FN Thomson Reuters Web of Science™ VR 1.0 PT J AU TSUTSUI, T FUJINO, T KODAMA, S TAINSKY, MA BOYD, J BARRETT, JC AF TSUTSUI, T FUJINO, T KODAMA, S TAINSKY, MA BOYD, J BARRETT, JC TI AFLATOXIN B-1-INDUCED IMMORTALIZATION OF CULTURED SKIN FIBROBLASTS FROM A PATIENT WITH LI-FRAUMENI SYNDROME SO CARCINOGENESIS LA English DT Article ID WILD-TYPE P53; UNSCHEDULED DNA-SYNTHESIS; FAMILIAL CANCER SYNDROME; HAMSTER EMBRYO CELLS; GENE AMPLIFICATION; TRANSFORMATION; INDUCTION; INVITRO; LINES AB To examine the mechanisms of immortalization in human cells, normal human diploid fibroblasts (WHE-7) and skin fibroblasts from a patient with Li-Fraumeni syndrome (MDAH 087) and a mutant p53 allele were treated with aflatoxin B-1 (AFB(1)). Exogenous metabolic activation of AFB(1) with rat liver post-mitochondrial supernatant (PMS) was used and the optimal treatment conditions needed were determined by the inducibility of unscheduled DNA synthesis. The same degree of cytotoxicity was observed with MDAH 087 cells and normal WHE-7 cells treated with AFB(1) at 0.1, 0.3 or 1 mu g/ml for 2 h with a 2% PMS mixture. All WHE-7 cell cultures (AFB(1)-treated and controls) failed to escape from senescence, whereas three out of nine AFB(1)-treated cultures of MDAH 087 cells escaped senescence, MDAH 087 cells treated with 0.1 mu g/ mi of AFB(1) two or three times initially decreased in growth similar to 40 days [10 population doublings (PD)] after the first treatment. However, the cells recovered with faster growth rates after similar to 100 additional days and grew continuously. Both cultures were immortal, defined as continuous growth for over 300 PD. Cells treated once with 0.3 mu g/ml of AFB(1) also escaped senescence, although they had about a 230 day time lag before restoration of cell growth. The three AFB(1)-treated cell lines exhibited altered morphologies, chromosome aberrations (numerical and structural aberrations) and loss of the wild-type p53 allele. Although immortal, the cells were non-tumorigenic in nude mice. Spontaneous immortalization of untreated MDAH 087 was not observed in this study. The results indicate that AFB(1) treatment of cells from a Li-Fraumeni patient, but not cells from normal individuals, can induce immortalization. This model may be useful for studying mechanisms of chemically induced immortalization. C1 NIEHS,MOLEC CARCINOGENESIS LAB,ENVIRONM CARCINOGENESIS PROGRAM,RES TRIANGLE PK,NC 27709. NIPPON DENT UNIV TOKYO,SCH DENT,DEPT PHARMACOL,CHIYODA KU,TOKYO 102,JAPAN. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT TUMOR BIOL,HOUSTON,TX 77030. NR 37 TC 28 Z9 28 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1995 VL 16 IS 1 BP 25 EP 34 DI 10.1093/carcin/16.1.25 PG 10 WC Oncology SC Oncology GA QE196 UT WOS:A1995QE19600004 PM 7834802 ER PT J AU KOPPSCHNEIDER, A PORTIER, CJ AF KOPPSCHNEIDER, A PORTIER, CJ TI CARCINOMA FORMATION IN NMRI MOUSE SKIN PAINTING STUDIES IS A PROCESS SUGGESTING GREATER-THAN-2 STAGES SO CARCINOGENESIS LA English DT Article ID ENZYME-ALTERED FOCI; TUMOR PROMOTION; QUANTITATIVE-ANALYSIS; CARCINOGENESIS; MODEL; PAPILLOMAS; PROGRESSION; CANCER; BIRTH; RATES AB The two-stage model of carcinogenesis, which incorporates clonal growth of intermediate cells, has gained increasing attention in recent years. It was formulated to match tumor incidence data and expanded to encompass observations made in initiation - promotion carcinogenicity experiments. Mouse skin experiments are perceived as supporting this model, with papillomas representing the intermediate cells and carcinomas representing the malignant cells. In this manuscript, the two-stage model is applied to data concerning papilloma and carcinoma formation from an initiation-promotion NMRI mouse skin painting experiment which included stop-promotion. It is shown that the model is not compatible with these data if all papillomas are considered premalignant lesions. The model was modified to allow for a heterogeneous population of papillomas. In this case, unless one assumes that premalignant and terminally benign papillomas are morphologically different in the sense that both types of papillomas at detection limit contain distinct numbers of actively dividing initiated cells, the model predicts larger numbers of papillomas at the end of the experiment than were actually observed. The best explanation is that the model is not in accordance with these data and that the data indicate the need for stages between initiated and malignant cells. C1 NIEHS,QUANTITAT & COMP BIOL LAB,RES TRIANGLE PK,NC 27709. RP KOPPSCHNEIDER, A (reprint author), DEUTSCH KREBSFORSCHUNGSZENTRUM,POSTFACH 101949,D-69009 HEIDELBERG,GERMANY. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 29 TC 17 Z9 18 U1 1 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1995 VL 16 IS 1 BP 53 EP 59 DI 10.1093/carcin/16.1.53 PG 7 WC Oncology SC Oncology GA QE196 UT WOS:A1995QE19600007 PM 7834805 ER PT J AU VANSTEE, EW SLOANE, RA SIMMONS, JE MOORMAN, MP BRUNNEMANN, KD AF VANSTEE, EW SLOANE, RA SIMMONS, JE MOORMAN, MP BRUNNEMANN, KD TI ENDOGENOUS FORMATION OF N-NITROSOMORPHOLINE IN MICE FROM (NO2)-N-15 BY INHALATION AND MORPHOLINE BY GAVAGE SO CARCINOGENESIS LA English DT Article ID NITROGEN-DIOXIDE; NITROSAMINE FORMATION; LIVER-MICROSOMES; NITRITE; NITRATE; DISPOSITION; INVIVO; SALIVA; SYSTEM; AMINES AB Male CD-1 mice were exposed to an nominal concentration of 20 p.p.m. of N-15-nitrogen dioxide ((NO2)-N-15) for 6 h/day for 4 days and for 2 h on the day 5, and to 1 g morpholine/kg body wt by gavage daily for five consecutive days, N-Nitrosomorpholine (NMOR) was found in whole mice, stomachs, skins with hair, and remains. The sum of individual tissue concentrations measured separately was 3421 ng/tissue, where the average skin weighed 4.3 g, the average stomach weighed 1.0 g and the average remains weighed 22.2 g. The average whole mouse weighed 27.7 g and contained a total of 3903 ng of NMOR. The concentration of NMOR was highest in the skin, nest highest in the stomach, and lowest in the remains. However, the total quantity of NMOR per tissue, while highest in the skin (83%), was nest highest in the remains (14.8%) and lowest in the stomach (2.2%), GC-MS analysis served to distinguish between the NMOR of (NO2)-N-15 origin and that of other origin. All of the NMOR in the whole mouse homogenates was identified as (15)NMOR In the stomach 73% was identified as (14)NMOR, representing 1.6% of the total NMOR in the mouse, and 27% as (15)NMOR, representing 0.6% of the total NMOR in the mouse, N-Nitrosamine formation in vivo is discussed as a possibly ongoing mammalian process. C1 NIEHS,RES TRIANGLE PK,NC 27709. US EPA,RES TRIANGLE PK,NC 27711. AMER HLTH FDN,NAYLOR DANA INST DIS PREVENT,VALHALLA,NY 10595. NR 24 TC 11 Z9 11 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1995 VL 16 IS 1 BP 89 EP 92 DI 10.1093/carcin/16.1.89 PG 4 WC Oncology SC Oncology GA QE196 UT WOS:A1995QE19600012 PM 7834809 ER PT B AU BREWER, HB AF BREWER, HB BE Gallo, LL TI CURRENT CONCEPTS OF THE PLASMA LIPOPROTEINS AND THEIR ROLE IN ATHEROSCLEROSIS SO CARDIOVASCULAR DISEASE 2: CELLULAR AND MOLECULAR MECHANISMS, PREVENTION, AND TREATMENT SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 14th Washington International Spring Symposium on Cardiovascular Disease - Cellular and Molecular Mechanisms, Prevention, and Treatment CY JUN 06-10, 1994 CL GEORGE WASHINGTON UNIV, WASHINGTON, DC SP GEORGE WASHINGTON UNIV MED CTR HO GEORGE WASHINGTON UNIV DE ATHEROSCLEROSIS; APOLIPOPROTEINS; DYSLIPOPROTEINEMIAS C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44992-7 J9 GWUMC DEPT PY 1995 BP 31 EP 40 PG 10 WC Biochemistry & Molecular Biology; Cardiac & Cardiovascular Systems SC Biochemistry & Molecular Biology; Cardiovascular System & Cardiology GA BC99M UT WOS:A1995BC99M00004 ER PT B AU KARANIAN, JW KIM, HY SALEM, N AF KARANIAN, JW KIM, HY SALEM, N BE Gallo, LL TI BIOSYNTHESIS OF DOCOSANOIDS BY HUMAN PLATELET - CARDIOVASCULAR PROPERTIES SO CARDIOVASCULAR DISEASE 2: CELLULAR AND MOLECULAR MECHANISMS, PREVENTION, AND TREATMENT SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 14th Washington International Spring Symposium on Cardiovascular Disease - Cellular and Molecular Mechanisms, Prevention, and Treatment CY JUN 06-10, 1994 CL GEORGE WASHINGTON UNIV, WASHINGTON, DC SP GEORGE WASHINGTON UNIV MED CTR HO GEORGE WASHINGTON UNIV C1 NIAAA,DICBR,MEMBRANE BIOCHEM & BIOPHYS LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44992-7 J9 GWUMC DEPT PY 1995 BP 269 EP 277 PG 9 WC Biochemistry & Molecular Biology; Cardiac & Cardiovascular Systems SC Biochemistry & Molecular Biology; Cardiovascular System & Cardiology GA BC99M UT WOS:A1995BC99M00033 ER PT B AU REMALEY, AT SCHUMACHER, UK BREWER, HB HOEG, JM AF REMALEY, AT SCHUMACHER, UK BREWER, HB HOEG, JM BE Gallo, LL TI ISOLATION OF NOVEL GENES REGULATED BY DIETARY CHOLESTEROL BY A PCR-BASED SUBTRACTION LIBRARY SO CARDIOVASCULAR DISEASE 2: CELLULAR AND MOLECULAR MECHANISMS, PREVENTION, AND TREATMENT SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 14th Washington International Spring Symposium on Cardiovascular Disease - Cellular and Molecular Mechanisms, Prevention, and Treatment CY JUN 06-10, 1994 CL GEORGE WASHINGTON UNIV, WASHINGTON, DC SP GEORGE WASHINGTON UNIV MED CTR HO GEORGE WASHINGTON UNIV C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44992-7 J9 GWUMC DEPT PY 1995 BP 327 EP 332 PG 6 WC Biochemistry & Molecular Biology; Cardiac & Cardiovascular Systems SC Biochemistry & Molecular Biology; Cardiovascular System & Cardiology GA BC99M UT WOS:A1995BC99M00041 ER PT B AU GORDON, DJ AF GORDON, DJ BE Gallo, LL TI CHOLESTEROL AND MORTALITY - WHAT CAN META-ANALYSIS TELL US SO CARDIOVASCULAR DISEASE 2: CELLULAR AND MOLECULAR MECHANISMS, PREVENTION, AND TREATMENT SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 14th Washington International Spring Symposium on Cardiovascular Disease - Cellular and Molecular Mechanisms, Prevention, and Treatment CY JUN 06-10, 1994 CL GEORGE WASHINGTON UNIV, WASHINGTON, DC SP GEORGE WASHINGTON UNIV MED CTR HO GEORGE WASHINGTON UNIV C1 NHLBI,DIV HEART & VASC DIS,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44992-7 J9 GWUMC DEPT PY 1995 BP 333 EP 340 PG 8 WC Biochemistry & Molecular Biology; Cardiac & Cardiovascular Systems SC Biochemistry & Molecular Biology; Cardiovascular System & Cardiology GA BC99M UT WOS:A1995BC99M00042 ER PT J AU AKIYAMA, SK AOTA, S YAMADA, KM AF AKIYAMA, SK AOTA, S YAMADA, KM TI FUNCTION AND RECEPTOR SPECIFICITY OF A MINIMAL 20-KILODALTON CELL ADHESIVE FRAGMENT OF FIBRONECTIN SO CELL ADHESION AND COMMUNICATION LA English DT Article DE FIBRONECTIN; INTEGRINS; CELL ADHESION; CELL MIGRATION ID SITE-DIRECTED MUTAGENESIS; HUMAN-PLASMA FIBRONECTIN; BINDING DOMAIN; MONOCLONAL-ANTIBODIES; PROTEOLYTIC FRAGMENTS; SINGLE GENE; INTEGRIN; ATTACHMENT; MIGRATION; SEQUENCE AB Previous studies have reached conflicting conclusions about the minimal size and sequences of the fibronectin cell-adhesive domain necessary for retention of high cell adhesive activity. We have expressed a recombinant 20 kDa cell-binding fragment of human fibronectin consisting of the ninth and tenth type III modules, which includes the Arg Gly-Asp (RGD) cell recognition site and a second cell adhesive domain that acts synergistically with the RGD site. This polypeptide retained a similar activity as a larger 110 kDa fibronectin fragment when used in soluble form in inhibition assays, but it displayed low cell adhesive activity if assayed after direct adsorption to a plastic substrate. However, adhesive function was restored if the fragment was bound to a non-inhibitory anti-fibronectin antibody pre-adsorbed to the plastic substrate. The antibody-bound fragment also promoted cell migration. Both cell spreading and migration were specifically mediated by the alpha(5) beta(1) integrin. Affinity columns containing immobilized 20 kDa cell-binding fragment effectively bound alpha(5)-, alpha(3)-, and alpha(v)-containing fibronectin-binding integrins. In contrast, an immobilized 11.5 kDa fragment that contained the RGD sequence but lacked the synergistic sequence was bound only poorly by as-containing fibronectin receptor integrins, even though the alpha(3)- and alpha(v)- containing integrins bound readily. Our results indicate that the manner in which adhesion proteins are presented to cells is important and that most cell adhesive activity is retained in a minimal 20 kDa segment of fibronectin. RP AKIYAMA, SK (reprint author), NIDR,DEV BIOL LAB,BLDG 30,BETHESDA,MD 20892, USA. OI Yamada, Kenneth/0000-0003-1512-6805 NR 52 TC 49 Z9 49 U1 0 U2 5 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1061-5385 J9 CELL ADHES COMMUN JI Cell Adhes. Commun. PY 1995 VL 3 IS 1 BP 13 EP 25 DI 10.3109/15419069509081275 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QK178 UT WOS:A1995QK17800002 PM 7538414 ER PT J AU Yamada, S Brown, KE Yamada, KM AF Yamada, S Brown, KE Yamada, KM TI Differential mRNA regulation of integrin subunits alpha(V), beta(1), beta(3), and beta(5) during mouse embryonic organogenesis SO CELL ADHESION AND COMMUNICATION LA English DT Article DE integrins; mouse embryos; mRNA expression; in situ hybridization; organogenesis ID CELL-ADHESION MOLECULES; AMINO-ACID-SEQUENCES; FIBRONECTIN RECEPTOR; INSITU HYBRIDIZATION; EXTRACELLULAR-MATRIX; COLLAGEN RECEPTOR; MESSENGER-RNAS; EXPRESSION; IDENTIFICATION; LAMININ AB Cell interactions with extracellular matrices play important roles in morphogenetic processes during embryonic development. Extracellular matrix receptors of the integrin family have been implicated in these steps. Recent studies indicate that a variety of integrins can be differentially expressed during development, consistent with diverse roles for integrins in embryogenesis. The present study compares the expression patterns of several major members of the alpha(v) integrin subfamily, focusing on mRNA expression of alpha(v), beta(1), beta(3), and beta(5) subunits during mouse embryonic organogenesis using Northern blot analysis and in situ hybridization. The alpha(v) and beta(1) subunits showed widespread tissue expression, although most tissues expressed alpha(v) at relatively low or basal levels. The mRNA for beta(5) was also expressed in a variety of embryonic organs and showed unusual localization patterns in certain organs. Striking, high-level expression of beta(5) transcripts was detected in the ependymal layer of the central nervous system, glomeruli of the kidney, epicardial region of the heart, and in the tooth germs, suggesting specific functions for this molecule during morphogenetic events in these organs. In contrast, few beta(3) transcripts were expressed during mid-gestation mouse embryogenesis except in megakaryocytes within the embryonic liver. These observations of differing expression spectra suggest that members of the alpha(v) integrin subfamily have distinct roles and also suggests that they have different transcriptional regulation. The beta(5) integrin is unique in its degree of tissue-specific mRNA regulation associated with morphogenesis of embryonic organs. C1 NIDR,DEV BIOL LAB,NIH,BETHESDA,MD 20892. NR 70 TC 31 Z9 33 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1061-5385 J9 CELL ADHES COMMUN JI Cell Adhes. Commun. PY 1995 VL 3 IS 4 BP 311 EP & DI 10.3109/15419069509081016 PG 18 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UN014 UT WOS:A1995UN01400004 PM 8821033 ER PT S AU STANLEY, JR AF STANLEY, JR BE Marsh, J Goode, JA TI DEFECTIVE CELL-CELL ADHESION IN THE EPIDERMIS SO CELL ADHESION AND HUMAN DISEASE SE CIBA FOUNDATION SYMPOSIA LA English DT Article; Proceedings Paper CT Symposium on Cell Adhesion and Human Disease CY MAY 17-19, 1994 CL CIBA FDN, LONDON, ENGLAND SP Ciba Fdn HO CIBA FDN ID PEMPHIGUS FOLIACEUS AUTOANTIBODIES; CONSTITUTIVE TRANSMEMBRANE GLYCOPROTEIN; VULGARIS ANTIGEN; CADHERIN FAMILY; BIOCHEMICAL-IDENTIFICATION; DESMOSOMAL GLYCOPROTEIN; PLASMINOGEN-ACTIVATOR; MR-165000 DESMOGLEIN; PASSIVE TRANSFER; FOGO SELVAGEM AB The disastrous effects of loss of epidermal cell adhesion are epitomized by the life-threatening blistering skin diseases pemphigus foliaceus and pemphigus vulgaris. Clinical and experimental observations show that loss of cell adhesion is induced by these patients' autoantibodies. Pemphigus foliaceus antigen is desmoglein 1 (dsg-1), a desmosomal transmembrane glycoprotein limited in distribution to stratified squamous epithelia. It is linked to plakogoblin, a desmosomal plaque protein. Molecular cloning has shown that desmogleins are members of the cadherin gene superfamily. The originally described cadherins (e.g. E-cadherin) are transmembrane, calcium-dependent, hemophilic adhesion molecules. Pemphigus vulgaris antigen is a 130 kDa glycoprotein also linked to plakoglobin. Molecular cloning has shown that pemphigus vulgaris antigen is also a desmoglein, dsg-3. Antibodies against pemphigus vulgaris antigen subdomains homologous to the binding subdomains of classical cadherins cause loss of epidermal cell adhesion, which suggests that desmogleins mediate adhesion, although direct evidence for this is lacking. The extracellular domain of pemphigus vulgaris antigen cannot substitute in function for that of E-cadherin. Future studies should address the cell biological function of desmogleins. RP STANLEY, JR (reprint author), NCI,DERMATOL BRANCH,BLDG 10,ROOM 12N238,BETHESDA,MD 20892, USA. NR 64 TC 14 Z9 14 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, ENGLAND PO19 7UD SN 0300-5208 BN 0-471-95279-6 J9 CIBA F SYMP PY 1995 VL 189 BP 107 EP 123 PG 17 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD31P UT WOS:A1995BD31P00008 PM 7587627 ER PT J AU ORNBERG, RL FURUYA, S COPING, G KUIJPERS, GAJ AF ORNBERG, RL FURUYA, S COPING, G KUIJPERS, GAJ TI GRANULE SWELLING IN STIMULATED BOVINE ADRENAL CHROMAFFIN CELLS - REGULATION BY INTERNAL GRANULE PH SO CELL AND TISSUE RESEARCH LA English DT Article DE EXOCYTOSIS; CHROMAFFIN CELLS; CATECHOLAMINE SECRETION; MEMBRANE FUSION; FREEZE SUBSTITUTION; COW ID PHOSPHOLIPID-BILAYER MEMBRANES; MAST-CELLS; CATECHOLAMINE RELEASE; SECRETORY GRANULES; INTRACELLULAR PH; MEDULLARY CELLS; OSMOTIC FORCES; EXOCYTOSIS; FUSION; CALCIUM AB Adrenal medullary chromaffin cells secrete catecholamines through exocytosis of their intracellular chromaffin granules. Osmotic granule swelling has been implicated to play a role in the generation of membrane stress associated with the fusion of the granule membrane. However, controversy exists as to whether swelling occurs before or after the actual fusion event. Using morphometric methods we have determined the granule diameter distributions in rapidly frozen, freeze-substituted chromaffin cells. Our measurements show that intracellular chromaffin granules increase in size from an average of 234 nm to 274 nm or 277 nm in cells stimulated to secrete with nicotine or high external K+, respectively. Granule swelling occurs before the formation of membrane contact. Ammonium chloride, an agent which inhibits stimulated catecholamine secretion by approximately 50% by altering the intragranular pH, also inhibits granule swelling. In addition, ammonium chloride-treated secreting cells shaw more granule-plasma membrane contacts than untreated secreting cells. Sodium propionate induces granule swelling in the absence of secretagogue and has been shown to enhance nicotine- and high K+- induced catecholamine release. These results indicate that in adrenal chromaffin cells granule swelling is an essential step in exocytosis before fusion pore formation, and is related to the pH of the granule environment. RP ORNBERG, RL (reprint author), NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892, USA. NR 40 TC 16 Z9 16 U1 0 U2 1 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 JAN PY 1995 VL 279 IS 1 BP 85 EP 92 DI 10.1007/BF00300694 PG 8 WC Cell Biology SC Cell Biology GA PW835 UT WOS:A1995PW83500009 PM 7895265 ER PT J AU ROTH, BJ YAGODIN, SV HOLTZCLAW, L RUSSELL, JT AF ROTH, BJ YAGODIN, SV HOLTZCLAW, L RUSSELL, JT TI A MATHEMATICAL-MODEL OF AGONIST-INDUCED PROPAGATION OF CALCIUM WAVES IN ASTROCYTES SO CELL CALCIUM LA English DT Article ID INOSITOL TRISPHOSPHATE; CA2+ OSCILLATIONS; RELEASE; CA-2+; CELLS AB In astrocytes, calcium signals evoked by neurotransmitters appear as waves within single cells, which spread to other cells in the network. Recent analysis has shown that waves are initiated at a single invariant site in the cell and propagated within the cell in a nonlinear and saltatory manner by regenerative amplification at specific predestined cellular sites, In order to gain insight into local cellular waves and wave collisions we have developed a mathematical model of cellular wave amplification loci. This model is in good agreement with experimental data which includes: ambient calcium gradients in resting cells, wave origination and local amplification and generation of local waves, As observed in experiments, the model also predicts that different locations in the cell can have different frequencies of oscillation. The amplification loci are thought to be specialized areas of the endoplasmic reticulum membrane containing a higher density or higher sensitivity of IP3 receptors, Our analysis suggests that the cellular loci act as weakly coupled oscillators each with its intrinsic latency and frequency of oscillation. Thus the appearance of the propagated calcium wave may be a reflection of these differences rather than an actual diffusional wave propagation. C1 NICHHD,MOLEC & CELLULAR NEUROPHYSIOL LAB,NEURONAL SECRETORY SYST SECT,BETHESDA,MD 20892. NICHHD,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RI Roth, Bradley/A-4920-2008 NR 19 TC 35 Z9 35 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0143-4160 J9 CELL CALCIUM JI Cell Calcium PD JAN PY 1995 VL 17 IS 1 BP 53 EP 64 DI 10.1016/0143-4160(95)90102-7 PG 12 WC Cell Biology SC Cell Biology GA QD294 UT WOS:A1995QD29400006 PM 7553781 ER PT J AU TOPOL, LZ MARX, M CALOTHY, G BLAIR, DG AF TOPOL, LZ MARX, M CALOTHY, G BLAIR, DG TI TRANSFORMATION-RESISTANT MOS REVERTANT IS UNABLE TO ACTIVATE MAP KINASE KINASE IN RESPONSE TO V-MOS OR V-RAF SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID MURINE SARCOMA-VIRUS; PROTO-ONCOGENE PRODUCT; XENOPUS-OOCYTES; 3T3 CELLS; INVITRO; THREONINE; PHOSPHORYLATION; MATURATION; TYROSINE; TUBULIN AB To study the mechanism by which v-mos induces cell transformation, we generated a transformed rat cell line (DTM) containing two functional copies of mos, one encoding the p37(v-mos) of the mi wild-type strain of Moloney murine sarcoma virus (Mo-MuSV) and the other the p85(gag-mos) fusion protein of the ts110 mutant of Moloney murine sarcoma virus. Subsequently, we isolated a revertant cell line (F-1) following transfection of DTM with a mutant retroviral construct (plC4Neo) carrying a selectable marker. Like DTM, the F-1 revertant contained two integrated copies of v-mos, expressed mos containing viral RNA, and contained rescuable transforming viruses. The revertant did not grow in soft agar, showed a greatly reduced ability to form tumors in nude mice, and exhibited organized tubulin and actin structures similar to those found in normal cells. Revertant cells were resistant to retransformation by v-mos and v-raf but could be retransformed by v-ras. MAP kinase (ERK-2) and MAP kinase kinase (MKK-1) activity, which are constitutively elevated in v-mos- and v-raf-transformed cells, exhibits levels in the F-1 revertant similar to those seen in nontransformed cells. F-1 and normal REF-1 cells express elevated levels of protein phosphatases in comparison to DTM cells. In vivo treatment with okadaic acid, a potent protein phosphatase inhibitor, leads to an increase in MKK-1 and MAP kinase activity in F-1 cells but not in REF-1. The results support the hypothesis that mos acts through the MAP kinase cascade (MKK-1 and ERK-2) to induce cell transformation and that blocking v-mos activation of that cascade (possibly because of increased levels of phosphatase) prevents transformation. C1 CTR UNIV ORSAY,INST CURIE BIOL,F-91405 ORSAY,FRANCE. RP TOPOL, LZ (reprint author), NCI,MOLEC ONCOL LAB,POB B,FREDERICK,MD 21702, USA. NR 67 TC 8 Z9 8 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 JAN PY 1995 VL 6 IS 1 BP 27 EP 38 PG 12 WC Cell Biology SC Cell Biology GA QA648 UT WOS:A1995QA64800004 PM 7718484 ER PT J AU BIES, J MUKHOPADHYAYA, R PIERCE, J WOLFF, L AF BIES, J MUKHOPADHYAYA, R PIERCE, J WOLFF, L TI ONLY LATE, NONMITOTIC STAGES OF GRANULOCYTE DIFFERENTIATION IN 32DCL3 CELLS ARE BLOCKED BY ECTOPIC EXPRESSION OF MURINE C-MYB AND ITS TRUNCATED FORMS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID V-MYB; MESSENGER-RNA; NUCLEOTIDE-SEQUENCE; MYELOID-LEUKEMIA; DNA-BINDING; CONSTITUTIVE EXPRESSION; ERYTHROLEUKEMIA-CELLS; CELLULAR PROGENITOR; GENE-EXPRESSION; LEUCINE-ZIPPER AB In murine leukemia virus-induced myeloid leukemias, insertional mutagenesis of the c-myb locus has been shown to occur frequently. Proto-oncogene activation is achieved in most leukemias by integration of murine leukemia virus upstream of exons 3 or 4 or by integration into exon 9 with consequent truncation of the protein. The present study investigates the effect of ectopic expression of full-length c-myb or c-myb containing amino- or carboxyl-terminal truncations (minus 47 and 248 amino acids, respectively) on