMODIUM-FALCIPARUM 175-KILODALTON ERYTHROCYTE BINDING ANTIGEN AND INVASION OF MURINE ERYTHROCYTES REQUIRES N-ACETYLNEURAMINIC ACID BUT NOT ITS O-ACETYLATED FORM SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE PLASMODIUM-FALCIPARUM; RED CELL; MEROZOITE; RECEPTOR; SIALIC ACID ID MOUSE ERYTHROCYTES; MALARIAL PARASITES; MEROZOITE INVASION; INFLUENZA-VIRUS; C-VIRUSES; RECEPTOR; PROTEINS; SURFACE; IDENTIFICATION; GLYCOPROTEIN AB Sialic acid on human erythrocytes is involved in invasion by the human malaria parasite, Plasmodium falciparum. Mouse erythrocytes were used as a reagent to explore the question of whether erythrocyte sialic acid functions as a nonspecific negative charge or whether the sialic acid is a necessary structural part of the receptor for merozoites. Human erythrocytes contain N-acetylneuraminic acid (Neu5Ac), whereas mouse erythrocytes, which are also invaded by P. falciparum merozoites, contain 9-O-acetyl-N-acetylneuraminic acid (Neu5,9Ac2) and N-glycoloylneuraminic acid (Neu5Gc), in addition to Neu5Ac. We compared the effects of sialidase and influenza C virus esterase treatments of mouse erythrocytes on invasion and the binding of a 175-kDa P. falciparum protein (EBA- 1 75), a sialic acid-dependent malaria ligand implicated in the invasion process. Sialidase-treated mouse erythrocytes were refractory to invasion by P. falciparum merozoites and failed to bind EBA-175. Influenza C virus esterase, which converts Neu5,9Ac2 to Neu5Ac, increased both invasion efficiency and EBA-175 binding to mouse erythrocytes. Thus, the parasite and EBA-175 discriminate between Neu5Ac and Neu5,9Ac2, that is, the C-9 acetyl group interferes with EBA-175 binding and invasion by P. falciparum merozoites. This indicates that sialic acid is part of a receptor for invasion. C1 NIAID,PARASIT DIS LAB,BLDG 4,ROOM 126,BETHESDA,MD 20892. DNAX RES INST MOLEC & CELLULAR BIOL INC,RES INST,PALO ALTO,CA. CUNY MT SINAI SCH MED,DEPT MICROBIOL,NEW YORK,NY 10029. UNIV KIEL,INST BIOCHEM,W-2300 KIEL 1,GERMANY. WALTER REED ARMY MED CTR,DEPT IMMUNOL,WASHINGTON,DC 20307. OI Palese, Peter/0000-0002-0337-5823 NR 30 TC 60 Z9 61 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-6851 J9 MOL BIOCHEM PARASIT JI Mol. Biochem. Parasitol. PD MAR PY 1992 VL 51 IS 1 BP 49 EP 54 DI 10.1016/0166-6851(92)90199-T PG 6 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA HG814 UT WOS:A1992HG81400006 PM 1565137 ER PT J AU ADAM, RD YANG, YM NASH, TE AF ADAM, RD YANG, YM NASH, TE TI THE CYSTEINE-RICH PROTEIN GENE FAMILY OF GIARDIA-LAMBLIA - LOSS OF THE CRP170 GENE IN AN ANTIGENIC VARIANT SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SURFACE PROTEIN; SEQUENCE; DNA; NUCLEOTIDE AB Giardia lamblia trophozoites demonstrate variable expression of a repertoire of cysteine-rich surface antigens in vitro and in vivo. The size of the repertoire has been estimated at 20 to 184, and specific variants can be detected after approximately 12 generations of in vitro growth for the WB isolate. In earlier studies, we cloned a portion of the gene for a 170-kDa surface antigen (CRP170) and demonstrated by DNA sequencing that it was cysteine rich (12%) and contained 2.6 copies of a tandemly repeated 195-bp pair sequence. The clone hybridized to multiple bands on a Southern blot of G. lamblia DNA in a pattern that was variable among the cloned lines but did not correlate with expression of CRP170. We have now cloned a nearly full length cDNA as well as genomic clones for CRP170 from the WBA6 cloned isolate. In addition, we have isolated a cDNA clone from the WB1269 line (expressing CRP72), an antigenic variant which was derived from WBA6. Sequence analysis of the CRP170 and CRP72 genes revealed marked C-terminal amino acid homology, suggesting a conserved functional role such as membrane anchoring. The CRP170 repeat oligonucleotide hybridized to a stairstep of bands approximately 6 kb in size on HindIII-digested WBA6 DNA representing the expressed cop(ies) of CRP170. In contrast, there was no hybridization to a fragment of similar size in WB1269, suggesting that WB1269 trophozoites have lost the expressed copy of the CRP170 gene. C1 UNIV ARIZONA,DEPT MICROBIOL IMMUNOL,TUCSON,AZ 85724. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. RP ADAM, RD (reprint author), UNIV ARIZONA,DEPT INTERNAL MED,INFECT DIS SECT,TUCSON,AZ 85724, USA. FU NIAID NIH HHS [R29AI28551] NR 37 TC 40 Z9 40 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1992 VL 12 IS 3 BP 1194 EP 1201 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HE838 UT WOS:A1992HE83800029 PM 1545800 ER PT J AU DAGOSTINO, DM FELBER, BK HARRISON, JE PAVLAKIS, GN AF DAGOSTINO, DM FELBER, BK HARRISON, JE PAVLAKIS, GN TI THE REV PROTEIN OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PROMOTES POLYSOMAL ASSOCIATION AND TRANSLATION OF GAG/POL AND VPU/ENV MESSENGER-RNAS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HTLV-I REX; TARGET SEQUENCE; GENE-EXPRESSION; TRANS-ACTIVATOR; RESPONSIVE ELEMENT; RIBOSOMAL-RNA; ENZYMATIC AMPLIFICATION; FUNCTIONAL-ANALYSIS; SECONDARY STRUCTURE; BETA-ACTIN AB Biochemical examination of the Rev-dependent expression of gag mRNAs produced from gag-Rev-responsive element (RRE) expression plasmids showed a large discrepancy between the level of cytoplasmic gag mRNA and the produced Gag protein. Significant levels of the mRNA produced in the absence of Rev were localized in the cytoplasm, while very low levels of Gag protein were produced. In the presence of Rev, the levels of mRNA increased by 4- to 16-fold, while the Gag protein production increased by 800-fold. These findings indicated that in addition to promoting nucleus-to-cytoplasm transport, Rev increased the utilization of cytoplasmic viral mRNA. Poly(A) selection and in vitro translation of cytoplasmic gag mRNA verified that the mRNA produced in the absence of Rev was functional. To analyze the translational defect in the absence of Rev, we examined the association of the cytoplasmic gag mRNA with ribosomes. gag mRNA produced in the absence of Rev was excluded from polysomes, while gag mRNA produced in the presence of Rev was associated with polysomes and produced Gag protein. These observations showed that the presence of Rev was required for efficient loading of gag mRNA onto polysomes. This effect required the presence of the RRE on the mRNA. Analysis of mRNAs produced from a rev-minus proviral clone confirmed that the presence of Rev promoted polysomal loading of both gag/pol and vpu/env mRNAs. The localization of gag mRNA was also examined by in situ hybridization. This analysis showed that in the presence of Rev, most of the gag mRNA was found in the cytoplasm, while in the absence of Rev, most of the gag mRNA was found in the nucleus and in the region surrounding the nucleus. These results suggest that a substantial fraction of the gag mRNA is retained in distinct cytoplasmic compartments in the absence and presence of Rev. These findings indicate that the presence of Rev is required along the entire mRNA transport and utilization pathway for the stabilization, correct localization, and efficient translation of RRE-containing mRNAs. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, HUMAN RETROVIRUS SECT, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, HUMAN RETROVIRUS PATHOGENESIS GRP, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N01-CO-74101] NR 72 TC 176 Z9 179 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1992 VL 12 IS 3 BP 1375 EP 1386 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HE838 UT WOS:A1992HE83800050 PM 1545819 ER PT J AU WONG, ML WEISS, SRB GOLD, PW DOI, SQ BANERJEE, S LICINIO, J LAD, R POST, RM SMITH, MA AF WONG, ML WEISS, SRB GOLD, PW DOI, SQ BANERJEE, S LICINIO, J LAD, R POST, RM SMITH, MA TI INDUCTION OF CONSTITUTIVE HEAT-SHOCK PROTEIN-73 MESSENGER-RNA IN THE DENTATE GYRUS BY SEIZURES SO MOLECULAR BRAIN RESEARCH LA English DT Article DE HEAT SHOCK PROTEIN; MESSENGER RNA; COCAINE; KINDLING; ELECTROCONVULSIVE SEIZURE; DENTATE GYRUS; HIPPOCAMPUS; INSITU HYBRIDIZATION ID GRANULE CELLS; STATUS EPILEPTICUS; COATED VESICLES; GENE-EXPRESSION; RAT-BRAIN; STRESS; HSP70; HYPERTHERMIA; COLCHICINE; CLONING AB We examined the effects of generalized seizures on heat shock protein (hsp) mRNA induction in the rat brain using in situ hybridization. Seizures induced by electroconvulsive shock, electrical or cocaine kindling caused a selective induction of the constitutive hsp 73 gene in the dentate gyrus. In these seizure paradigms, not thought to induce widespread tissue damage, neither the heat-inducible hsp 72 gene nor a member of the hsp 90 family (hsp 84) were induced. Hsp 73 may play a role in the adaptation and/or in the maintainence of dentate granule cell integrity following seizures. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BLDG 36,ROOM 2D 15,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NIDDK,METAB DIS BRANCH,BETHESDA,MD 20892. NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. RI Wong, Ma-Li/D-7903-2011; Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 38 TC 25 Z9 25 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD MAR PY 1992 VL 13 IS 1-2 BP 19 EP 25 DI 10.1016/0169-328X(92)90040-I PG 7 WC Neurosciences SC Neurosciences & Neurology GA HH368 UT WOS:A1992HH36800003 PM 1315915 ER PT J AU YOUNG, WS LIGHTMAN, SL AF YOUNG, WS LIGHTMAN, SL TI CHRONIC STRESS ELEVATES ENKEPHALIN EXPRESSION IN THE RAT PARAVENTRICULAR AND SUPRAOPTIC NUCLEI SO MOLECULAR BRAIN RESEARCH LA English DT Article DE STRESS; OPIOID; HYPOTHALAMUS; VASOPRESSIN; OXYTOCIN ID CORTICOTROPIN-RELEASING FACTOR; PREPROENKEPHALIN MESSENGER-RNA; OPIATE RECEPTORS; NERVE-TERMINALS; METHIONINE ENKEPHALIN; MAGNOCELLULAR NEURONS; INSITU HYBRIDIZATION; POSTERIOR PITUITARY; STIMULATED RELEASE; OPIOID RECEPTOR AB Numerous studies have implicated opioids in the regulation of hypothalamic functions. Dynorphin, which is co-expressed with vasopressin in the magnocellular neurons of the paraventricular and supraoptic nuclei, is co-regulated with vasopressin in response to hyperosmolality and appears to inhibit vasopressin and oxytocin release from the posterior pituitary. Enkephalin is present in paraventricular parvocellular neurons and its expression is elevated in response to various stresses. However, enkephalin's presence and roles in paraventricular and supraoptic magnocellular neurons are uncertain. By giving rats daily intraperitoneal injections of hypertonic saline for up to 12 days, we induced a marked increase in enkephalin expression in magnocellular neurons of the paraventricular and supraoptic nuclei, beyond what develops from drinking hypertonic saline. Our results suggest that enkephalin expression in both vasopressin and oxytocin neurons may increase in response to chronic stresses and provide another source of enkephalin in addition to the parvocellular neurons. RP YOUNG, WS (reprint author), NIMH,CELL BIOL LAB,BLDG 36,ROOM 2D10,BETHESDA,MD 20892, USA. RI Young, W Scott/A-9333-2009 OI Young, W Scott/0000-0001-6614-5112 NR 57 TC 43 Z9 43 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD MAR PY 1992 VL 13 IS 1-2 BP 111 EP 117 DI 10.1016/0169-328X(92)90050-L PG 7 WC Neurosciences SC Neurosciences & Neurology GA HH368 UT WOS:A1992HH36800013 PM 1349719 ER PT J AU HURD, YL BROWN, EE FINLAY, JM FIBIGER, HC GERFEN, CR AF HURD, YL BROWN, EE FINLAY, JM FIBIGER, HC GERFEN, CR TI COCAINE SELF-ADMINISTRATION DIFFERENTIALLY ALTERS MESSENGER-RNA EXPRESSION OF STRIATAL PEPTIDES SO MOLECULAR BRAIN RESEARCH LA English DT Note DE COCAINE; DOPAMINE; PEPTIDE; STRIATUM ID IDENTIFIED STRIATONIGRAL NEURONS; D1 DOPAMINE RECEPTOR; SUBSTANCE-P; RAT; DYNORPHIN; PATHWAY; ENKEPHALIN; METABOLISM; NUCLEUS; NIGRA AB The influence of cocaine self-administration on the expression of messenger RNAs for dynorphin, enkephalin and substance P was analyzed in the rat striatum with in situ hybridization histochemistry. Cocaine, an indirect dopamine agonist, was found to differentially affect the levels of mRNA encoding these neuropeptides in different subregions of the striatum. Following a 7 day period of variable free access to cocaine, dynorphin and substance P mRNA levels were elevated throughout the striatum, but the increases were substantially greater in the dorsal striatum than in the nucleus accumbens. Enkephalin mRNA was not significantly altered in the dorsal striatum but was slightly elevated in the nucleus accumbens. These results suggest that cocaine self-administration has differential effects on striatonigral and striatopallidal projection neurons, and that these effects vary in subregions of the striatum. C1 NIMH,CELL BIOL LAB,BLDG 36,RM 2D 10,BETHESDA,MD 20892. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. UNIV BRITISH COLUMBIA,DEPT PSYCHIAT,DIV NEUROL SCI,VANCOUVER V6T 1W5,BC,CANADA. NR 36 TC 180 Z9 181 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD MAR PY 1992 VL 13 IS 1-2 BP 165 EP 170 DI 10.1016/0169-328X(92)90058-J PG 6 WC Neurosciences SC Neurosciences & Neurology GA HH368 UT WOS:A1992HH36800021 ER PT J AU LIU, YH TENG, CT AF LIU, YH TENG, CT TI ESTROGEN RESPONSE MODULE OF THE MOUSE LACTOFERRIN GENE CONTAINS OVERLAPPING CHICKEN OVALBUMIN UP-STREAM PROMOTER TRANSCRIPTION FACTOR AND ESTROGEN RECEPTOR-BINDING ELEMENTS SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID DNA-BINDING; C-JUN; GLUCOCORTICOID RECEPTOR; SEQUENCE; UPSTREAM; COUP; ENHANCER; PROTEIN; AP-1; LACTOTRANSFERRIN AB Transcription of the lactoferrin gene is stimulated by estrogen in mouse uterus. To study direct estrogen regulation of this gene at the molecular level, we cloned and analyzed the 5'-flanking region of the mouse lactoferrin gene. Sequence analysis revealed a putative estrogen-responsive element (ERE) overlapping with a chicken ovalbumin up-stream promoter (COUP) element located at position -349 to -329 from the transcription initiation site. The ERE element differed from the consensus ERE sequence by one nucleotide at the second position of the 3' half of the element (G to A); the COUP element differed by one nucleotide from the chicken COUP element. Synthetic oligonucleotide containing the mouse lactoferrin COUP/ERE element was inserted into the reporter chloramphenicol acetyltransferase vector, then transiently transfected into human endometrium carcinoma RL95-2 cells to assess hormone responsiveness. We found that the COUP/ERE element confers estrogen action to both homologous and heterologous promoters. Nuclear proteins from diethylstilbestrol-treated mouse uteri and proteins from estrogen receptor expression vector-transfected RL95-2 whole cell extract bound in vitro to COUP/ERE element specifically, as assessed by band-shift assay. By using antibodies specific to the estrogen receptor and the COUP transcription factor, we demonstrated that both proteins were present in mouse uterine tissue and interacted specifically with the COUP/ERE element, as shown by the superband shift. Competition experiments with specific ERE or COUP oligonucleotides also confirmed the interaction between lactoferrin COUP/ERE element with the estrogen receptor and the COUP transcription factor. Therefore, we named this sequence mERM, the mouse lactoferrin estrogen response module. C1 NIEHS,REPROD & DEV TOXICOL LAB,POB 12233,MD 1301,RES TRIANGLE PK,NC 27709. NR 49 TC 83 Z9 83 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD MAR PY 1992 VL 6 IS 3 BP 355 EP 364 DI 10.1210/me.6.3.355 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HM714 UT WOS:A1992HM71400006 PM 1584212 ER PT J AU OSHIMA, H SIMONS, SS AF OSHIMA, H SIMONS, SS TI MODULATION OF TRANSCRIPTION FACTOR ACTIVITY BY A DISTANT STEROID MODULATORY ELEMENT SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID TYROSINE AMINOTRANSFERASE GENE; RAT HEPATOMA-CELLS; BOX BINDING-FACTOR; DNA-BINDING; GLUCOCORTICOID RECEPTOR; CYCLIC-AMP; PROGESTERONE-RECEPTOR; BIOLOGICAL-ACTIVITY; ESTROGEN-RECEPTOR; FACTORS INTERACT AB Variations in the biological activity of antisteroids, as determined by their percent agonist activity, is a well known but poorly understood phenomenon. For example, in tyrosine aminotransferase (TAT) induction by the antiglucocorticoid dexamethasone 21-mesylate in rat hepatoma tissue culture cells, the percent agonist activity varies with the density of cultured cells. A 21-basepair sequence of the rat TAT gene has now been isolated which confers all of the induction properties of the endogenous TAT gene to homologous and heterologous promoters and genes. We call this 21-basepair sequence, which acts in concert with a trans-acting factor identified by gel shift experiments, a glucocorticoid modulatory element. The changes in induction properties were found to be independent of the fold induction by dexamethasone, thus arguing that the GME does not synergize with the glucocorticoid response element. A model incorporating this new element is advanced which can explain the observed variations of TAT induction and may be generally applicable for the mechanism of action of other steroid hormones. C1 NIDDKD,MOLEC & CELLULAR BIOL LAB,STEROID HORMONES SECT,BLDG 8,ROOM B2A-07,BETHESDA,MD 20892. NR 55 TC 56 Z9 55 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD MAR PY 1992 VL 6 IS 3 BP 416 EP 428 DI 10.1210/me.6.3.416 PG 13 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HM714 UT WOS:A1992HM71400013 PM 1584217 ER PT J AU PARKER, KC SILVER, ML WILEY, DC AF PARKER, KC SILVER, ML WILEY, DC TI AN HLA-A2/BETA-2-MICROGLOBULIN-PEPTIDE COMPLEX ASSEMBLED FROM SUBUNITS EXPRESSED SEPARATELY IN ESCHERICHIA-COLI SO MOLECULAR IMMUNOLOGY LA English DT Article ID TOXIC LYMPHOCYTES-T; CLASS-I MOLECULES; HISTOCOMPATIBILITY ANTIGENS; SURFACE EXPRESSION; MATRIX PROTEIN; BINDING-SITE; PEPTIDE; HLA-A2; RECOGNITION; ASSOCIATION AB The human class I histocompatibility antigen HLA-A2 has been assembled from subunits expressed separately in E. coli. A peptide that is known to be recognized by human cytotoxic T lymphocytes (CTLs) in association with HLA-A2 is a necessary component of the reconstitution mixture. The N-terminal extracellular fragment of the HLA-A2 heavy chain is initially synthesised as an insoluble aggregate. The aggregate is solubilized in denaturant, mixed with the influenza nucleoprotein 85-94 decapeptide (NP peptide), and diluted into a solution containing human beta-2-microglobulin (beta-2m) isolated from the E. coli periplasm. The HLA-A2 heavy chain becomes soluble in physiological solutions if both beta-2m and the NP peptide are present. The reconstituted HLA-A2 complex is recognised by a monoclonal antibody that is specific for the native HLA-A2/beta-2m heterodimer, and is also recognised by a monoclonal antibody that recognises beta-2m. When other peptides known from CTL studies to associate with HLA-A2 are used. a significantly lower yield of reconstituted complex is obtained. The isoelectric point of the reconstituted complex depends on which peptide is used. confirming that the peptide is a component of the reconstituted complex. C1 HARVARD UNIV,HOWARD HUGHES MED INST,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. RP PARKER, KC (reprint author), NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892, USA. OI Parker, Kenneth/0000-0002-6282-2478 NR 36 TC 19 Z9 28 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD MAR PY 1992 VL 29 IS 3 BP 371 EP 378 DI 10.1016/0161-5890(92)90024-R PG 8 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA HJ527 UT WOS:A1992HJ52700010 PM 1557046 ER PT J AU YUN, YP CASAZZA, JP SOHN, DH VEECH, RL SONG, BJ AF YUN, YP CASAZZA, JP SOHN, DH VEECH, RL SONG, BJ TI PRETRANSLATIONAL ACTIVATION OF CYTOCHROME-P450IIE DURING KETOSIS INDUCED BY A HIGH-FAT DIET SO MOLECULAR PHARMACOLOGY LA English DT Article ID N-NITROSODIMETHYLAMINE DEMETHYLASE; RABBIT LIVER-MICROSOMES; GROWTH-HORMONE; INDUCIBLE FORM; DIABETIC RAT; ISOZYME 3A; ETHANOL; ACETONE; INDUCTION; METABOLISM AB Ethanol-inducible cytochrome P450 (P450IIE) is reported to be induced by ketosis. In the present study, the effects of a high fat diet on P450IIE induction and the relationship between ketone body concentration and P450IIE induction were studied by the following: 1) measurement of the activity of aniline hydroxylase, 2) immunoblot analysis for P450IIE protein, and 3) Northern blot analysis for P450IIE mRNA. The enzyme activities (aniline hydroxylase) in hepatic and renal microsomes were elevated about 2-3-fold by feeding with a high fat diet for 3 days. The increases in enzyme activities were also accompanied by 3-fold increases in immunoreactive P450IIE protein and its mRNA. In contrast, no differences were observed for the catalytic activities of N-alkoxyresorufin dealkylases or the amounts of immunoreactive P450IA and P450IIC, indicating a specific induction of P450IIE by high fat feeding. Furthermore, the increases in the levels of P450IIE mRNA correlated positively (r = 0.73) with plasma concentrations of acetoacetate and beta-hydroxybutyrate but not with that of acetone, which induces P450IIE without changing its mRNA level. Our data thus indicated that P450IIE induction during the ketosis of a high fat feeding appears to be due to pretranslational activation and that is similar to the induction mechanism of fasted and diabetic animals. C1 NIAAA,METAB & MOLEC BIOL LAB,12501 WASHINGTON AVE,ROCKVILLE,MD 20852. NR 40 TC 71 Z9 75 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD MAR PY 1992 VL 41 IS 3 BP 474 EP 479 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HL473 UT WOS:A1992HL47300007 PM 1545775 ER PT J AU SOERGEL, DG YASUMOTO, T DALY, JW GUSOVSKY, F AF SOERGEL, DG YASUMOTO, T DALY, JW GUSOVSKY, F TI MAITOTOXIN EFFECTS ARE BLOCKED BY SK-AND-F-96365, AN INHIBITOR OF RECEPTOR-MEDIATED CALCIUM ENTRY SO MOLECULAR PHARMACOLOGY LA English DT Article ID RAT PHEOCHROMOCYTOMA CELLS; PHOSPHOINOSITIDE BREAKDOWN; INOSITOL PHOSPHATES; TUMOR PROMOTER; CA-2+ ENTRY; MEMBRANE; SYNAPTOSOMES; THAPSIGARGIN; GENERATION; HYDROLYSIS AB The dinoflagellate toxin maitotoxin (MTX) elicited a sustained increase of [Ca2+]i in C6 glioma cells. This response was inhibited by SK&F 96365, a blocker of receptor-mediated calcium entry. In C6 cells, endothelin-1 elicited a rapid but transient increase in [Ca2+]i, followed by a smaller sustained increase. SK&F 96365 inhibited the sustained increase in [Ca2+]i. In both C6 glioma cells and RIN insulinoma cells, MTX elicited a marked influx of Ca-45(2+). SK&F 96365 inhibited MTX-induced Ca-45(2+) influx by 95% at 30-mu-M. The L-type calcium channel blocker nifedipine, even at 10-mu-M, inhibited MTX-induced calcium uptake by only 20% in RIN cells and by only 10% in C6 cells. MTX elicited calcium-dependent phosphoinositide breakdown in both C6 and RIN cells. In both cell lines, the MTX-induced phosphoinositide breakdown was inhibited by 90% by SK&F 96365 at 30-mu-M. Endothelin-1 and carbamylcholine elicited phosphoinositide breakdown in C6 cells and RIN cells, respectively. The stimulations were unaffected by the presence of SK&F 96365 up to 100-mu-M. In RIN insulinoma cells, MTX elicited calcium-dependent release of insulin. SK&F 96365 at 30-mu-M inhibited MTX-induced insulin release by 75%, whereas nifedipine, even at 30-mu-M, inhibited release by only 10%. The blockade of MTX-induced responses by SK&F 96365 indicates that MTX increases intracellular calcium by interacting directly with a calcium-entry system that is similar, in its sensitivity to SK&F 96365, to the calcium-entry system activated by receptors that elicit phosphoinositide breakdown. Activation of phospholipase C and hormone release by MTX also are blocked by SK&F 96365 and, thus, may be secondary to the activation of such a calcium-entry system. C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. TOHOKU UNIV,FAC AGR,SENDAI,MIYAGI 980,JAPAN. NR 25 TC 75 Z9 75 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD MAR PY 1992 VL 41 IS 3 BP 487 EP 493 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HL473 UT WOS:A1992HL47300009 PM 1312215 ER PT J AU COSTA, T OGINO, Y MUNSON, PJ ONARAN, HO RODBARD, D AF COSTA, T OGINO, Y MUNSON, PJ ONARAN, HO RODBARD, D TI DRUG EFFICACY AT GUANINE NUCLEOTIDE-BINDING REGULATORY PROTEIN-LINKED RECEPTORS - THERMODYNAMIC INTERPRETATION OF NEGATIVE ANTAGONISM AND OF RECEPTOR ACTIVITY IN THE ABSENCE OF LIGAND SO MOLECULAR PHARMACOLOGY LA English DT Article ID ADENYLATE-CYCLASE SYSTEM; TERNARY COMPLEX MODEL; OPIOID RECEPTORS; D2-DOPAMINE RECEPTOR; ADENOSINE RECEPTORS; ANTERIOR-PITUITARY; RESPONSE CURVES; AGONIST; MEMBRANES; GTP AB The mutual effects that a hormonal ligand (H) and a guanine nucleotide regulatory protein (G protein) exert on each other when simultaneously occupying distinct sites of the receptor molecule (R) can be viewed as the molecular mechanism of drug efficacy. These effects are predictable on the basis of a model assuming that the ternary complex between the three partners (HRG) reaches equilibrium in the membrane [J. Biol. Chem. 255:7108-7117 (1980)]. Ligands can be classified as agonists, neutral antagonists, or negative antagonists, depending on whether they enhance, leave unchanged, or reduce, respectively, the spontaneous tendency of R to interact with G. Using this model and the assumption that the G protein response observed in membranes reflects the sum of ligand-independent (RG) and ligand-dependent (HRG) receptor-G protein complexes, we can explain virtually all the phenomenology reported earlier for opioid receptor-mediated stimulation of GTPase, i.e., 1) existence of ligands with both "positive" and "negative" intrinsic activity (the latter termed negative antagonists), 2) equipotency of neutral antagonists for the competitive blockade of the responses elicited both by agonists and by negative antagonists, and 3) apparent heterogeneity of binding sites for the binding isotherms of negative antagonists. The ternary complex model can also explain the differential effects of sodium on ligand binding and ligand-dependent GTPase activity, if we assume that this ion reduces the stability constant between receptor and G protein in membranes. Computer simulations predict that a negative antagonist exhibits a discrepancy between "biological" K(i) (obtained by Schild plots) and true dissociation constant for the receptor, which increases as the fraction of "precoupled" receptors in the membrane increases. The demonstration of negative antagonism is definitive evidence for the existence of receptor coupling (hence activity) in the absence of ligand. Using this experimental paradigm, we show here that spontaneous receptor activity occurs in isolated membranes but not in intact NG108-15 cells. C1 NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. RP COSTA, T (reprint author), NIH,DIV COMP RES & TECHNOL,ABS,BLDG 12A,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. OI costa, tommaso/0000-0002-8729-3357 NR 33 TC 255 Z9 255 U1 1 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD MAR PY 1992 VL 41 IS 3 BP 549 EP 560 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HL473 UT WOS:A1992HL47300016 PM 1312216 ER PT J AU LUFT, R RALL, JE ROTHSCHILD, MA GORDIS, E GLICK, S ROSSELIN, G PALLOTTA, J AF LUFT, R RALL, JE ROTHSCHILD, MA GORDIS, E GLICK, S ROSSELIN, G PALLOTTA, J TI REMINISCENCES AND REFLECTIONS SO MOUNT SINAI JOURNAL OF MEDICINE LA English DT Article C1 NIDDKD,BETHESDA,MD. UNIV MIAMI,RADIOL,MIAMI,FL 33152. VET AFFAIRS MED CTR,NUCL MED SERV,MIAMI,FL. NIAAA,ROCKVILLE,MD 20852. BEN GURION UNIV NEGEV,INTERNAL MED,BEER SHEVA,ISRAEL. CTR RECH PARIS ST ANTOINE,PARIS,FRANCE. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02215. RP LUFT, R (reprint author), KAROLINSKA INST,ENDOCRINOL,S-10401 STOCKHOLM 60,SWEDEN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOUNT SINAI HOSPITAL PI NEW YORK PA BOX 1094 ONE GUSTAVE L LEVY PLACE ATTN: CIRCULATION ASST, NEW YORK, NY 10029-6574 SN 0027-2507 J9 MT SINAI J MED JI Mt. Sinai J. Med. PD MAR PY 1992 VL 59 IS 2 BP 97 EP 100 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA HL058 UT WOS:A1992HL05800002 ER PT J AU GORDIS, E AF GORDIS, E TI SCIENCE AND SOCIAL-POLICY SO MOUNT SINAI JOURNAL OF MEDICINE LA English DT Article ID LIVER-TRANSPLANTATION RP GORDIS, E (reprint author), NIAAA,5600 FISHERS LANE,ROOM 16-105,ROCKVILLE,MD 20857, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU MOUNT SINAI HOSPITAL PI NEW YORK PA BOX 1094 ONE GUSTAVE L LEVY PLACE ATTN: CIRCULATION ASST, NEW YORK, NY 10029-6574 SN 0027-2507 J9 MT SINAI J MED JI Mt. Sinai J. Med. PD MAR PY 1992 VL 59 IS 2 BP 108 EP 110 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA HL058 UT WOS:A1992HL05800004 PM 1574061 ER PT J AU WOODGATE, R AF WOODGATE, R TI CONSTRUCTION OF A UMUDC OPERON SUBSTITUTION MUTATION IN ESCHERICHIA-COLI SO MUTATION RESEARCH LA English DT Article DE ESCHERICHIA-COLI; SOS MUTAGENESIS; UMUDC OPERON; LAMBDA-GTL-LAMBDA-B; GENE REPLACEMENT ID CHEMICAL MUTAGENESIS; ULTRAVIOLET-LIGHT; GENE; DEFICIENT; MUTANTS; REPAIR; UV AB Using a specialized transducing lambda phage, the umuDC operon of Escherichia coli was deleted and replaced with the chloramphenicol acetyltransferase gene. The DELTA(umuDC)595::cat mutation was subsequently transferred by generalized P1 transduction into a variety of genetic backgrounds. It is concluded that the UmuD,C proteins, which are normally required for inducible mutagenesis, are not essential for cell survival. RP WOODGATE, R (reprint author), NICHHD,VIRUSES & CELLULAR BIOL SECT,BLDG 6,ROOM 1A13,BETHESDA,MD 20892, USA. NR 14 TC 104 Z9 104 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD MAR PY 1992 VL 281 IS 3 BP 221 EP 225 DI 10.1016/0165-7992(92)90012-7 PG 5 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HH592 UT WOS:A1992HH59200012 PM 1371846 ER PT J AU TIZABI, Y AGUILERA, G GILAD, GM AF TIZABI, Y AGUILERA, G GILAD, GM TI AGE-RELATED REDUCTION IN PITUITARY CORTICOTROPIN-RELEASING HORMONE RECEPTORS IN 2 RAT STRAINS SO NEUROBIOLOGY OF AGING LA English DT Article DE AGING; HYPOTHALAMIC-PITUITARY ADRENAL AXIS; CRH RECEPTOR; ACTH; RAT STRAINS ID OLD MALE-RATS; ADRENOCORTICAL AXIS; ACTH-SECRETION; STRESS; CORTICOSTERONE; SENSITIVITY; INHIBITION; BINDING AB Open field behavior and age-related changes in anterior pituitary corticotropin-releasing hormone (CRH) receptors, as well as plasma ACTH levels, were measured in two inbred rat strains. The strains utilized were Wistar Kyoto (WKY) and Brown-Norway (BN), the former characterized by shorter life-span and hyper-reactivity to stressors as compared to the latter. Behaviorally, WKY rats showed hyper-responsivity to a novel environment as indicated by their delay in entering the open field, increased grooming, reduced rearing, and reduced locomotion. These strain-dependent behavioral differences were not affected by aging. The binding capacity of CRH receptors was similar in both strains and Bmax values were decreased (25-27%) with aging, with no changes in Kd values. In contrast, plasma ACTH levels were 67% higher in WKY than in BN rats but did not change with aging. Thus, despite pituitary CRH receptor down regulation, plasma ACTH levels following decapitation were sustained during aging. This suggests the presence of some compensatory factors in the hypothalamic-pituitary axis regulation which sustain ACTH response during aging. Furthermore, the findings indicate that higher plasma ACTH levels and hyper-reactivity to a novel environment are inversely correlated with longevity in the rat. C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. RP TIZABI, Y (reprint author), HOWARD UNIV,COLL MED,DEPT PHARMACOL,WASHINGTON,DC 20059, USA. NR 23 TC 37 Z9 38 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD MAR-APR PY 1992 VL 13 IS 2 BP 227 EP 230 DI 10.1016/0197-4580(92)90034-U PG 4 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA HL796 UT WOS:A1992HL79600005 PM 1326090 ER PT J AU HEUSER, IJE BARONTI, F MARIN, CA MA, N MERRIAM, GR CHASE, TN MOURADIAN, MM AF HEUSER, IJE BARONTI, F MARIN, CA MA, N MERRIAM, GR CHASE, TN MOURADIAN, MM TI GROWTH-HORMONE SECRETION IN ALZHEIMERS-DISEASE - 24-HOUR PROFILE OF BASAL LEVELS AND RESPONSE TO STIMULATION AND SUPPRESSION STUDIES SO NEUROBIOLOGY OF AGING LA English DT Article DE ALZHEIMERS DISEASE; BASAL GROWTH-HORMONE SECRETION; GROWTH-HORMONE-RELEASING HORMONE; CLONIDINE; SOMATOSTATIN; SMATOSTAIN-ANALOG SMS-201-995 ID SENILE DEMENTIA; SOMATOSTATIN; CLONIDINE; NEUROPEPTIDES; INJECTION; RELEASE; RATS AB The 24-h growth hormone secretory pattern and GH response to growth hormone releasing hormone, the alpha(2)-adrenoceptor agonist clonidine and the somatostatin-analogue SMS 201-995 were evaluated in 9 patients with Alzheimer's disease and 9 age- and body mass-matched control subjects. The secretory profile did not differentiate between patients and controls. Both secreted the largest amount of GH during the early nighthours between 22.00-02.00, whereas the majority of daytime GH levels were below the assay's detection limit (0.4 ng/ml). No difference was found in GH response to GHRH between patients and controls. All subjects showed significantly enhanced GH secretion after GHRH. Dividing the patients into two groups according to age-of-onset (< 60 years >), there was a trend toward larger GH responses to GHRH for the early-onset group. No other parameter differentiated the groups. GH levels after clonidine were blunted in all subjects but one AD patient, probably due to an age-dependent attenuation frequently observed in subjects over 45 years of age. Finally, the administration of the somatostatin-analogue did