granulocyte differentiation in vitro. Recombinant myb retroviruses were used to infect an interleukin 3-dependent progenitor cell line, 32Dcl3, which undergoes terminal differentiation to mature neutrophilic granulocytes in the presence of granulocyte colony-stimulating factor. Overexpression of c-myb did not abrogate the interleukin 3 dependency of the parental cell line. However, cells expressing all forms of c-myb were blocked at an intermediate stage of granulocyte differentiation and continued to proliferate in the presence of granulocyte colony-stimulating factor. After 14 days in medium with granulocyte colony-stimulating factor, myb-expressing cultures predominantly consisted of promyelocytes with some myelocytes and almost undetectable numbers of neutrophilic granulocytes. This suggested that early stages of granulocyte differentiation were not inhibited, a finding that was further supported by the induction of myeloperoxidase, a biochemical marker of promyelocytes. Interestingly, the expression of lactoferrin, known to be a marker of late stages of granulocyte differentiation, was completely inhibited in the cells infected with myb viruses. It was concluded that c-myb expression blocked granulocyte differentiation to the terminal mitotic stages and that deletion of the NH2-terminal 47 amino acids and/or the COOH-terminal 248 amino acids of c-myb neither enhanced nor diminished this effect. C1 NCI,GENET LAB,BETHESDA,MD 20892. NCI,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. NR 63 TC 46 Z9 46 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 JAN PY 1995 VL 6 IS 1 BP 59 EP 68 PG 10 WC Cell Biology SC Cell Biology GA QA648 UT WOS:A1995QA64800007 PM 7536440 ER PT J AU JAEGER, RG JAEGER, MMM ARAUJO, VC KACHAR, B AF JAEGER, RG JAEGER, MMM ARAUJO, VC KACHAR, B TI ANALYSIS OF THE INTERDEPENDENT LOCALIZATION OF VIMENTIN AND MICROTUBULES IN NEOPLASTIC MYOEPITHELIAL CELLS SO CELL MOTILITY AND THE CYTOSKELETON LA English DT Article DE CYTOSKELETON; INTERMEDIATE FILAMENTS; VIMENTIN; MICROTUBULES; MYOEPITHELIAL CELLS; IMMUNOFLUORESCENCE ID INTERMEDIATE FILAMENT REORGANIZATION; CULTURED-CELLS; PROTEINS; ASSOCIATION; IMMUNOFLUORESCENCE; ORGANIZATION; FIBROBLASTS; EXPRESSION; MOVEMENTS; DYNAMICS AB Salivary gland neoplastic myoepithelial cells in culture form very thin cytoplasmic processes in which the vimentin network is well dispersed. These vimentin filaments can be individually visualized by immunofluorescence. In this study, we have analyzed the role of microtubules in the distension and organization of the vimentin filament network found in these cells. We find that vimentin filaments colocalize along microtubules; however, a significant number of filaments can also be found in microtubule-free domains. Additionally, vimentin filaments are absent from large domains of microtubule-rich domains. Treatment of neoplastic myepithelial cells with the microtubule inhibitor nocodazole did not cause any retraction of the distended vimentin network. This observation suggests that the structural integrity of microtubules is not important for the stability of the vimentin network. Combining procedures for transient disruption of vimentin filaments and microtubules we observed that, in the absence of microtubules, the vimentin network could reassemble in the perinuclear region but was unable to extend toward the cell periphery. The dispersion of vimentin filaments to the peripheral regions of the cytoplasm could only be observed upon microtubule reassembly. This indicates that microtubules are not required for the stability of the vimentin network, but the dispersion of vimentin filaments to the peripheral cytoplasm depends on active interactions with microtubules. (C) 1995 Wiley-Liss, Inc. C1 NIDOCD,CELLULAR BIOL LAB,BETHESDA,MD. UNIV SAO PAULO,SCH DENT,DEPT ORAL PATHOL,BR-05508 SAO PAULO,BRAZIL. RI Marques, Marcia/F-3780-2012; Araujo, Vera /G-3586-2014; Jaeger, Ruy/G-8230-2011 OI Marques, Marcia/0000-0002-9398-1252; NR 33 TC 6 Z9 6 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0886-1544 J9 CELL MOTIL CYTOSKEL JI Cell Motil. Cytoskeleton PY 1995 VL 32 IS 4 BP 289 EP 298 DI 10.1002/cm.970320405 PG 10 WC Cell Biology SC Cell Biology GA TH106 UT WOS:A1995TH10600004 PM 8608607 ER PT J AU MCNAIRY, SA AF MCNAIRY, SA TI MESSAGE FROM THE DIRECTOR OF THE RCMI PROGRAM SO CELLULAR AND MOLECULAR BIOLOGY LA English DT Editorial Material RP MCNAIRY, SA (reprint author), NIH,NATL CTR RES RESOURCES,MINOR INST PROGRAM RES CTR,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CELLULAR & MOLECULAR BIOLOGY PI NOISY-LE-GRAND PA PROF R WEGMANN RESIDENCE HAUSSMANN 1 AVENUE DU PAVE NEUF, 93160 NOISY-LE-GRAND, FRANCE SN 0145-5680 J9 CELL MOL BIOL JI Cell. Mol. Biol. PY 1995 VL 41 SU 1 BP SIII EP & PG 0 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA RA778 UT WOS:A1995RA77800002 PM 8574135 ER PT J AU YANAGIHARA, R SAITOU, N NERURKAR, VR SONG, KJ BASTIAN, I FRANCHINI, G GAJDUSEK, DC AF YANAGIHARA, R SAITOU, N NERURKAR, VR SONG, KJ BASTIAN, I FRANCHINI, G GAJDUSEK, DC TI MOLECULAR PHYLOGENY AND DISSEMINATION OF HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I VIEWED WITHIN THE CONTEXT OF PRIMATE EVOLUTION AND HUMAN MIGRATION SO CELLULAR AND MOLECULAR BIOLOGY LA English DT Article; Proceedings Paper CT 4th RCMI International AIDS Symposium CY NOV 03-04, 1994 CL SAN JUAN, PR SP RES CTR MINORITY INST DE RETROVIRIDAE; GENETIC DIVERSITY; PHYLOGENETIC TREE; SAHUL; SUNDA; MELANESIA; AUSTRALIA; WALLACEA; PLEISTOCENE ID PAPUA-NEW-GUINEA; NUCLEOTIDE-SEQUENCE ANALYSIS; ANCIENT HUMAN-POPULATIONS; LEUKEMIA-LYMPHOMA VIRUS; DIFFERENT GEOGRAPHICAL REGIONS; HUMAN PAPILLOMAVIRUS TYPE-16; JAPANESE ENCEPHALITIS-VIRUS; WESTERN PACIFIC REGION; HUMAN OCCUPATION SITE; HTLV-1 ISOLATE MT-2 AB .A renewed interest in the emergence and evolution of the primate T-cell lymphotropic viruses has followed the discovery of genetically distinct variants of human T-cell lymphotropic virus type I (HTLV-I) in Melanesia and Australia. Phylogenetic trees based on selected regions of the gag, pol, env and pX genes of HTLV-I from widely separated geographic regions and of simian T-cell lymphotropic virus type I (STLV-I) from African and Asian catarrhines, constructed using the neighbor-joining and maximum parsimony methods, indicated that the Australo-Melanesian and cosmopolitan strains of HTLV-I have evolved along separate geographically dependent lineages, with African STLV-I strains clustering with cosmopolitan HTLV-I strains and Asian STLV-I strains diverging from the common ancestral virus before the Australo-Melanesian HTLVI strains. When viewed within the context of non-human primate evolution and human occupation of Australia and Melanesia, the rate of molecular change of HTLV-I and STLV-I is approximately 2.5-6.8 x 10(-7) substitutions per site per year. Overall, the sequence and phylogenetic analyses are in accord with interspecies virus transmission among non-human primates, as well as between non-human primates and humans, with independent evolution of HTLV-I in Southeast Asia and in Africa, and with dissemination of HTLV-I by forced or voluntary movements of human populations. The immunosuppressive and T-cell activation properties of HTLV-I places at added risk these Australian Aboriginal and Melanesian populations, some of which are in imminent threat of infection with human immunodeficiency virus type 1. C1 NATL INST GENET,EVOLUT GENET LAB,MISHIMA,SHIZUOKA 411,JAPAN. UNIV HAWAII,PACIFIC BIOMED RES CTR,RETROVIROL RES LAB,HONOLULU,HI 96822. MENZIES SCH HLTH RES,DARWIN,NT 0811,AUSTRALIA. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RP YANAGIHARA, R (reprint author), NINCDS,CENT NERVOUS SYST STUDIES LAB,BLDG 36,RM 5B-21,BETHESDA,MD 20892, USA. NR 111 TC 18 Z9 18 U1 1 U2 3 PU CELLULAR & MOLECULAR BIOLOGY PI NOISY-LE-GRAND PA PROF R WEGMANN RESIDENCE HAUSSMANN 1 AVENUE DU PAVE NEUF, 93160 NOISY-LE-GRAND, FRANCE SN 0145-5680 J9 CELL MOL BIOL JI Cell. Mol. Biol. PY 1995 VL 41 SU 1 BP S145 EP S161 PG 17 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA RA778 UT WOS:A1995RA77800019 PM 8574142 ER PT J AU SHALIT, M SEKHSARIA, S MALECH, HL AF SHALIT, M SEKHSARIA, S MALECH, HL TI MODULATION OF GROWTH AND DIFFERENTIATION OF EOSINOPHILS FROM HUMAN PERIPHERAL-BLOOD CD34(+) CELLS BY IL5 AND OTHER GROWTH-FACTORS SO CELLULAR IMMUNOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; HUMAN HEMATOPOIETIC PROGENITORS; NECROSIS-FACTOR-ALPHA; INTERFERON-GAMMA; PROLIFERATION; INTERLEUKIN-3; INHIBITION; CULTURES; INVITRO; TARGET AB Small numbers of CD34(+) primitive hematopoietic progenitors are found in normal human peripheral blood. These cells differentiate to myeloid or lymphoid lineage under the influence of different growth factors. We investigated the effects of IL5 and other growth factors on the production of eosinophils from peripheral blood CD34(+) cells. CD34(+) cells were enriched from normal donors by apheresis and positive selection using an affinity column and plated in agarose with different combinations of cytokines. At 14 days of growth a triple stain technique was used to identify eosinophil, monocyte, and neutrophil colonies. IL5 alone did not support colony growth from CD34(+) cells. In contrast, GM-CSF and IL3 alone or together without added IL5 supported the generation of more than 50% pure eosinophil colonies. Addition of IL5 did not change the total number of colonies, but increased the fraction of pure eosinophil colonies to over 70%. Addition of G-CSF reduced the percentage of eosinophil colonies and increased the percentage of neutrophil colonies. Under the best conditions for eosinophil colony growth (IL3 + GM-CSF + IL5), the addition of interferon-alpha or bacterial lipopolysaccharide inhibited colony growth by 51 and 58%, respectively. Addition of interferon-gamma, tumor necrosis factor-alpha, or dexamethasone had no effect on eosinophil colonies. Since IL5 alone did not support colony growth from CD34(+) cells, we determined when IL5-responsive cells appeared in culture. Cells were grown initially with IL3 + GM-CSF in suspension, washed, and plated in agarose with IL5 alone. Only when progenitors were grown at least 3 days could IL5 serve as the single growth factor supporting pure eosinophil colony growth (47 colonies/10(4) cells plated at Day 3 and 134 colonies/10(4) cells at Day 7). We used neutralizing anti-IL5 antibodies to demonstrate that this late acting IL5 growth effect was specific, and that differentiation of eosinophils in the presence of IL3 + GMCSF was IL5 independent. Using reverse-transcriptase polymerase chain reaction, the mRNA encoding the eosinophil-specific protein eosinophil peroxidase (EPO) was not detected in Day 0 CD34(+) cells, but was demonstrated by Day 3 of culture. We conclude that within 3 days of culture, peripheral blood CD34(+) cells can become committed to the eosinophil lineage as demonstrated by responsiveness to IL5 and production of EPO transcripts. (C) 1995 Academic Press,Inc. RP SHALIT, M (reprint author), NIAID,HOST DEF LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 30 TC 49 Z9 50 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD JAN PY 1995 VL 160 IS 1 BP 50 EP 57 DI 10.1016/0008-8749(95)80008-7 PG 8 WC Cell Biology; Immunology SC Cell Biology; Immunology GA QF321 UT WOS:A1995QF32100007 PM 7531118 ER PT J AU CRITCHFIELD, JM ZUNIGAPFLUCKER, JC LENARDO, MJ AF CRITCHFIELD, JM ZUNIGAPFLUCKER, JC LENARDO, MJ TI PARAMETERS CONTROLLING THE PROGRAMMED DEATH OF MATURE MOUSE T-LYMPHOCYTES IN HIGH-DOSE SUPPRESSION SO CELLULAR IMMUNOLOGY LA English DT Article ID ANTIGEN-STIMULATED SUICIDE; PROLIFERATIVE RESPONSE; FINE SPECIFICITY; CYTOCHROME-C; CELL; APOPTOSIS; RECOGNITION; ACTIVATION; CLONES; MICE AB We have characterized parameters of both T cells and antigen-presenting cells (APCs) that influence high-dose suppression due to apoptosis. Blockade of interleukin-2 (IL-2) utilization is shown to inhibit both proliferation and the ensuing death. An analysis of sublines of a mature T cell clone demonstrates a correlation between IL-2 receptor cr chain (IL-BR) induction, increased proliferation, and greater suppression at high antigen doses. Profound loss of cells at high antigen dose was found to require at least 48 to 72 hr to develop. Antigen add-back experiments showed that strong T cell receptor reengagement of activated, cycling cells was essential for proliferative suppression and cell loss. Increasing the ratio of APC:T lymphocytes to 50:1 augmented cell death. For antigen-induced death of lymph node T cells, fresh T-depleted splenocytes were more effective than splenocytes that had been irradiated or treated with mitomycin C. Thus, T lymphocyte apoptosis at high antigen doses is a function of the activation response of the T lymphocyte as well as the efficiency of antigen presentation by the APC. These results strengthen the theory that apoptosis takes part in a feedback regulatory mechanism that has been called propricoidal regulation, which limits T cell expansion at high antigen doses. (C) 1995 Academic Press, Inc. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. RI Zuniga-Pflucker, Juan/H-1295-2012; OI Zuniga-Pflucker, Juan Carlos/0000-0003-2538-3178 NR 26 TC 31 Z9 33 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD JAN PY 1995 VL 160 IS 1 BP 71 EP 78 DI 10.1016/0008-8749(95)80011-7 PG 8 WC Cell Biology; Immunology SC Cell Biology; Immunology GA QF321 UT WOS:A1995QF32100010 PM 7531119 ER PT J AU THOMPSON, DC PERERA, K LONDON, R AF THOMPSON, DC PERERA, K LONDON, R TI QUINONE METHIDE FORMATION FROM PARA ISOMERS OF METHYLPHENOL (CRESOL), ETHYLPHENOL, AND ISOPROPYLPHENOL - RELATIONSHIP TO TOXICITY SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID BUTYLATED HYDROXYTOLUENE; GLUTATHIONE; ALKYLATION; REACTIVITY; OXIDATION; EUGENOL; RATS AB The oxidative metabolism and toxicity of the para isomers of methylphenol (cresol), ethylphenol, and isopropylphenol were studied using male Sprague-Dawley rat liver microsomes and precision-cut liver slices. Reactive intermediates from each compound were trapped using radiolabeled glutathione and were detected and quantified by HPLC. Conjugates were collected and their structures determined by fast atom bombardment mass spectrometry and proton nuclear magnetic resonance. During microsomal incubations each test compound formed monoglutathione conjugates with structures which are consistent with the formation of quinone methide intermediates. In each case the glutathione moiety was attached to the benzylic carbon on the alkyl side chain of the phenol. With ethylphenol, which has a prochiral benzylic carbon, two isomeric conjugates were detected. The rate of formation of the glutathione conjugates in liver slice incubations was 4-isopropylphenol > 4-ethylphenol > 4-methylphenol. This correlated with the toxicity of the three compounds in liver slices. At equimolar concentrations 4-isopropylphenol was the most toxic while 4-methylphenol was the least toxic. Depletion of intracellular glutathione was observed in the presence of each test compound which preceded cell death. Enhancement of cellular thiol levels with N-acetylcysteine protected cells from the toxic effects of all three compounds as did inhibition of cytochrome P450 activity with metyrapone. These results suggest the formation of quinone methide intermediates from three alkylphenols during oxidative metabolism and demonstrate a correlation between the amount of reactive intermediate formed and toxicity observed in liver slices. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RP THOMPSON, DC (reprint author), TEXAS A&M UNIV,COLL MED,DEPT MED PHARMACOL & TOXICOL,COLLEGE STN,TX 77843, USA. FU NIEHS NIH HHS [5 R29 ES06016] NR 18 TC 66 Z9 66 U1 0 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0893-228X J9 CHEM RES TOXICOL JI Chem. Res. Toxicol. PD JAN-FEB PY 1995 VL 8 IS 1 BP 55 EP 60 DI 10.1021/tx00043a007 PG 6 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA QD305 UT WOS:A1995QD30500008 PM 7703367 ER PT J AU PAGE, JE SZELIGA, J AMIN, S HECHT, SS DIPPLE, A AF PAGE, JE SZELIGA, J AMIN, S HECHT, SS DIPPLE, A TI MUTATIONAL SPECTRA FOR 5,6-DIMETHYLCHRYSENE 1,2-DIHYDRODIOL 3,4-EPOXIDES IN THE SUPF GENE OF PSP189 SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID DIOL-EPOXIDES; DIHYDRODIOL-EPOXIDES; SHUTTLE VECTOR; DNA ADDUCTS; MOUSE SKIN; BENZOPHENANTHRENE; ADENINE; 5-METHYLCHRYSENE; 1,2-EPOXIDES; SPECIFICITY AB Dihydrodiol epoxides from 5,6-dimethylchrysene exhibit properties similar to those of fjord region-containing hydrocarbon derivatives in that they react extensively with deoxyadenosine residues in DNA and consequently generate substantial numbers of mutations at AT pairs as well as GC pairs. The syn-dihydrodiol epoxide favors reaction with deoxyadenosine (68% of adducts) to a greater extent than does the anti-dihydrodiol epoxide (52% of adducts), and point mutations at AT pairs (72% for syn- and 45% for anti-dihydrodiol epoxide) follow the same trend. A novel feature of the mutagenicity of the 5,6-dimethylchrysene derivatives is that they exhibit a higher fraction of AT --> GC transitions (28% and 26% for syn and anti, respectively) than has been seen for other hydrocarbon derivatives to date. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702. AMER HLTH FDN,VALHALLA,NY 10950. OI Hecht, Stephen/0000-0001-7228-1356 FU NCI NIH HHS [N01-CO-46000, N01-CP-21115] NR 30 TC 13 Z9 13 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0893-228X J9 CHEM RES TOXICOL JI Chem. Res. Toxicol. PD JAN-FEB PY 1995 VL 8 IS 1 BP 143 EP 147 DI 10.1021/tx00043a019 PG 5 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA QD305 UT WOS:A1995QD30500020 PM 7703358 ER PT J AU LANSBURY, PT AF LANSBURY, PT TI THE CHEMISTRY OF SCRAPIE INFECTION - IMPLICATIONS OF THE ICE-9 METAPHOR SO CHEMISTRY & BIOLOGY LA English DT Article ID PRION DISEASES; AMYLOID FORMATION; PRP ACCUMULATION; CONGO RED; INHIBITION; PROTEIN; CONVERSION; RESISTANT; FIBRILS; FORM AB The transmissible spongiform encephalopathies pose an increasing problem for animal, and perhaps human, health. The infectious agent seems to tack a nucleic acid component, posing the question of how it can reproduce. A model of reproduction by nucleated polymerization suggests a number of-novel approaches to the problem. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. RP LANSBURY, PT (reprint author), MIT,DEPT CHEM,CAMBRIDGE,MA 02139, USA. NR 44 TC 117 Z9 118 U1 0 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 1074-5521 J9 CHEM BIOL JI Chem. Biol. PD JAN PY 1995 VL 2 IS 1 BP 1 EP 5 DI 10.1016/1074-5521(95)90074-8 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QJ331 UT WOS:A1995QJ33100001 PM 9383397 ER PT B AU ADAMS, HR CHANNING, MA DIVEL, JE DUNN, BB KIESEWETTER, DO PLASCJAK, P REGDOS, SL SIMPSON, NR ECKELMAN, WC AF ADAMS, HR CHANNING, MA DIVEL, JE DUNN, BB KIESEWETTER, DO PLASCJAK, P REGDOS, SL SIMPSON, NR ECKELMAN, WC BE Emran, AM TI Trend analysis of quality control data SO CHEMISTS' VIEWS OF IMAGING CENTERS LA English DT Proceedings Paper CT American-Chemical-Society Symposium on Chemists Views of Imaging Centers/206th ACS National Meeting CY AUG 22-27, 1993 CL CHICAGO, IL SP Amer Chem Soc, Div Nucl Chem & Technol, US DOE, Off Hlth & Environm Res, Int Atom Energy Agcy, Vienna, Bioscan Inc, Washington, CTI Inc, Knoxville, GE Med Syst, Milwaukee, Isotech Inc, Miamisburg, Isotex Inc, Houston C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT POSITRON EMISS TOMOGR,BETHESDA,MD 20892. NR 0 TC 5 Z9 5 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44912-9 PY 1995 BP 175 EP 188 PG 14 WC Chemistry, Inorganic & Nuclear; Nuclear Science & Technology; Pharmacology & Pharmacy; Radiology, Nuclear Medicine & Medical Imaging SC Chemistry; Nuclear Science & Technology; Pharmacology & Pharmacy; Radiology, Nuclear Medicine & Medical Imaging GA BD92S UT WOS:A1995BD92S00021 ER PT B AU PIPPIN, CC GANSOW, OA BRECHBIEL, MW KOCH, L MOLINET, R VANGEEL, J APOSTOLIDIS, C GEERLINGS, MW SCHEINBERG, DA AF PIPPIN, CC GANSOW, OA BRECHBIEL, MW KOCH, L MOLINET, R VANGEEL, J APOSTOLIDIS, C GEERLINGS, MW SCHEINBERG, DA BE Emran, AM TI Recovery of Bi-213 from an Ac-225 cow: Application to the radiolabeling of antibodies with Bi-213 SO CHEMISTS' VIEWS OF IMAGING CENTERS LA English DT Proceedings Paper CT American-Chemical-Society Symposium on Chemists Views of Imaging Centers/206th ACS National Meeting CY AUG 22-27, 1993 CL CHICAGO, IL SP Amer Chem Soc, Div Nucl Chem & Technol, US DOE, Off Hlth & Environm Res, Int Atom Energy Agcy, Vienna, Bioscan Inc, Washington, CTI Inc, Knoxville, GE Med Syst, Milwaukee, Isotech Inc, Miamisburg, Isotex Inc, Houston C1 NCI,RADIAT ONCOL BRANCH,CHEM SECT,BETHESDA,MD 20892. NR 0 TC 5 Z9 5 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44912-9 PY 1995 BP 315 EP 322 PG 8 WC Chemistry, Inorganic & Nuclear; Nuclear Science & Technology; Pharmacology & Pharmacy; Radiology, Nuclear Medicine & Medical Imaging SC Chemistry; Nuclear Science & Technology; Pharmacology & Pharmacy; Radiology, Nuclear Medicine & Medical Imaging GA BD92S UT WOS:A1995BD92S00035 ER PT J AU LENFANT, C AF LENFANT, C TI TASK-FORCE ON RESEARCH IN CARDIOPULMONARY DYSFUNCTION IN CRITICAL CARE MEDICINE SO CIRCULATION LA English DT Editorial Material RP LENFANT, C (reprint author), NHLBI,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 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 JAN 1 PY 1995 VL 91 IS 1 BP 1 EP 7 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA PZ555 UT WOS:A1995PZ55500001 PM 7805189 ER PT J AU RIHAL, CS EAGLE, KA MICKEL, MC FOSTER, ED SOPKO, G GERSH, BJ AF RIHAL, CS EAGLE, KA MICKEL, MC FOSTER, ED SOPKO, G GERSH, BJ TI SURGICAL THERAPY FOR CORONARY-ARTERY DISEASE AMONG PATIENTS WITH COMBINED CORONARY-ARTERY AND PERIPHERAL VASCULAR-DISEASE SO CIRCULATION LA English DT Article DE BYPASS; PERIPHERAL VASCULAR DISEASE; CORONARY DISEASE; SURGERY ID CAROTID ENDARTERECTOMY; MYOCARDIAL-INFARCTION; BYPASS-SURGERY; HEART-DISEASE; 5-YEAR SURVIVAL; LATE MORTALITY; MORBIDITY; OPERATIONS; RISK; REVASCULARIZATION AB Background Among patients with combined coronary artery and peripheral vascular disease, long-term benefits of surgical therapy compared with medical therapy for coronary artery disease are unknown. Methods and Results Using prospectively collected data from the Coronary Artery Surgery Study registry, we performed a retrospective cohort analysis of 1834 patients (mean age, 56 years; 20% women) with both coronary artery and peripheral vascular disease and evaluated their long-term outcomes. Of these patients, 986 received (nonrandomly) coronary artery bypass graft surgery, and 848 were treated medically. Perioperative mortality was 4.2% (2.9% in the absence of peripheral vascular disease; P = .02). In a mean follow-up period of 10.4 years, 1100 deaths occurred (80% due to cardiovascular causes). For the surgical group, 4-, 8-, 12-, and 16-year estimated probabilities of survival were 88%, 72%, 55%, and 41%, respectively, and 73%, 57%, 44%, and 34%, respectively, for the medical group (P < .0001). Multivariate analysis demonstrated that type of therapy was independently associated with survival (P = .0001; chi(2) = 15.34). Subgroup analysis suggested that benefits of surgical treatment on survival were limited to patients with three-vessel coronary artery disease and were inversely related to ejection fraction. Survival free of death or myocardial infarction was also significantly better among the surgical group. Type of therapy was significantly associated with occurrence of late events (P = .01; chi(2)=6.55). Subgroup analysis again demonstrated that beneficial effects of surgery were limited to patients with three-vessel coronary artery disease and were inversely related to ejection fraction. Conclusions Surgical treatment provides long-term benefit for certain subgroups of patients with combined coronary artery and peripheral arterial vascular disease. C1 MAYO CLIN & MAYO FDN, DIV CARDIOVASC DIS & INTERNAL MED, ROCHESTER, MN 55905 USA. MASSACHUSETTS GEN HOSP, DEPT CLIN CARDIOL, BOSTON, MA 02114 USA. UNIV WASHINGTON, DEPT BIOSTAT, SEATTLE, WA 98195 USA. ALBANY MED COLL, ALBANY, NY USA. NHLBI, CARDIAC DIS BRANCH, BETHESDA, MD 20892 USA. NR 51 TC 69 Z9 71 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD JAN 1 PY 1995 VL 91 IS 1 BP 46 EP 53 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA PZ555 UT WOS:A1995PZ55500009 PM 7805218 ER PT J AU LAZAROUS, DF SCHEINOWITZ, M SHOU, M HODGE, E RAJANAYAGAM, MAS HUNSBERGER, S ROBISON, WG STIBER, JA CORREA, R EPSTEIN, SE UNGER, EF AF LAZAROUS, DF SCHEINOWITZ, M SHOU, M HODGE, E RAJANAYAGAM, MAS HUNSBERGER, S ROBISON, WG STIBER, JA CORREA, R EPSTEIN, SE UNGER, EF TI EFFECTS OF CHRONIC SYSTEMIC ADMINISTRATION OF BASIC FIBROBLAST GROWTH-FACTOR ON COLLATERAL DEVELOPMENT IN THE CANINE HEART SO CIRCULATION LA English DT Article DE CIRCULATION; PHARMACOKINETICS; PEPTIDES, GROWTH SUBSTANCES ID BLOOD-FLOW MEASUREMENTS; CORONARY ANASTOMOSES; RAT-HEART; PROLIFERATION; LOCALIZATION; ARTERIES AB Background Recently we reported that intracoronary administration of basic fibroblast growth factor (bFGF), a patent angiogenic peptide, increases collateral blood flow in dogs subjected to progressive left circumflex coronary artery (LCx) occlusion. The aim of the present study was to examine the effect of systemically administered bFGF