not render conclusive results, since spontaneous decline of GH concentration was already beginning 2 hours before the drug was given and continued steadily throughout the observation period. In conclusion, patients with only mild to moderate degree of Alzheimer's disease have no prominent changes in GH regulation. C1 MAX PLANCK INST PSYCHIAT,INST CLIN,KRAEPELINSTR 10,W-8000 MUNICH 40,GERMANY. NINCDS,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. OI Mouradian, M. Maral/0000-0002-9937-412X NR 36 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD MAR-APR PY 1992 VL 13 IS 2 BP 255 EP 260 DI 10.1016/0197-4580(92)90037-X PG 6 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA HL796 UT WOS:A1992HL79600008 PM 1522942 ER PT J AU DUNCAN, MW MARKEY, SP WEICK, BG PEARSON, PG ZIFFER, H HU, YL KOPIN, IJ AF DUNCAN, MW MARKEY, SP WEICK, BG PEARSON, PG ZIFFER, H HU, YL KOPIN, IJ TI 2-AMINO-3-(METHYLAMINO)PROPANOIC ACID (BMAA) BIOAVAILABILITY IN THE PRIMATE SO NEUROBIOLOGY OF AGING LA English DT Article DE BMAA; ALS-PD; CYCADS; GUAM; BIOAVAILABILITY; PRIMATES ID AMYOTROPHIC LATERAL SCLEROSIS; MOTOR-NEURON DISEASE; PARKINSONISM-DEMENTIA; UNLIKELY CAUSE; CYCAD USE; NEUROTOXIN; GUAM; FOOD AB 2-Amino-3-(methylamino)-propanoic acid (BMAA) is a low potency excitatory amino acid present in the cycad plant that has been proposed as a factor in the high incidence of amyotrophic lateral sclerosis-parkinsonism dementia (ALS-PD) in the western Pacific region. We employed stable isotopic forms of BMAA to assess the oral bioavailability of this compound in cynomologus monkeys (n = 3). The stable isotope labeled BMAA ([N-15]-BMAA) was injected i.v. at the same time that the unlabeled compound was administered orally. Both forms of BMAA were then quantified in a 48h urine sample by gas chromatography-mass spectrometry (GC/MS). Following oral dosing, 80% of the administered BMAA was absorbed into the systemic circulation; thus, oral bioavailability was high and other routes of administration could not result in significantly higher circulating levels of BMAA for a given administered dose. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NINCDS,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892. NIMH,ANALYT BIOCHEM SECT,BETHESDA,MD 20892. NINCDS,ANIM HLTH & CARE SECT,BETHESDA,MD 20892. NR 20 TC 10 Z9 10 U1 1 U2 5 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD MAR-APR PY 1992 VL 13 IS 2 BP 333 EP 337 DI 10.1016/0197-4580(92)90047-2 PG 5 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA HL796 UT WOS:A1992HL79600018 PM 1522948 ER PT J AU AKUNNE, HC JOHANNESSEN, JN DECOSTA, BR RICE, KC ROTHMAN, RB AF AKUNNE, HC JOHANNESSEN, JN DECOSTA, BR RICE, KC ROTHMAN, RB TI MPTP LESIONS OF THE NIGROSTRIATAL DOPAMINERGIC PROJECTION DECREASE [H-3] 1-[1-(2-THIENYL)CYCLOHEXYL]-PIPERIDINE BINDING TO PCP SITE-2 - FURTHER EVIDENCE THAT PCP SITE-2 IS ASSOCIATED WITH THE BIOGENIC-AMINE REUPTAKE COMPLEX SO NEUROCHEMICAL RESEARCH LA English DT Article DE PHENCYCLIDINE; DOPAMINE; MPTP; RECEPTORS; PCP RECEPTOR ID HIGH-AFFINITY; GBR-12935 BINDING; TRANSPORT COMPLEX; H-3 GBR-12935; RAT-BRAIN; RECEPTOR AB Our previous studies have demonstrated that, using membranes of guinea pig brain, [H-3]1-[1-(2-thienyl)cyclohexyl]piperidine ([H-3]TCP) labels not only the phencyclidine binding site associated with the NMDA receptor (PCP site 1), but also a second high affinity binding site which is associated with the biogenic amine reuptake carrier (termed PCP site 2). To test this hypothesis, the binding of [H-3]GBR12935 to the dopamine transporter, and [H-3]TCP binding to PCP sites 1 and 2 were measured in caudates harvested from control, MPTP-treated and reserpine-treated dogs. MPTP treatment decreased dopamine levels by over 99%, decreased [H-3]GBR12935 binding by over 90%, decreased [H-3]TCP binding to PCP site 2 by about 50%, and had no significant effect on [H-3]TCP binding to PCP site 1. These data are consistent with the hypothesis that a portion of PCP site 2 is associated with dopaminergic nerve terminals in dog caudate. C1 NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224. NIDDK,MED CHEM LAB,BETHESDA,MD 20892. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. US FDA,CTR FOOD SAFETY & APPL NUTR,DIV TOXICOL,WASHINGTON,DC 20204. NR 14 TC 8 Z9 8 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0364-3190 J9 NEUROCHEM RES JI Neurochem. Res. PD MAR PY 1992 VL 17 IS 3 BP 261 EP 264 DI 10.1007/BF00966668 PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HE806 UT WOS:A1992HE80600007 PM 1320214 ER PT J AU HANBAUER, I GRILLI, M AF HANBAUER, I GRILLI, M TI MOLECULAR MECHANISMS INVOLVED IN TRANSPORT AND RELEASE OF DOPAMINE IN PRIMARY CULTURES OF MESENCEPHALIC NEURONS SO NEUROCHEMISTRY INTERNATIONAL LA English DT Article; Proceedings Paper CT SATELLITE MEETING ON DOPAMINERGIC SYSTEMS AND THEIR REGULATION, AT THE 11TH INTERNATIONAL CONGRESS OF PHARMACOLOGY CY JUL 08-11, 1990 CL COMO, ITALY SP CNR, ITALIAN SOC PHARM, C GOLGI FDN, ABBOTT LABS, GLAXO GRP RES, FIDIA, GLAXO, KNOLL, LILLY RES LABS, L P B PHARM INST ID CA-2+ CHANNELS; UPTAKE SITES; BINDING; NOREPINEPHRINE; STRIATUM; MEMBRANE; COCAINE; AMINES RP HANBAUER, I (reprint author), NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892, USA. NR 23 TC 3 Z9 3 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-0186 J9 NEUROCHEM INT JI Neurochem. Int. PD MAR PY 1992 VL 20 SU S BP S101 EP S105 PG 5 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HL803 UT WOS:A1992HL80300019 PM 1365405 ER PT J AU JOSEPH, JA ROTH, GS AF JOSEPH, JA ROTH, GS TI LOSS OF MUSCARINIC REGULATION OF STRIATAL DOPAMINE FUNCTION IN SENESCENCE SO NEUROCHEMISTRY INTERNATIONAL LA English DT Article; Proceedings Paper CT SATELLITE MEETING ON DOPAMINERGIC SYSTEMS AND THEIR REGULATION, AT THE 11TH INTERNATIONAL CONGRESS OF PHARMACOLOGY CY JUL 08-11, 1990 CL COMO, ITALY SP CNR, ITALIAN SOC PHARM, C GOLGI FDN, ABBOTT LABS, GLAXO GRP RES, FIDIA, GLAXO, KNOLL, LILLY RES LABS, L P B PHARM INST ID RECIPROCAL INHIBITORY CONTROL; MEMORY DEFICITS; RAT-BRAIN; AGED RATS; EFFECTOR SYSTEMS; RECEPTORS; RELEASE; ACETYLCHOLINE; AGONIST; CORTEX RP JOSEPH, JA (reprint author), NIA,GERONTOL RES CTR,MOLEC PHYSIOL & GENET SECT,BALTIMORE,MD 21224, USA. NR 44 TC 3 Z9 3 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-0186 J9 NEUROCHEM INT JI Neurochem. Int. PD MAR PY 1992 VL 20 SU S BP S237 EP S240 PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HL803 UT WOS:A1992HL80300045 PM 1365433 ER PT J AU SIBLEY, DR MONSMA, FJ MCVITTIE, LD GERFEN, CR BURCH, RM MAHAN, LC AF SIBLEY, DR MONSMA, FJ MCVITTIE, LD GERFEN, CR BURCH, RM MAHAN, LC TI MOLECULAR NEUROBIOLOGY OF DOPAMINE RECEPTOR SUBTYPES SO NEUROCHEMISTRY INTERNATIONAL LA English DT Article; Proceedings Paper CT SATELLITE MEETING ON DOPAMINERGIC SYSTEMS AND THEIR REGULATION, AT THE 11TH INTERNATIONAL CONGRESS OF PHARMACOLOGY CY JUL 08-11, 1990 CL COMO, ITALY SP CNR, ITALIAN SOC PHARM, C GOLGI FDN, ABBOTT LABS, GLAXO GRP RES, FIDIA, GLAXO, KNOLL, LILLY RES LABS, L P B PHARM INST ID EXPRESSION; CLONING; CDNA; RAT; D1 C1 NOVA PHARMACEUT CORP,BALTIMORE,MD 21224. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP SIBLEY, DR (reprint author), NINCDS,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892, USA. NR 14 TC 14 Z9 14 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-0186 J9 NEUROCHEM INT JI Neurochem. Int. PD MAR PY 1992 VL 20 SU S BP S17 EP S22 PG 6 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HL803 UT WOS:A1992HL80300005 PM 1365419 ER PT J AU COIRINI, H JOHNSON, AE SCHUMACHER, M MCEWEN, BS AF COIRINI, H JOHNSON, AE SCHUMACHER, M MCEWEN, BS TI SEX-DIFFERENCES IN THE REGULATION OF OXYTOCIN RECEPTORS BY OVARIAN-STEROIDS IN THE VENTROMEDIAL HYPOTHALAMUS OF THE RAT SO NEUROENDOCRINOLOGY LA English DT Article DE OXYTOCIN RECEPTORS; VENTROMEDIAL NUCLEUS; SEX DIFFERENCE; ESTRADIOL; ESTROGEN; PROGESTERONE; OVARIAN STEROIDS; HYPOTHALAMUS ID PROGESTIN RECEPTORS; FEMALE RATS; GONADOTROPIN-RELEASE; INDUCED FACILITATION; MATERNAL-BEHAVIOR; TIME COURSE; ESTRADIOL; BINDING; RECEPTIVITY; INDUCTION AB The facilitation of sexual receptivity by oxytocin (OT) in female rats is related to the regulation of oxytocin receptors (OTR) by ovarian steroids in the ventromedial nuclei (VMN) of the hypothalamus. In a previous study, we have shown that estradiol benzoate (EB) causes a twofold increase in OTR binding in the VMN. Progesterone (P) then modulates levels of the estrogen-induced OTR and increases the area occupied by the receptors by acting on the neuronal membrane. In the present study, we compared the effects of EB and P on OTR binding between males and females. In both sexes, EB increased the density of OTR and the area covered by the receptors at the level of the medial and caudal VMN. In estrogen-primed females, P further increased OTR levels in the medial VMN and the area covered by OTR at the level of the caudal VMN. By contrast, P did not modulate OTR binding in estrogen-primed males. Thus, the behavioral insensitivity of male rats to ovarian hormones, in particular to P, may be related to sex differences affecting the modulation of OTR binding. C1 ROCKEFELLER UNIV, NEUROENDOCRINOL LAB, 1230 YORK AVE, NEW YORK, NY 10021 USA. NIMH, COMPARAT STUDIES BRAIN & BEHAV SECT, CLIN SCI LAB, POOLESVILLE, MD USA. RI Schumacher, Michael/G-3581-2013 FU FIC NIH HHS [TW04103]; NINDS NIH HHS [NS07080] NR 39 TC 37 Z9 37 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 EI 1423-0194 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD MAR PY 1992 VL 55 IS 3 BP 269 EP 275 DI 10.1159/000126125 PG 7 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA HH467 UT WOS:A1992HH46700005 PM 1323800 ER PT J AU PASCUALLEONE, A COHEN, LG SHOTLAND, LI DANG, N PIKUS, A WASSERMANN, EM BRASILNETO, JP VALLSSOLE, J HALLETT, M AF PASCUALLEONE, A COHEN, LG SHOTLAND, LI DANG, N PIKUS, A WASSERMANN, EM BRASILNETO, JP VALLSSOLE, J HALLETT, M TI NO EVIDENCE OF HEARING-LOSS IN HUMANS DUE TO TRANSCRANIAL MAGNETIC STIMULATION SO NEUROLOGY LA English DT Article ID TEMPORARY THRESHOLD SHIFT; SUSCEPTIBILITY; IMPULSES; HAZARD AB Prompted by the description of hearing loss in rabbits exposed to the acoustic artifact of magnetic stimulation, we compared the results of audiologic studies before and after exposure to transcranial magnetic stimulation in humans. We found no evidence of temporary or permanent threshold shifts in any of the subjects, even in those exposed to transcranial magnetic stimulation repeatedly for several years. Risk of hearing loss from the acoustic artifact of magnetic stimulation, as evaluated by audiograms, tympanograms, acoustic reflexes, and auditory evoked potentials, seems to be small in humans. C1 NINCDS,HUMAN CORTICAL PHYSIOL UNIT,BLDG 10,ROOM 5N226,BETHESDA,MD 20892. NINCDS,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. NIDOCD,CLIN AUDIOL UNIT,BETHESDA,MD. RI Pascual-Leone, Alvaro/G-6566-2011 NR 37 TC 60 Z9 61 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR PY 1992 VL 42 IS 3 BP 647 EP 651 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA HJ992 UT WOS:A1992HJ99200034 PM 1549231 ER PT J AU HYDE, TM AARONSON, BA RANDOLPH, C RICKLER, KC WEINBERGER, DR AF