on collateral blood flow and to assess its pharmacokinetics and potential side effects. Methods and Results Forty-seven dogs were subjected to progressive ameroid-induced occlusion of the LCx, an intervention known to induce the development of collateral vessels. In phase I of the investigation, dogs were randomized to receive bFGF 1.74 mg/d (n=10) or saline (n=9) as a left atrial injection for 4 weeks. Relative collateral blood flow was assessed serially with radiolabeled microspheres in the conscious state during maximal coronary vasodilatation. Initiation of bFGF treatment was temporally associated with a marked acceleration of collateral development; however, collateral flow in control dogs improved toward the end of the study, approaching that of bFGF-treated dogs at the 38-day end point. Phase II of the investigation was a three-armed study of extended duration to determine whether bFGF caused a sustained increase in collateral function. Dogs were randomized to receive bFGF 1.74 mg/d for 9 weeks (n=7), bFGF 1.74 mg/d for 5 weeks followed by placebo for 4 weeks (n-11), or placebo for 9 weeks (n=10). Relative and absolute collateral blood flow were assessed serially with microspheres during maximal coronary vasodilatation. Between the 10th and 17th days after ameroid placement, bFGF-treated dogs exhibited marked improvement in collateral flow such that maximal collateral conductance exceeded that of controls by 24% at the 5-week crossover point. Final collateral conductance was similar in dogs receiving bFGF for 5 and 9 weeks despite withdrawal of treatment in the former group. bFGF administration was associated with a 21% increase in final collateral conductance as well as a 49% increase in collateral zone vascular density. Prolonged bFGF administration was also associated with a decrease in arterial pressure, moderate thrombocytopenia, and moderate, reversible anemia. Conclusions Systemic administration of bFGF enhanced collateral conductance in dogs with progressive single-vessel coronary occlusion. The beneficial effect of bFGF occurred primarily between the 7th and 14th days of therapy, and regression of collateral development was not noted after withdrawal of treatment. The present investigation provides impetus to the concept that collateral development can be enhanced pharmacologically-specifically by bFGF-raising the possibility that such an intervention might eventually be applied clinically. C1 NHLBI,CARDIOL BRANCH,EXPTL PHYSIOL & PHARMACOL SECT,BETHESDA,MD 20892. NHLBI,BIOSTAT RES BRANCH,BETHESDA,MD 20892. NHLBI,PATHOL BRANCH,BETHESDA,MD 20892. NEI,BETHESDA,MD 20892. NR 30 TC 181 Z9 187 U1 2 U2 5 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JAN 1 PY 1995 VL 91 IS 1 BP 145 EP 153 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA PZ555 UT WOS:A1995PZ55500022 PM 7805195 ER PT J AU PALKOVITS, M MEZEY, E FODOR, M GANTEN, D BAHNER, U GEIGER, H HEIDLAND, A AF PALKOVITS, M MEZEY, E FODOR, M GANTEN, D BAHNER, U GEIGER, H HEIDLAND, A TI NEUROTRANSMITTERS AND NEUROPEPTIDES IN THE BARORECEPTOR REFLEX ARC - CONNECTIONS BETWEEN THE NUCLEUS OF THE SOLITARY TRACT AND THE VENTROLATERAL MEDULLA-OBLONGATA IN THE RAT SO CLINICAL AND EXPERIMENTAL HYPERTENSION LA English DT Article; Proceedings Paper CT Satellite Symposium on Neural Mechanisms in Hypertension CY MAR 16-18, 1994 CL AYERS ROCK, AUSTRALIA DE NUCLEUS OF THE SOLITARY TRACT; VENTROLATERAL MEDULLA OBLONGATA; GLUTAMATE; TYROSINE HYDROXYLASE; ANGIOTENSINOGEN MESSENGER-RNA; ATRIAL NATRIURETIC POLYPEPTIDE ID CENTRAL NERVOUS-SYSTEM; IMMUNOREACTIVE NEURONS; ANGIOTENSIN-II; BRAIN-STEM; CARDIOVASCULAR CONTROL; PRESSOR AREA; PROJECTIONS; PATHWAY; CELLS; LOCALIZATION AB The primary baroreceptor area (nucleus of the solitary tract - NTS) is anatomically interconnected with the rostral (''vasomotor area'') and the caudal (''vasodepressor area'') ventrolateral medulla by a well-defined are of neuronal pathways. The chemical character and the direction of these pathways have been investigated with immunohistochemical and neurochemical techniques in intact and brainstem-operated rats. The transection of the neuronal are resulted in an accumulation of tyrosine hydroxylase immunoreactivity in a small group of cells in the NTS adjacent to the area postrema, ipsilateral to the knife cut. Decreased angiotensinogen mRNA and atrial natriuretic peptide concentrations were measured in the ventrolateral medulla after the cut, and an accumulation of angiotensin II-immunoreactivity was found in neuronal perikarya in the ipsilateral NTS. Intracranial vagotomy caused marked depletions in glutamate levels in the subcommissural portion of the NTS and in the caudal ventrolateral medulla but nowhere else in the brainstem investigated including the rostral ventrolateral medulla. C1 NIH,CELL BIOL LAB,BETHESDA,MD 20892. MAX DELBRUCK CTR MOLEC MED,DEPT PHARMACOL,O-1115 BERLIN,GERMANY. UNIV WURZBURG,DEPT NEPHROL,MED CLIN,W-8700 WURZBURG,GERMANY. RP PALKOVITS, M (reprint author), SEMMELWEIS UNIV MED,SCH MED,NEUROMORPHOL LAB,H-1450 BUDAPEST,HUNGARY. RI Palkovits, Miklos/F-2707-2013; OI Palkovits, Miklos/0000-0003-0578-0387 NR 33 TC 15 Z9 15 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1064-1963 J9 CLIN EXP HYPERTENS JI Clin. Exp. Hypertens. PD JAN-FEB PY 1995 VL 17 IS 1-2 BP 101 EP 113 DI 10.3109/10641969509087058 PG 13 WC Pharmacology & Pharmacy; Peripheral Vascular Disease SC Pharmacology & Pharmacy; Cardiovascular System & Cardiology GA QD972 UT WOS:A1995QD97200010 PM 7735261 ER PT J AU VANDENBERG, C GUAN, XY VONHOFF, D JENKINS, R BITTNER, M GRIFFIN, C KALLIONIEMI, O VISAKORPI, T MCGILL, J HERATH, J EPSTEIN, J SAROSDY, M MELTZER, P TRENT, J AF VANDENBERG, C GUAN, XY VONHOFF, D JENKINS, R BITTNER, M GRIFFIN, C KALLIONIEMI, O VISAKORPI, T MCGILL, J HERATH, J EPSTEIN, J SAROSDY, M MELTZER, P TRENT, J TI DNA-SEQUENCE AMPLIFICATION IN HUMAN PROSTATE-CANCER IDENTIFIED BY CHROMOSOME MICRODISSECTION - POTENTIAL PROGNOSTIC IMPLICATIONS SO CLINICAL CANCER RESEARCH LA English DT Article ID ALLELIC LOSS; E-CADHERIN; CARCINOMA; GENE; EXPRESSION; DELETION; CELLS; GENERATION; PROBES; MYC AB The primary aim of this report was to examine the significance of increased DNA sequence copy number (gene amplification) in human prostate cancers, Three methodologies (chromosome microdissection, comparative genomic hybridization, and fluorescence in situ hybridization) were combined to (a) identify a common region of gene amplification in human prostate cells and (b) evaluate in patient samples the prevalence of this genetic change in both primary and recurrent prostate samples, The results of chromosome microdissection revealed a common amplified band region (8q24.1-24.2) in two prostate cases with cytological evidence of gene amplification (double minutes), Fluorescence in situ hybridization using the 8q microdissection probe was performed on fresh tumor touch preparations from 44 randomly selected prostatectomy specimens, Amplification of DNA sequences from 8q24 was observed in 4 (9%) of 44 cases, Four of the 44 patients in this series presented with a positive lymph node at initial diagnosis and 3 of these 4 patients showed 8q amplification, Because of this finding, comparative genomic hybridization and fluorescence ill situ hybridization were performed on tumor cells from nine prostate cancer patients with recurrent disease, In eight of nine cases a gain of DNA sequences encompassing 8q24 was observed, Taken together with other evidence implicating 8q gain in prostate cancer progression, these results suggest that the analysis of this genetic change may have diagnostic utility as a marker of prostate cancer progression. C1 NCHGR, CANC GENET LAB, BETHESDA, MD 20892 USA. UNIV TEXAS, HLTH SCI CTR, SAN ANTONIO, TX 78284 USA. MAYO CLIN & MAYO FDN, GENET LAB, ROCHESTER, MN 55905 USA. JOHNS HOPKINS UNIV, CTR ONCOL, BALTIMORE, MD 21287 USA. TAMPERE UNIV HOSP, DEPT LAB MED, TAMPERE, FINLAND. CANC THERAPY & RES CTR S TEXAS, SAN ANTONIO, TX 78229 USA. RI Guan, Xin-Yuan/A-3639-2009; Kallioniemi, Olli/H-5111-2011; Kallioniemi, Olli/H-4738-2012 OI Guan, Xin-Yuan/0000-0002-4485-6017; Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332 FU NCI NIH HHS [UO1-CA-48405, P20CA58225] NR 34 TC 87 Z9 87 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 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN PY 1995 VL 1 IS 1 BP 11 EP 18 PG 8 WC Oncology SC Oncology GA RJ523 UT WOS:A1995RJ52300003 PM 9815882 ER PT J AU GOLDBERG, MR HEIMBROOK, DC RUSSO, P SAROSDY, MF GREENBERG, RE GIANTONIO, BJ LINEHAN, WM WALTHER, M FISHER, HAG MESSING, E CRAWFORD, ED OLIFF, AI PASTAN, IH AF GOLDBERG, MR HEIMBROOK, DC RUSSO, P SAROSDY, MF GREENBERG, RE GIANTONIO, BJ LINEHAN, WM WALTHER, M FISHER, HAG MESSING, E CRAWFORD, ED OLIFF, AI PASTAN, IH TI PHASE-I CLINICAL-STUDY OF THE RECOMBINANT ONCOTOXIN TP40 IN SUPERFICIAL BLADDER-CANCER SO CLINICAL CANCER RESEARCH LA English DT Article ID GROWTH-FACTOR RECEPTOR; TRANSITIONAL-CELL-CARCINOMA; PSEUDOMONAS EXOTOXIN; PROTEIN; EXPRESSION; ALPHA; CYTOTOXICITY; MANAGEMENT; TUMORS AB Transforming growth factor alpha-Pseudomonas exotoxin-40 (TP40) is a hybrid fusion protein that selectively binds to cancer cells that express the epidermal growth factor receptor, TP40 is then internalized and kills these cells by virtue of its Pseudomonas exotoxin-derived domains, We studied the safety and short-term antitumor activity of intravesical TP40 in 43 patients with refractory superficial bladder cancer, These patients had resected T-a/T-1 disease (n = 19), visible T-a or T-1 lesions (n = 11), or carcinoma in situ (n = 13), Patients were treated with increasing dose levels of TP40 at 0.15, 0.3, 0.6, 1.2, 2.4, 4.8, or 9.6 mg/week for 6 weeks and evaluated by comparing pretreatment and posttreatment cystoscopic examinations, cytology, and histopathology, All TP40 doses were well tolerated, No evidence of antitumor activity was seen in any of the patients with T-a or T-1 lesions, However, 8 of 9 patients with evaluable carcinoma in situ were judged by histopathology of multiple biopsy specimens to exhibit clinical improvement following TP40 therapy, In most of these responsive patients, cystoscopic examination supported the histopathological findings, although cytology of urine and bladder washings persistently demonstrated malignant cells, Therefore, TP40 appears to be a well-tolerated biological agent that may prove to have utility in treating carcinoma in situ of the bladder. C1 MERCK SHARP & DOHME LTD, RES LABS, W POINT, PA 19486 USA. MEM SLOAN KETTERING CANC CTR, NEW YORK, NY 10021 USA. UNIV TEXAS, HLTH SCI CTR, SAN ANTONIO, TX 78284 USA. FOX CHASE CANC CTR, PHILADELPHIA, PA 19111 USA. NCI, BETHESDA, MD 20892 USA. ALBANY MED COLL, ALBANY, NY 12208 USA. UNIV WISCONSIN, SCH MED, MADISON, WI 53706 USA. UNIV COLORADO, CTR HLTH SERV, DENVER, CO 80262 USA. NR 19 TC 50 Z9 54 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN PY 1995 VL 1 IS 1 BP 57 EP 61 PG 5 WC Oncology SC Oncology GA RJ523 UT WOS:A1995RJ52300008 PM 9815887 ER PT J AU GUDAS, JM NGUYEN, H KLEIN, RC KATAYOSE, D SETH, P COWAN, KH AF GUDAS, JM NGUYEN, H KLEIN, RC KATAYOSE, D SETH, P COWAN, KH TI DIFFERENTIAL EXPRESSION OF MULTIPLE MDM2 MESSENGER-RNAS AND PROTEINS IN NORMAL AND TUMORIGENIC BREAST EPITHELIAL-CELLS SO CLINICAL CANCER RESEARCH LA English DT Article ID WILD-TYPE P53; ESTROGEN-RECEPTOR CONTENT; CANCER CELLS; PROGESTERONE RECEPTORS; GENE AMPLIFICATION; HUMAN SARCOMAS; MUTATIONS; GROWTH; LINE; MCF-7 AB The MDM2 gene is a nuclear phosphoprotein that is regulated by p53 and functions, in one capacity, to inhibit the transcriptional activity of the wild-type p53 protein, Multiple MDM2 transcripts were detected in human breast epithelial cells. In estrogen receptor-negative normal, immortal, and tumorigenic breast epithelial cells, we found a good correlation between MDM2 mRNA levels and expression of wild-type p53, When wild-type p53 was overexpressed in estrogen receptor-negative tumor cells containing a mutant or no endogenous p53, MDM2 mRNA levels increased significantly, indicating that wild-type p53 positively influences MDM2 mRNA levels in these tumor cells, Because all estrogen receptor-positive breast tumor cells had high MDM2 mRNA levels regardless of the status of their endo genous p53 protein, other factors likely influence MDM2 expression in these cells, Distinct MDM2 proteins (range, M(r) 54,000-68,000 and 90,000-100,000, respectively) were differentially expressed in human breast epithelial cells. The lower molecular weight MDM2 proteins were most abundant in the normal mammary cells but present at varying levels in many of the tumor cells examined, MDM2 was a nuclear protein; however, nuclear staining intensity did not always correlate with the amount of MDM2-immunoreactive protein as determined by Western blot analysis, This discrepancy suggests that MDM2 interacts with novel cellular proteins in different kinds of breast epithelial cells. RP GUDAS, JM (reprint author), NCI,DIV CANC TREATMENT,MED BRANCH,MED BREAST CANC SECT,BLDG 10,ROOM 12N226,BETHESDA,MD 20892, USA. NR 52 TC 70 Z9 70 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 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN PY 1995 VL 1 IS 1 BP 71 EP 80 PG 10 WC Oncology SC Oncology GA RJ523 UT WOS:A1995RJ52300010 PM 9815889 ER PT J AU WAKEFIELD, LM LETTERIO, JJ CHEN, T DANIELPOUR, D ALLISON, RSH PAI, LH DENICOFF, AM NOONE, MH COWAN, KH OSHAUGHNESSY, JA SPORN, MB AF WAKEFIELD, LM LETTERIO, JJ CHEN, T DANIELPOUR, D ALLISON, RSH PAI, LH DENICOFF, AM NOONE, MH COWAN, KH OSHAUGHNESSY, JA SPORN, MB TI TRANSFORMING GROWTH-FACTOR-BETA-1 CIRCULATES IN NORMAL HUMAN PLASMA AND IS UNCHANGED IN ADVANCED METASTATIC BREAST-CANCER SO CLINICAL CANCER RESEARCH LA English DT Article ID PROGRAMMED CELL-DEATH; FACTOR-BETA; EXPRESSION; INVIVO; THROMBOGLOBULIN; CARCINOMA; RAT; LOCALIZATION; TGF-BETA-1; PROSTATE AB A method has been developed to determine true plasma transforming growth factor beta (TGF-beta) levels by using the platelet alpha granule-specific marker, platelet factor 4, to correct for the TGF-beta contributed by platelets degranulated en vivo. TGF-beta levels were measured on acid-ethanol extracts of human plasma using isoform-specific sandwich enzyme-linked immunosorbent assays, Normal human subjects had 4.1 +/- 2.0 ng/ml TGF-beta 1 (range, 2.0-12.0; n = 42), <0.2 ng/ml TGF-beta 2, and <0.1 ng/ml TGF-beta 3 in their plasma, There were no significant changes with age or with hormonal status, but any given individual showed fluctuations of up to 3-fold in measured plasma TGF-beta levels due to unknown factors, Of 28 patients with advanced metastatic breast cancer, 2 had greatly elevated TGF-beta 1 levels, while the rest were in the normal range, The presence of physiologically significant levels of TGF-beta 1 in the plasmas of normal human subjects may indicate previously unsuspected endocrine roles for this peptide, while TGF-beta 2 and TGF-beta 3 appear to act only in a local autocrine/paracrine fashion. C1 NCI,MED BRANCH,BETHESDA,MD 20892. RP WAKEFIELD, LM (reprint author), NCI,CHEMOPREVENT LAB,BLDG 41,ROOM B1111,41 LIB DR MSC 5055,BETHESDA,MD 20892, USA. NR 39 TC 132 Z9 132 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 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN PY 1995 VL 1 IS 1 BP 129 EP 136 PG 8 WC Oncology SC Oncology GA RJ523 UT WOS:A1995RJ52300016 PM 9815895 ER PT J AU GOLDBERGER, BA LOEWENTHAL, B DARWIN, WD CONE, EJ AF GOLDBERGER, BA LOEWENTHAL, B DARWIN, WD CONE, EJ TI INTRASUBJECT VARIATION OF CREATININE AND SPECIFIC-GRAVITY MEASUREMENTS IN CONSECUTIVE URINE SPECIMENS OF HEROIN USERS SO CLINICAL CHEMISTRY LA English DT Letter C1 NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. NR 7 TC 28 Z9 28 U1 0 U2 2 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 JAN PY 1995 VL 41 IS 1 BP 116 EP 117 PG 2 WC Medical Laboratory Technology SC Medical Laboratory Technology GA QA212 UT WOS:A1995QA21200025 PM 7813059 ER PT J AU SIVAPARVATHI, M SAWAYA, R WANG, SW RAYFORD, A YAMAMOTO, M LIOTTA, LA NICOLSON, GL RAO, JS AF SIVAPARVATHI, M SAWAYA, R WANG, SW RAYFORD, A YAMAMOTO, M LIOTTA, LA NICOLSON, GL RAO, JS TI OVEREXPRESSION AND LOCALIZATION OF CATHEPSIN-B DURING THE PROGRESSION OF HUMAN GLIOMAS SO CLINICAL & EXPERIMENTAL METASTASIS LA English DT Article DE CYSTEINE PROTEASES; EXTRACELLULAR MATRIX; GLIOBLASTOMA MULTIFORME; INVASION ID PLASMINOGEN-ACTIVATOR; BRAIN-TUMORS; TISSUE; CELLS; PROTEINASE; METALLOPROTEINASE; IDENTIFICATION; EXTRACTION; MODULATION; SECRETION AB Degradation of the extracellular matrix is a prerequisite for acquisition of the invasive phenotype. Several proteinases released by invading tumor cells appear to participate in the focal degradation of extracellular matrix proteins, Using an enzyme-linked immunosorbent assay, enzymatic assays, Western and Nothern blotting techniques, we determined whether increased levels of the cysteine protease cathepsin B correlated with the progression and invasion of human gliomas, The amount of cathepsin B activity and protein content were highest in glioblastomas, lower in anaplastic astrocytomas and lowest in normal brain tissue and low-grade gliomas, There were significantly higher amounts of Mr 25000 and 26000 bands in glioblastoma and anaplastic astrocytoma than in normal brain and low-grade glioma tissue extracts as determined by Western blotting with anti-cathepsin antibodies, In addition, cathepsin B transcripts were overexpressed in anaplastic astrocytoma (about two- to three-fold), in glioblastoma (about eight- to 10-fold), compared with normal brain tissue and low-grade glioma, Immunohistochemical staining for cathepsin B showed intense immunoreactivity in tumor and endothelial cells of glioblastomas and anaplastic astrocytomas but only weak immunoreactivity in low-grade glioma and normal brain tissues, Therefore, we conclude that cathepsin B expression is greatest in highly malignant astrocytomas, especially in glioblastomas, and is correlated with the malignant progression of astrocytomas. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT NEUROSURG,HOUSTON,TX 77030. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT TUMOR BIOL,HOUSTON,TX 77030. NCI,PATHOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA 44352, CA 56792] NR 34 TC 87 Z9 89 U1 1 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0262-0898 J9 CLIN EXP METASTAS JI Clin. Exp. Metastasis PD JAN PY 1995 VL 13 IS 1 BP 49 EP 56 DI 10.1007/BF00144018 PG 8 WC Oncology SC Oncology GA QD792 UT WOS:A1995QD79200006 PM 7820956 ER PT J AU MOHANAM, S WANG, SW RAYFORD, A YAMAMOTO, M SAWAYA, R NAKAJIMA, M LIOTTA, LA NICOLSON, GL STETLERSTEVENSON, WG RAO, JS AF MOHANAM, S WANG, SW RAYFORD, A YAMAMOTO, M SAWAYA, R NAKAJIMA, M LIOTTA, LA NICOLSON, GL STETLERSTEVENSON, WG RAO, JS TI EXPRESSION OF TISSUE INHIBITORS OF METALLOPROTEINASES - NEGATIVE REGULATORS OF HUMAN GLIOBLASTOMA INVASION IN-VIVO SO CLINICAL & EXPERIMENTAL METASTASIS LA English DT Article DE GLIOBLASTOMA MULTIFORME; INVASION; MATRIX; METALLOPROTEINASES; METASTASIS; TISSUE INHIBITORS OF METALLOPROTEINASES ID HUMAN-BRAIN-TUMORS; IV COLLAGENASE; DEGRADING METALLOPROTEINASES; MATRIX METALLOPROTEINASE; 72-KDA GELATINASE; COMPLEX-FORMATION; GLIOMA-CELLS; TIMP-2; STROMELYSIN; FIBROBLASTS AB Tissue inhibitors of metalloproteinases (TIMPs) are negative regulators of matrix metalloproteinases (MMPs) which degrade major components of the extracellular matrix, The aberrant expression of TIMPs is believed to represent an important modulating factor in the invasive capacity of human tumors, In the present study we analyzed the expression of TIMPs in human brain tumor tissue samples by an enzyme-linked immunosorbent assay (ELISA) and by Northern blotting analysis, Quantitation of TIMP-1 and TIMP-2 by ELISA demonstrated low levels of TIMP-1 and TIMP-2 proteins in glioblastomas, and moderate levels in anaplastic astrocytomas compared with normal brain tissues low-grade gliomas and metastatic tumors (renal and breast carcinomas and melanomas), Northern blot analysis of TIMP-1 transcripts demonstrated higher expression in meningioma, normal brain tissues and other metastatic tumors than in anaplastic astrocytoma and glioblastoma, Two distinct transcripts of 1.0 and 3.5 kb were observed for TIMP-2 mRNA in normal brain tissue and in tumor extracts, In addition, TIMP-2 mRNA expression was lower in glioblastoma and anaplastic astrocytoma than in meningioma, normal brain tissues and metastatic tumors, These findings suggest that down-regulation of both TIMP-1 and TIMP-2 contributes significantly to the invasive potential of human glioblastoma multiforme and anaplastic astrocytomas. C1 UNIV TEXAS,MD ANDERSON CANCER CTR,DEPT NEUROSURG,HOUSTON,TX 77030. UNIV TEXAS,MD ANDERSON CANCER CTR,DEPT TUMOR BIOL,HOUSTON,TX 77030. NCI,PATHOL LAB,BETHESDA,MD 20892. UNIV TOKYO,DEPT BIOACT SUBST,TOKYO,JAPAN. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 FU NCI NIH HHS [CA 44352, CA 56792] NR 34 TC 85 Z9 88 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0262-0898 J9 CLIN EXP METASTAS JI Clin. Exp. Metastasis PD JAN PY 1995 VL 13 IS 1 BP 57 EP 62 DI 10.1007/BF00144019 PG 6 WC Oncology SC Oncology GA QD792 UT WOS:A1995QD79200007 PM 7820957 ER PT J AU ZHOU, P THOMASSEN, MJ PETTAY, J DEODHAR, SD BARNA, BP AF ZHOU, P THOMASSEN, MJ PETTAY, J DEODHAR, SD BARNA, BP TI HUMAN MONOCYTES PRODUCE MONOCYTE CHEMOATTRACTANT PROTEIN-1 (MCP-1) IN RESPONSE TO A SYNTHETIC PEPTIDE DERIVED FROM C-REACTIVE PROTEIN SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID TUMORICIDAL ACTIVITY; ALVEOLAR MACROPHAGES; RHEUMATOID-ARTHRITIS; ENDOTHELIAL-CELLS; HUMAN-FIBROBLASTS; GENE-EXPRESSION; ACTIVATION; CYTOKINE; PURIFICATION; GENERATION AB We reported previously that a synthetic peptide (RS-83277) derived from human C-reactive protein (CRP) augmented human monocyte/macrophage tumoricidal activity and cytokine production. RS-83287, a synthetic peptide derived from a different CRP site, was ineffective. Because chemoattractant properties have been attributed to some CRP-derived peptides, we hypothesized that RS-83277, in addition to activating effects, might promote human monocyte chemotaxis. Results indicated that neither CRP peptide RS-83277 nor RS-83287 was, itself, a chemoattractant. RS-83277, but not RS-83287, however, elicited time-dependent production of monocyte chemoattractant activity in conditioned media (CM) of cultured human mononuclear leukocytes and purified, adherent monocytes (RIG). CM from nonadherent MO contained no activity, indicating that adherence was required for monocyte response. Monocyte chemoattractant activity was dose-dependent and was removed by treatment with immobilized antibody to human monocyte chemoattractant protein 1 (MCP-1) but not by irrelevant IgG. These results indicate that a specific peptide segment of CRP acts upon human adherent monocytes to promote production of the autocrine chemotactic and activating factor MCP-1. Data suggest that degraded CRP represents a complex source of biologically active peptides which, among other effects, may amplify monocyte recruitment to sites of injury, (C) 1995 Academic Press, Inc. C1 CLEVELAND CLIN FDN,DEPT CLIN PATHOL,CLEVELAND,OH 44195. NIAID,CLIN INVEST LAB,BETHESDA,MD 20814. CLEVELAND CLIN FDN,DEPT PULM & CRIT CARE MED,CLEVELAND,OH 44195. CLEVELAND CLIN FDN,RES INST,CLEVELAND,OH 44195. FU NCI NIH HHS [CA-54248, CA-49950] NR 32 TC 18 Z9 18 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD JAN PY 1995 VL 74 IS 1 BP 84 EP 88 DI 10.1006/clin.1995.1012 PG 5 WC Immunology; Pathology SC Immunology; Pathology GA PY460 UT WOS:A1995PY46000012 PM 7994930 ER PT J AU MARQUES, AR KWONCHUNG, KJ HOLLAND, SM TURNER, ML GALLIN, JI AF MARQUES, AR KWONCHUNG, KJ HOLLAND, SM TURNER, ML GALLIN, JI TI SUPPURATIVE CUTANEOUS GRANULOMATA CAUSED BY MICROASCUS-CINEREUS IN A PATIENT WITH CHRONIC GRANULOMATOUS-DISEASE SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID SCOPULARIOPSIS-BREVICAULIS; IMMUNOCOMPROMISED HOST; INFECTION; FUNGI; LESIONS; SOILS AB We describe a patient with chronic granulomatous disease who presented with erythematous papular skin lesions on the chest, back, and arm, Examination of biopsy specimens from the lesions on the arm and back showed suppurative granulomata in association with acute and chronic inflammation, Histopathologic examination of a specimen from the lesion on the arm revealed fungal elements, and cultures yielded Microascus cinereus. The patient was treated with 2.5 g of intravenous amphotericin B, and the lesions resolved. We report what is, to our knowledge, the first case of invasive disease due solely to M, cinereus. C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 29 TC 20 Z9 20 U1 0 U2 1 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 JAN PY 1995 VL 20 IS 1 BP 110 EP 114 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA QC639 UT WOS:A1995QC63900019 PM 7727636 ER PT B AU LEKSTROMHIMES, JA STRAUS, SE AF LEKSTROMHIMES, JA STRAUS, SE BE Sacks, SL Straus, SE Whitley, RJ Griffiths, PD TI Varicella-zoster virus infections in the normal and immunocompromised host SO CLINICAL MANAGEMENT OF HERPES VIRUSES LA English DT Proceedings Paper CT Update 94 - Clinical Management of Herpes Virus Infections CY JAN, 1994 CL WHISTLER, CANADA SP Int Soc Antiviral Res, Amer Social Hlth Assoc, Univ Brit Columbia Fac Med Continuing Med Educ Off, SmithKline Beecham Pharm, Wellcome Fdn, Burroughs Wellcome Inc, Syntex Res RP NIAID,CLIN INVEST LAB,MED VIROL SECT,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU I O S PRESS PI AMSTERDAM PA VAN DIEMENSTRAAT 94, 1013 CN AMSTERDAM, NETHERLANDS BN 90-5199-227-0 PY 1995 BP 175 EP 192 PG 18 WC Infectious Diseases; Virology SC Infectious Diseases; Virology GA BE12E UT WOS:A1995BE12E00010 ER PT J AU GERFEN, CR AF GERFEN, CR TI DOPAMINE-RECEPTOR FUNCTION IN THE BASAL GANGLIA SO CLINICAL NEUROPHARMACOLOGY LA English DT Article; Proceedings Paper CT Symposium on Dopamine Receptor Subtypes in Neurological and Psychiatric Diseases CY JUL 17-19, 1994 CL KALAMAZOO, MI DE PARKINSONS DISEASE; D-1- AND D-2-RECEPTOR SUBTYPES; DIRECT AND INDIRECT STRIATAL PATHWAYS; GENE REGULATION ID ANTI-SCHIZOPHRENIC DRUGS; NIGRA PARS RETICULATA; RAT STRIATAL NEURONS; SUBSTANTIA-NIGRA; C-FOS; GLOBUS-PALLIDUS; MOTOR CONTROL; INTRACELLULAR INJECTION; OCULOMOTOR FUNCTIONS; MATRIX COMPARTMENTS AB Clinical disorders that affect the basal ganglia, such as Parkinson's disease, are believed to result from an imbalance in the activity of the two main output pathways of the striatum, the direct and indirect striatal output pathways. Dopamine (DA) modulates the activity of these pathways through the select distribution of the D-1 and D-2 DA-receptor subtypes on neurons, which give rise to the direct and indirect striatal output pathways, respectively. Studies employing quantitative in situ hybridization histochemistry have been used to analyze changes in levels of gene-regulated peptides and immediate early genes in direct and indirect striatal output neurons in response to selective D-1-and D-2-agonist treatments. D-2-receptor activation reverses and D-1-receptor activation increases gene regulation in indirect and direct striatal output neurons, respectively. These findings suggest that functional activity in the two output pathways of the striatum are oppositely regulated by DA by segregation of the D-1- and D-2-receptor subtypes on different striatal neuron populations. A proposed pharmacologic strategy for the treatment of Parkinson's disease based on these findings is suggested. RP GERFEN, CR (reprint author), NIMH,CELL BIOL LAB,NEUROANAT SECT,BLDG 10,ROOM 2D-10,BETHESDA,MD 20892, USA. NR 51 TC 31 Z9 31 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-5664 J9 CLIN NEUROPHARMACOL JI Clin. Neuropharmacol. PY 1995 VL 18 SU 1 BP S162 EP S177 PG 16 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA RD909 UT WOS:A1995RD90900018 ER PT J AU LILLRANK, SM LIPSKA, BK WEINBERGER, DR AF LILLRANK, SM LIPSKA, BK WEINBERGER, DR TI NEURODEVELOPMENTAL ANIMAL-MODELS OF SCHIZOPHRENIA SO CLINICAL NEUROSCIENCE LA English DT Article DE SCHIZOPHRENIA; NEURODEVELOPMENT; ANIMAL MODEL; HIPPOCAMPUS ID APOMORPHINE-INDUCED STEREOTYPY; INDUCED LOCOMOTOR-ACTIVITY; PREFRONTAL CORTEX; HIPPOCAMPAL DAMAGE; DOPAMINE-RECEPTORS; NUCLEUS-ACCUMBENS; PRENATAL EXPOSURE; MONOZYGOTIC TWINS; RATS; LESIONS AB One difficulty in reproducing the core neurobiological features of schizophrenia in experimental animals is that most neurobiological data about the illness are inconclusive: neither the inducing conditions nor the neurobiological mechanisms have been made clear. We review the advantages and limitations of animal models of schizophrenia based on neurodevelopmental hypotheses that implicate early, probably prenatal age, as the time at which the fundamental disease process occurs. These models, although principally founded on circumstantial clinical evidence of early developmental neuropathology, seem to reproduce a surprisingly broad spectrum of prominent neurobiological aspects of the disorder, and may help explain mechanisms that underlie the pathophysiology of this illness. In particular, the model based on neonatal excitotoxic hippocampal damage has provided data indicating the neurobiological plausibility of the notion that a developmental cortical defect has a delayed effect on cortical function and dopamine regulation (i.e., the neurodevelopmental hypothesis). (C) 1995 Wiley-Liss, Inc. RP LILLRANK, SM (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. RI Lipska, Barbara/E-4569-2017 NR 94 TC 54 Z9 55 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1065-6766 J9 CLIN NEUROSCI JI Clin. Neurosci. PY 1995 VL 3 IS 2 BP 98 EP 104 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA RL568 UT WOS:A1995RL56800007 PM 7583625 ER PT J AU GOLDMAN, D AF GOLDMAN, D TI CANDIDATE GENES IN ALCOHOLISM SO CLINICAL NEUROSCIENCE LA English DT Article DE ADH2; ALDH2; GENETIC POLYMORPHISMS; SEROTONIN RECEPTOR; DOPAMINE RECEPTOR ID DOPAMINE RECEPTOR GENOTYPE; MONOAMINE OXIDASE-A; ALLELIC ASSOCIATION; 5-HYDROXYINDOLEACETIC ACID; GEL-ELECTROPHORESIS; SEROTONIN RECEPTOR; AMINE METABOLITES; POPULATION; LINKAGE; BEHAVIOR AB Individual alleles identified by candidate gene analysis have been shown to profoundly influence certain complex behavioral syndromes including vulnerability to alcoholism. The alcohol and aldehyde dehydrogenase polymorphisms, ADH2(2) and ALDH2(2), respectively, are associated with lower vulnerability to alcoholism both in the Orient and also in North America among populations of Taiwanese and Koreans who have immigrated there. Protein structural Variants have recently been identified for a series of genes involved in dopamine and serotonin function. Three dopamine receptors exhibit such structural variants, and these include the DRD2 dopamine receptor, which has three relatively rare amino acid substitutions. Structural polymorphisms were detected in five serotonin receptors (5HT(1A), 5HT(1Db), 5HT(2A), 5HT(2C) and 5HT(7)). Association studies between neurotransmitter gene variants and alcoholism are at an earlier stage than with ADH2(2)/ALDH2(2), but results are thus far negative (dopamine DRD4 receptor), equivocal (dopamine DRD2 receptor), or preliminary (tryptophan hydroxylase, 5HT(2c) and 5 HT1Db). (C) 1995 Wiley-Liss, Inc. RP GOLDMAN, D (reprint author), NIAAA,NEUROGENET LAB,FLOW BLDG ROOM 2,12501 WASHINGTON AVE,ROCKVILLE,MD 20852, USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 80 TC 39 Z9 39 U1 2 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1065-6766 J9 CLIN NEUROSCI JI Clin. Neurosci. PY 1995 VL 3 IS 3 BP 174 EP 181 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA TH242 UT WOS:A1995TH24200005 PM 8612062 ER PT J AU KEENAN, RM HATSUKAMI, DK PENTEL, PR THOMPSON, TN GRILLO, MA AF KEENAN, RM HATSUKAMI, DK PENTEL, PR THOMPSON, TN GRILLO, MA TI EVIDENCE THAT COTININE IS PSYCHOACTIVE - REPLY SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Letter C1 UNIV MINNESOTA,SCH MED,DEPT PSYCHIAT,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT MED,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT PHARMACOL,MINNEAPOLIS,MN 55455. RP KEENAN, RM (reprint author), NIDA,ADDICT RES CTR,CLIN PHARMACOL BRANCH,POB 5180,BALTIMORE,MD 21224, USA. NR 1 TC 0 Z9 0 U1 1 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 1995 VL 57 IS 1 BP 95 EP 97 DI 10.1016/0009-9236(95)90272-4 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QC629 UT WOS:A1995QC62900014 ER PT S AU Halpern, JL Neale, EA AF Halpern, JL Neale, EA BE Montecucco, C TI Neurospecific binding, internalization, and retrograde axonal transport SO CLOSTRIDIAL NEUROTOXINS: THE MOLECULAR PATHOGENESIS OF TETANUS AND BOTULISM SE Current Topics in Microbiology and Immunology LA English DT Review ID BOTULINUM TYPE-A; TETANUS TOXIN BINDING; SPINAL-CORD NEURONS; NEUROTOXIN FORMS CHANNELS; PLANAR LIPID BILAYERS; RAT-BRAIN MEMBRANES; DIPHTHERIA-TOXIN; FRAGMENT-C; HEAVY-CHAIN; BREFELDIN-A C1 NICHHD, NIH, DEV NEUROBIOL LAB, BETHESDA, MD 20892 USA. RP Halpern, JL (reprint author), US FDA, CTR BIOL EVALUAT & RES,DIV BACTERIAL PROD,BLDG 29, ROOM 103, 8800 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 147 TC 82 Z9 83 U1 0 U2 1 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0070-217X BN 3-540-58452-8 J9 CURR TOP MICROBIOL JI Curr.Top.Microbiol.Immunol. PY 1995 VL 195 BP 221 EP 241 PG 21 WC Immunology; Microbiology; Neurosciences SC Immunology; Microbiology; Neurosciences & Neurology GA BF67W UT WOS:A1995BF67W00010 PM 8542755 ER PT J AU Donaldson, JG Radhakrishna, H Peters, PJ AF Donaldson, JG Radhakrishna, H Peters, PJ TI The ARF GTPases: Defining roles in membrane traffic and organelle structure SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT Cold Spring Harbor Symposia on Quantitative Biology - Protein Kinesis: The Dynamics of Protein Trafficking and Stability CY 1995 CL COLD SPRING HARBOR, NY ID ADP-RIBOSYLATION FACTOR; GTP-BINDING-PROTEIN; COP-COATED VESICLES; GOLGI MEMBRANES; BREFELDIN-A; PHOSPHOLIPASE-D; GUANINE-NUCLEOTIDE; ACTIVATING PROTEIN; BETA-COP; COATOMER C1 UNIV UTRECHT,DEPT CELL BIOL,UTRECHT,NETHERLANDS. RP Donaldson, JG (reprint author), NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892, USA. NR 45 TC 14 Z9 14 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1995 VL 60 BP 229 EP 234 PG 6 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA VA125 UT WOS:A1995VA12500025 PM 8824395 ER PT J AU Burns, ME Beushausen, SA Chin, GJ Tang, D DeBello, WM Dresbach, T OConnor, V Schweizer, FE Wang, SSH Whiteheart, SW Hawkey, LA Betz, H Augustine, GJ AF Burns, ME Beushausen, SA Chin, GJ Tang, D DeBello, WM Dresbach, T OConnor, V Schweizer, FE Wang, SSH Whiteheart, SW Hawkey, LA Betz, H Augustine, GJ TI Proteins involved in synaptic vesicle docking and fusion SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT Cold Spring Harbor Symposia on Quantitative Biology - Protein Kinesis: The Dynamics of Protein Trafficking and Stability CY 1995 CL COLD SPRING HARBOR, NY ID RAB EFFECTOR DOMAIN; SQUID GIANT SYNAPSE; NEUROTRANSMITTER RELEASE; TRANSMITTER RELEASE; CA2+-DEPENDENT EXOCYTOSIS; SYNTHETIC PEPTIDE; MEMBRANE-FUSION; TRANSPORT; SYNAPTOTAGMIN; INHIBITION C1 NIH, BETHESDA, MD 20892 USA. MAX PLANCK INST BRAIN RES, DEPT NEUROCHEM, D-60496 FRANKFURT, GERMANY. UNIV KENTUCKY, MED CTR, DEPT BIOCHEM, LEXINGTON, KY 40536 USA. RP Burns, ME (reprint author), DUKE UNIV, MED CTR, DEPT NEUROBIOL, DURHAM, NC 27710 USA. RI Augustine, George/J-9228-2013; OI Whiteheart, Sidney/0000-0001-5577-0473 FU NIGMS NIH HHS [GM-07184]; NIMH NIH HHS [MH-11073]; NINDS NIH HHS [NS-21624] NR 61 TC 4 Z9 4 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI COLD SPRING HARBOR PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1995 VL 60 BP 337 EP 348 PG 12 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA VA125 UT WOS:A1995VA12500037 PM 8824407 ER PT J AU Gottesman, S Wickner, S Jubete, Y Singh, SK Kessel, M Maurizi, M AF Gottesman, S Wickner, S Jubete, Y Singh, SK Kessel, M Maurizi, M TI Selective, energy-dependent proteolysis in Escherichia coli SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT Cold Spring Harbor Symposia on Quantitative Biology - Protein Kinesis: The Dynamics of Protein Trafficking and Stability CY 1995 CL COLD SPRING HARBOR, NY ID HEAT-SHOCK PROTEIN; ATP-BINDING SITES; CLP PROTEASE; MYXOCOCCUS-XANTHUS; LON PROTEASE; SACCHAROMYCES-CEREVISIAE; SPECIFICITY COMPONENT; MOLECULAR CHAPERONES; MUTATIONAL ANALYSIS; SEQUENCE-ANALYSIS C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NIAMSD,STRUCT BIOL LAB,BETHESDA,MD 20892. RP Gottesman, S (reprint author), NCI,MOL BIOL LAB,BETHESDA,MD 20892, USA. NR 70 TC 27 Z9 27 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1995 VL 60 BP 533 EP 548 PG 16 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA VA125 UT WOS:A1995VA12500056 PM 8824426 ER PT J AU Zimmerberg, J Vogel, SS Whalley, T Plonsky, I Sokoloff, A Chanturia, A Chernomordik, LV AF Zimmerberg, J Vogel, SS Whalley, T Plonsky, I Sokoloff, A Chanturia, A Chernomordik, LV TI Intermediates in membrane fusion SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT Cold Spring Harbor Symposia on Quantitative Biology - Protein Kinesis: The Dynamics of Protein Trafficking and Stability CY 1995 CL COLD SPRING HARBOR, NY ID SEA-URCHIN EGG; INTRACELLULAR PROTEIN-TRANSPORT; PHOSPHOLIPID-BILAYER MEMBRANES; CORTICAL-GRANULE EXOCYTOSIS; CALCIUM-TRIGGERED FUSION; VIRAL ENVELOPE PROTEIN; GTP-DEPENDENT FUSION; INFLUENZA HEMAGGLUTININ; MAST-CELLS; ENDOPLASMIC-RETICULUM RP Zimmerberg, J (reprint author), NICHHD,LAB THEORET & PHYS BIOL,NIH,BETHESDA,MD 20892, USA. RI Vogel, Steven/A-3585-2012; OI Whalley, Tim/0000-0003-3362-0006; Vogel, Steven/0000-0002-3005-2667 NR 67 TC 8 Z9 8 U1 0 U2 2 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1995 VL 60 BP 589 EP 599 PG 11 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA VA125 UT WOS:A1995VA12500062 PM 8824432 ER PT S AU ROBBINS, JB SCHNEERSON, R VANN, WF BRYLA, DA FATTOM, A AF ROBBINS, JB SCHNEERSON, R VANN, WF BRYLA, DA FATTOM, A BE Williams, JC Goldenthal, KL Burns, DL Lewis, BP TI PREVENTION OF SYSTEMIC INFECTIONS CAUSED BY GROUP-B STREPTOCOCCUS AND STAPHYLOCOCCUS-AUREUS BY MULTIVALENT POLYSACCHARIDE-PROTEIN CONJUGATE VACCINES SO COMBINED VACCINES AND SIMULTANEOUS ADMINISTRATION: CURRENT ISSUES AND PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Combined Vaccines and Simultaneous Administration: Current Issues and Perspectives CY JUL 28-30, 1993 CL BETHESDA, MD SP US FDA, Ctr Biol Evaluat & Res, Natl Vaccine Program Off, NIH, NIAID, Ctr Dis Control & Prevent, WHO ID INFLUENZAE TYPE-B; CAPSULAR POLYSACCHARIDE; PREGNANT-WOMEN; STRUCTURAL DETERMINATION; IMMUNOLOGICAL PROPERTIES; MONOCLONAL-ANTIBODIES; III POLYSACCHARIDE; IGG ANTIBODY; EXOTOXIN-A; IMMUNOGENICITY C1 US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD 20892. UNIVAX BIOL INC,ROCKVILLE,MD 20852. RP ROBBINS, JB (reprint author), NICHHD,BETHESDA,MD 20892, USA. NR 66 TC 18 Z9 18 U1 1 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-863-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 754 BP 68 EP 82 DI 10.1111/j.1749-6632.1995.tb44439.x PG 15 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Multidisciplinary Sciences SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Science & Technology - Other Topics GA BD16V UT WOS:A1995BD16V00010 PM 7625682 ER PT S AU GERMAIN, RN AF GERMAIN, RN BE Williams, JC Goldenthal, KL Burns, DL Lewis, BP TI THE BIOCHEMISTRY AND CELL BIOLOGY OF ANTIGEN PRESENTATION BY MHC CLASS-I AND CLASS-II MOLECULES - IMPLICATIONS FOR DEVELOPMENT OF COMBINATION VACCINES SO COMBINED VACCINES AND SIMULTANEOUS ADMINISTRATION: CURRENT ISSUES AND PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Combined Vaccines and Simultaneous Administration: Current Issues and Perspectives CY JUL 28-30, 1993 CL BETHESDA, MD SP US FDA, Ctr Biol Evaluat & Res, Natl Vaccine Program Off, NIH, NIAID, Ctr Dis Control & Prevent, WHO ID MAJOR HISTOCOMPATIBILITY COMPLEX; LIPOSOME-ENCAPSULATED ANTIGENS; INVARIANT CHAIN EXPRESSION; CYTOTOXIC LYMPHOCYTES-T; HLA-DR MOLECULES; SELF-PEPTIDES; SURFACE EXPRESSION; RECEPTOR GENES; MICE LACKING; BINDING RP GERMAIN, RN (reprint author), NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BLDG 10,ROOM 11N311,BETHESDA,MD 20892, USA. NR 58 TC 41 Z9 42 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-863-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 754 BP 114 EP 125 DI 10.1111/j.1749-6632.1995.tb44444.x PG 12 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Multidisciplinary Sciences SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Science & Technology - Other Topics GA BD16V UT WOS:A1995BD16V00015 PM 7625645 ER PT S AU EHRHARDT, RO STROBER, W AF EHRHARDT, RO STROBER, W BE Williams, JC Goldenthal, KL Burns, DL Lewis, BP TI THE ROLE OF SIGA+B CELLS IN ORAL IMMUNITY SO COMBINED VACCINES AND SIMULTANEOUS ADMINISTRATION: CURRENT ISSUES AND PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Combined Vaccines and Simultaneous Administration: Current Issues and Perspectives CY JUL 28-30, 1993 CL BETHESDA, MD SP US FDA, Ctr Biol Evaluat & Res, Natl Vaccine Program Off, NIH, NIAID, Ctr Dis Control & Prevent, WHO ID GROWTH-FACTOR-BETA; MYELIN BASIC-PROTEIN; HUMAN B-CELLS; T-CELLS; IMMUNOGLOBULIN-A; MICE; IMMUNODEFICIENCY; TOLERIZATION; TRANSCRIPTS; EXPRESSION RP EHRHARDT, RO (reprint author), NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BLDG 10,ROOM 11N 234-246,BETHESDA,MD 20892, USA. NR 20 TC 3 Z9 3 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-863-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 754 BP 138 EP 142 DI 10.1111/j.1749-6632.1995.tb44446.x PG 5 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Multidisciplinary Sciences SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Science & Technology - Other Topics GA BD16V UT WOS:A1995BD16V00017 PM 7625647 ER PT S AU VOGEL, FR AF VOGEL, FR BE Williams, JC Goldenthal, KL Burns, DL Lewis, BP TI IMMUNOLOGICAL ADJUVANTS FOR MODERN VACCINE FORMULATIONS SO COMBINED VACCINES AND SIMULTANEOUS ADMINISTRATION: CURRENT ISSUES AND PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Combined Vaccines and Simultaneous Administration: Current Issues and Perspectives CY JUL 28-30, 1993 CL BETHESDA, MD SP US FDA, Ctr Biol Evaluat & Res, Natl Vaccine Program Off, NIH, NIAID, Ctr Dis Control & Prevent, WHO ID ANTIBODY-RESPONSE; IMMUNIZATION; LIPOSOMES; INDUCTION; MICE; IMMUNOADJUVANTS; STIMULATION; PROTEIN; ISCOMS; HOST AB Many of today's candidate vaccines are composed of synthetic, recombinant, or highly purified subunit antigens. Vaccines composed of these purified subunits generally are considered to be safer than traditional whole-killed or live-attenuated vaccines. Often, however, purified subunit vaccines are inherently less immunogenic. Immunologic adjuvants are agents that act to generally enhance specific immune responses to vaccine antigens. Formulating experimental vaccines with potent immunologic adjuvants is an attractive approach for amplifying and directing immune responses to highly purified antigens incorporated into combination vaccines containing one or more of these immunogens. Alum adjuvants, consisting of aluminum salts, first described in the 1920s, remain the only adjuvants in United States licensed vaccine formulations. Novel adjuvants now undergoing preclinical and clinical testing with experimental subunit vaccines include detoxified lipid A, adjuvant emulsions, liposomes, biodegradable microspheres, muramyl peptides, and saponins. Such adjuvants have been shown to elicit cytotoxic T-cell responses as well as antibody to subunit antigens. Some of these adjuvants also have been shown to lower the threshold levels of antigen necessary to evoke immune responses. Reducing the needed dose of antigens through the use of novel adjuvants should facilitate the design of multivalent and combination vaccines that incorporate multiple antigens. In this paper I describe several types of immunologic adjuvants now being evaluated in experimental retroviral vaccines. I also discuss the mechanisms of adjuvanticity and the standardization of adjuvant safety testing. RP VOGEL, FR (reprint author), NIAID,VACCINE & PREVENT RES PROGRAM,DIV AIDS,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 30 TC 30 Z9 31 U1 0 U2 4 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-863-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 754 BP 153 EP 160 DI 10.1111/j.1749-6632.1995.tb44448.x PG 8 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Multidisciplinary Sciences SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Science & Technology - Other Topics GA BD16V UT WOS:A1995BD16V00019 PM 7625649 ER PT S AU BERZOFSKY, JA AF BERZOFSKY, JA BE Williams, JC Goldenthal, KL Burns, DL Lewis, BP TI DESIGNING PEPTIDE VACCINES TO BROADEN RECOGNITION AND ENHANCE POTENCY SO COMBINED VACCINES AND SIMULTANEOUS ADMINISTRATION: CURRENT ISSUES AND PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Combined Vaccines and Simultaneous Administration: Current Issues and Perspectives CY JUL 28-30, 1993 CL BETHESDA, MD SP US FDA, Ctr Biol Evaluat & Res, Natl Vaccine Program Off, NIH, NIAID, Ctr Dis Control & Prevent, WHO ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-SEROPOSITIVE INDIVIDUALS; CYTOTOXIC T-LYMPHOCYTES; CLASS-I H-2K(B); ENVELOPE PROTEIN; 3-DIMENSIONAL STRUCTURE; SYNTHETIC PEPTIDES; CELL RECOGNITION; VIRAL ENVELOPE; BINDING MOTIF RP BERZOFSKY, JA (reprint author), NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BLDG 10 ROOM 6B-12,BETHESDA,MD 20892, USA. NR 41 TC 17 Z9 17 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-863-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 754 BP 161 EP 168 DI 10.1111/j.1749-6632.1995.tb44449.x PG 8 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Multidisciplinary Sciences SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Science & Technology - Other Topics GA BD16V UT WOS:A1995BD16V00020 PM 7625650 ER PT S AU CLEMENS, J BRENNER, R RAO, M AF CLEMENS, J BRENNER, R RAO, M BE Williams, JC Goldenthal, KL Burns, DL Lewis, BP TI INTERACTIONS BETWEEN PRP-T VACCINE AGAINST HAEMOPHILUS-INFLUENZAE TYPE-B AND CONVENTIONAL INFANT VACCINES - LESSONS FOR FUTURE STUDIES OF SIMULTANEOUS IMMUNIZATION AND COMBINED VACCINES SO COMBINED VACCINES AND SIMULTANEOUS ADMINISTRATION: CURRENT ISSUES AND PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Combined Vaccines and Simultaneous Administration: Current Issues and Perspectives CY JUL 28-30, 1993 CL BETHESDA, MD SP US FDA, Ctr Biol Evaluat & Res, Natl Vaccine Program Off, NIH, NIAID, Ctr Dis Control & Prevent, WHO ID PROTEIN CONJUGATE VACCINE; CAPSULAR POLYSACCHARIDE; CLINICAL-TRIALS; EFFICACY; CHILDREN; IMMUNOGENICITY; ANTIBODIES RP CLEMENS, J (reprint author), NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892, USA. NR 32 TC 12 Z9 12 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-863-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 754 BP 255 EP 266 DI 10.1111/j.1749-6632.1995.tb44458.x PG 12 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Multidisciplinary Sciences SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Science & Technology - Other Topics GA BD16V UT WOS:A1995BD16V00029 PM 7625660 ER PT S AU BLACKWELDER, WC AF BLACKWELDER, WC BE Williams, JC Goldenthal, KL Burns, DL Lewis, BP TI SIMILARITY EQUIVALENCE TRIALS FOR COMBINATION VACCINES SO COMBINED VACCINES AND SIMULTANEOUS ADMINISTRATION: CURRENT ISSUES AND PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Combined Vaccines and Simultaneous Administration: Current Issues and Perspectives CY JUL 28-30, 1993 CL BETHESDA, MD SP US FDA, Ctr Biol Evaluat & Res, Natl Vaccine Program Off, NIH, NIAID, Ctr Dis Control & Prevent, WHO ID COMPARATIVE BIOAVAILABILITY TRIALS; SAMPLE-SIZE DETERMINATION; APPROXIMATE INTERVAL ESTIMATION; SIDED TESTS PROCEDURE; CLINICAL-TRIALS; BIOEQUIVALENCE ASSESSMENT; BINOMIAL PARAMETERS; NULL HYPOTHESIS; RELATIVE RISK; DIFFERENCE RP BLACKWELDER, WC (reprint author), NIAID,SOLAR BLDG,ROOM 3A03,BETHESDA,MD 20892, USA. NR 34 TC 26 Z9 26 U1 2 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-863-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 754 BP 321 EP 328 DI 10.1111/j.1749-6632.1995.tb44465.x PG 8 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Multidisciplinary Sciences SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases; Science & Technology - Other Topics GA BD16V UT WOS:A1995BD16V00036 PM 7625668 ER PT B AU Berson, A AF Berson, A BE Murray, A TI A standard for automated ECG analysis - Are we ready? SO COMPUTERS IN CARDIOLOGY 1995 LA English DT Proceedings Paper CT 22nd Annual Scientific Meeting of Computers in Cardiology CY SEP 10-13, 1995 CL VIENNA, AUSTRIA SP NIH, Div Comp Res & Technol, European Soc Cardiol, IEEE, Eng Med & Biol Soc C1 NHLBI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU I E E E PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 BN 0-7803-3053-6 J9 COMPUT CARDIOL PY 1995 BP 45 EP 46 DI 10.1109/CIC.1995.482567 PG 2 WC Computer Science, Interdisciplinary Applications; Engineering, Biomedical SC Computer Science; Engineering GA BF05B UT WOS:A1995BF05B00012 ER PT B AU Callicott, JH Weinberger, DR AF Callicott, JH Weinberger, DR BE Brunello, N Racagni, G Langer, SZ Mendlewicz, J TI Schizophrenia and intracortical 'dysconnection': New insights about pathophysiology and mechanisms of antipsychotic treatment SO CRITICAL ISSUES IN THE TREATMENT OF SCHIZOPHRENIA SE INTERNATIONAL ACADEMY FOR BIOMEDICAL AND DRUG RESEARCH LA English DT Proceedings Paper CT Workshop on Critical Issues in the Treatment of Schizophrenia CY MAR 10-12, 1995 CL FLORENCE, ITALY RP Callicott, JH (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND BN 3-8055-6199-7 J9 INT ACAD B JI Int.Acad.Biomed.Drug Res. PY 1995 VL 10 BP 66 EP 76 PG 11 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA BF26U UT WOS:A1995BF26U00008 ER PT J AU GRONENBORN, AM CLORE, GM AF GRONENBORN, AM CLORE, GM TI STRUCTURES OF PROTEIN COMPLEXES BY MULTIDIMENSIONAL HETERONUCLEAR MAGNETIC-RESONANCE SPECTROSCOPY SO CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Review DE MULTIDIMENSIONAL NMR; PROTEIN COMPLEXES; DNA COMPLEXES; SOLUTION STRUCTURE ID 3-DIMENSIONAL NMR-SPECTROSCOPY; RESTRAINED MOLECULAR-DYNAMICS; DNA-BINDING DOMAIN; PANCREATIC TRYPSIN-INHIBITOR; LAC REPRESSOR HEADPIECE; PULSED-FIELD GRADIENTS; DISTANCE GEOMETRY; CRYSTAL-STRUCTURE; HIGH-RESOLUTION; STEREOSPECIFIC ASSIGNMENTS AB With the advent of multidimensional heteronuclear-edited and -filtered NMR experiments, the field of three-dimensional structure determination by NMR has again increased in scope, making it possible to move the technology beyond the approximately 