HYDE, TM AARONSON, BA RANDOLPH, C RICKLER, KC WEINBERGER, DR TI RELATIONSHIP OF BIRTH-WEIGHT TO THE PHENOTYPIC-EXPRESSION OF GILLES-DE-LA-TOURETTES SYNDROME IN MONOZYGOTIC TWINS SO NEUROLOGY LA English DT Article ID LA-TOURETTES SYNDROME; TRANSFUSION SYNDROME; IDENTICAL-TWINS; CONCORDANT; HANDEDNESS; CRITERIA; PAIRS; TICS AB We studied 16 pairs of monozygotic twins (mean age, 12.8 +/- 1.4 years; age range, 8 to 26 years; sex, 12 male pairs, four female pairs) in whom at least one twin had Gilles de la Tourette's syndrome (TS) to determine the concordance rates for TS and tic disorders and to examine environmental factors accounting for intrapair differences in tic severity. In this cohort, the concordance rate for TS was 56%, and the concordance rate for tic disorders was 94%, supporting a primary genetic basis for TS and tic disorders with a high rate of penetrance for the gene. Thirteen of the pairs had differing birth weights and the lower birth-weight twin had a higher tic score in 12 of these pairs. The magnitude of the intrapair birth-weight difference (BWD) strongly predicted the magnitude of the intrapair tic score difference. The difference in tic severity could not be explained by any postnatal medical events. These findings suggest that crucial events affecting the phenotypic expression of TS occur in utero and that the factors causing the BWD also are related to tic severity. RP HYDE, TM (reprint author), ST ELIZABETH HOSP,NIMH,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA. NR 48 TC 139 Z9 143 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR PY 1992 VL 42 IS 3 BP 652 EP 658 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA HJ992 UT WOS:A1992HJ99200035 PM 1549232 ER PT J AU BOJA, JW MARKHAM, L PATEL, A UHL, G KUHAR, MJ AF BOJA, JW MARKHAM, L PATEL, A UHL, G KUHAR, MJ TI EXPRESSION OF A SINGLE DOPAMINE TRANSPORTER CDNA CAN CONFER 2 COCAINE BINDING-SITES SO NEUROREPORT LA English DT Article DE DOPAMINE TRANSPORTER; COCAINE BINDING SITE; [H-3]WIN 35,428; CDNA; TRANSFECTED COS CELLS ID RECEPTORS AB RADIOLABELED cocaine analogs can bind to low and high affinity sites on striatal dopamine transporters (DAT). Recently, a cDNA encoding a rat brain dopamine transporter pDAT1 has been cloned. COS cells transfected with the pDAT1 in a eukaryotic expression vector express both a high (K(D) = 3.4 nM) and low affinity (K(D) = 163.6 nM) cocaine binding sites, suggesting that both sites are provided by a single gene product. C1 NIDA,ADDICT RES CTR,MOLEC NEUROBIOL LAB,POB 5180,BALTIMORE,MD. NIDA,ADDICT RES CTR,MOLEC PHARMACOL LAB,BALTIMORE,MD. JOHNS HOPKINS UNIV,DEPT NEUROL,NEUROSCI BRANCH,BALTIMORE,MD 21224. NR 8 TC 46 Z9 47 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD MAR PY 1992 VL 3 IS 3 BP 247 EP 248 DI 10.1097/00001756-199203000-00007 PG 2 WC Neurosciences SC Neurosciences & Neurology GA HM185 UT WOS:A1992HM18500007 PM 1515577 ER PT J AU ROGAN, WJ GLADEN, BC AF ROGAN, WJ GLADEN, BC TI NEUROTOXICOLOGY OF PCBS AND RELATED-COMPOUNDS SO NEUROTOXICOLOGY LA English DT Article; Proceedings Paper CT 3RD MEETING OF THE INTERNATIONAL NEUROTOXICOLOGY ASSOC CY JUL 01-05, 1991 CL PARMA, ITALY SP INT NEUROTOXICOL ASSOC DE POLYCHLOROBIPHENYL COMPOUNDS; POLYCHLORINATED DIBENZOFURANS; NERVOUS SYSTEM DISEASES; CHEMICALLY INDUCED; CHILD DEVELOPMENT; NEUROTOXICOLOGY; REVIEWS ID POLYCHLORINATED-BIPHENYLS PCBS; HUMAN-MILK; EXPOSURE; CONTAMINANTS; CONGENERS; CHILDREN; DOPAMINE; LESIONS; INUTERO; WORKERS AB Polychlorinated biphenyls (PCBs) are a family of 209 chemicals with two linked phenyl rings and variable chlorination. They are clear oils at room temperature. They were produced from the 1930s until banned in the 1970s because of toxicity and evidence of widespread environmental contamination. They were used mostly as insulators in electrical equipment; their widespread occurrence in the environment is more a consequence of uncontrolled disposal than of deliberate dissemination. In Asia, there have been two outbreaks of poisoning due to cooking oil contaminated by thermally degraded PCBs. Studies in workers exposed chronically to "clean" PCBs, workers exposed acutely to thermally degraded PCBs in clean-up of fires, and adult patients in Asia who ingested contaminated rice oil consistently show slowed nerve conduction and sometimes show headache, lassitude, and other CNS symptoms. In children exposed to background levels in the US, those with the highest transplacental exposure show hypotonia and hyporeflexia at birth and slowed motor development through age two, a defect in visual memory processing at 7 mon, and defects in short term memory at 4 years. Despite the presence of PCBs in breast milk, no association between breast milk exposure and any measured outcome has been seen other than lower activity levels at 4 years among long term breast fed children at the highest PCB levels. In Asia, children who were in utero at or after the 1968 exposure in Japan or the 1979 exposure in Taiwan showed clinically evident developmental delay. In Taiwan, the children were shown to have a variety of ectodermal defects, but the association between these defects and developmental delay was weak. In several species of laboratory animals, PCBs administered to the pregnant mother or perinatally produce impairments in learning and hyperactivity in the young. The mechanism by which PCBs produce damage to the brain or to peripheral nerves is unknown; PCBs alter dopamine concentrations in the CNS, interfere with (especially neonatal) thyroid function, and in one experiment caused the formation of peninsular projections around anterior horn cells like those seen in Werdnig Hoffman paralysis. Thus far, developmental impairment in children has been documented to occur at levels far below any other form of morbidity associated with PCBs in humans, and there are now two independent studies showing such delay at levels of PCBs commonly encountered by the general population. This makes the regulation of PCBs problematic, since clean-up of the large amounts already in the environment will be extremely expensive. C1 NIEHS,STAT & BIOMATH BRANCH,RES TRIANGLE PK,NC 27709. RP ROGAN, WJ (reprint author), NIEHS,EPIDEMIOL BRANCH,MAIL DROP A305,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Rogan, Walter/I-6034-2012 OI Rogan, Walter/0000-0002-9302-0160 NR 44 TC 116 Z9 117 U1 1 U2 10 PU INTOX PRESS INC PI LITTLE ROCK PA PO BOX 24865, LITTLE ROCK, AR 72221 SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD SPR PY 1992 VL 13 IS 1 BP 27 EP 35 PG 9 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA HN298 UT WOS:A1992HN29800004 PM 1508429 ER PT J AU BOGUSKI, MS HARDISON, RC SCHWARTZ, S MILLER, W AF BOGUSKI, MS HARDISON, RC SCHWARTZ, S MILLER, W TI ANALYSIS OF CONSERVED DOMAINS AND SEQUENCE MOTIFS IN CELLULAR REGULATORY PROTEINS AND LOCUS-CONTROL REGIONS USING NEW SOFTWARE TOOLS FOR MULTIPLE ALIGNMENT AND VISUALIZATION SO NEW BIOLOGIST LA English DT Article DE COMPUTER SOFTWARE; GTPASE-ACTIVATING PROTEINS; LOCUS CONTROL REGIONS; MULTIPLE SEQUENCE ALIGNMENT; PRENYLATION; FARNESYLTRANSFERASE; SEQUENCE MOTIFS; SRC HOMOLOGY DOMAINS ID BETA-GLOBIN LOCUS; GTPASE-ACTIVATING PROTEIN; DOMINANT CONTROL REGION; RECEPTOR TYROSINE KINASES; TRANSGENIC MICE; GENE-PRODUCT; SACCHAROMYCES-CEREVISIAE; PEPTIDE-BINDING; ERYTHROID-CELLS; CDNA CLONING C1 PENN STATE UNIV,INST MOLEC EVOLUTIONARY GENET,UNIV PK,PA 16802. NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20892. PENN STATE UNIV,DEPT MOLEC & CELL BIOL,UNIV PK,PA 16802. PENN STATE UNIV,DEPT COMP SCI,UNIV PK,PA 16802. RI Hardison, Ross/G-1142-2010 OI Hardison, Ross/0000-0003-4084-7516 FU NIDDK NIH HHS [DK01589, DK27635]; NLM NIH HHS [R01 LM05110] NR 59 TC 34 Z9 35 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4674 J9 NEW BIOL PD MAR PY 1992 VL 4 IS 3 BP 247 EP 260 PG 14 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA JR311 UT WOS:A1992JR31100010 PM 1581291 ER PT J AU HILL, MN SCHRON, EB AF HILL, MN SCHRON, EB TI OPPORTUNITIES FOR NURSE RESEARCHERS IN CLINICAL-TRIALS SO NURSING RESEARCH LA English DT Editorial Material C1 NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,CLIN TRIALS BRANCH,BETHESDA,MD 20892. RP HILL, MN (reprint author), JOHNS HOPKINS UNIV,SCH NURSING,BALTIMORE,MD 21218, USA. NR 18 TC 6 Z9 6 U1 0 U2 0 PU AMER J NURSING CO PI NEW YORK PA 555 W 57TH ST, NEW YORK, NY 10019-2961 SN 0029-6562 J9 NURS RES JI Nurs. Res. PD MAR-APR PY 1992 VL 41 IS 2 BP 114 EP 116 PG 3 WC Nursing SC Nursing GA HL944 UT WOS:A1992HL94400011 PM 1549515 ER PT J AU STRATTON, P MOFENSON, LM WILLOUGHBY, AD AF STRATTON, P MOFENSON, LM WILLOUGHBY, AD TI HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION IN PREGNANT-WOMEN UNDER CARE AT AIDS CLINICAL-TRIALS CENTERS IN THE UNITED-STATES SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID ZIDOVUDINE; DECISIONS AB The federal government supports a nationwide network of medical centers to evaluate promising therapies against the human immunodeficiency virus (HIV) and the opportunistic infections and cancers that characterize AIDS. Forty-five obstetricians from the 49 medical centers receiving federal research support for the conduct of AIDS-related clinical trials, in preparation for a meeting, provided summary information about the number and clinical status of the known HIV-infected pregnant women under their care and the prenatal screening policies for HIV infection at their institutions. In the 12-month period before December 1989, an estimated 1000-1801 HIV-infected women delivered at these centers. The majority (82%) were asymptomatic, 12% were symptomatic, and 6% had AIDS. Routine T-cell testing of infected women was done as part of prenatal care in only 30 of 45 centers. Pneumocystis carinii pneumonia was reported in 35 women. Zidovudine was administered during pregnancy in 29 women. Formal prenatal screening policies have been implemented at the majority (43 of 45) of the medical centers. Most of the infected women identified at these centers chose to continue the pregnancy. With the increasing incidence of HIV infection in women, information concerning the clinical and immunologic state of pregnant infected women and the present use of antiretroviral and other related therapeutics during pregnancy can guide the approach to women's health care and is crucial to the design and implementation of AIDS clinical trials. RP STRATTON, P (reprint author), NICHHD,PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH,EXECUT PLAZA S,ROOM 450,BETHESDA,MD 20892, USA. OI Mofenson, Lynne/0000-0002-2818-9808 NR 24 TC 13 Z9 14 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD MAR PY 1992 VL 79 IS 3 BP 364 EP 368 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA HF011 UT WOS:A1992HF01100007 PM 1738515 ER PT J AU SPERLING, RS STRATTON, P AF SPERLING, RS STRATTON, P TI TREATMENT OPTIONS FOR HUMAN IMMUNODEFICIENCY VIRUS-INFECTED PREGNANT-WOMEN SO OBSTETRICS AND GYNECOLOGY LA English DT Review ID PNEUMOCYSTIS-CARINII PNEUMONIA; PLACEBO-CONTROLLED TRIAL; AIDS-RELATED COMPLEX; TRIMETHOPRIM-SULFAMETHOXAZOLE; AZIDOTHYMIDINE AZT; DOUBLE-BLIND; PROPHYLAXIS; PENTAMIDINE; EFFICACY; DISEASE AB The increasing seroprevalence of human immunodeficiency virus (HIV) among women of reproductive age and the risks of vertical transmission of HIV have led to recommendations for routine prenatal HIV counseling and testing. The incentive to undergo such testing is related not only to fetal concerns, but also to the potential benefit of early and comprehensive therapy for women. Treatments that should be considered for use during pregnancy include the antiretroviral agent zidovudine and prophylactic agents to prevent Pneumocystis carinii pneumonia, the most common opportunistic infection seen in patients progressing to AIDS. Assessment of the risks and benefits of these treatments during pregnancy is complex and requires discussions between physician and patient. This paper reviews current information and provides recommendations for incorporating therapies into obstetric practice. C1 MT SINAI MED CTR,DEPT OBSTET GYNECOL & REPROD SCI,NEW YORK,NY 10029. NICHHD,PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH,BETHESDA,MD 20892. FU NIAID NIH HHS [UO1-AI-27667] NR 39 TC 33 Z9 33 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD MAR PY 1992 VL 79 IS 3 BP 443 EP 448 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA HF011 UT WOS:A1992HF01100024 PM 1738529 ER PT J AU KOCHEL, T RICE, NR AF KOCHEL, T RICE, NR TI V-REL- AND C-REL- PROTEIN COMPLEXES BIND TO THE NF-KAPPA-B SITE INVITRO SO ONCOGENE LA English DT Article ID AVIAN RETICULOENDOTHELIOSIS VIRUS; TRANSFORMED LYMPHOID-CELLS; TUMOR-NECROSIS-FACTOR; TRANSCRIPTIONAL ACTIVATOR; ONCOGENE ENCODES; GENE; DNA; FIBROBLASTS; EXPRESSION; NUCLEAR AB Previous work by others has revealed homology between the rel oncogene and the transcription factor NF-kappa-B. Further, in vitro-translated v-rel protein and c-rel protein are able to bind to an oligonucleotide containing the kappa-B binding site. Unlike the in vitro-translated product, cellular Rel protein exists in high molecular weight complexes with several other proteins. In this report we show that immunopurified cellular complexes containing the v-rel protein and/or the c-rel protein are also able to bind to an oligonucleotide containing the kappa-B site. These cellular complexes are heterogeneous in size, and all sizes appeared to have binding activity. UV cross-linking demonstrated that the Rel proteins themselves were bound to the DNA. Thus it is likely that the Rel proteins play a direct role in transcriptional regulation. C1 NCI,FREDERICK CANC RES & DEV CTR,MOLECUL VIROL & CARCINOGENESIS LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 39 TC 12 Z9 12 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR PY 1992 VL 7 IS 3 BP 567 EP 572 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HK005 UT WOS:A1992HK00500025 PM 1549370 ER PT J AU ENGELKE, W RUTTIMANN, UE TSUCHIMOCHI, M BACHER, JD AF ENGELKE, W RUTTIMANN, UE TSUCHIMOCHI, M BACHER, JD TI AN EXPERIMENTAL-STUDY OF NEW DIAGNOSTIC METHODS FOR THE EXAMINATION OF OSSEOUS LESIONS IN THE TEMPOROMANDIBULAR-JOINT SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS LA English DT Article ID DIGITAL SUBTRACTION RADIOGRAPHY; BONE-SCINTIGRAPHY AB Digital subtraction radiography, tomosynthesis, bone uptake of radionuclide, and arthroscopy were evaluated for detection and quantification of bony lesions induced unilaterally in the condyles of six dogs. A stereotaxic head-holder facilitated acquisition of reproducible radiographs suitable for subtraction and for circular tomosynthesis. Bone uptake of technetium-99m methylene diphosphonate was measured with a hand-held collimated miniature detector. Arthroscopy was performed with an arthroscope of 2.4 mm diameter. Bone defect mass determined by subtraction radiography correlated highly (r = 0.92, p < 0.001) with the calcium content of removed bone measured by atomic spectroscopy. Both subtraction radiography and tomosynthesis indicated reshaping of the condyle into a more anterior position over a 10-week follow-up period. Radionuclide uptake was significantly elevated (p < 0.04) from 2 to 10 weeks after surgery and correlated (r = 0.73, p < 0.05) with regained bone mass measured by subtraction radiography. Arthroscopy revealed progressive degeneration of cartilage with denudation in the fossa. Both radiographic techniques demonstrated the lesions and bone remodeling, but only subtraction provided quantitative results. Radionuclide uptake predicted quantitatively future bone mass changes, and arthroscopy revealed cartilage and soft tissue status not otherwise observable. C1 NIDR,DIAGNOST SYST BRANCH,BETHESDA,MD 20892. NIH,VET MED & SURG SECT,VET RESOURCES BRANCH,SURG UNIT,BETHESDA,MD 20892. NR 32 TC 14 Z9 14 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1079-2104 J9 ORAL SURG ORAL MED O JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. PD MAR PY 1992 VL 73 IS 3 BP 348 EP 359 DI 10.1016/0030-4220(92)90134-C PG 12 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HJ297 UT WOS:A1992HJ29700021 PM 1545968 ER PT J AU SNOW, JB AF SNOW, JB TI FROM THE NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article RP SNOW, JB (reprint author), NIDCD,BLDG 31,ROOM 3C-02,BETHESDA,MD 20892, USA. 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 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD MAR PY 1992 VL 106 IS 3 BP 311 EP 314 PG 4 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA HJ155 UT WOS:A1992HJ15500022 PM 1589225 ER PT J AU GRACELY, RH AF GRACELY, RH TI EVALUATION OF MULTIDIMENSIONAL PAIN SCALES SO PAIN LA English DT Article ID QUESTIONNAIRE; SENSATIONS; ANALGESIA RP GRACELY, RH (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 10,ROOM IN-103,BETHESDA,MD 20892, USA. NR 17 TC 59 Z9 60 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD MAR PY 1992 VL 48 IS 3 BP 297 EP 300 DI 10.1016/0304-3959(92)90076-N PG 4 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA HM571 UT WOS:A1992HM57100001 PM 1594252 ER PT J AU ZEIGLER, D LYNCH, SA MUIR, J BENJAMIN, J MAX, MB AF ZEIGLER, D LYNCH, SA MUIR, J BENJAMIN, J MAX, MB TI TRANSDERMAL CLONIDINE VERSUS PLACEBO IN PAINFUL DIABETIC NEUROPATHY SO PAIN LA English DT Article DE CONTROLLED CLINICAL TRIALS; ADRENERGIC AGONISTS; ANALGESIA; PAIN; NOREPINEPHRINE ID RELIEVES POSTHERPETIC NEURALGIA; EPIDURAL CLONIDINE; CANCER PAIN; ANALGESIA; AMITRIPTYLINE; HYPERALGESIA AB In a randomized, double-blind, 2-period crossover study, 24 patients with pain due to diabetic polyneuropathy received transdermal clonidine, 0.3 mg/day, and placebo patches, each for 6 weeks. Pain was assessed daily by a 13-word descriptor list. Mean daily pain scores for the 6th week, the primary outcome variable, averaged 13% lower with clonidine than with placebo (95% conf. lim. for clonidine effect: 29% reduction to 3% increase in pain), which was not statistically significant (P = 0.11, 2-tailed paired t test). After this study, however, 9 patients who wished to continue clonidine had single (3 patients) or multiple (6 patients) cycles of clonidine withdrawal and rechallenge. Seven of 9 patients consistently reported return of pain with patch withdrawal followed by relief upon retreatment. One patient had an equivocal response, and the other patient had no relief upon retreatment. The 7 responders appeared similar to the other 17 patients in pain quality and neurological exam. We conclude that there may be a subset of patients with diabetic polyneuropathy who respond to transdermal clonidine. Further research is needed to identify features of neuropathic pain that predict drug response and to develop study designs that are more sensitive to a response in a subset of patients. C1 NIDR, NEUROBIOL & ANESTHESIOL BRANCH,PAIN RES CLIN, BLDG 10,ROOM 3C-405, BETHESDA, MD 20892 USA. NIH, DEPT CLIN CTR NURSING, BETHESDA, MD 20892 USA. WALTER REED ARMY MED CTR, DEPT PHYS MED & REHABIL, WASHINGTON, DC 20307 USA. NR 31 TC 53 Z9 54 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 EI 1872-6623 J9 PAIN JI Pain PD MAR PY 1992 VL 48 IS 3 BP 403 EP 408 DI 10.1016/0304-3959(92)90092-P PG 6 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA HM571 UT WOS:A1992HM57100017 PM 1594263 ER PT J AU WATERS, AP MCCUTCHAN, TF AF WATERS, AP MCCUTCHAN, TF TI PLASMODIUM-FALCIPARUM - BIRDS TO HUMANS SO PARASITOLOGY TODAY LA English DT Letter C1 NIH,PARASIT DIS LAB,MALARIA SECT,BLDG 4,BETHESDA,MD 20892. RP WATERS, AP (reprint author), LEIDEN UNIV,DEPT PARASITOL,MALARIA SECT,POSTBUS 9605,2300 RC LEIDEN,NETHERLANDS. RI Waters, Andy/C-9377-2009 OI Waters, Andy/0000-0001-8900-2982 NR 10 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0169-4758 J9 PARASITOL TODAY JI Parasitol. Today PD MAR PY 1992 VL 8 IS 3 BP 91 EP 92 DI 10.1016/0169-4758(92)90245-W PG 2 WC Parasitology SC Parasitology GA HF600 UT WOS:A1992HF60000010 PM 15463581 ER PT J AU LAUER, RM BARNESS, LA CLARK, R DECKELBAUM, RJ FINBERG, L KWITEROVICH, PO MCBRIDE, PE SCHIEKEN, RM SCOTT, LW STRONG, JP WEIDMAN, WH ZIEGLER, EE CLEEMAN, JI ERNST, N HARLAN, WR RIFKIND, B ROSSOUW, JE QUINTADLER, L MCNEIL, CT AF LAUER, RM BARNESS, LA CLARK, R DECKELBAUM, RJ FINBERG, L KWITEROVICH, PO MCBRIDE, PE SCHIEKEN, RM SCOTT, LW STRONG, JP WEIDMAN, WH ZIEGLER, EE CLEEMAN, JI ERNST, N HARLAN, WR RIFKIND, B ROSSOUW, JE QUINTADLER, L MCNEIL, CT TI NATIONAL CHOLESTEROL EDUCATION-PROGRAM (NCEP) - HIGHLIGHTS OF THE REPORT OF THE EXPERT PANEL ON BLOOD CHOLESTEROL LEVELS IN CHILDREN AND ADOLESCENTS SO PEDIATRICS LA English DT Editorial Material C1 NHLBI,NCEP,BLDG 31,ROOM 4A05,BETHESDA,MD 20892. NR 0 TC 289 Z9 305 U1 0 U2 4 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAR PY 1992 VL 89 IS 3 BP 495 EP 501 PG 7 WC Pediatrics SC Pediatrics GA HG529 UT WOS:A1992HG52900026 ER PT J AU LAUER, RM BARNESS, LA CLARK, R DECKELBAUM, RJ FINBERG, L KWITEROVICH, PO MCBRIDE, PE SCHIEKEN, RM SCOTT, LW STRONG, JP WEIDMAN, WH ZIEGLER, EE CLEEMAN, JI ERNST, N HARLAN, WR RIFKIND, B ROSSOUW, JE QUINTADLER, L MCNEIL, CT AF LAUER, RM BARNESS, LA CLARK, R DECKELBAUM, RJ FINBERG, L KWITEROVICH, PO MCBRIDE, PE SCHIEKEN, RM SCOTT, LW STRONG, JP WEIDMAN, WH ZIEGLER, EE CLEEMAN, JI ERNST, N HARLAN, WR RIFKIND, B ROSSOUW, JE QUINTADLER, L MCNEIL, CT TI NATIONAL CHOLESTEROL EDUCATION-PROGRAM - REPORT OF THE EXPERT-PANEL-ON-BLOOD-CHOLESTEROL-LEVELS-IN-CHILDREN-AND-ADOLESCENTS SO PEDIATRICS LA English DT Review ID CORONARY HEART-DISEASE; HIGH-DENSITY LIPOPROTEIN; HYPERCHOLESTEROLEMIC SCHOOL-CHILDREN; FAMILY HISTORY DEFINITIONS; CANCER PRONE PEDIGREES; MIDDLE-AGED MEN; CARDIOVASCULAR-DISEASE; RISK-FACTORS; SERUM-CHOLESTEROL; MYOCARDIAL-INFARCTION C1 UNIV WISCONSIN,CTR CLIN SCI,MADISON,WI 53706. UNIV KANSAS,MED CTR,SCH NURSING,KANSAS CITY,KS 66103. UNIV KANSAS,MED CTR,SCH MED,KANSAS CITY,KS 66103. COLUMBIA UNIV,DEPT PEDIAT,DIV GASTROENTEROL & NUTR,NEW YORK,NY 10027. SUNY DOWNSTATE MED CTR,DEPT PEDIAT,BROOKLYN,NY. JOHNS HOPKINS UNIV,SCH MED,LIPID RES ATHEROSCLEROSIS UNIT,BALTIMORE,MD 21205. UNIV WISCONSIN,SCH MED,DEPT FAMILY MED & PRACTICE,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT MED,DIV CARDIOL,MADISON,WI 53706. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PEDIAT CARDIOL,RICHMOND,VA 23298. BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. LOUISIANA STATE UNIV,MED CTR,DEPT PATHOL,NEW ORLEANS,LA 70112. MAYO CLIN & MAYO FDN,PEDIAT CARDIOL SECT,ROCHESTER,MN 55905. UNIV IOWA,COLL MED,DEPT PEDIAT,IOWA CITY,IA 52242. NHLBI,NATL CHOLESTEROL EDUC PROGRAM,BETHESDA,MD 20892. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. NHLBI,DIV HEART & VASC DIS,LIPID METAB ATHEROGENESIS BRANCH,BETHESDA,MD 20892. UNIV RES CORP,BETHESDA,MD. RP LAUER, RM (reprint author), UNIV IOWA HOSP & CLIN,DIV PEDIAT CARDIOL,IOWA CITY,IA 52242, USA. NR 240 TC 0 Z9 0 U1 1 U2 4 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAR PY 1992 VL 89 IS 3 SU S BP R1 EP & PG 0 WC Pediatrics SC Pediatrics GA HH026 UT WOS:A1992HH02600001 ER PT J AU TSUTSUMI, K STROMBERG, C SAAVEDRA, JM AF TSUTSUMI, K STROMBERG, C SAAVEDRA, JM TI CHARACTERIZATION OF ANGIOTENSIN-II RECEPTOR SUBTYPES IN THE RAT SPLEEN SO PEPTIDES LA English DT Article DE RENIN ANGIOTENSIN SYSTEM; ANGIOTENSIN RECEPTORS; IMMUNE SYSTEM; DUP-753; CGP-42112-A; PD-123177; DITHIOTHREITOL; AT(1) RECEPTORS ID MONONUCLEAR CELL REACTIVITY; BINDING-SITES; THYMIDINE INCORPORATION; MAMMALIAN SPLEEN; AUTORADIOGRAPHY; IDENTIFICATION; INNERVATION; SUPPRESSION; BRAIN; GLAND AB Quantitative autoradiography was used to determine the subtype of ANG receptors in the red pulp of the rat spleen. The AT1 antagonist DuP 753 competed for ANG binding with high affinity; binding was abolished by dithiothreitol. The AT2 competitor CGP 42112 A showed lower affinity, and the AT2 competitor PD 123177 did not affect binding at 10(-5) M. These data indicated the presence of only AT1 receptors. AT1 receptor number was similar in immature (2 weeks old) and adult (8 weeks old) rats. Binding was sensitive to guanine nucleotides, suggesting an association with G-proteins. Angiotensin II, at a dose of 10(-7) M, stimulated inositol phosphate formation 33% over control values in spleen from 8-week-old rats. This effect was significantly blocked by 10(-5) M DuP 753. We suggest a possible role of AT1 receptors in the regulation of splenic volume, blood flow, and lymphocyte function. RP TSUTSUMI, K (reprint author), NIMH,CLIN SCI LAB,PHARMACOL SECT,BLDG 10,ROOM 2D-45,BETHESDA,MD 20892, USA. NR 31 TC 26 Z9 27 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0196-9781 J9 PEPTIDES JI Peptides PD MAR-APR PY 1992 VL 13 IS 2 BP 291 EP 296 DI 10.1016/0196-9781(92)90111-F PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA HW886 UT WOS:A1992HW88600014 PM 1329044 ER PT J AU BITAR, MS KEIS, AF OWUSU, SE MULVEN, R DESOUZA, EB AF BITAR, MS KEIS, AF OWUSU, SE MULVEN, R DESOUZA, EB TI IMPAIRMENT OF ALBUTEROL-INDUCED SUPPRESSION OF FOOD-INTAKE IN DIABETES-MELLITUS SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE DIABETES; INGESTIVE BEHAVIOR; BETA-ADRENOCEPTORS; ALBUTEROL ID BETA-ADRENERGIC RECEPTORS; RAT-BRAIN; QUANTITATIVE AUTORADIOGRAPHY; BETA-2-ADRENERGIC RECEPTORS; NOREPINEPHRINE METABOLISM; PITUITARY; INHIBITION; INSULIN AB Albuterol (salbutamol), a beta(2) adrenoreceptor agonist, produced a dose-dependent decrease in food intake in Sprague-Dawley male control rats. This phenomenon appeared to be impaired in streptozotocin (STZ) diabetic rats. The density of beta(2) adrenoreceptors in the ventromedial hypothalamic nucleus was increased as a function of diabetes. In contrast, a decrease in the ventromedial hypothalamic 5-hydroxyindoleacetic acid (5-HIAA) concentration, an indicator of serotonin (5-hydroxytryptamine; 5-HT) release or turnover rate, was observed in this disease state. Neither the beta(2) adrenoreceptor level nor 5-HT turnover rate was altered in the periventricular hypothalamic nucleus of STZ diabetic rats. The concentrations of 5-HT in both hypothalamic nuclei were unchanged in these animals. Neurochemical and behavioral abnormalities featured in the diabetic state were reversed with institution of insulin therapy. These data conclude that diabetes-related impairment in the anorexic action of albuterol may be due to derangements in ventromedial hypothalamic beta(2) adrenoreceptor function. C1 NIDA,NEUROSCI BRANCH, NEUROBIOL LAB,BALTIMORE,MD 21224. RP BITAR, MS (reprint author), PENN COLL PODIATR MED,DEPT BIOMED SCI,PHARMACOL SECT,PHILADELPHIA,PA 19107, USA. NR 38 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD MAR PY 1992 VL 41 IS 3 BP 483 EP 487 DI 10.1016/0091-3057(92)90361-I PG 5 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA HN238 UT WOS:A1992HN23800003 PM 1374915 ER PT J AU JASKIW, GE WEINBERGER, DR AF JASKIW, GE WEINBERGER, DR TI IBOTENIC ACID LESIONS OF MEDIAL PREFRONTAL CORTEX AUGMENT SWIM-STRESS-INDUCED LOCOMOTION SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Note DE PREFRONTAL CORTEX; IBOTENIC ACID; STRESS; SWIM; LOCOMOTION; DOPAMINE; RAT ID NUCLEUS ACCUMBENS; RAT; AMPHETAMINE; INCREASE; STIMULI; DOPAC AB Locomotor activity of rats with sham or ibotenic acid lesions of the medial prefrontal cortex (MPFC) was assessed after animals were exposed to a 15-min swim or control stress. Swim-stress-induced locomotor activity was augmented in the MPFC-lesioned rats. These and other data suggest that lesions of the MPFC are followed by an exaggeration of the normal behavioral response to stress. Dysregulation of dopamine transmission in the basal ganglia may be involved. C1 NIMH,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,NIMH RES CTR,WASHINGTON,DC 20032. NR 19 TC 35 Z9 35 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD MAR PY 1992 VL 41 IS 3 BP 607 EP 609 DI 10.1016/0091-3057(92)90380-X PG 3 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA HN238 UT WOS:A1992HN23800022 PM 1584841 ER PT J AU RESZKA, K LOWN, JW CHIGNELL, CF AF RESZKA, K LOWN, JW CHIGNELL, CF TI PHOTOSENSITIZATION BY ANTICANCER AGENTS .10. ORTHO-SEMIQUINONE AND SUPEROXIDE RADICALS PRODUCED DURING ANTHRAPYRAZOLE-SENSITIZED OXIDATION OF CATECHOLS SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID ELECTRON-SPIN RESONANCE; SINGLET MOLECULAR-OXYGEN; VISIBLE-LIGHT; PHOTOLYSIS; COMPLEXES; IONS AB Photosensitized oxidation of catechol, 3,4-dihydroxybenzoic acid (DHBA), 3,4-dihydroxydihydrocinnamic acid (DHCA), and 3,4-dihydroxy-phenylalanine (DOPA) by novel anticancer agents, anthrapyrazoles (AP), has been studied employing EPR and the spin trapping technique. The formation of o-semiquinone radicals, the one-electron oxidation products of the catechols, stabilized in the form of zinc ion complexes, has been demonstrated. Rate constants for the disproportionation of the semiquinone radical/Zn2+ complexes in (DMSO)/acetate buffer (pH 4.5, 1:1 vol/vol; 100 mM Zn2+) mixture have been determined to be 0.35 x 10(4), 14 x 10(4), 8.8 x 10(4) and 3 x 10(4) M-1 s-1 for catechol, DHBA, DHCA and DOPA respectively. The presence of oxygen enhanced rather than inhibited the photogeneration of the o-semiquinone radicals and facilitated their EPR detection, The EPR spectrum of the superoxide radical adduct with the spin trap 5,5-dimethyl-1-pyrroline-N-oxide was observed for the first time during photosensitized oxidation of the catechols in acidic aqueous solutions and in DMSO/acetate buffer mixture. C1 UNIV ALBERTA,DEPT CHEM,EDMONTON T6G 2G2,ALBERTA,CANADA. RP RESZKA, K (reprint author), NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709, USA. NR 25 TC 13 Z9 13 U1 0 U2 3 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD MAR PY 1992 VL 55 IS 3 BP 359 EP 366 DI 10.1111/j.1751-1097.1992.tb04248.x PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HG514 UT WOS:A1992HG51400004 PM 1313979 ER PT J AU MUSIAL, F CROWELL, MD FRENCH, AW AF MUSIAL, F CROWELL, MD FRENCH, AW TI THE EFFECT OF FEEDING ON DEFECATION BEHAVIOR IN PIGS SO PHYSIOLOGY & BEHAVIOR LA English DT Note DE PIGS; DEFECATION; FEEDING; RECTAL BALLOON DISTENSION; PRESSURE; VOLUME; COMPLIANCE ID YUCATAN MINIATURE PIG; GASTROCOLONIC RESPONSE; COLONIC RESPONSE; MOTOR-ACTIVITY; INTESTINE; PATTERN AB The effect of eating on defecation behaviour was investigated in four 20-30 kg pigs. Rectal distention stimulation was performed pre- and postprandially at 10 cm from the anus with a 5 cm latex balloon. Volume was increased in steps of 10 ml up to 200 ml of air or until balloon defecation. Dependent measures were volume, rectal pressure, determined with a solid state pressure transducer inside the balloon probe, rectal compliance, and an index of distention induced contractile activity. The volume and pressure required to elicit defecation was significantly lower after feeding (p < 0.01). Distention induced contractile activity was significantly increased near defecation threshold, but pre- and postprandial conditions were not different. There was no difference in rectal compliance pre- and postprandially. These results suggest that eating lowers defecation threshold in terms of distention volume and rectal pressure, and that these changes are not dependent on altered rectal compliance or changes in distention induced motor activity. C1 FRANCIS SCOTT KEY MED CTR,DIV DIGEST DIS,4940 EASTERN AVE,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT MED PSYCHIAT,BALTIMORE,MD 21224. NIA,GERONTOL RES INST,BALTIMORE,MD 21224. NR 19 TC 10 Z9 10 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD MAR PY 1992 VL 51 IS 3 BP 643 EP 646 DI 10.1016/0031-9384(92)90190-D PG 4 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA HN239 UT WOS:A1992HN23900028 PM 1523240 ER PT J AU KIMM, SYS PAYNE, GH LAKATOS, E WEBBER, LS GREENBLATT, J AF KIMM, SYS PAYNE, GH LAKATOS, E WEBBER, LS GREENBLATT, J TI PRIMARY CARE PHYSICIANS AND CHILDRENS BLOOD CHOLESTEROL SO PREVENTIVE MEDICINE LA English DT Article ID RISK-FACTORS; DISEASE C1 NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. PROSPECT ASSOCIATES,ROCKVILLE,MD 20850. LOUISIANA STATE UNIV,MED CTR,SCH MED,NEW ORLEANS,LA 70112. RP KIMM, SYS (reprint author), UNIV PITTSBURGH,SCH MED,DEPT CLIN EPIDEMIOL & PREVENT MED,M200 SCAIFE,PITTSBURGH,PA 15261, USA. FU NHLBI NIH HHS [N01-HC-65070] NR 16 TC 7 Z9 7 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 0091-7435 J9 PREV MED JI Prev. Med. PD MAR PY 1992 VL 21 IS 2 BP 191 EP 202 DI 10.1016/0091-7435(92)90018-D PG 12 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA HK684 UT WOS:A1992HK68400004 PM 1579554 ER PT J AU PERKINS, ND SCHMID, RM DUCKETT, CS LEUNG, K RICE, NR NABEL, GJ AF PERKINS, ND SCHMID, RM DUCKETT, CS LEUNG, K RICE, NR NABEL, GJ TI DISTINCT COMBINATIONS OF NF-KAPPA-B-SUBUNITS DETERMINE THE SPECIFICITY OF TRANSCRIPTIONAL ACTIVATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DNA BINDING; C-REL GENE; TRANSACTIVATION ID HUMAN IMMUNODEFICIENCY VIRUS; ENHANCER-BINDING-PROTEIN; REGULATORY SEQUENCE; GENE-EXPRESSION; REL; PROMOTER; NUCLEAR; CELLS; TRANSACTIVATION; TRANSFORMATION AB The nuclear factor that binds to the kappa-light-chain enhancer of B cells (NF-kappa-B) is a transcription factor that regulates the expression of a variety of cellular and viral genes. NF-kappa-B is composed of distinct subunits, and at least four independent genes (p105, p100, p65, and c-rel) have been isolated that encode related proteins that bind kappa-B sites. Because it is possible that specific interactions of different subunits can allow selective gene activation, we have characterized the specificity of transcriptional activation by various combinations of these subunits. When tested alone, an almost-equal-to 49-kDa form (p49) of the p100 protein bound weakly to kappa-B, but p49 associated with p65 to bind efficiently to this site. Furthermore, p49 acted in combination with either p65 or a Rel/VP16 fusion protein to activate kappa-B-dependent transcription in Jurkat T leukemia cells. The p49/p65 or p49/Rel combination stimulated transcription mediated by the canonical kappa-B site but did not stimulate reporter genes containing interleukin 2 receptor-alpha or major histocompatibility complex kappa-B elements, despite its ability to bind to these sites. Transactivation mediated by the p49/p100 and p65 NF-kappa-B proteins is therefore sensitive to minor changes in the sequence of the kappa-B site. Specificity determined by the association of NF-kappa-B subunits provides a mechanism to selectively regulate variant kappa-B sites associated with different cellular and viral genes. C1 UNIV MICHIGAN,MED CTR,HOWARD HUGHES MED INST,DEPT INTERNAL MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,HOWARD HUGHES MED INST,DEPT BIOL CHEM,ANN ARBOR,MI 48109. NCI,FREDERICK CANC RES DEV CTR,APPL BIOSCI LABS,BASIC RES PROGRAM,FREDERICK,MD 21702. ST GEORGE HOSP,LONDON,ENGLAND. FU NCI NIH HHS [N01-CO74101]; NIAID NIH HHS [AI26865, AI29179] NR 31 TC 260 Z9 261 U1 0 U2 2 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 1 PY 1992 VL 89 IS 5 BP 1529 EP 1533 DI 10.1073/pnas.89.5.1529 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HG681 UT WOS:A1992HG68100003 PM 1542644 ER PT J AU ARISPE, N ROJAS, E HARTMAN, J SORSCHER, EJ POLLARD, HB AF ARISPE, N ROJAS, E HARTMAN, J SORSCHER, EJ POLLARD, HB TI INTRINSIC ANION CHANNEL ACTIVITY OF THE RECOMBINANT 1ST NUCLEOTIDE BINDING FOLD DOMAIN OF THE CYSTIC-FIBROSIS TRANSMEMBRANE REGULATOR PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CHLORIDE CHANNEL; CYSTIC FIBROSIS TRANSMEMBRANE REGULATOR; RECONSTITUTION ID FORMS CALCIUM CHANNELS; BILAYER-MEMBRANES; GENE; IDENTIFICATION; FUSION AB The first nucleotide binding fold (NBF-1) from the cystic fibrosis transmembrane regulator (CFTR) has been expressed in bacteria and found to bind ATP and to express anion channel activity when reconstituted onto a planar lipid bilayer. This evidence suggests that the NBF forms the anion-selective portion of the CFTR channel. We also found that the recombinant NBF-1 anion channel is blocked by ATP (1 mM), under which condition it appears to have a minimal conductance of almost-equal-to 9 pS and an ohmic current-voltage relationship. We further found that the recombinant NBF-1 bearing the DELTA-F508 mutation has nearly identical anion channel activity to that of the wild-type protein but can be distinguished from wild type under bianionic conditions with chloride and gluconate. We conclude from these data that the anion channel activity of the recombinant NBF-1 could represent all or part of the anion conductance mechanism of CFTR and that the role of the ATP binding by the NBF could be to modulate this anion channel activity. C1 NIDDKD,CELL BIOL & GENET LAB,BLDG 8,ROOM 401,BETHESDA,MD 20892. UNIV ALABAMA,SCH MED,DEPT MED,BIRMINGHAM,AL 35294. UNIV ALABAMA,SCH MED,DEPT PHYSIOL & BIOPHYS,BIRMINGHAM,AL 35294. NR 27 TC 58 Z9 58 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 1 PY 1992 VL 89 IS 5 BP 1539 EP 1543 DI 10.1073/pnas.89.5.1539 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HG681 UT WOS:A1992HG68100005 PM 1371876 ER PT J AU SEFTOR, REB SEFTOR, EA GEHLSEN, KR STETLERSTEVENSON, WG BROWN, PD RUOSLAHTI, E HENDRIX, MJC AF SEFTOR, REB SEFTOR, EA GEHLSEN, KR STETLERSTEVENSON, WG BROWN, PD RUOSLAHTI, E HENDRIX, MJC TI ROLE OF THE ALPHA-V-BETA-3 INTEGRIN IN HUMAN-MELANOMA CELL INVASION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE VITRONECTIN RECEPTOR; VITRONECTIN; SIGNAL TRANSDUCTION; COLLAGENASE-IV ID ARG-GLY-ASP; FIBRONECTIN RECEPTOR; BASEMENT-MEMBRANE; EXPERIMENTAL METASTASIS; TRANSFORMED PHENOTYPE; ADHESION MOLECULES; SYNTHETIC PEPTIDES; IV COLLAGENASE; ALPHA-V; EXPRESSION AB The human melanoma cell line A375M expresses the vitronectin receptor (alpha(v)beta-3 integrin) on its cell surface. Treatment of A375M cells with either polyclonal or monoclonal anti-alpha(v)beta-3 antibodies resulted in stimulation of invasion through basement membrane matrices in vitro. Similar treatment of these cells with a monoclonal anti-alpha(v) antibody, which does not inhibit the adhesive function of the alpha(v)beta-3 antigen, also stimulated invasion; however, anti-beta-3 antibody treatment had no effect. Furthermore, pretreatment of the cells with vitronectin or addition of vitronectin to the basement membrane matrix also resulted in stimulation of invasion. Similar treatments with fibronectin receptor antibody or fibronectin had no effect on invasion. Analysis of type IV collagenase expression in cells treated with anti-alpha(v)beta-3 antibody showed higher levels of both the secreted 72-kDa enzyme and its mRNA. Signal transduction through the alpha(v)beta-3 integrin could underlie the elevated expression of metalloproteinase and the enhanced invasion of A375M cells through basement membrane matrices. C1 UNIV ARIZONA, ARIZONA CANC CTR, TUCSON, AZ 85724 USA. LA JOLLA INST EXPTL MED, LA JOLLA, CA 92037 USA. LA JOLLA CANC RES FDN, CANC RES CTR, LA JOLLA, CA 92037 USA. NCI, PATHOL LAB, BETHESDA, MD 20892 USA. RP SEFTOR, REB (reprint author), UNIV ARIZONA, DEPT ANAT, TUCSON, AZ 85724 USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 FU NCI NIH HHS [CA28896, CA42507]; NCRR NIH HHS [2S07RR05675-22] NR 46 TC 423 Z9 426 U1 4 U2 7 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 1 PY 1992 VL 89 IS 5 BP 1557 EP 1561 DI 10.1073/pnas.89.5.1557 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HG681 UT WOS:A1992HG68100009 PM 1371877 ER PT J AU KOPP, JB KLOTMAN, ME ADLER, SH BRUGGEMAN, LA DICKIE, P MARINOS, NJ ECKHAUS, M BRYANT, JL NOTKINS, AL KLOTMAN, PE AF KOPP, JB KLOTMAN, ME ADLER, SH BRUGGEMAN, LA DICKIE, P MARINOS, NJ ECKHAUS, M BRYANT, JL NOTKINS, AL KLOTMAN, PE TI PROGRESSIVE GLOMERULOSCLEROSIS AND ENHANCED RENAL ACCUMULATION OF BASEMENT-MEMBRANE COMPONENTS IN MICE TRANSGENIC FOR HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GENES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HIV-ASSOCIATED NEPHROPATHY; KAPOSIS-SARCOMA; TAT PROTEIN; DISEASE; LESIONS; CELLS; CHILDREN; COLLAGEN; LAMININ; KIDNEY AB Patients infected with human immunodeficiency virus type 1 (HIV-1) develop a renal syndrome characterized by proteinuria, renal failure, and focal segmental glomerulosclerosis. By using a noninfectious HIV-1 DNA construct lacking the gag and pol genes, three transgenic mouse lines have been generated that develop a syndrome remarkably similar to the human disease. In the present study, we have characterized in detail one of these lines, Tg26. In Tg26 mice, proteinuria was detectable at almost-equal-to 24 days of age, followed by severe nephrotic syndrome and rapid progression to end-stage renal failure. Renal histology showed focal segmental glomerulosclerosis and microcystic tubular dilatation. Indirect immunofluorescence studies demonstrated increased accumulation of the basement membrane components laminin, collagen type IV, and heparan sulfate proteoglycan. The viral protein Rev was present in sclerotic glomeruli. Northern blot analysis of total renal RNA showed expression of viral genes prior to the appearance of histologic renal disease, with greatly diminished viral gene expression late in the disease course. Kidneys from transgenic mice expressed increased steady-state levels of collagen alpha-1(IV) mRNA when glomerulosclerosis was present. We conclude that the presence of HIV-1 genes is associated with progressive renal dysfunction and glomerulosclerosis in transgenic mice. C1 NIDR,ORAL MED LAB,BETHESDA,MD 20892. NIDR,ANIM CARE UNIT,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIH,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,BETHESDA,MD 20892. RP KOPP, JB (reprint author), NIDR,DEV BIOL LAB,BLDG 30,ROOM 430,BETHESDA,MD 20892, USA. RI klotman, mary/A-1921-2016; OI Kopp, Jeffrey/0000-0001-9052-186X NR 23 TC 227 Z9 228 U1 1 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 1 PY 1992 VL 89 IS 5 BP 1577 EP 1581 DI 10.1073/pnas.89.5.1577 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HG681 UT WOS:A1992HG68100013 PM 1542649 ER PT J AU SICA, A TAN, TH RICE, N KRETZSCHMAR, M GHOSH, P YOUNG, HA AF SICA, A TAN, TH RICE, N KRETZSCHMAR, M GHOSH, P YOUNG, HA TI THE C-REL PROTOONCOGENE PRODUCT C-REL BUT NOT NF-KAPPA-B BINDS TO THE INTRONIC REGION OF THE HUMAN INTERFERON-GAMMA GENE AT A SITE RELATED TO AN INTERFERON-STIMULABLE RESPONSE ELEMENT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MULTIPLE NUCLEAR FACTORS; IMMUNE INTERFERON; ONCOGENE ENCODES; T-CELLS; EXPRESSION; DNA; ENHANCER; TRANSCRIPTION; PROTEINS; TRANSACTIVATION AB Interferon-gamma (IFN-gamma) is an important immunoregulatory protein that is expressed usually only in large granular lymphocytes and T cells. The gene encoding IFN-gamma was previously found to contain an intronic enhancer element that was not tissue-specific in its activity, despite the restricted expression of the intact IFN-gamma-encoding gene. Using nuclear extracts from the human T-cell line Jurkat, we have now identified two protein-binding regions in this intronic enhancer element. One of the protected regions has strong partial identity to the NF-kappa-B site present in the promoter region of the human interleukin 2-encoding gene. Based on this observation and recent reports of the interaction of the c-rel protooncogene product (c-Rel) with NF-kappa-B sites, we determined whether c-Rel could interact with the intronic enhancer element in the human IFN-gamma genomic DNA. Most surprisingly, gel-shift analysis, using c-Rel expressed in Escherichia coli established that c-Rel binds specifically to the IFN-gamma intronic DNA but not to the interleukin 2-like NF-kappa-B site. Additional studies with antibodies prepared against c-Rel peptides verified specificity of the interaction of c-Rel with this binding site. In addition, using an affinity-purified p50 subunit of the NF-kappa-B complex, we observed that the p50 protein did not bind to this additional c-Rel-binding site. Furthermore, nucleotide sequence analysis of this DNA region revealed a strong similarity of the additional c-Rel-binding site to a previously identified IFN-stimulable response element. These data show that c-Rel can interact with DNA regions distinct from that recognized by NF-kappa-B and may, in fact, be involved in transcriptional regulation of the IFN-stimulable genes via the IFN-stimulable response element. C1 NCI,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LAB,BASIC RES PROGRAM,FREDERICK,MD 21702. ROCKEFELLER UNIV,BIOCHEM & MOLEC BIOL LAB,NEW YORK,NY 10021. RI Tan, Tse-Hua/E-3983-2010 OI Tan, Tse-Hua/0000-0003-4969-3170 FU NCI NIH HHS [N01-CO-74102, N01-CO-74101] NR 39 TC 111 Z9 115 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 1 PY 1992 VL 89 IS 5 BP 1740 EP 1744 DI 10.1073/pnas.89.5.1740 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HG681 UT WOS:A1992HG68100046 PM 1542667 ER EF