10 kDa limit inherent to conventional two-dimensional NMR to systems upto potentially 35 to 40 kDa. This article outlines the basic strategies for solving three-dimensional structures of larger systems, in particular, protein complexes and multimeric proteins using three- and four-dimensional NMR spectroscopy, summarizes the key experiments, and illustrates the power of these methods using several examples of protein-DNA, protein-peptide complexes, and oligomeric proteins from the authors' laboratories. RP GRONENBORN, AM (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 2,BETHESDA,MD 20892, USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 156 TC 59 Z9 59 U1 1 U2 7 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 SN 1040-9238 J9 CRIT REV BIOCHEM MOL JI Crit. Rev. Biochem. Molec. Biol. PY 1995 VL 30 IS 5 BP 351 EP & DI 10.3109/10409239509083489 PG 0 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TC731 UT WOS:A1995TC73100001 PM 8575189 ER PT J AU MILNER, JA BLUMBERG, JB ERNST, N HATHCOCK, JN ZIEGLER, RG KOHLMEIER, L BLACKBURN, G DICHTER, C AF MILNER, JA BLUMBERG, JB ERNST, N HATHCOCK, JN ZIEGLER, RG KOHLMEIER, L BLACKBURN, G DICHTER, C TI RESPONSE PANEL ON THE IMPACT OF NUTRIENT AND NONNUTRIENT ANTIOXIDANTS ON CANCER AND CARDIOVASCULAR-DISEASE SO CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION LA English DT Discussion C1 TUFTS UNIV,USDA,HUMAN NUTR RES CTR AGING,BOSTON,MA 02111. NHLBI,BETHESDA,MD 20892. US FDA,DIV SCI & APPL TECHNOL,OFF SPECIAL NUTR,LAUREL,MD 20708. NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. HARVARD UNIV,DEACONESS HOSP,SCH MED,BOSTON,MA. UNIV N CAROLINA,CHAPEL HILL,NC. RP MILNER, JA (reprint author), PENN STATE UNIV,DEPT NUTR,126 HENDERSON BLDG S,UNIVERSITY PK,PA 16802, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 SN 1040-8398 J9 CRIT REV FOOD SCI JI Crit. Rev. Food Sci. Nutr. PY 1995 VL 35 IS 1-2 BP 99 EP 110 PG 12 WC Food Science & Technology; Nutrition & Dietetics SC Food Science & Technology; Nutrition & Dietetics GA QG096 UT WOS:A1995QG09600010 ER PT J AU MCMILLIAN, MK HONG, JS AF MCMILLIAN, MK HONG, JS TI REGULATION OF PREPROENKEPHALIN EXPRESSION IN ASTROCYTES - IS THERE A ROLE FOR GLIA-DERIVED OPIOID-PEPTIDES IN REACTIVE GLIOSIS SO CRITICAL REVIEWS IN NEUROBIOLOGY LA English DT Review DE ASTROCYTES; GLIOSIS; ENKEPHALIN; PREPROENKEPHALIN; NF-KAPPA B; CYTOKINES; GENE REGULATION; TRANSCRIPTION FACTORS ID PROENKEPHALIN GENE-EXPRESSION; NERVE GROWTH-FACTOR; SPINAL-CORD INJURY; NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; RAT GLIOMA-CELLS; CULTURED ASTROCYTES; MESSENGER-RNA; INTERLEUKIN-1 PRODUCTION; PERITONEAL-MACROPHAGES AB Cultured glial cells synthesize a number of neuropeptides, growth factors, cytokines, and other factors that are not detectable in resting glia in the adult brain but that appear in response to brain injury. Enkephalin-containing peptides are produced and released by cultured astrocytes and glioma cell lines, which have provided convenient model systems to study the regulation of the preproenkephalin gene. The purpose of this review is to examine data suggesting that reactive astrocytes produce enkephalin-contaning peptides, the regulatory processes that may be involved, and possible functions of glia-derived peptides in reactive gliosis. C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709. NR 109 TC 0 Z9 0 U1 0 U2 0 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, STE 1202, NEW YORK, NY 10016-7892 SN 0892-0915 J9 CRIT REV NEUROBIOL JI Crit. Rev. Neurobiol. PY 1995 VL 9 IS 1 BP 91 EP 103 PG 13 WC Neurosciences SC Neurosciences & Neurology GA RF691 UT WOS:A1995RF69100004 ER PT J AU DATILES, MB LASA, MS PODGOR, MJ HERNANDEZGALILEA, E MAGNO, BV AF DATILES, MB LASA, MS PODGOR, MJ HERNANDEZGALILEA, E MAGNO, BV TI MEASUREMENT ERROR IN ASSESSING THE SIZE OF CORTICAL CATARACTS FROM RETROILLUMINATION PHOTOGRAPHS SO CURRENT EYE RESEARCH LA English DT Article DE CORTICAL CATARACTS; RETROILLUMINATION PHOTOGRAPHS; MEASUREMENT ERROR; COMPUTER PLANIMETRY; SAMPLE SIZE ESTIMATES; HUMAN ID POSTERIOR SUBCAPSULAR CATARACTS; LENS OPACITIES; ANALYSIS SYSTEM; CLASSIFICATION; NUCLEAR AB This study describes a new method of quantifying anteriorly located cortical cataracts using retroillumination photographs and computer planimetry. Cortical cataracts were graded clinically and then photographed using the Neitz retroillumination camera twice by each of 2 photographers. The cataract outlines were traced onto a transparent overlay, and computer planimetry was performed using a Scan Maker 600ZS, a MAC II Computer and specially developed software. We estimated the measurement error of the method and its associated effect on sample size estimates for clinical studies. We calculated that the variability in this technique would contribute about 21 additional subjects to overall sample size estimates in studies comparing the mean areas of cortical opacities. In many studies this would be a small addition to total sample size requirements. This technique provides clinically useful measurements of the size of a cortical opacity as seen on a retroillumination photograph. This may be useful for future clinical studies on natural progression of cortical cataracts as well as for clinical trials of anticataract drugs. C1 NEI,BETHESDA,MD 20892. OI Datiles, Manuel III B./0000-0003-4660-1664 NR 17 TC 0 Z9 0 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 JAN PY 1995 VL 14 IS 1 BP 19 EP 26 DI 10.3109/02713689508999910 PG 8 WC Ophthalmology SC Ophthalmology GA QD616 UT WOS:A1995QD61600003 PM 7720402 ER PT S AU Hsu, YPP Schuback, DE Tivol, EA Shalish, C Murphy, DL Breakefield, XO AF Hsu, YPP Schuback, DE Tivol, EA Shalish, C Murphy, DL Breakefield, XO BE Yu, PM Tipton, KF Boulton, AA TI Analysis of MAOA mutations in humans SO CURRENT NEUROCHEMICAL AND PHARMACOLOGICAL ASPECTS OF BIOGENIC AMINES SE PROGRESS IN BRAIN RESEARCH LA English DT Article; Proceedings Paper CT International Joint Meeting of the 6th Amine Oxidase Workshop/5th Trace Amine Conference CY AUG, 1994 CL SASKATOON, CANADA SP Int Soc Neurochem, Burroughs Wellcome, Canada, Ciba Geigy Canada, Ciba Geigy Ltd, Basel, Chiesi Pharm, Italy, Eli Lilly Canada, Nordic Merrell Dow, Canada, Orion Corp, Finland, Rhone Poulenc Pharma, Canada, Synthelabo Res, France, Upjohn Canada ID MONOAMINE OXIDASE-A; NORRIE DISEASE; PARKINSONS-DISEASE; X-CHROMOSOME; PRENATAL-DIAGNOSIS; PEPTIDE SEQUENCES; MOLECULAR-BASIS; ENZYME-ACTIVITY; CANDIDATE GENE; HUMAN-LIVER C1 VET ADM MED CTR,W ROXBURY,MA 02132. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. NR 59 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 BN 0-444-81938-X J9 PROG BRAIN RES PY 1995 VL 106 BP 67 EP 75 PG 9 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BF87C UT WOS:A1995BF87C00007 PM 8584675 ER PT J AU CHANG, AC MCAREAVEY, D FANANAPAZIR, L AF CHANG, AC MCAREAVEY, D FANANAPAZIR, L TI IDENTIFICATION OF PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY AT HIGH-RISK FOR SUDDEN-DEATH SO CURRENT OPINION IN CARDIOLOGY LA English DT Article AB Patients with hypertrophic cardiomyopathy are at increased risk for sudden death. Recent studies have improved our ability to risk-stratify such patients and have elucidated several potential mechanisms of sudden death and syncope. Certain noninvasive tests, such as signal-averaged electrocardiography and measurements of cardiac autonomic function and QT/QT dispersion, are often abnormal in hypertrophic cardiomyopathy, but are not useful for risk stratification. Myocardial ischemia determined by exercise thallium scintigraphy, however, identifies young patients with hypertrophic cardiomyopathy who are at high risk for cardiac arrest and syncope. Nonsustained ventricular tachycardia on ambulatory Holter monitoring in the absence of symptoms of impaired consciousness is associated with a benign prognosis and is not predictive of sudden death. Conversely, ventricular tachycardia induced at electrophysiologic study identifies adult patients with hypertrophic cardiomyopathy who subsequently experience sudden death. Finally, characterization of the natural history of the genetic defects will increasingly become an integral part of risk evaluation in hypertrophic cardiomyopathy. RP CHANG, AC (reprint author), NHLBI,CARDIOL BRANCH,INHERITED CARDIAC DIS SECT,ROOM 7B-14,BLDG 10,10 CTR DR,MSC 1650,BETHESDA,MD 20892, USA. NR 0 TC 27 Z9 28 U1 0 U2 0 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 0268-4705 J9 CURR OPIN CARDIOL JI Curr. Opin. Cardiol. PD JAN PY 1995 VL 10 IS 1 BP 9 EP 15 DI 10.1097/00001573-199501000-00003 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QB629 UT WOS:A1995QB62900002 PM 7787270 ER PT J AU GOLDBERG, TE BERMAN, KF WEINBERGER, DR AF GOLDBERG, TE BERMAN, KF WEINBERGER, DR TI NEUROPSYCHOLOGY AND NEUROPHYSIOLOGY OF SCHIZOPHRENIA SO CURRENT OPINION IN PSYCHIATRY LA English DT Article ID CEREBRAL BLOOD-FLOW; I-123 IMP SPECT; EMISSION TOMOGRAPHY; MEMORY; CLOZAPINE; RECEPTORS; PSYCHOSIS; BLOCKADE; EPILEPSY; MODEL AB Distinctive profiles of neuropsychological impairment and neurophysiological abnormalities exist in schizophrenia. At the cognitive level, these impairments appear to involve various aspects of working, semantic, and secondary memory. Some of these deficits may be unresponsive to neuroleptic medication. Functional neuroimaging has indicated a pattern of cerebral frontal hypoactivity and temporal hyperactivity consistent with the cognitive findings. Taken together, these results may begin to account for the frequent and often severe morbidity associated with the disorder. RP GOLDBERG, TE (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,DIRP,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. NR 45 TC 10 Z9 10 U1 6 U2 8 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0951-7367 J9 CURR OPIN PSYCHIATR JI Curr. Opin. Psychiatr. PD JAN PY 1995 VL 8 IS 1 BP 34 EP 40 DI 10.1097/00001504-199501000-00009 PG 7 WC Psychiatry SC Psychiatry GA QL951 UT WOS:A1995QL95100009 ER PT J AU BREIER, A AF BREIER, A TI THE MANAGEMENT OF TREATMENT-RESISTANT SCHIZOPHRENIA SO CURRENT OPINION IN PSYCHIATRY LA English DT Article ID CLOZAPINE-INDUCED AGRANULOCYTOSIS; NEGATIVE SYMPTOMS; DOUBLE-BLIND; PSYCHIATRIC-SYMPTOMS; RISPERIDONE; SEROTONIN-S2; FLUPHENAZINE; OUTPATIENTS; HALOPERIDOL; INPATIENTS AB Several important developments in the pharmacotherapy of treatment-resistant schizophrenia have occurred over the past year. These developments include the resolution of questions related to the clinical application and safety of clozapine, the widespread introduction of risperidone, and new approaches to the treatment of negative symptoms and cognitive impairment. These developments will be critically examined and future challenges for the management of treatment-resistant schizophrenia will be discussed. RP BREIER, A (reprint author), NIMH,EXPTL THERAPEUT BRANCH,NIH 10-4N212,9000 ROCKVILLE PIKE,10 CTR DR MSC 13,BETHESDA,MD 20892, USA. NR 25 TC 1 Z9 1 U1 1 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0951-7367 J9 CURR OPIN PSYCHIATR JI Curr. Opin. Psychiatr. PD JAN PY 1995 VL 8 IS 1 BP 41 EP 44 DI 10.1097/00001504-199501000-00010 PG 4 WC Psychiatry SC Psychiatry GA QL951 UT WOS:A1995QL95100010 ER PT B AU NEWMAN, JD AF NEWMAN, JD BE Zimmermann, E Newman, JD Jurgens, U TI Vocal ontogeny in macaques and marmosets: Convergent and divergent lines of development SO CURRENT TOPICS IN PRIMATE VOCAL COMMUNICATION LA English DT Proceedings Paper CT XIV Congress of the International-Primatological-Society CY AUG 16-21, 1992 CL STRASBOURG, FRANCE SP Int Primatol Soc C1 NICHHD,COMPARAT ETHOL LAB,POOLESVILLE,MD 20837. NR 0 TC 19 Z9 19 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45064-X PY 1995 BP 73 EP 97 PG 25 WC Behavioral Sciences; Zoology SC Behavioral Sciences; Zoology GA BD38P UT WOS:A1995BD38P00004 ER PT B AU BIBEN, M BERNHARDS, D AF BIBEN, M BERNHARDS, D BE Zimmermann, E Newman, JD Jurgens, U TI Vocal ontogeny of the squirrel monkey, Saimiri boliviensis peruviensis SO CURRENT TOPICS IN PRIMATE VOCAL COMMUNICATION LA English DT Proceedings Paper CT XIV Congress of the International-Primatological-Society CY AUG 16-21, 1992 CL STRASBOURG, FRANCE SP Int Primatol Soc C1 NICHHD,COMPARAT ETHOL LAB,BETHESDA,MD 20892. NR 0 TC 8 Z9 8 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45064-X PY 1995 BP 99 EP 120 PG 22 WC Behavioral Sciences; Zoology SC Behavioral Sciences; Zoology GA BD38P UT WOS:A1995BD38P00005 ER PT J AU LYU, MS ADAMSON, MC ZHA, H REMMERS, E KOZAK, CA AF LYU, MS ADAMSON, MC ZHA, H REMMERS, E KOZAK, CA TI LINKAGE AND SYNTENY HOMOLOGIES BETWEEN HUMAN-CHROMOSOME-7 AND 7 MOUSE CHROMOSOMES SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD. NIAMSD,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 71 IS 1 BP 26 EP 26 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA RL266 UT WOS:A1995RL26600014 ER PT J AU PROCHAZKA, M THOMPSON, DB KNOWLER, WC BENNETT, PH BOGARDUS, C SCHERER, SW TSUI, LC AF PROCHAZKA, M THOMPSON, DB KNOWLER, WC BENNETT, PH BOGARDUS, C SCHERER, SW TSUI, LC TI LINKAGE AND ASSOCIATION OF MARKERS AT 7Q21.3-]Q22.1 WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS (NIDDM) IN PIMA-INDIANS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIDDKD,PHOENIX,AZ. HOSP SICK CHILDREN,DEPT GENET,TORONTO,ON M5G 1X8,CANADA. RI Tsui, Lap-chee/A-1081-2010 NR 0 TC 4 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 71 IS 1 BP 30 EP 30 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA RL266 UT WOS:A1995RL26600023 ER PT J AU ZIMONJIC, DB REZANKA, LJ EVANS, CH POLYMEROPOULOS, MH TRENT, JM POPESCU, NC AF ZIMONJIC, DB REZANKA, LJ EVANS, CH POLYMEROPOULOS, MH TRENT, JM POPESCU, NC TI MAPPING OF THE IMMUNE INTERFERON-GAMMA GENE (IFNG) TO CHROMOSOME BAND 12Q14BY FLUORESCENCE IN-SITU HYBRIDIZATION SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID INSITU HYBRIDIZATION; GROWTH-FACTOR; LOCALIZATION AB The human immune interferon gamma gene (IFNG) was localized to chromosome band 12q14 by fluorescence in situ hybridization. This correction of a previous localization resolves the discrepancy between the syntenic maps of human chromosome 12 and mouse chromosome 10 and facilitates linkage analysis and identification of gene interactions near this region of chromosome 12 as well as further genetic studies of interferon-gamma immune-associated diseases. C1 NCI,DIV CANC ETIOL,BIOL LAB,BETHESDA,MD 20892. NIH,NATL CTR HUMAN GENOME RES,GENET DIS RES LAB,BETHESDA,MD 20892. NIH,NATL CTR HUMAN GENOME RES,CANC CYTOGENET LAB,BETHESDA,MD 20892. NR 14 TC 14 Z9 16 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 71 IS 3 BP 247 EP 248 DI 10.1159/000134119 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA TD385 UT WOS:A1995TD38500010 PM 7587386 ER PT J AU ALDAZ, CM YEUNG, RS LATIF, F LERMAN, MI XIAO, G TRONO, D WALKER, CL AF ALDAZ, CM YEUNG, RS LATIF, F LERMAN, MI XIAO, G TRONO, D WALKER, CL TI COLOCALIZATION OF THE RAT HOMOLOG OF THE VONHIPPEL-LINDAU (VHL) GENE AND THE PLASMA-MEMBRANE CA++ TRANSPORTING ATPASE-ISOFORM-2 (ATP2B2) GENE TO RAT CHROMOSOME BANDS 4Q41.3-]42.1 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID RENAL-CELL CARCINOMA; SMALL REGION; NORWAY RAT; EKER RAT; LOCALIZATION; CANCER; MOUSE; IDENTIFICATION; HYBRIDIZATION; NORVEGICUS AB Using fluorescence in situ hybridization, we localized the rat homolog of the von Hippel-Lindau gene (Vhl) to rat chromosome band 4q41.3-->q42.1. We also mapped the gene encoding the plasma membrane Ca++-transporting ATPase isoform 2 (Atp2b2) to the same chromosome subregion. These two genes together with Raf1 appear to be members of a large syntenic gene cluster that maps to human chromosome bands 3p25 --> p26, mouse chromosome bands 6 C3 --> E, and rat chromosome bands 4q41 --> q42. Cytogenetic analysis of NRK 52E cells derived from immortalized normal rat kidney epithelial cells revealed an inverted duplication of the region containing this gene cluster. C1 FOX CHASE CANC CTR,INST CANC RES,PHILADELPHIA,PA 19111. NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. RP ALDAZ, CM (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,DEPT CARCINOGENESIS,SMITHVILLE,TX 78957, USA. FU NCI NIH HHS [CA63613, CA48922] NR 27 TC 5 Z9 5 U1 0 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 71 IS 3 BP 253 EP 256 DI 10.1159/000134121 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA TD385 UT WOS:A1995TD38500012 PM 7587388 ER PT J AU SHIPLEY, JM BIRDSALL, S CLARK, J CREW, J GILL, S LINEHAN, M GNARRA, J FISHER, S CRAIG, IW COOPER, CS AF SHIPLEY, JM BIRDSALL, S CLARK, J CREW, J GILL, S LINEHAN, M GNARRA, J FISHER, S CRAIG, IW COOPER, CS TI MAPPING THE X-CHROMOSOME BREAKPOINT IN 2 PAPILLARY RENAL-CELL CARCINOMA CELL-LINES WITH A T(X-1)(P11.2-Q21.2) AND THE FIRST REPORT OF A FEMALE CASE SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID SHORT ARM; ADENOCARCINOMA; CYTOGENETICS; TRANSCRIPTION; MARKERS; CHILD; GENE AB A t(X;1)(p11.2;q21.2) has been reported in cases of papillary renal cell tumors arising in males. In this study two cell fines derived from this tumor type have been used to indicate the breakpoint region on the X chromosome. Both cell lines have the translocation in addition to other rearrangements and one is derived from the first female case to be reported with the t(X;1)(p11.2;q21.2). Fluorescence in situ hybridization (FISH) has been used to position YACs belonging to contigs in the Xp11.2 region relative to the breakpoint. When considered together with detailed mapping information from the Xp11.2 region the position of the breakpoint in both cell lines was suggested as follows: Xpter --> Xp11.23 - OATL1 - GATA1 - WAS - TFE3 - SYP - t(X;1) - DXS255 - CLCN5 - DXS146 - OATL2 - Xp11.22 --> Xcen. The breakpoint was determined to lie in an uncloned region between SYP and a YAC called FTDM/1 which extends 1 Mb distal to DXS255. These results are contrary to the conclusion from previous FISH studies that the breakpoint was near the OATL2 locus, but are consistent with, and considerably refine, the position that had been established by molecular analysis. C1 NCI,UROL ONCOL SECT,BETHESDA,MD 20892. UNIV OXFORD,DEPT BIOCHEM,GENET LAB,OXFORD OX1 3QU,ENGLAND. RP SHIPLEY, JM (reprint author), INST CANC RES,MOLEC CYTOGENET LAB,F BLOCK,15 COTSWALD RD,SUTTON SM2 5NG,SURREY,ENGLAND. RI Fisher, Simon/E-9130-2012 OI Fisher, Simon/0000-0002-3132-1996 NR 36 TC 42 Z9 42 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 71 IS 3 BP 280 EP 284 DI 10.1159/000134127 PG 5 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA TD385 UT WOS:A1995TD38500018 PM 7587394 ER PT J AU TRENT, JM WILTSHIRE, R SU, LK NICOLAIDES, NC VOGELSTEIN, B KINZLER, KW AF TRENT, JM WILTSHIRE, R SU, LK NICOLAIDES, NC VOGELSTEIN, B KINZLER, KW TI THE GENE FOR THE APC-BINDING PROTEIN BETA-CATENIN (CTNNB1) MAPS TO CHROMOSOME 3P22, A REGION FREQUENTLY ALTERED IN HUMAN MALIGNANCIES SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID CELL CARCINOMA; MUTATIONS; CANCER; IDENTIFICATION; HETEROZYGOSITY; GENERATION; DELETION; TUMORS; LOCUS; LUNG AB beta-Catenin is one of the E-cadherin associated proteins involved in the process of cellular adhesion. It has recently been shown to interact with the APC protein whose gene is known to be mutated in the germline of familial adenomatous polyposis patients. This interaction implies that beta-catenin is a potential regulator of the APC gene. The localization of the human beta-catenin gene (CTNNB1) to chromosome 3p22, by fluorescent in situ hybridization (FISH), has linked the gene to a region that is frequently altered in several human malignancies. The location of the gene and the protein interactions suggest the importance of beta-catenin in the etiology of various human cancers. C1 UNIV MICHIGAN,SCH MED,DEPT HUMAN GENET,ANN ARBOR,MI 48109. JOHNS HOPKINS UNIV,SCH MED,DEPT ONCOL,BALTIMORE,MD 21205. RP TRENT, JM (reprint author), NIH,NATL CTR HUMAN GENOME RES,CANC GENET LAB,BLDG 49,RM 4A22,49 CONVENT DR,MSC 4470,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA-57345] NR 22 TC 22 Z9 23 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 71 IS 4 BP 343 EP 344 DI 10.1159/000134136 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA TJ854 UT WOS:A1995TJ85400002 PM 8521721 ER PT J AU LEDBETTER, DH AF LEDBETTER, DH TI MOLECULAR CYTOGENETICS - DOSAGE AND IMPRINTING EFFECTS IN HUMAN-DEVELOPMENT SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 71 IS 4 BP 392 EP 392 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA TJ854 UT WOS:A1995TJ85400012 ER PT J AU ADAMSON, MC KOZAK, CA AF ADAMSON, MC KOZAK, CA TI LINKAGE AND SYNTENY HOMOLOGIES BETWEEN HUMAN-CHROMOSOME-13 AND MOUSE CHROMOSOME-5, CHROMOSOME-8 AND CHROMOSOME-14 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 70 IS 1-2 BP 17 EP 17 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QX326 UT WOS:A1995QX32600002 ER PT J AU HABETS, GGM VANDERKAMMEN, RA JENKINS, NA GILBERT, DJ COPELAND, NG HAGEMEIJER, A COLLARD, JG AF HABETS, GGM VANDERKAMMEN, RA JENKINS, NA GILBERT, DJ COPELAND, NG HAGEMEIJER, A COLLARD, JG TI THE INVASION-INDUCING TIAM1 GENE MAPS TO HUMAN-CHROMOSOME BAND 21Q22 AND MOUSE CHROMOSOME-16 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID ACUTE MYELOID-LEUKEMIA AB The murine invasion-inducing Tiam1 gene maps to the distal end of chromosome 16, 3.8 cM centromeric of the Ets2 gene. TIAM1, the human homolog of Tiam1, maps to the syntenic region (q22) on human chromosome 21. The gene order in 21q22 is cen-TIAM1-AML1-ERG-ETS2-tel. C1 NETHERLANDS CANC INST,DIV CELL BIOL,1066 CX AMSTERDAM,NETHERLANDS. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. ERASMUS UNIV ROTTERDAM,DEPT CELL BIOL & GENET,3000 DR ROTTERDAM,NETHERLANDS. FU NCI NIH HHS [N01-CO-74101] NR 13 TC 14 Z9 15 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 70 IS 1-2 BP 48 EP 51 DI 10.1159/000133989 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QX326 UT WOS:A1995QX32600029 PM 7736788 ER PT J AU SLORACH, EM POLYMEROPOULOS, MH EVANS, KL SEAWRIGHT, A FLETCHER, JM PORTEOUS, DJ BROOKES, AJ AF SLORACH, EM POLYMEROPOULOS, MH EVANS, KL SEAWRIGHT, A FLETCHER, JM PORTEOUS, DJ BROOKES, AJ TI REGIONAL LOCALIZATION OF 19 BRAIN EXPRESSED SEQUENCE TAGS TO HUMAN-CHROMOSOME-11 USING PCR AMPLIFICATION OF SOMATIC-CELL HYBRID DNAS SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID GENES; MARKERS; ASSIGNMENT; GLOBIN AB Expressed sequence tags (ESTs) provide an efficient route to the identification of genes involved in normal development and in disease. PCR amplification of somatic cell hybrid DNAs was used to localise 22 brain-derived ESTs to subregions of human chromosome 11. Problems encountered with the standardised PCR conditions were overcome by optimising the annealing temperatures and the use of ''touchdown'' PCR. Amplification of the correct target sequence allowed the mapping of 19 ESTs, 8 to the short arm and 11 to the long arm of chromosome 11. No definitive localisation could be determined for the three remaining ESTs. C1 ST ELIZABETH HOSP,CTR NEUROSCI,NIMH,BIOCHEM GENET LAB,WASHINGTON,DC 20032. RP SLORACH, EM (reprint author), WESTERN GEN HOSP,MRC,HUMAN GENET UNIT,MOLEC GENET SECT,CREWE RD,EDINBURGH EH4 2XU,MIDLOTHIAN,SCOTLAND. RI Evans, Kathryn /I-5910-2012; Porteous, David/C-7289-2013 OI Porteous, David/0000-0003-1249-6106 NR 19 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 70 IS 1-2 BP 71 EP 75 DI 10.1159/000133995 PG 5 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QX326 UT WOS:A1995QX32600035 PM 7736794 ER PT J AU MATHEW, P MORRIS, SW KANE, JR SHURTLEFF, SA PASQUINI, M JENKINS, NA GILBERT, DJ COPELAND, NG AF MATHEW, P MORRIS, SW KANE, JR SHURTLEFF, SA PASQUINI, M JENKINS, NA GILBERT, DJ COPELAND, NG TI LOCALIZATION OF THE MURINE HOMOLOG OF THE ANAPLASTIC LYMPHOMA KINASE (ALK) GENE ON MOUSE CHROMOSOME-17 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID MAP AB The murine homolog of the human anaplastic lymphoma kinase gene, which encodes a membrane-spanning receptor tyrosine kinase in the insulin receptor kinase subfamily, was assigned to mouse Chromosome 17 by interspecific backcross analysis. This assignment further confirms the homology between a portion of the distal Chromosome 17 and the short arm of human chromosome 2 and extends this region in the mouse by an additional 3 cM. C1 ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL ONCOL, MEMPHIS, TN 38101 USA. ST JUDE CHILDRENS RES HOSP, DEPT PATHOL, MEMPHIS, TN 38101 USA. NCI, FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB, ABL,BASIC RES PROGRAM, FREDERICK, MD 21702 USA. RP MATHEW, P (reprint author), ST JUDE CHILDRENS RES HOSP, DEPT EXPTL ONCOL, 332 N LAUDERDALE, BOX 318, MEMPHIS, TN 38101 USA. FU NCI NIH HHS [P30 CA21765, N01-CO-74101, CA01702] NR 6 TC 9 Z9 11 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 70 IS 1-2 BP 143 EP 144 DI 10.1159/000134080 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QX326 UT WOS:A1995QX32600051 PM 7736780 ER PT J AU BLOUIN, JL CHRISTIE, D CHAKRAVARTI, A LEDBETTER, D MORRIS, MA GOS, A CHEN, HM ROSSIER, C ANTONARAKIS, SE AF BLOUIN, JL CHRISTIE, D CHAKRAVARTI, A LEDBETTER, D MORRIS, MA GOS, A CHEN, HM ROSSIER, C ANTONARAKIS, SE TI SHORT SEQUENCE REPEAT POLYMORPHISM(S) IN THE TELOMERE OF THE LONG ARM OF HUMAN-CHROMOSOME-21 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV GENEVA,SCH MED,DIV MED GENET,CH-1211 GENEVA,SWITZERLAND. CANTONAL HOSP,GENEVA,SWITZERLAND. CASE WESTERN RESERVE UNIV,DEPT GENET,CLEVELAND,OH 44106. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 70 IS 3-4 BP 168 EP 168 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA RG533 UT WOS:A1995RG53300009 ER PT J AU SUMARSONO, S TYMMS, M CORRICK, C WILSON, T LAHOUD, M KOLA, R PAPAS, TS SETH, A KOLA, I AF SUMARSONO, S TYMMS, M CORRICK, C WILSON, T LAHOUD, M KOLA, R PAPAS, TS SETH, A KOLA, I TI MICE TRANSGENIC FOR THE ETS2 PROTOONCOGENE DEVELOP A SUBSET OF PHENOTYPIC ABNORMALITIES FOUND IN DOWN-SYNDROME SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MONASH UNIV,INST REPROD & DEV,MOLEC EMBRYOL & BIRTH DEFECTS LAB,CLAYTON,VIC,AUSTRALIA. MED UNIV S CAROLINA,HOLLINGS ONCOL CTR,CTR MOLEC & STRUCT BIOL,CHARLESTON,SC 29425. NCI,MOLEC ONCOL LAB,FREDERICK,MD. RI Lahoud, Mireille/F-1299-2013 NR 0 TC 0 Z9 0 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 70 IS 3-4 BP 181 EP 181 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA RG533 UT WOS:A1995RG53300052 ER PT J AU BELL, DW TAGUCHI, T JENKINS, NA GILBERT, DJ COPELAND, NG GILKS, CB ZWEIDLERMCKAY, P GRIMES, HL TSICHLIS, PN TESTA, JR AF BELL, DW TAGUCHI, T JENKINS, NA GILBERT, DJ COPELAND, NG GILKS, CB ZWEIDLERMCKAY, P GRIMES, HL TSICHLIS, PN TESTA, JR TI CHROMOSOMAL LOCALIZATION OF A GENE, GFI1, ENCODING A NOVEL ZINC-FINGER PROTEIN REVEALS A NEW SYNTENIC REGION BETWEEN MAN AND RODENTS SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID FLUORESCENCE INSITU HYBRIDIZATION; TUMOR PROGRESSION; DNA-SEQUENCES; LINKAGE MAP; MOUSE; ACTIVATION; LYMPHOMAS; DELETION; 1P AB The Gfi1 gene encodes a zinc finger protein which binds DNA and is involved in transcriptional regulation. Gfi1 was assigned to the central portion of mouse Chr 5 by interspecific backcross mapping and to human chromosome band 1p22 and rat chromosome band 14p22 by fluorescence in situ hybridization (FISH). Comparative mapping data presented here describes a new syntenic region between man and rodents. C1 FOX CHASE CANC CTR,DEPT MED ONCOL,MOLEC CYTOGENET SECT,PHILADELPHIA,PA 19111. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD. UNIV BRITISH COLUMBIA,DEPT PATHOL,VANCOUVER,BC,CANADA. OI Zweidler-McKay, Patrick/0000-0001-6621-523X; Grimes, H. Leighton/0000-0001-8162-6758 FU NCI NIH HHS [N01-CO-74101, CA56110, CA45745] NR 17 TC 49 Z9 49 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 70 IS 3-4 BP 263 EP 267 DI 10.1159/000134048 PG 5 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA RG533 UT WOS:A1995RG53300075 PM 7789186 ER PT J AU OHARA, B JENKINS, NA GILBERT, DJ COPELAND, NG SHOWS, TB EDDY, RL BOHLEN, P KOVESDI, I AF OHARA, B JENKINS, NA GILBERT, DJ COPELAND, NG SHOWS, TB EDDY, RL BOHLEN, P KOVESDI, I TI CHROMOSOMAL ASSIGNMENT OF THE HEPARIN-BINDING CYTOKINE GENES MDK AND PTN IN MOUSE AND MAN SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID HUMAN PLEIOTROPHIN GENE; GENOMIC ORGANIZATION; LEUKEMIA-VIRUS; LINKAGE MAP; LOCALIZATION; MK; DIFFERENTIATION; REGION AB MDK and PTN are two members of a family of heparin-binding cytokines thought to be involved in a number of developmental processes. The locations for these genes were determined in man and mouse using somatic cell hybrid analysis and interspecific backcross analysis. Human MDK was mapped to 11p13-->p11. MDK in the mouse (Mdk) was mapped to a syntenic region of mouse Chromosome 2. A pseudogene of Mdk was mapped to mouse Chromosome 11. The closely related human gene PTN was mapped to a separate location on human chromosome region 7q22-->qter. C1 ROSWELL PK MEM INST,DEPT HUMAN GENET,BUFFALO,NY. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD. RP OHARA, B (reprint author), AMER CYANAMID CO,LEDERLE LABS,DIV MED RES,MOLEC BIOL RES SECT,BLDG 205,ROOM 217,PEARL RIVER,NY 10965, USA. FU NCI NIH HHS [N01-CO-74101] NR 20 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 69 IS 1-2 BP 40 EP 43 DI 10.1159/000133934 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QF045 UT WOS:A1995QF04500010 PM 7835084 ER PT J AU MOORE, KJ TESTA, JR FRANCKE, U MILATOVICH, A COPELAND, NG JENKINS, NA AF MOORE, KJ TESTA, JR FRANCKE, U MILATOVICH, A COPELAND, NG JENKINS, NA TI CLONING AND REGIONAL ASSIGNMENT OF THE HUMAN MYOSIN HEAVY-CHAIN-12 (MYH12) GENE TO CHROMOSOME BAND-15Q21 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID FLUORESCENCE INSITU HYBRIDIZATION; DNA-SEQUENCES; UNCONVENTIONAL MYOSIN; PARENTAL ORIGIN; PRADER-WILLI; LINKAGE MAP; MOUSE; LOCALIZATION; BRAIN; LOCUS AB Sequences encoding 1,235 bp of the human myosin heavy chain 12 (MYH12) gene have been cloned from a human brain cDNA library by PCR amplification. The human sequence is 95.8% identical to the mouse sequence at the amino acid level, indicating that the MYH12 gene has been evolutionarily well conserved. Somatic cell hybrid analysis and in situ hybridization place the MYH12 gene on human chromosome 15, at band q21, and extend distally the known region of chromosome 15 linkage homology on mouse chromosome 9. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. FOX CHASE CANC CTR,DEPT MED ONCOL,PHILADELPHIA,PA 19111. STANFORD UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT GENET,STANFORD,CA 94305. STANFORD UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT PEDIAT,STANFORD,CA 94305. FU NCI NIH HHS [N01-CO-74101, CA-45745]; NHGRI NIH HHS [R01-HG00298] NR 30 TC 11 Z9 12 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 69 IS 1-2 BP 53 EP 58 DI 10.1159/000133937 PG 6 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QF045 UT WOS:A1995QF04500013 PM 7835087 ER PT J AU HUANG, B MEYER, JM JACKSONCOOK, C AF HUANG, B MEYER, JM JACKSONCOOK, C TI HERITABILITY ESTIMATES AND HETEROMORPHIC DISTRIBUTION OF THE ISOSCHIZOMERS MBOI AND SAU3AL SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 69 IS 1-2 BP 114 EP 114 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QF045 UT WOS:A1995QF04500027 ER PT J AU SARGENT, L DRAGAN, Y BAHNUB, N WILEY, J SATTLER, C SCHROEDER, P SATTLER, G JORDAN, VC PITOT, H AF SARGENT, L DRAGAN, Y BAHNUB, N WILEY, J SATTLER, C SCHROEDER, P SATTLER, G JORDAN, VC PITOT, H TI TAMOXIFEN INDUCES HEPATIC ANEUPLOIDY AND MITOTIC SPINDLE DISRUPTION AFTER A SINGLE IN-VIVO ADMINISTRATION TO FEMALE SPRAGUE-DAWLEY RATS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706. E CAROLINA UNIV,DEPT MED GENET,GREENVILLE,NC 27834. UNIV ILLINOIS,CHICAGO,IL. RI Jordan, V. Craig/H-4491-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 69 IS 1-2 BP 125 EP 126 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QF045 UT WOS:A1995QF04500073 ER PT J AU COX, DW BILLINGSLEY, GD BALE, AE DONISKELLER, H EDWARDS, JH LITT, M MCBRIDE, W PERSICHETTI, F SPURR, NK WEBER, JL WEISSENBACH, J WHITE, RL AF COX, DW BILLINGSLEY, GD BALE, AE DONISKELLER, H EDWARDS, JH LITT, M MCBRIDE, W PERSICHETTI, F SPURR, NK WEBER, JL WEISSENBACH, J WHITE, RL TI CEPH CONSORTIUM MAP OF CHROMOSOME-14 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID HUMAN GENOME; LINKAGE MAP AB Families from the linkage panel of Centre d'Etude du Polymorphisme Humain have been used to generate a linkage map containing 68 loci; 13 genes, 33 di- and 4 tetranucleotide repeats, one oligonucleotide ligation assay (OLA), and 17 RFLPs. This map integrates markers from several previous maps, and has undergone further error checking. 43 loci have been placed with odds of 1000:1 or greater, five with odds of 100:1, with an average interval of 3.5 cM. An additonal 20 loci have been placed within defined intervals. C1 YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06510. UNIV IOWA,IOWA CITY,IA. WASHINGTON UNIV,SCH MED,DEPT GENET,ST LOUIS,MO 63110. UNIV OXFORD,DEPT BIOCHEM,OXFORD OX1 3QU,ENGLAND. OREGON HLTH SCI UNIV,DEPT BIOCHEM,PORTLAND,OR 97201. NCI,BIOCHEM LAB,BETHESDA,MD 20892. NCI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV ROME,DEPT BIOL,ROME,ITALY. IMPERIAL CANC RES FUND,CLARE HALL LABS,LONDON,HERTS,ENGLAND. MARSHFIELD MED RES FDN,CTR MED GENET,MARSHFIELD,WI 54449. INST PASTEUR,PARIS,FRANCE. UNIV UTAH,HOWARD HUGHES MED INST,ECCLES INST HUMAN GENET,SALT LAKE CITY,UT. RP COX, DW (reprint author), HOSP SICK CHILDREN,RES INST,DEPT GENET,555 UNIV AVE,TORONTO,ON M5G 1X8,CANADA. NR 14 TC 9 Z9 9 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 69 IS 3-4 BP 175 EP 178 DI 10.1159/000133955 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QT857 UT WOS:A1995QT85700003 PM 7698005 ER PT J AU PAPPAS, GJ THOMPSON, E BURGESS, A GREENWOOD, A TRENT, JM AF PAPPAS, GJ THOMPSON, E BURGESS, A GREENWOOD, A TRENT, JM TI GENERATION AND MOLECULAR CYTOGENETIC CHARACTERIZATION OF A RADIATION REDUCTION HYBRID PANEL FOR HUMAN-CHROMOSOME-6 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID HUMAN-MALIGNANT MELANOMA; SOMATIC-CELL HYBRIDS; LONG ARM; PROBES AB A neo(R) marked chromosome-6 containing hybrid (D113JA) was used to generate a panel of 15 radiation-reduced hybrid cell lines. The panel was constructed by irradiating microcells isolated from D113JA at 800 or 8000 rads, providing different levels of chromosome 6 retention. These hybrids have been systematically analyzed using interspersed repetitive elements, previously assigned markers for chromosome 6, and fluorescent in situ hybridization (FISH). As expected, G418 selection has favored the retention of fragments near the insertion site of the neo(R) gene (6q16). The panel as constituted provides an important resource for regional assignment of molecular markers, especially to regions on 6q. C1 NIH,NATL CTR HUMAN GENOME RES,CANC GENET LAB,BETHESDA,MD 20892. UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. NR 20 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 69 IS 3-4 BP 201 EP 206 DI 10.1159/000133963 PG 6 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QT857 UT WOS:A1995QT85700011 PM 7698012 ER PT J AU MODI, WS FARRAR, WL HOWARD, OMZ AF MODI, WS FARRAR, WL HOWARD, OMZ TI CONFIRMED ASSIGNMENT OF A NOVEL HUMAN TYROSINE KINASE GENE (JAK1A) TO 1P32.3-]P31.3 BY NONISOTOPIC IN-SITU HYBRIDIZATION SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID PROTEIN-KINASE AB JAK1A is a recently isolated class 3 (nonreceptor) tyrosine kinase that has catalytic domain sequence homology with other kinases and is known to be ubiquitously expressed in all human tissues thus far examined. The gene for this enzyme had previously been localized to chromosome 1 using somatic cell hybrids and linkage analyses. In the present study, fluorescence in situ hybridization was utilized to confirm its localization and regionally assign the gene to chromosome region 1p32.3-->p31.3. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. RP MODI, WS (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. RI Howard, O M Zack/B-6117-2012 OI Howard, O M Zack/0000-0002-0505-7052 FU NCI NIH HHS [N01-CO-74102] NR 11 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 69 IS 3-4 BP 232 EP 234 DI 10.1159/000133971 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QT857 UT WOS:A1995QT85700019 PM 7698020 ER PT J AU PIONTEK, K MULLER, HW FISCHER, U GOTTERT, E BATZER, MA MELTZER, PS TRENT, JM MEESE, E AF PIONTEK, K MULLER, HW FISCHER, U GOTTERT, E BATZER, MA MELTZER, PS TRENT, JM MEESE, E TI GENERATION AND CHARACTERIZATION OF A HUMAN-CHROMOSOME 6-SPECIFIC HNCDNA LIBRARY FROM A SOMATIC-CELL HYBRID SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID TRANSCRIBED SEQUENCES; ALU-PCR; RAPID GENERATION; MAPPING PANEL; REGION; GENE; DNA; IDENTIFICATION; CLONING; PROBES AB Chromosome specific cDNA libraries are a useful source of candidate genes for disorders which have been linked to particular chromosomes. Here, we report the generation of a cDNA library made from a somatic cell hybrid retaining chromosome 6 as its only human component. In order to ascertain the chromosomal location of cDNAs the library was amplified by inter-Alu-PCR and used as probe for competitive in situ suppression (CISS). To identify human specific cDNA clones the library was screened with PD39, a highly human specific Alu consensus probe. Out of 350,000 clones 360 were found to hybridize with PD39. Nucleotide sequences were determined for 40 clones with inserts larger than 500 basepairs (bp) and a sequence comparison was performed at the National Center for Biotechnology Information using BLASTN. One clone was shown to be identical to Manganese Superoxide Dismutase (MnSOD/SOD2) which has previously been assigned to chromosome 6q25. Localization of 11 clones was determined using PCR and clone-specific primer pairs on a hybrid mapping panel DNA set. Two PCR-localized clones and five additional clones were localized by fluorescence in situ hybridization. Transcripts for five clones were identified by RT-PCR. The generation of chromosome 6-specific hncDNAs from a somatic cell hybrid should aid in the identification of disease-associated genes localized on this chromosome. C1 UNIV HOSP SAAR,SCH MED,DEPT HUMAN GENET,D-66421 HOMBURG,GERMANY. NATL CTR HUMAN GENOME RES,BETHESDA,MD. LAWRENCE LIVERMORE NATL LAB,CTR HUMAN GENOME,BIOL & BIOTECHNOL RES PROGRAM,LIVERMORE,CA. NR 36 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 69 IS 3-4 BP 273 EP 278 DI 10.1159/000133978 PG 6 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA QT857 UT WOS:A1995QT85700026 PM 7698027 ER PT J AU VAMVAKOPOULOS, NC MODI, WS FLOROS, J AF VAMVAKOPOULOS, NC MODI, WS FLOROS, J TI MAPPING THE HUMAN PULMONARY SURFACTANT-ASSOCIATED PROTEIN-B GENE (SFTP3) TO CHROMOSOME 2P12-]P11.2 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID RESPIRATORY-DISTRESS SYNDROME; SP-A GENE; LUNGS; CDNA AB Pulmonary surfactant, a lipoprotein complex is essential for normal lung function. The non-serum surfactant-associated proteins, SP-A, SP-B, and SP-C, play important roles in the biology of pulmonary surfactant. We have mapped the human SP-B gene (SFTP3) to chromosome 2, band 2p12 --> p11.2 by fluorescent in situ hybridization. C1 PENN STATE UNIV,COLL MED,DEPT CELLULAR & MOLEC PHYSIOL,HERSHEY,PA 17033. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS DEV PROGRAM,FREDERICK,MD. FU NHLBI NIH HHS [HL 34788] NR 22 TC 32 Z9 33 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 68 IS 1-2 BP 8 EP 10 DI 10.1159/000133878 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PQ322 UT WOS:A1995PQ32200003 PM 7956367 ER PT J AU SAITO, F SASAKI, S CHEPELINSKY, AB FUSHIMI, K MARUMO, F IKEUCHI, T AF SAITO, F SASAKI, S CHEPELINSKY, AB FUSHIMI, K MARUMO, F IKEUCHI, T TI HUMAN AQP2 AND MIP GENES, 2 MEMBERS OF THE MIP FAMILY, MAP WITHIN CHROMOSOME BAND-12Q13 ON THE BASIS OF 2-COLOR FISH SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID MAJOR INTRINSIC PROTEIN; INSITU HYBRIDIZATION; WATER CHANNEL; MEMBRANE-PROTEIN; AQUAPORIN-CHIP; LENS; CLONING; LOCALIZATION; RESOLUTION; MARKERS AB The human AQP2 (collecting duct water channel, aquaporin 2) gene encodes a 271 amino acid protein and is a member of the MIP (major intrinsic protein of lens fiber) gene family. Using two-color fluorescence in situ hybridization on high-resolution R-banded chromosomes and human genomic DNA clones for AQP2 and MIP as probes, we found that both genes mapped closely within the human chromosome region 12q13. C1 TOKYO MED & DENT UNIV,SCH MED,DEPT INTERNAL MED,TOKYO 113,JAPAN. NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. RP SAITO, F (reprint author), TOKYO MED & DENT UNIV,MED RES INST,DEPT CYTOGENET,BUNKYO KU,1-5-45 YUSHIMA,TOKYO 113,JAPAN. NR 28 TC 27 Z9 27 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 68 IS 1-2 BP 45 EP 48 DI 10.1159/000133885 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PQ322 UT WOS:A1995PQ32200010 PM 7525161 ER PT J AU POPESCU, NC ZIMONJIC, DB ALBOR, A NOTARIO, V AF POPESCU, NC ZIMONJIC, DB ALBOR, A NOTARIO, V TI LOCALIZATION OF THE TP53 GENE ON SYRIAN-HAMSTER CHROMOSOME-9 BY FLUORESCENCE IN-SITU HYBRIDIZATION SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID BANDING PATTERNS AB Mutations of the Tp53 tumor suppressor gene have been detected in 50% of all human cancers. The normal Tp53 gene product acts as a negative regulator of cell division or is associated with abnormal growth in certain differentiated cell types. The Tp53 gene was mapped by FISH to Syrian hamster chromosome 9 bands qb2.2-->2.3 using a genomic DNA probe with a high degree of sequence identity to the human Tp53 gene. C1 GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,DEPT RADIAT MED,DIV EXPTL CARCINOGENESIS,WASHINGTON,DC 20007. NCI,BIOL LAB,BETHESDA,MD 20892. NR 14 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 68 IS 1-2 BP 71 EP 73 DI 10.1159/000133893 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PQ322 UT WOS:A1995PQ32200018 PM 7956364 ER PT J AU VOROBIEVA, N PROTOPOPOV, A PROTOPOPOVA, M KASHUBA, V ALLIKMETS, RL MODI, W ZABAROVSKY, ER KLEIN, G KISSELEV, L GRAPHODATSKY, A AF VOROBIEVA, N PROTOPOPOV, A PROTOPOPOVA, M KASHUBA, V ALLIKMETS, RL MODI, W ZABAROVSKY, ER KLEIN, G KISSELEV, L GRAPHODATSKY, A TI LOCALIZATION OF HUMAN ARF2 AND NCK GENES AND 13 OTHER NOTI-LINKING CLONES TO CHROMOSOME-3 BY FLUORESCENCE IN-SITU HYBRIDIZATION SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID RENAL-CELL CARCINOMA; HUMAN GENOME; CPG ISLANDS; LUNG-CANCER; SHORT ARM; MARKERS; HETEROZYGOSITY; CONSTRUCTION; DELETION; INSITU AB Two human genes containing NotI sites, ADP-ribosylation factor (ARF2) and melanoma NCK protein, were mapped by fluorescence in situ hybridization to 3p21.2-->p21.1 and 3q21, respectively. Thirteen other NotI-linking clones, representing sequence tagged sites, were also mapped to different regions of human chromosome 3. Two of these clones that contain sequences 80% homologous to the rat tropoelastin gene and brain Cl- channel protein CLC-2 gene probably represent new human genes closely related to the known rat genes. C1 KAROLINSKA INST,CTR MICROBIOL & TUMOR BIOL,DEPT TUMOR BIOL,S-17177 STOCKHOLM,SWEDEN. RUSSIAN ACAD SCI,INST CYTOL & GENET,SIBERIAN BRANCH,NOVOSIBIRSK 630090,RUSSIA. UKRAINIAN ACAD SCI,INST MOLEC BIOL & GENET,KIEV 252627,UKRAINE. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RUSSIAN ACAD SCI,VA ENGELHARDT MOLEC BIOL INST,MOSCOW,RUSSIA. RI Zabarovsky, Eugene/A-6645-2010; Graphodatsky, Alexander/B-4922-2010; Vorobieva, Nadezhda/N-6461-2015 OI Graphodatsky, Alexander/0000-0002-8282-1085; FU NCI NIH HHS [5 R01 CA14054-15] NR 23 TC 23 Z9 23 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 68 IS 1-2 BP 91 EP 94 DI 10.1159/000133898 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PQ322 UT WOS:A1995PQ32200023 PM 7956370 ER PT J AU DU, Y REMMERS, EF ZHA, H GOLDMUNTZ, EA MATHERN, P CROFFORD, LJ SZPIRER, J SZPIRER, C WILDER, RL AF DU, Y REMMERS, EF ZHA, H GOLDMUNTZ, EA MATHERN, P CROFFORD, LJ SZPIRER, J SZPIRER, C WILDER, RL TI GENETIC-MAP OF 8 MICROSATELLITE MARKERS COMPRISING 2 LINKAGE GROUPS ON RAT CHROMOSOME-6 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID MOUSE; ASSIGNMENT AB Five genes and three anonymous DNA loci were mapped to rat chromosome 6 by genetic linkage and somatic cell hybrid analyses. The eight loci were all identified by PCR-based microsatellite polymorphism analysis and were characterized in 40 F-2 intercross progeny of Fischer (F344/N) and Lewis (LEW/N) inbred rats for segregation analysis. These markers formed two linkage groups spanning, respectively, 58.1 cM and 4.0 cM. The first linkage group is comprised of two anonymous DNA loci and four genes with the following map order and distances: D6Cep8 (previously D3)-17.9 cM-D6Arb309-2.5 cM-Vsnl1 (neural visinin-like protein)-20.4 cM-Prkar2b (type II beta regulatory subunit of cAMP-dependent protein kinase)-8.8 cM-Fkhl1 (forkhead-like transcription factor BF-1)-8.5 cM-Rnu1c(18-3A U1 RNA). The second linkage group is comprised of one gene, Ckb (creatine kinase, brain) and one anonymous DNA locus, D6Arb54, separated by 4.0 cM. For each marker, two to eight alleles were detected in a panel of 16 inbred rat strains (ACI/N, BN/SsN, BUF/N, DA/Bk1, F344/N, LER/N, LEW/N, LOU/MN, MNR/N, MR/N, SHR/N, SR/Jr, SS/Jr, WBB1/N, WBB2/N, and WKY/N). Comparative mapping information indicated that rat chromosome 6 exhibits syntenic conservation with mouse chromosome 12. Homologs of the rat chromosome 6 loci have been identified on human chromosomes 2, 7, and 14. C1 UNIV LIBRE BRUXELLES,DEPT MOLEC BIOL,RHODE ST GENESE,BELGIUM. RP DU, Y (reprint author), NIAMSD,ARTHRIT & RHEUMATISM BRANCH,BLDG 10,ROOM 9N228,BETHESDA,MD 20892, USA. RI Crofford, Leslie/J-8010-2013 NR 20 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 68 IS 1-2 BP 107 EP 111 DI 10.1159/000133901 PG 5 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PQ322 UT WOS:A1995PQ32200026 PM 7956346 ER PT J AU ZABAROVSKY, ER KASHUBA, VI ALLIKMETS, RL VOROBIEVA, NV PEKARSKY, Y BANNIKOV, V GIZATULLIN, R ZABAROVSKA, VI ERLANDSSON, R PAULSSON, N DOMNINSKY, D ZAKHARYEV, V LERMAN, M MODI, WW DEAN, M GRAFODATSKY, AS RYNDITCH, A STANBRIDGE, EJ GARDINER, K KISSELEV, L KLEIN, G AF ZABAROVSKY, ER KASHUBA, VI ALLIKMETS, RL VOROBIEVA, NV PEKARSKY, Y BANNIKOV, V GIZATULLIN, R ZABAROVSKA, VI ERLANDSSON, R PAULSSON, N DOMNINSKY, D ZAKHARYEV, V LERMAN, M MODI, WW DEAN, M GRAFODATSKY, AS RYNDITCH, A STANBRIDGE, EJ GARDINER, K KISSELEV, L KLEIN, G TI MAPPING OF HUMAN-CHROMOSOME-3 USING NOTI LINKING CLONES AS LANDMARKS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 KAROLINSKA INST,CTR MICROBIOL & TUMOR BIOL,STOCKHOLM,SWEDEN. VA ENGELHARDT MOLEC BIOL INST,MOSCOW 117984,RUSSIA. INST MOLEC BIOL & GENET,KIEV,UKRAINE. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS & IMMUNOBIOL LAB,FREDERICK,MD 21702. NOVOSIBIRSK CYTOL & GENET INST,NOVOSIBIRSK,RUSSIA. ELEANOR ROOSEVELT INST,DENVER,CO. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. CALIF COLL MED,DEPT MICROBIOL & MOLEC GENET,IRVINE,CA. RI Zabarovsky, Eugene/A-6645-2010; Vorobieva, Nadezhda/N-6461-2015 NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 68 IS 3-4 BP 141 EP 141 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PX890 UT WOS:A1995PX89000008 ER PT J AU AKSENTIJEVICH, I CHEN, X BALOW, JE LEVY, E PRAS, E GARDNER, D PRAS, M FISCHELGHODSIAN, N KUPELIAN, A SHOHAT, M ROTTER, JI SHEN, Y RICHARDS, RI CALLEN, DF DOGGETT, NA LIU, P BLAKE, T SHELTON, D GUMUCIO, D KASTNER, DL AF AKSENTIJEVICH, I CHEN, X BALOW, JE LEVY, E PRAS, E GARDNER, D PRAS, M FISCHELGHODSIAN, N KUPELIAN, A SHOHAT, M ROTTER, JI SHEN, Y RICHARDS, RI CALLEN, DF DOGGETT, NA LIU, P BLAKE, T SHELTON, D GUMUCIO, D KASTNER, DL TI REFINED LOCALIZATION OF THE GENE CAUSING FAMILIAL MEDITERRANEAN FEVER SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIAMS,ARB,BETHESDA,MD. HELLER INST MED RES,TEL HASHOMER,ISRAEL. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. BEILINSON MED CTR,PETAH TIQWA,ISRAEL. ADELAIDE WOMENS & CHILDRENS HOSP,ADELAIDE,SA,AUSTRALIA. LOS ALAMOS NATL LAB,LOS ALAMOS,NM. NIH,NCHGR,LGT,BETHESDA,MD. UNIV MICHIGAN,ANN ARBOR,MI 48109. RI Liu, Paul/A-7976-2012; Callen, David/G-1975-2012 OI Liu, Paul/0000-0002-6779-025X; NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 68 IS 3-4 BP 178 EP 178 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PX890 UT WOS:A1995PX89000052 ER PT J AU KOZMAN, HM KEITH, TP GERKEN, S DONISKELLER, H WHITE, RL WEISSENBACH, J AKSENTIJEVICH, I KASTNER, DL VERGNAUD, G KIDD, K GUSELLA, J JEFFREYS, A SUTHERLAND, GR MULLEY, JC AF KOZMAN, HM KEITH, TP GERKEN, S DONISKELLER, H WHITE, RL WEISSENBACH, J AKSENTIJEVICH, I KASTNER, DL VERGNAUD, G KIDD, K GUSELLA, J JEFFREYS, A SUTHERLAND, GR MULLEY, JC TI THE CEPH CONSORTIUM LINKAGE MAP OF HUMAN-CHROMOSOME-16 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 WOMENS & CHILDRENS HOSP,DEPT CYTOGENET & MOLEC GENET,ADELAIDE,SA,AUSTRALIA. WASHINGTON UNIV,SCH MED,DEPT GENET,ST LOUIS,MO 63110. UNIV UTAH,HOWARD HUGHES MED INST,SALT LAKE CITY,UT. INST PASTEUR,PARIS,FRANCE. NIAMSD,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD 20892. CTR ETUD BOUCHET,F-91710 VERT LE PETIT,FRANCE. YALE UNIV,SCH MED,DEPT HUMAN GENET,NEW HAVEN,CT 06510. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV LEICESTER,DEPT GENET,LEICESTER LE1 7RH,LEICS,ENGLAND. RI Sutherland, Grant/D-2606-2012; Vergnaud, Gilles/P-1304-2015 OI Vergnaud, Gilles/0000-0003-0913-194X NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1995 VL 68 IS 3-4 BP 182 EP 182 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PX890 UT WOS:A1995PX89000066 ER PT J AU EGAWA, M MAENO, M KUNG, HF SCHWABE, M AF EGAWA, M MAENO, M KUNG, HF SCHWABE, M TI EXPRESSION OF THE HUMAN INTERLEUKIN-6 RECEPTOR ALPHA-CHAIN IN XENOPUS-LAEVIS OOCYTES SO CYTOKINE LA English DT Article DE IL-6 RECEPTOR; XENOPUS LAEVIS; PROTEIN EXPRESSION ID IL-6 SIGNAL TRANSDUCER; LEUKEMIA-INHIBITORY FACTOR; STIMULATORY FACTOR-II; TYROSINE KINASE; GROWTH-HORMONE; ONCOSTATIN-M; GP130; CYTOKINES; BINDING; CELLS AB We investigated the biochemical properties of the 80 kDa binding subunit (gp80) of the human interleukin 6 receptor (IL-6R) in the genetic environment of the amphibian Xenopus laevis. In vitro transcribed mRNA encoding full length human gp80 was microinjected into Xenopus laevis stage VI oocytes. Protein expression was monitored by iodinated IL-6 and human gp80-specific monoclonal antibodies (mAb) PM1 and MT18. Maximal IL-6 binding activity was observed between 36-42 h after injection. Scatchard analysis indicated that gp80-injected oocytes expressed two independent classes of IL-g binding sites of high- (K-d1 = 9 x 10(-11) M, 20 x 10(6) sites/cell) and low-affinity (K-d2 = 2 X 10(-9) M, 70.3 x 10(6) sites/cell). PM1 but not MT18 completely inhibited IL-6 binding to injected eggs. Our data suggest that the human IL-6R alpha-subunit gp80 is sufficient to confer high- and low-affinity IL-6 binding to Xenopus laevis oocytes. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,BIOCHEM PHYSIOL LAB,FREDERICK,MD 21702. NR 37 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4666 J9 CYTOKINE JI Cytokine PD JAN PY 1995 VL 7 IS 1 BP 83 EP 88 DI 10.1006/cyto.1995.1011 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA QF135 UT WOS:A1995QF13500011 PM 7749071 ER PT B AU TombranTink, J AF TombranTink, J BE Anderson, RE LaVail, MM Hollyfield, JG TI Function, age-related expression and molecular characterization of PEDF, a neurotrophic serpin secreted bu human RPE cells SO DEGENERATIVE DISEASES OF THE RETINA LA English DT Proceedings Paper CT 6th International Symposium on Retinal Degenerations CY NOV 04-09, 1994 CL JERUSALEM, ISRAEL C1 NEI,LRCMB,BETHESDA,MD 20892. NEI,LRCMB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45137-9 PY 1995 BP 51 EP 60 PG 10 WC Ophthalmology SC Ophthalmology GA BE44M UT WOS:A1995BE44M00006 ER PT S AU Majewska, MD AF Majewska, MD BE Bellino, FL Daynes, RA Hornsby, PJ Lavrin, DH Nestler, JE TI Neuronal actions of dehydroepiandrosterone - Possible roles in brain development, aging, memory, and affect SO DEHYDROEPIANDROSTERONE (DHEA) AND AGING SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Dehydroepiandrosterone (DHEA) and Aging CY JUN 17-19, 1995 CL WASHINGTON, D.C. SP New York Acad Sci, NIA, NIAMS, NCI, Diag Syst Labs Inc, Glaxo Wellcome Inc, Glenn Fdn Med Res, Henry & Lucy Moses Fund Inc, Merck Res Labs, Paradigm Biosci Inc, Pfizer Cent Res, Wyeth Ayerst Res ID GABA-A RECEPTOR; SUBUNIT MESSENGER-RNAS; LONG-TERM POTENTIATION; RAT-BRAIN; PREGNENOLONE-SULFATE; MICE; PROGESTERONE; ANTAGONIST; MODULATION; STEROIDS RP NATL INST DRUG ABUSE, MEDICAT DEV DIV, 5600 FISHERS LANE, RM 11A-55, ROCKVILLE, MD 20857 USA. NR 86 TC 127 Z9 131 U1 0 U2 4 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-005-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 774 BP 111 EP 120 DI 10.1111/j.1749-6632.1995.tb17375.x PG 10 WC Endocrinology & Metabolism; Geriatrics & Gerontology; Multidisciplinary Sciences SC Endocrinology & Metabolism; Geriatrics & Gerontology; Science & Technology - Other Topics GA BF30Y UT WOS:A1995BF30Y00008 PM 8597451 ER PT S AU Lane, MA Ingram, DK Roth, GS AF Lane, MA Ingram, DK Roth, GS BE Bellino, FL Daynes, RA Hornsby, PJ Lavrin, DH Nestler, JE TI Effects of aging and long-term calorie restriction on DHEA and DHEA sulfate in rhesus monkeys SO DEHYDROEPIANDROSTERONE (DHEA) AND AGING SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Dehydroepiandrosterone (DHEA) and Aging CY JUN 17-19, 1995 CL WASHINGTON, DC SP New York Acad Sci, NIA, NIAMS, NCI, Diag Syst Labs Inc, Glaxo Wellcome Inc, Glenn Fdn Med Res, Henry & Lucy Moses Fund Inc, Merck Res Labs, Paradigm Biosci Inc, Pfizer Cent Res, Wyeth Ayerst Res RP Lane, MA (reprint author), NIA,GERONTOL RES CTR,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 7 TC 10 Z9 10 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 1-57331-005-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 774 BP 319 EP 322 PG 4 WC Endocrinology & Metabolism; Geriatrics & Gerontology; Multidisciplinary Sciences SC Endocrinology & Metabolism; Geriatrics & Gerontology; Science & Technology - Other Topics GA BF30Y UT WOS:A1995BF30Y00031 PM 8597476 ER PT S AU Wolkowitz, OM Reus, VI Roberts, E Manfredi, F Chan, T Ormiston, S Johnson, R Canick, J Brizendine, L Weingartner, H AF Wolkowitz, OM Reus, VI Roberts, E Manfredi, F Chan, T Ormiston, S Johnson, R Canick, J Brizendine, L Weingartner, H BE Bellino, FL Daynes, RA Hornsby, PJ Lavrin, DH Nestler, JE TI Antidepressant and cognition-enhancing effects of DHEA in major depression SO DEHYDROEPIANDROSTERONE (DHEA) AND AGING SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Dehydroepiandrosterone (DHEA) and Aging CY JUN 17-19, 1995 CL WASHINGTON, DC SP New York Acad Sci, NIA, NIAMS, NCI, Diag Syst Labs Inc, Glaxo Wellcome Inc, Glenn Fdn Med Res, Henry & Lucy Moses Fund Inc, Merck Res Labs, Paradigm Biosci Inc, Pfizer Cent Res, Wyeth Ayerst Res ID DEHYDROEPIANDROSTERONE SULFATE; MEMORY C1 CITY HOPE NATL MED CTR,DEPT NEUROBIOCHEM,DUARTE,CA 91010. NIAAA,BETHESDA,MD 20892. RP Wolkowitz, OM (reprint author), UNIV CALIF SAN FRANCISCO,DEPT PSYCHIAT,SAN FRANCISCO,CA 94143, USA. RI reus, victor/I-7923-2015 OI reus, victor/0000-0002-8193-5697 NR 7 TC 61 Z9 63 U1 0 U2 5 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 1-57331-005-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 774 BP 337 EP 339 PG 3 WC Endocrinology & Metabolism; Geriatrics & Gerontology; Multidisciplinary Sciences SC Endocrinology & Metabolism; Geriatrics & Gerontology; Science & Technology - Other Topics GA BF30Y UT WOS:A1995BF30Y00037 PM 8597481 ER PT S AU Lubet, RA Mccormick, DM Gordon, GM Grubbs, C Lei, XD Prough, RA Steele, VE Kelloff, GJ Thomas, CF Moon, RD AF Lubet, RA Mccormick, DM Gordon, GM Grubbs, C Lei, XD Prough, RA Steele, VE Kelloff, GJ Thomas, CF Moon, RD BE Bellino, FL Daynes, RA Hornsby, PJ Lavrin, DH Nestler, JE TI Effects of dehydroepiandrosterone on MNU-induced breast cancer in Sprague-Dawley rats SO DEHYDROEPIANDROSTERONE (DHEA) AND AGING SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Dehydroepiandrosterone (DHEA) and Aging CY JUN 17-19, 1995 CL WASHINGTON, DC SP New York Acad Sci, NIA, NIAMS, NCI, Diag Syst Labs Inc, Glaxo Wellcome Inc, Glenn Fdn Med Res, Henry & Lucy Moses Fund Inc, Merck Res Labs, Paradigm Biosci Inc, Pfizer Cent Res, Wyeth Ayerst Res C1 JOHNS HOPKINS UNIV,CTR ONCOL,BALTIMORE,MD 21205. UNIV ILLINOIS,CHICAGO,IL. UNIV ALABAMA,BIRMINGHAM,AL 35294. UNIV LOUISVILLE,LOUISVILLE,KY 40292. RP Lubet, RA (reprint author), NCI,BETHESDA,MD 20892, USA. NR 1 TC 3 Z9 3 U1 0 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 1-57331-005-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 774 BP 340 EP 341 PG 2 WC Endocrinology & Metabolism; Geriatrics & Gerontology; Multidisciplinary Sciences SC Endocrinology & Metabolism; Geriatrics & Gerontology; Science & Technology - Other Topics GA BF30Y UT WOS:A1995BF30Y00038 PM 8597482 ER PT S AU Inaba, K Inaba, M WitmerPack, M Hathcock, K Hodes, R Steinman, RM AF Inaba, K Inaba, M WitmerPack, M Hathcock, K Hodes, R Steinman, RM BE Banchereau, J Schmitt, D TI Expression of B7 costimulator molecules on mouse dendritic cells SO DENDRITIC CELLS IN FUNDAMENTAL AND CLINICAL IMMUNOLOGY, VOL 2 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 3rd International Symposium on Dendritic Cells in Fundamental and Clinical Immunology CY JUN 19-23, 1994 CL ANNECY, FRANCE ID EPIDERMAL LANGERHANS CELLS; COLONY-STIMULATING FACTOR; MACROPHAGES; POPULATIONS; INVITRO; CULTURE; MATURE C1 KANSAI MED UNIV,DEPT PATHOL,MORIGUCHI,OSAKA 530,JAPAN. NIAID,BETHESDA,MD 20205. ROCKEFELLER UNIV,CELLULAR PHYSIOL & IMMUNOL LAB,NEW YORK,NY 10021. RP Inaba, K (reprint author), KYOTO UNIV,FAC SCI,DEPT ZOOL,KYOTO 606,JAPAN. RI Steinman, Ralph/F-7729-2012 NR 18 TC 34 Z9 34 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45078-X J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 378 BP 65 EP 70 PG 6 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BE35J UT WOS:A1995BE35J00013 PM 8526146 ER PT S AU Borkowski, TA Farr, AG Nelson, AJ Udey, MC AF Borkowski, TA Farr, AG Nelson, AJ Udey, MC BE Banchereau, J Schmitt, D TI Identification of a novel cell surface protein expressed by murine epidermal Langerhans cells and some lymphoid dendritic cells SO DENDRITIC CELLS IN FUNDAMENTAL AND CLINICAL IMMUNOLOGY, VOL 2 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 3rd International Symposium on Dendritic Cells in Fundamental and Clinical Immunology CY JUN 19-23, 1994 CL ANNECY, FRANCE ID MOUSE; THYMUS C1 UNIV WASHINGTON,DEPT BIOL STRUCT,SEATTLE,WA 98195. RP Borkowski, TA (reprint author), NCI,DERMATOL BRANCH,BETHESDA,MD 20892, USA. FU NIA NIH HHS [AG 04360]; NIAID NIH HHS [AI 24137] NR 11 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45078-X J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 378 BP 93 EP 95 PG 3 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BE35J UT WOS:A1995BE35J00019 PM 8526153 ER PT S AU Katz, SI Aiba, S Cavani, A Enk, AH AF Katz, SI Aiba, S Cavani, A Enk, AH BE Banchereau, J Schmitt, D TI Early events in contact sensitivity SO DENDRITIC CELLS IN FUNDAMENTAL AND CLINICAL IMMUNOLOGY, VOL 2 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 3rd International Symposium on Dendritic Cells in Fundamental and Clinical Immunology CY JUN 19-23, 1994 CL ANNECY, FRANCE ID LANGERHANS CELLS; INDUCTION; ANTIGEN; IMMUNE; IL-10 C1 UNIFORMED SERV UNIV HLTH SCI,DEPT DERMATOL,BETHESDA,MD 20814. TOHOKU UNIV,DEPT DERMATOL,SENDAI,MIYAGI 980,JAPAN. UNIV MAINZ,DEPT DERMATOL,W-6500 MAINZ,GERMANY. RP Katz, SI (reprint author), NCI,DERMATOL BRANCH,BETHESDA,MD 20892, USA. NR 12 TC 2 Z9 2 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45078-X J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 378 BP 497 EP 500 PG 4 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BE35J UT WOS:A1995BE35J00112 PM 8526127 ER PT S AU GERSHON, ES AF GERSHON, ES BE Gessa, GL Fratta, W Pani, L Serra, G TI RECENT DEVELOPMENTS IN GENETICS OF BIPOLAR ILLNESS SO DEPRESSION AND MANIA: FROM NEUROBIOLOGY TO TREATMENT SE ADVANCES IN BIOCHEMICAL PSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT Symposium on Depression, at the 8th Sardinian Conference on Neuroscience CY MAY, 1995 CL VILLASIMIUS, ITALY SP Gunther Fdn ID MANIC-DEPRESSIVE ILLNESS; X-CHROMOSOME MARKERS; OLD ORDER AMISH; TYROSINE-HYDROXYLASE POLYMORPHISMS; MAJOR AFFECTIVE-DISORDER; LINKAGE ANALYSIS; RECEPTOR GENE; CLOSE LINKAGE; AUSTRALIAN PEDIGREES; CHRISTMAS DISEASE RP GERSHON, ES (reprint author), NIMH,CLIN NEUROGENET BRANCH,BLDG 10,BETHESDA,MD 20892, USA. NR 69 TC 2 Z9 2 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA E WASHINGTON SQ, PHILADELPHIA, PA 19105 SN 0065-2229 BN 0-7817-0307-7 J9 ADV BIOCHEM PSYCHOPH PY 1995 VL 49 BP 85 EP 98 PG 14 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA BD68F UT WOS:A1995BD68F00005 PM 7653336 ER PT J AU SCHMITT, JM YADLOWSKY, MJ BONNER, RF AF SCHMITT, JM YADLOWSKY, MJ BONNER, RF TI SUBSURFACE IMAGING OF LIVING SKIN WITH OPTICAL COHERENCE MICROSCOPY SO DERMATOLOGY LA English DT Article DE LIGHT; MICROSCOPY; IMAGING ID TISSUES; INVIVO AB Background: A new type of microscope has been developed for acquiring cross-sectional images of living skin noninvasively. It takes advantage of the short temporal coherence of a broad-band light source to reject scattered light. Because this microscope is still in an early stage of development, its potential as a diagnostic tool in dermatology has not yet been determined. Objective: This study was designed to explore potential applications of optical coherence microscopy in dermatology. The aim was to investigate the structures in skin that can be seen without staining or using sophisticated image-processing methods. Methods: A prototype fiberoptic microscope was assembled that uses a 1,300-nm light-emitting diode as a light source. Scans were obtained from the skin on the index finger and forearm. Subsurface structures were identified based on knowledge of the anatomy of normal healthy skin. Results: Structures located as deep as 1 mm below the surface of the skin could be imaged with a resolution of about 10 mu m in the axial and lateral dimensions. In optical slices taken perpendicular to the skin surface, the contours of the epidermal ridges and the boundary between the epidermis and dermis were readily observed. Conclusions: The results of this study suggest that an optical coherence microscope may have value as a diagnostic tool for cases in which visualization of subcellular details is not required. The resolution, contrast and scanning speed of the microscope need to be improved. C1 NIH,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RI Bonner, Robert/C-6783-2015 NR 20 TC 205 Z9 205 U1 0 U2 14 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 1995 VL 191 IS 2 BP 93 EP 98 PG 6 WC Dermatology SC Dermatology GA RU298 UT WOS:A1995RU29800004 PM 8520074 ER PT J AU TUR, E HOHL, D JETTEN, A PANIZZON, R FRENK, E AF TUR, E HOHL, D JETTEN, A PANIZZON, R FRENK, E TI MODIFICATION OF LATE EPIDERMAL DIFFERENTIATION IN PHOTOAGED SKIN TREATED WITH TOPICAL RETINOIC ACID CREAM SO DERMATOLOGY LA English DT Article DE CORNIFIED CELL ENVELOPE; RETINOIC ACID; PHOTOAGING; EPIDERMAL DIFFERENTIATION ID CORNIFIED ENVELOPE; TRANSGLUTAMINASE ACTIVITY; EXPRESSION PATTERNS; HUMAN KERATINOCYTES; CROSS-LINKING; LORICRIN; TISSUES; INVIVO; CELLS; COMPETENCE AB Background: Retinoic acid (RA) cream treatment alters epidermal proliferation and differentiation in photoaged skin. Objective: To study the changes in the expression of markers of epidermal differentiation in photoaged skin following RA cream treatment. Methods: Ten subjects with photoaged skin were examined before treatment and at regular intervals during 12 months of once daily application of 0.05% tretinoin cream over the left forearm. Paraffin-embedded biopsy sections from the forearm were stained with loricrin, filaggrin, involucrin and cornifin antisera in addition to hematoxylin and eosin, The various layers were measured using a calibrated optical micrometer, Results: The thickness of the epidermis increased rapidly, reaching a substantial increase after 1 month of retinoid cream application and retaining it during the following 12 months. The stratum granulosum achieved a transient but substantial increase after 1 and 3 months. Except involucrin, the ratio between the layers expressing the various markers of epidermal differentiation and the epidermis significantly increased following tretinoin cream treatment, Conclusion: RA. cream treatment not Only increases the thickness of the epidermis but also the programming of late terminal epidermal differentiation, as expressed by the markers studied. Thus, RA appears to affect both proliferation and differentiation of keratinocytes in vivo. C1 CHU VAUDOIS,DEPT DERMATOL,CH-1011 LAUSANNE,SWITZERLAND. TEL AVIV SOURASKY MED CTR,DEPT DERMATOL,TEL AVIV,ISRAEL. UNIV ZURICH HOSP,DEPT DERMATOL,CH-8091 ZURICH,SWITZERLAND. NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. OI Jetten, Anton/0000-0003-0954-4445 NR 36 TC 12 Z9 12 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 1995 VL 191 IS 2 BP 124 EP 128 PG 5 WC Dermatology SC Dermatology GA RU298 UT WOS:A1995RU29800010 PM 8520058 ER PT J AU FELSENFELD, AL KENNISON, JA AF FELSENFELD, AL KENNISON, JA TI POSITIONAL SIGNALING BY HEDGEHOG IN DROSOPHILA IMAGINAL DISC DEVELOPMENT SO DEVELOPMENT LA English DT Article DE DROSOPHILA; IMAGINAL DISC; HEDGEHOG; MOONRAT; SEGMENT POLARITY GENE; CELL SIGNALING ID SEGMENT-POLARITY GENE; CELL-CELL COMMUNICATION; REGULATORY ELEMENTS; HOMEOTIC GENES; PATCHED GENE; BETA FAMILY; EXPRESSION; WINGLESS; PROTEIN; TRANSCRIPTION AB We describe a dominant gain-of-function allele of the segment polarity gene hedgehog. This mutation causes ectopic expression of hedgehog mRNA in the anterior compartment of wing discs, leading to overgrowth of tissue in the anterior of the wing and partial duplication of distal wing structures. The posterior compartment of the wing is unaffected. Other imaginal derivatives are affected, resulting in duplications of legs and antennae and malformations of eyes. In mutant imaginal vying discs, expression of the decapentaplegic gene, which is implicated in the hedgehog signaling pathway, is also perturbed. The results suggest that hedgehog protein acts in the wing as a signal to instruct neighboring cells to adopt fates appropriate to the region of the wing just anterior to the compartmental boundary. RP FELSENFELD, AL (reprint author), NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892, USA. NR 46 TC 54 Z9 54 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD JAN PY 1995 VL 121 IS 1 BP 1 EP 10 PG 10 WC Developmental Biology SC Developmental Biology GA QD185 UT WOS:A1995QD18500001 PM 7867491 ER PT J AU SHARP, R BABYATSKY, MW TAKAGI, H TAGERUD, S WANG, TC BOCKMAN, DE BRAND, SJ MERLINO, G AF SHARP, R BABYATSKY, MW TAKAGI, H TAGERUD, S WANG, TC BOCKMAN, DE BRAND, SJ MERLINO, G TI TRANSFORMING GROWTH-FACTOR-ALPHA DISRUPTS THE NORMAL PROGRAM OF CELLULAR-DIFFERENTIATION IN THE GASTRIC-MUCOSA OF TRANSGENIC MICE SO DEVELOPMENT LA English DT Article DE TGF-ALPHA; STOMACH; PARIETAL CELL; CHIEF CELL; APOPTOSIS; MENETRIERS DISEASE; ACHLORHYDRIA; IN SITU HYBRIDIZATION; MOUSE ID ACID-SECRETION; MOUSE STOMACH; DEVELOPMENTAL EXPRESSION; MENETRIERS DISEASE; EPITHELIAL-CELLS; PRECURSOR CELLS; FUNDIC MUCOSA; TGF-ALPHA; RAT; PANCREAS AB Transforming growth factor alpha (TGF alpha) evokes diverse responses in transgenic mouse tissues in which it is overexpressed, including the gastric mucosa, which experiences aberrant growth and a coincident repression of hydrochloric acid production. Here we show that ectopically expressed TGF alpha induces an age-dependent cellular reorganization of the transgenic stomach, in which the surface mucous cell population in the gastric pit is greatly expanded at the expense of cells in the glandular base. Immunohistochemical analysis of BrdU incorporation into DNA demonstrated that although mature surface mucous cells were not proliferating, DNA synthesis was enhanced by approximately 67% in the glandular base and isthmus, where progenitor cells reside. RNA blot and in situ hybridization were employed to determine temporal and spatial expression patterns of specific markers representing a variety of exocrine and endocrine gastric cell types. Mature parietal and chief cells mere specifically depleted from the glandular mucosa, as judged by a 6- to 7-fold decrease in the expression of genes encoding H+,K+-ATPase, which is required for acid secretion, and pepsinogen C, respectively. The reduction of these markers coincided in time with the activation of TGF alpha transgene expression in the neonatal stomach. The rate of cell death in the glandular region was not overtly different. Significantly, the loss of parietal and chief cells occurred without a concomitant loss of their respective cellular precursors. In contrast to exocrine cells, D and G endocrine cells were much less severely affected, based on analysis of somatostatin and gastrin expression. Analysis of these dynamic changes indicates that TGF alpha can induce selective alterations in terminal differentiation and proliferation in the gastric mucosa, and suggests that TGF alpha plays an important physiological role in the normal regulation of epithelial cell renewal. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MED COLL GEORGIA,DEPT CELLULAR BIOL & ANAT,AUGUSTA,GA 30912. NR 49 TC 81 Z9 85 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD JAN PY 1995 VL 121 IS 1 BP 149 EP 161 PG 13 WC Developmental Biology SC Developmental Biology GA QD185 UT WOS:A1995QD18500014 PM 7867496 ER PT J AU PATTERTON, D HAYES, WP SHI, YB AF PATTERTON, D HAYES, WP SHI, YB TI TRANSCRIPTIONAL ACTIVATION OF THE MATRIX METALLOPROTEINASE GENE STROMELYSIN-3 COINCIDES WITH THYROID HORMONE-INDUCED CELL-DEATH DURING FROG METAMORPHOSIS SO DEVELOPMENTAL BIOLOGY LA English DT Article ID XENOPUS-LAEVIS; DEGRADING METALLOPROTEINASES; AMPHIBIAN METAMORPHOSIS; EXTRACELLULAR-MATRIX; CONNECTIVE-TISSUE; SMALL-INTESTINE; RECEPTOR; EXPRESSION; CARCINOMAS; PROTEIN AB A full-length cDNA was isolated for a thyroid hormone response gene in the metamorphosing frog intestine and shown by sequence analysis to be the frog homolog of the mammalian extracellular matrix metalloproteinase stromelysin-3 (ST3). Northern hybridization indicated that ST3 gene expression is differentially activated in tadpole tissues during metamorphosis. In the small intestine, in situ hybridization localized high levels of ST3 mRNA to fibroblast-like cells during thyroid hormone-induced metamorphosis. ST3 mRNA was undetectable in the intestine prior to metamorphosis, while high levels were present at the metamorphic climax. At this time, primary intestinal epithelial cells are known to undergo cell death and replacement by secondary epithelial cells, arguing that ST3 is involved in the modification of the extracellular matrix during apoptosis. ST3 mRNA was also expressed at high levels during tadpole tail resorption, but not in premetamorphic tail or developing hindlimb, further supporting a role for ST3 when tissue remodeling is accompanied by large-scale cell death. Premetamorphic tadpoles treated with thyroid hormone showed a similar but compressed time course of ST3 gene regulation, suggesting that thyroid hormone controls ST3 gene expression during metamorphosis. In contrast, during embryogenesis, ST3 was expressed before endogenous thyroid hormone is detectable, indicating that ST3 can also be regulated independently of thyroid hormone. These findings implicate that ST3 participates in the modification of the extracellular matrix during metamorphic apoptosis, but Northern analyses using heterologous probes raise the possibility that additional matrix metalloproteinases may also be involved. (C) 1995 Academic Press, Inc. C1 NICHHD, MOLEC EMBRYOL LAB, BETHESDA, MD 20892 USA. NICHHD, DEV NEUROBIOL LAB, BETHESDA, MD 20892 USA. NR 43 TC 136 Z9 137 U1 3 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN PY 1995 VL 167 IS 1 BP 252 EP 262 DI 10.1006/dbio.1995.1021 PG 11 WC Developmental Biology SC Developmental Biology GA QG553 UT WOS:A1995QG55300021 PM 7851646 ER PT J AU WELCH, JE BROWN, PR OBRIEN, DA EDDY, EM AF WELCH, JE BROWN, PR OBRIEN, DA EDDY, EM TI GENOMIC ORGANIZATION OF A MOUSE GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE GENE (GAPD-S) EXPRESSED IN POSTMEIOTIC SPERMATOGENIC CELLS SO DEVELOPMENTAL GENETICS LA English DT Article DE SPERMATOGENESIS; GLYCOLYSIS; GENE EXPRESSION; ENZYME; GLYCERALDEHYDE 3-PHOSPHATE DEHYDROGENASE ID MESSENGER-RIBONUCLEIC-ACID; NUCLEOTIDE-SEQUENCES; ROUND SPERMATIDS; HEXOKINASE; ALDOLASE; GLUCOSE; FAMILY; TRANSCRIPTION; METABOLISM; ADENOSINE AB The Gapd-s gene encodes an isoform of the glyceraldehyde 3-phosphate dehydrogenase enzyme expressed only in post-meiotic spermatogenic cells. Two clones containing the Gapd-s gene were isolated from a mouse genomic library. Sequencing and restriction enzyme analysis demonstrated that this single-copy gene contains 11 exons and spans 9596 base pairs. The locations of Gapd-s exons and introns are conserved when compared to the corresponding portions of the chicken and human somatic Gapd genes. The promoter region contains no TATA box, although there is a potential SP1 recognition site within exon 1. Like other TATA-less genes, primer extension analysis reveals some heterogeneity in the site of transcription initiation with Gapd-s transcripts initiating from three discrete sites. Northern analysis demonstrated that a 1.5-kb Gapd-s mRNA is expressed in the testis in at least three mammalian orders, indicating that the Gapd-s gene appeared early in mammalian evolution. Using GAPD-deficient bacteria, mouse GAPD-S was shown to be capable of functioning as a glycolytic enzyme. Since GAPD has been proposed to be a key enzyme regulating glycolysis in spermatogenic cells, GAPD-S may represent a potential target for toxicological or contraceptive agents affecting fertility by interfering with glycolysis. (C) 1995 Wiley-Liss, Inc. C1 UNIV N CAROLINA,REPROD BIOL LABS,CHAPEL HILL,NC. UNIV N CAROLINA,DEPT PEDIAT,CHAPEL HILL,NC. UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC. RP WELCH, JE (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,GAMETE BIOL SECT,BLDG 101,MAIL DROP C4-03,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU NCI NIH HHS [CA16086]; NICHD NIH HHS [HD-26485, P30-HD-18968, R01 HD026485] NR 47 TC 26 Z9 27 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 0192-253X J9 DEV GENET JI Dev. Genet. PY 1995 VL 16 IS 2 BP 179 EP 189 DI 10.1002/dvg.1020160210 PG 11 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA QQ214 UT WOS:A1995QQ21400009 PM 7736666 ER PT J AU ZHOU, YD DELAFONTAINE, P MARTIN, BM BERNSTEIN, KE AF ZHOU, YD DELAFONTAINE, P MARTIN, BM BERNSTEIN, KE TI IDENTIFICATION OF 2 POSITIVE TRANSCRIPTIONAL ELEMENTS WITHIN THE 91-BASE PAIR PROMOTER FOR MOUSE TESTIS ANGIOTENSIN-CONVERTING ENZYME (TESTIS ACE) SO DEVELOPMENTAL GENETICS LA English DT Article DE TESTIS ACE; POSITIVE PROMOTER ELEMENT; IN VITRO TRANSCRIPTION; TISSUE-SPECIFICITY ID 2 HOMOLOGOUS DOMAINS; MOLECULAR-CLONING; EXPRESSION; GENE; SPERMATOGENESIS; POLYMERASE; ISOZYME; SYSTEM AB Testis angiotensin-converting enzyme (testis ACE) is an isozyme of ACE only expressed by male germ cells during spermiogenesis. It is the result of a strong sperm-specific promoter found within the 12th intron of the somatic ACE gene. Previous studies have localized the boundaries of the mouse testis ACE promoter as being from -91 to -9, relative to the transcriptional start site, and have suggested two important DNA regulatory elements starting at positions -55 and -32. DNA constructs were made in which these motifs were either eliminated or substituted. Each construct was tested for its ability to promote transcription in vitro, using a rat testis nuclear extract. Disruption of either motif reduced in vitro transcription to about 30% of control levels, while mutations of both elements abolished transcription. Two sites were selected inside each motif and altered by point mutation. Each of four constructs, containing a mutation at -51, -48, -30, or -28; transcribed at 29% or less the efficiency of the parent construct. The DNA element at -55, TGAGGTCA, is homologous to a consensus cyclic AMP response element. The motif at -32, TCTTAT, is located at a position analogous to a TATA box. Substitution of the -32 motif with a consensus TATA box sequence, TATAAA, stimulated transcriptional activity about 3-fold. As measured by gel mobility shift, oligonucleotides encompassing the -32 motif and the consensus TATA box formed different DNA-protein complexes. However, the -32 motif oligo-nucleotide was recognized by nuclear proteins prepared from either liver or testis nuclei. In this example of a tissue-specific promoter that functions only during spermatogenesis, at least two DNA elements act synergistically during in vitro transcription, (C) 1995 Wiley-Liss, Inc. C1 EMORY UNIV,DEPT PATHOL,ATLANTA,GA 30322. EMORY UNIV,DEPT MED,ATLANTA,GA 30322. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. FU NHLBI NIH HHS [HL 47035]; NIDDK NIH HHS [DK39777, DK44280] NR 19 TC 13 Z9 13 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0192-253X J9 DEV GENET JI Dev. Genet. PY 1995 VL 16 IS 2 BP 201 EP 209 DI 10.1002/dvg.1020160212 PG 9 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA QQ214 UT WOS:A1995QQ21400011 PM 7736668 ER PT J AU LEIBOWITZ, MD BISWAS, C BRADY, EJ CONTI, M CULLINAN, CA HAYES, NS MANGANIELLO, VC SAPERSTEIN, R WANG, LH ZAFIAN, PT BERGER, J AF LEIBOWITZ, MD BISWAS, C BRADY, EJ CONTI, M CULLINAN, CA HAYES, NS MANGANIELLO, VC SAPERSTEIN, R WANG, LH ZAFIAN, PT BERGER, J TI A NOVEL INSULIN SECRETAGOGUE IS A PHOSPHODIESTERASE INHIBITOR SO DIABETES LA English DT Article ID PANCREATIC BETA-CELLS; CAMP PHOSPHODIESTERASE; HYPOGLYCEMIC ACTIVITY; CA2+ OSCILLATIONS; HORMONES; GLUCOSE; SECRETION; NUTRIENTS; RELEASE; CA-2+ AB The arylpiperazine L-686,398 was described as an oral hypoglycemic agent and is shown to be an insulin secretagogue in vitro. The characteristics of its activity were similar to those of the incretin glucagon-like peptide I (GLP-I). We demonstrate that both the peptide and L-686,398 increase the accumulation of cAMP in isolated ob/ob mouse pancreatic islet cells, but by different mechanisms. Although GLP-I activates adenylate cyclase, the arylpiperazine has no effect on this enzyme or on the binding of I-125-labeled GLS-I to its receptor on RINm5F rat insulinoma cell membranes. However, L-686,398 inhibits the total cAMP phosphodiesterase (PDE) activity in homogenates of ob/ob mouse pancreatic islets with an EC(50) of similar to 50 mu mol/l. To determine the mechanism of PDE inhibition by the arylpiperazine and to examine its specificity, we studied the kinetics of arylpiperazine inhibition of two recombinant PDEs. The arylpiperazine is a competitive inhibitor of both a human heart type III PDE and a rat type IV-D PDE. Inhibition of the type III and IV isozymes are characterized by K-i values of 27 and 5 mu mol/l, respectively. Although not extremely potent, the arylpiperazine does exhibit modest selectivity between these PDEs. The observation that L-686,398 acts as a PDE inhibitor suggests that exploration for beta-cell-specific PDE isoforms may reveal novel PDEs as targets for the development of therapeutically useful glucose-dependent insulin secretagogues. C1 MERCK & CO INC,MERCK SHARP & DOHME RES LABS,DEPT ENDOCRINE PHARMACOL,RAHWAY,NJ 07065. STANFORD UNIV,SCH MED,DIV REPROD BIOL,PALO ALTO,CA 94304. NHLBI,BIOCHEM PHYSIOL SECT,BETHESDA,MD 20892. RP LEIBOWITZ, MD (reprint author), MERCK & CO INC,MERCK SHARP & DOHME RES LABS,DEPT MOLEC ENDOCRINOL,POB 2000,ROOM 80N-31C,RAHWAY,NJ 07065, USA. NR 32 TC 30 Z9 30 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 JAN PY 1995 VL 44 IS 1 BP 67 EP 74 DI 10.2337/diabetes.44.1.67 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PZ998 UT WOS:A1995PZ99800011 PM 7813816 ER PT S AU Kador, PF Sato, S Neuenschwander, H Lizak, MJ Secchi, F Greentree, W Takahashi, Y AF Kador, PF Sato, S Neuenschwander, H Lizak, MJ Secchi, F Greentree, W Takahashi, Y BE Baba, S Kaneko, T TI Recent studies on the polyol pathway: The relationship between aldose reductase-catalyzed polyol production, retinopathy, and sorbitol dehydrogenase SO DIABETES 1994 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 15th International-Diabetes-Federation Congress CY NOV 06-11, 1994 CL KOBE, JAPAN SP Int Diabet Federat DE fructose; galactose; galactose-fed dogs; glucose; NMR; pericytes; sorbitol; trypsin digestion C1 NEI,LAB OCULAR THERAPEUT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81725-5 J9 INT CONGR SER PY 1995 VL 1100 BP 315 EP 320 PG 4 WC Endocrinology & Metabolism; Medicine, General & Internal SC Endocrinology & Metabolism; General & Internal Medicine GA BE46T UT WOS:A1995BE46T00052 ER PT S AU Rodbard, D Berger, M Pernick, N AF Rodbard, D Berger, M Pernick, N BE Baba, S Kaneko, T TI Computer, networking, and information systems to facilitate delivery of health care to patients with diabetes SO DIABETES 1994 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 15th International-Diabetes-Federation Congress CY NOV 06-11, 1994 CL KOBE, JAPAN SP Int Diabet Federat DE computers; diabetes mellitus; medical informatics; telemedicine C1 NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81725-5 J9 INT CONGR SER PY 1995 VL 1100 BP 800 EP 803 PG 2 WC Endocrinology & Metabolism; Medicine, General & Internal SC Endocrinology & Metabolism; General & Internal Medicine GA BE46T UT WOS:A1995BE46T00144 ER PT J AU BLANK, A GRAVE, GD METZGER, BE AF BLANK, A GRAVE, GD METZGER, BE TI EFFECTS OF GESTATIONAL DIABETES ON PERINATAL MORBIDITY REASSESSED - REPORT OF THE INTERNATIONAL WORKSHOP ON ADVERSE PERINATAL OUTCOMES OF GESTATIONAL DIABETES-MELLITUS, DECEMBER 3-4, 1992 SO DIABETES CARE LA English DT Editorial Material RP BLANK, A (reprint author), NICHHD,OFF RES REPORTING,BLDG 31,ROOM 2A32,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 45 Z9 45 U1 1 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JAN PY 1995 VL 18 IS 1 BP 127 EP 129 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QG882 UT WOS:A1995QG88200020 PM 7698033 ER PT J AU HARRIS, MI AF HARRIS, MI TI FREQUENCY OF ORAL GLUCOSE-TOLERANCE TESTING IN THE US SO DIABETES CARE LA English DT Letter ID BLOOD-GLUCOSE; UNITED-STATES; RELIABILITY C1 NIDDKD,NATL DIABET DATA GRP,BETHESDA,MD 20892. NR 14 TC 1 Z9 1 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JAN PY 1995 VL 18 IS 1 BP 134 EP 135 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QG882 UT WOS:A1995QG88200023 PM 7698036 ER PT S AU Sato, S Secchi, EF Lizak, MJ Fenner, W Kador, PF AF Sato, S Secchi, EF Lizak, MJ Fenner, W Kador, PF BE Hotta, N Greene, DA Ward, JD Sima, AAF Boulton, AJM TI Nerve changes in galactose-fed dogs SO DIABETIC NEUROPATHY: NEW CONCEPTS AND INSIGHTS SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 3rd International Symposium on Diabetic Neuropathy, as a Satellite Symposium of the 15th International-Diabetes-Federation Congress CY NOV 03-11, 1994 CL KOBE, JAPAN SP Int Diabetes Federat DE aldose reductase; sorbitol; galactosemia; aldose reductase inhibitor; neuropathy C1 NEI,NIH,LAB OCULAR THERAPEUT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-82098-1 J9 INT CONGR SER PY 1995 VL 1084 BP 321 EP 327 PG 7 WC Endocrinology & Metabolism; Medicine, General & Internal; Neurosciences; Pathology SC Endocrinology & Metabolism; General & Internal Medicine; Neurosciences & Neurology; Pathology GA BE78J UT WOS:A1995BE78J00048 ER PT J AU METZ, DC WEBER, HC ORBUCH, M STRADER, DB LUBENSKY, IA JENSEN, RT AF METZ, DC WEBER, HC ORBUCH, M STRADER, DB LUBENSKY, IA JENSEN, RT TI HELICOBACTER-PYLORI INFECTION - A REVERSIBLE CAUSE OF HYPERGASTRINEMIA AND HYPERCHLORHYDRIA WHICH MAY MIMIC ZOLLINGER-ELLISON-SYNDROME SO DIGESTIVE DISEASES AND SCIENCES LA English DT Note DE GASTRIC ACID HYPERSECRETION; DUODENAL ULCER; STOMACH; GASTRINOMA; ZOLLINGER-ELLISON SYNDROME ID GASTRIC-ACID SECRETION; DUODENAL-ULCER; SERUM GASTRIN; CAMPYLOBACTER-PYLORI; MANAGEMENT; RESECTION; HYPOCHLORHYDRIA; ERADICATION; DIAGNOSIS; SYMPTOMS C1 NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 41 TC 15 Z9 15 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 JAN PY 1995 VL 40 IS 1 BP 153 EP 159 DI 10.1007/BF02063959 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QC388 UT WOS:A1995QC38800028 PM 7821103 ER PT B AU Thoma, GR Berman, LE Long, LR AF Thoma, GR Berman, LE Long, LR BE Kuo, CCJ TI Data storage and organization for a general access xray image archive SO DIGITAL IMAGE STORAGE AND ARCHIVING SYSTEMS SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Digital Image Storage and Archiving Systems CY OCT 25-26, 1995 CL PHILADELPHIA, PA SP Soc Photo Opt Instrumentat Engineers DE digitized medical xrays; electronic xray archives; client server design; optical jukebox; RAID; image processing; multisocket transmission; Internet C1 NATL LIB MED,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1970-2 J9 P SOC PHOTO-OPT INS PY 1995 VL 2606 BP 59 EP 65 DI 10.1117/12.227267 PG 7 WC Computer Science, Artificial Intelligence; Computer Science, Hardware & Architecture; Computer Science, Information Systems; Optics SC Computer Science; Optics GA BE66U UT WOS:A1995BE66U00006 ER PT J AU COATES, RJ GREENBERG, RS LIU, MT CORREA, P HARLAN, LC REYNOLDS, P FENOGLIOPREISER, CM HAYNES, MA HANKEY, BF HUNTER, CP EDWARDS, BK AF COATES, RJ GREENBERG, RS LIU, MT CORREA, P HARLAN, LC REYNOLDS, P FENOGLIOPREISER, CM HAYNES, MA HANKEY, BF HUNTER, CP EDWARDS, BK TI ANATOMIC SITE DISTRIBUTION OF COLON-CANCER BY RACE AND OTHER COLON-CANCER RISK-FACTORS SO DISEASES OF THE COLON & RECTUM LA English DT Article DE COLON CANCER; SUBSITE; RACE; BLACKS; DIET; PARITY; HISTOLOGIC TYPE; GRADE ID LARGE-BOWEL-CANCER; MELBOURNE COLORECTAL-CANCER; SEX-DIFFERENCES; AGE; POPULATION; SUBSITE; EPIDEMIOLOGY; CARCINOMAS; ADENOMAS AB PURPOSE: Black patients with colon cancer are more likely to have poorer survival from colon cancer than are white patients. To determine whether anatomic site differences might contribute to survival differences, we compared anatomic site distributions of black and white patients. METHODS: As part of the Black/White Cancer Survival Study, we collected medical record data for 1,045 patients from Atlanta, New Orleans, and San Francisco/Oakland, newly diagnosed in 1985 or 1986 and interviewed 745 of them. RESULTS: In polychotomous logistic regression analysis, site was related to stage, grade, and histologic type and among women with age, parity, and possibly smoking. However, it was not related to race, except perhaps among men age 65 and older, among whom blacks were somewhat likely to have more transverse and distal, not proximal, cancer. These relations were consistent across subgroups and were independent of other factors examined. CONCLUSION: Results suggest that site differences are unlikely to contribute to poorer survival commonly observed among black colon cancer patients in the United States. C1 LOUISIANA STATE UNIV,DEPT PATHOL,NEW ORLEANS,LA. NCI,DIV CANC PREVENT & CONTROL,ROCKVILLE,MD. CALIF DEPT HLTH SERV,EMERYVILLE,CA. UNIV CINCINNATI,MED CTR,DEPT PATHOL & LAB MED,CINCINNATI,OH. RP COATES, RJ (reprint author), EMORY UNIV,ROLLINS SCH PUBL HLTH,DEPT EPIDEMIOL,DIV EPIDEMIOL,1518 CLIFTON RD NE,ATLANTA,GA 30322, USA. FU NCI NIH HHS [CN-35042-46, N01CN-45174, N01CN-05227] NR 63 TC 21 Z9 22 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0012-3706 J9 DIS COLON RECTUM JI Dis. Colon Rectum PD JAN PY 1995 VL 38 IS 1 BP 42 EP 50 DI 10.1007/BF02053856 PG 9 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA QD528 UT WOS:A1995QD52800009 PM 7813344 ER PT S AU LONDON, ED MUKHIN, A AF LONDON, ED MUKHIN, A BE Abood, LG Lajtha, A TI POLYAMINES AS ENDOGENOUS MODULATORS OF THE N-METHYL-D-ASPARTATE RECEPTOR SO DIVERSITY OF INTERACTING RECEPTORS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Functional Diversity of Interacting Receptors CY MAY 25-28, 1994 CL WASHINGTON, DC SP New York Acad Sci ID CENTRAL NERVOUS-SYSTEM; H-3 MK-801 BINDING; RAT-BRAIN; RECOGNITION SITE; XENOPUS OOCYTES; SPERMINE; COMPLEX; MK-801; IFENPRODIL; GLUTAMATE C1 JOHNS HOPKINS MED INST,DEPT RADIOL,BALTIMORE,MD 21205. UNIV MARYLAND,SCH MED,DEPT PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21201. RP LONDON, ED (reprint author), NIDA,DIV INTRAMURAL RES,INTRAMURAL RES PROGRAM,NEUROIMAGING & DRUG ACT SECT,POB 5180,BALTIMORE,MD 21224, USA. NR 26 TC 8 Z9 8 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-924-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 757 BP 430 EP 436 DI 10.1111/j.1749-6632.1995.tb17502.x PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics GA BD16W UT WOS:A1995BD16W00043 PM 7611700 ER PT J AU MEINSMA, R FERNANDEZSALGUERO, P VANKUILENBURG, ABP VANGENNIP, AH GONZALEZ, FJ AF MEINSMA, R FERNANDEZSALGUERO, P VANKUILENBURG, ABP VANGENNIP, AH GONZALEZ, FJ TI HUMAN POLYMORPHISM IN DRUG-METABOLISM - MUTATION IN THE DIHYDROPYRIMIDINE DEHYDROGENASE GENE RESULTS IN EXON SKIPPING AND THYMINE URACILUREA SO DNA AND CELL BIOLOGY LA English DT Article ID SEVERE 5-FLUOROURACIL TOXICITY; FAMILIAL PYRIMIDINEMIA; MONONUCLEAR-CELLS; CANCER-PATIENTS; DEFICIENCY; FLUOROURACIL; DEGRADATION; BLOOD AB A condition called thymine uracilurea has been described that is due to a lack of dihydropyrimidine dehydrogenase (DPD) activity. Cancer patients experiencing acute 5-fluorouracil toxicity also have lower-than-normal DPD activities. However, to date, the molecular basis of this disorder has not been addressed. In this study, the phenotype and genotype of a family that presents a patient showing no DPD activity was determined. Fibroblast mRNAs from the patient and four family members were subjected to reverse transcriptase polymerase chain reaction (RT-PCR) using primers generated from the human DPD cDNA sequence. DPD mRNA from the patient was found to lack a segment of 165 nucleotides that results from exon skipping. DPD mRNA from the parents and a sibling were found to be heterozygous for the deleted and the normal mRNA, while a brother had two normal transcripts. DPD activities and levels of DPD protein correlated with genotype; the deficient patient had no detectable DPD protein. PCR analysis of the genomic DNA from this family revealed that the defective mRNA is not due to a deletion of a portion of the gene that contains the exon, thus implying that the mutation is the result of an as yet nonidentified point mutation that causes faulty splicing. C1 UNIV AMSTERDAM,ACAD MED CTR,DEPT PEDIAT,1100 DE AMSTERDAM,NETHERLANDS. UNIV AMSTERDAM,ACAD MED CTR,DEPT CLIN CHEM,1100 DE AMSTERDAM,NETHERLANDS. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. OI Fernandez-Salguero, Pedro M./0000-0003-2839-5027 NR 23 TC 83 Z9 86 U1 0 U2 1 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 JAN PY 1995 VL 14 IS 1 BP 1 EP 6 DI 10.1089/dna.1995.14.1 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA QD520 UT WOS:A1995QD52000001 PM 7832988 ER PT B AU BRODER, S AF BRODER, S BE Cooper, GM Temin, RG Sugden, B TI Progress in the molecular medicine of cancer SO DNA PROVIRUS: HOWARD TEMIN'S SCIENTIFIC LEGACY LA English DT Proceedings Paper CT Howard Temin Commemorative Symposium - DNA Provirus CY OCT 13-15, 1994 CL MADISON, WI C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVE NW, WASHINGTON, DC 20005-4171 BN 1-55581-098-5 PY 1995 BP 129 EP 152 PG 24 WC Oncology; Genetics & Heredity; Microbiology; Virology SC Oncology; Genetics & Heredity; Microbiology; Virology GA BE26J UT WOS:A1995BE26J00010 ER PT B AU VARMUS, H AF VARMUS, H BE Cooper, GM Temin, RG Sugden, B TI Under the influence: From the provirus hypothesis to multistep carcinogenesis SO DNA PROVIRUS: HOWARD TEMIN'S SCIENTIFIC LEGACY LA English DT Proceedings Paper CT Howard Temin Commemorative Symposium - DNA Provirus CY OCT 13-15, 1994 CL MADISON, WI C1 NIH,OFF DIRECTOR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVE NW, WASHINGTON, DC 20005-4171 BN 1-55581-098-5 PY 1995 BP 185 EP 188 PG 4 WC Oncology; Genetics & Heredity; Microbiology; Virology SC Oncology; Genetics & Heredity; Microbiology; Virology GA BE26J UT WOS:A1995BE26J00013 ER PT B AU GALLO, RC AF GALLO, RC BE Cooper, GM Temin, RG Sugden, B TI Human retroviruses in the second decade: Some pathogenic mechanisms and approaches to their control SO DNA PROVIRUS: HOWARD TEMIN'S SCIENTIFIC LEGACY LA English DT Proceedings Paper CT Howard Temin Commemorative Symposium - DNA Provirus CY OCT 13-15, 1994 CL MADISON, WI C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVE NW, WASHINGTON, DC 20005-4171 BN 1-55581-098-5 PY 1995 BP 247 EP 269 PG 23 WC Oncology; Genetics & Heredity; Microbiology; Virology SC Oncology; Genetics & Heredity; Microbiology; Virology GA BE26J UT WOS:A1995BE26J00017 ER PT J AU Clark, AD JacoboMolina, A Clark, P Hughes, SH Arnold, E AF Clark, AD JacoboMolina, A Clark, P Hughes, SH Arnold, E TI Crystallization of human immunodeficiency virus type 1 reverse transcriptase with and without nucleic acid substrates, inhibitors, and an antibody fab fragment SO DNA REPLICATION SE METHODS IN ENZYMOLOGY LA English DT Review ID DOUBLE-STRANDED DNA; ANGSTROM RESOLUTION; CRYSTAL-STRUCTURE; ESCHERICHIA-COLI; TIBO DERIVATIVES; COMPLEX; RESISTANCE; INVITRO; EXPRESSION; MUTATIONS C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD 21701. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. RP Clark, AD (reprint author), RUTGERS STATE UNIV,CTR ADV BIOTECHNOL & MED,PISCATAWAY,NJ 08854, USA. FU NCI NIH HHS [N01-CO-74101] NR 35 TC 21 Z9 21 U1 0 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 262 BP 171 EP 185 PG 17 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA BE40P UT WOS:A1995BE40P00015 PM 8594346 ER PT S AU Bebenek, K Kunkel, TA AF Bebenek, K Kunkel, TA BE Campbell, JL TI Analyzing fidelity of DNA polymerases SO DNA REPLICATION SE Methods in Enzymology LA English DT Review ID MUTATIONAL SPECIFICITY; INSERTION FIDELITY; ESCHERICHIA-COLI; INVITRO; MUTAGENESIS; FRAMESHIFT; FRAGMENT; ASSAY RP NIEHS, MOLEC GENET LAB, RES TRIANGLE PK, NC 27709 USA. NR 19 TC 180 Z9 181 U1 0 U2 6 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 0-12-182163-3 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 262 BP 217 EP 232 PG 16 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA BE40P UT WOS:A1995BE40P00018 PM 8594349 ER PT J AU Capson, TL Benkovic, SJ Nossal, NG AF Capson, TL Benkovic, SJ Nossal, NG TI Photochemical cross-linking of DNA replication proteins at primer terminus SO DNA REPLICATION SE METHODS IN ENZYMOLOGY LA English DT Review ID ACCESSORY PROTEINS; SACCHAROMYCES-CEREVISIAE; POLYMERASE; IDENTIFICATION; COMPLEX; 5'-TRIPHOSPHATE; TEMPLATE; SUBUNIT; ACIDS; GENE C1 PENN STATE UNIV,DEPT CHEM,UNIVERSITY PK,PA 16802. NIDDKD,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. RP Capson, TL (reprint author), UNIV UTAH,DEPT CHEM,SALT LAKE CITY,UT 84132, USA. NR 23 TC 3 Z9 3 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 262 BP 449 EP 456 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA BE40P UT WOS:A1995BE40P00034 PM 8594369 ER PT J AU Nossal, NG Hinton, DM Hobbs, LJ Spacciapoli, P AF Nossal, NG Hinton, DM Hobbs, LJ Spacciapoli, P TI Purification of bacteriophage T4 DNA replication proteins SO DNA REPLICATION SE METHODS IN ENZYMOLOGY LA English DT Review ID ESCHERICHIA-COLI; ACCESSORY PROTEINS; GENE-41 PROTEIN; RNA-POLYMERASE; ATP HYDROLYSIS; EXPRESSED PROTEIN; PRIMASE-HELICASE; PRIMER-TEMPLATE; LEADING-STRAND; INVITRO RP Nossal, NG (reprint author), NIDDKD,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 61 TC 34 Z9 34 U1 1 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 262 BP 560 EP 584 PG 25 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA BE40P UT WOS:A1995BE40P00043 PM 8594379 ER PT J AU SETO, D SETO, J DESHPANDE, P HOOD, L AF SETO, D SETO, J DESHPANDE, P HOOD, L TI DMSO RESOLVES CERTAIN COMPRESSIONS AND SIGNAL DROPOUTS IN FLUORESCENT DYE-LABELED PRIMER-BASED DNA-SEQUENCING REACTIONS SO DNA SEQUENCE LA English DT Article DE DMSO; DNA; FLUORESCENCE; SEQUENCING; COMPRESSIONS; SIGNAL DROPOUTS ID POLYMERASE; IMPROVEMENT; RESOLUTION; IONS AB Automated base calling algorithms are more sensitive to the quality of the DNA sequencing data than are the labor intensive visual methods of base calling. To improve this quality, data from DNA sequencing reactions halle been compared in order to determine the effects of the inclusion of dimethyl sulfoxide (DMSO). Inclusion of 10% DMSO into the reaction cocktail resolves at least one type of sequence compression. This compression may be due to the lack of ability in T7 DNA polymerase to read through certain sequences correctly. The poor quality of these data is seen as radioactive bands or fluorescent signal peaks that have an abnormal alignment, either in the wrong order or as single bands/peaks. The inclusion of DMSO also resolves sequences where the peak signal is absent or severely diminished, leading to a ''gap'' in the chromatogram profile. DMSO is better than deaza-dITP for resolving certain compressions. Addition of DMSO is a cheaper and more efficient method for high-throughput DNA sequencing than repeating reactions with base analogs. C1 UNIV WASHINGTON,DEPT MOLEC BIOTECHNOL FJ20,SEATTLE,WA 98195. CALTECH,DIV BIOL 14775,PASADENA,CA 91125. NIDDK,BETHESDA,MD 20892. FU NHGRI NIH HHS [HG00356]; NIGMS NIH HHS [GM 13039] NR 31 TC 10 Z9 10 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-5179 J9 DNA SEQUENCE JI DNA Seq. PY 1995 VL 5 IS 3 BP 131 EP & DI 10.3109/10425179509029352 PG 0 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QL807 UT WOS:A1995QL80700001 PM 7612923 ER PT J AU BRADY, JP PIATIGORSKY, J AF BRADY, JP PIATIGORSKY, J TI A NOVEL CDNA ISOLATED FROM THE MOUSE EYE LENS ENCODING A PROTEIN WITH ZINC FINGERS AND A KRAB DOMAIN SO DNA SEQUENCE LA English DT Note DE KRAB DOMAIN; LENS; MOUSE; NUCLEOTIDE SEQUENCE; PCR; ZINC FINGERS ID GENE; KRUPPEL; FAMILY AB A cDNA clone, pMLZ-8, was isolated from a newborn mouse eye lens cDNA library using a consensus zinc finger oligonucleotide hybridization probe. The cDNA contains an open reading frame that conceptually encodes a 606 amino acid protein. The protein possesses a ''KRAB'' domain at its amino-terminus and has a carboxy-terminal region with fifteen consensus C2H2 zinc fingers. PCR analysis reveals the presence of pMLZ-8 mRNA in lens, liver, kidney, spleen, and brain of newborn mice. C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 17 TC 2 Z9 2 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-5179 J9 DNA SEQUENCE JI DNA Seq. PY 1995 VL 5 IS 6 BP 389 EP 392 DI 10.3109/10425179509020871 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA TB219 UT WOS:A1995TB21900008 PM 8777319 ER PT S AU NIRENBERG, M NAKAYAMA, K NAKAYAMA, N KIM, Y MELLERICK, D WANG, LH WEBBER, KO LAD, R AF NIRENBERG, M NAKAYAMA, K NAKAYAMA, N KIM, Y MELLERICK, D WANG, LH WEBBER, KO LAD, R BE Chambers, DA TI THE NK-2 HOMEOBOX GENE AND THE EARLY DEVELOPMENT OF THE CENTRAL-NERVOUS-SYSTEM OF DROSOPHILA SO DNA: THE DOUBLE HELIX: PERSPECTIVE AND PROSPECTIVE AT FORTY YEARS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on DNA: The Double Helix - Forty Years, Perspective and Prospective CY OCT 13-16, 1993 CL CHICAGO, IL SP New York Acad Sci, Univ Illinois Chicago, Green Coll, Univ Oxford ID SINGLE-MINDED GENE; DORSAL VENTRAL AXIS; LOOP-HELIX PROTEINS; OF-SPLIT COMPLEX; TRANSCRIPTIONAL REGULATION; NUCLEAR-LOCALIZATION; EARLY NEUROGENESIS; PATTERN-FORMATION; DEPENDENT MANNER; PROGENITOR CELLS C1 NHLBI, MOLEC CARDIOL LAB, BETHESDA, MD 20892 USA. KANAZAWA UNIV, CANC RES INST, DEPT IMMUNOBIOL, KANAZAWA, ISHIKAWA 920, JAPAN. NCI, MOLEC BIOL LAB, BETHESDA, MD 20892 USA. HOSP UNIV PENN, DEPT PSYCHIAT, PHILADELPHIA, PA 19104 USA. RP NHLBI, BIOCHIM GENET LAB, BLDG 10, BETHESDA, MD 20892 USA. NR 80 TC 30 Z9 31 U1 1 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-906-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 758 BP 224 EP 242 DI 10.1111/j.1749-6632.1995.tb24830.x PG 19 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics GA BD16X UT WOS:A1995BD16X00025 PM 7625694 ER PT S AU PASTAN, IH PAI, LH BRINKMANN, U FITZGERALD, DJ AF PASTAN, IH PAI, LH BRINKMANN, U FITZGERALD, DJ BE Chambers, DA TI RECOMBINANT TOXINS - NEW THERAPEUTIC AGENTS FOR CANCER SO DNA: THE DOUBLE HELIX: PERSPECTIVE AND PROSPECTIVE AT FORTY YEARS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on DNA: The Double Helix - Forty Years, Perspective and Prospective CY OCT 13-16, 1993 CL CHICAGO, IL SP New York Acad Sci, Univ Illinois Chicago, Green Coll, Univ Oxford ID PSEUDOMONAS EXOTOXIN; IMMUNOTOXINS; DOMAINS; B3 RP PASTAN, IH (reprint author), NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BLDG 37,ROOM 4E16,BETHESDA,MD 20892, USA. NR 10 TC 42 Z9 43 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-906-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 758 BP 345 EP 354 DI 10.1111/j.1749-6632.1995.tb24840.x PG 10 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics GA BD16X UT WOS:A1995BD16X00033 PM 7625703 ER PT J AU COMPTON, WM LAMB, RJ FLETCHER, BW AF COMPTON, WM LAMB, RJ FLETCHER, BW TI RESULTS OF THE NIDA TREATMENT DEMONSTRATION GRANTS COCAINE WORKGROUP - CHARACTERISTICS OF COCAINE USERS AND HIV RISK BEHAVIORS SO DRUG AND ALCOHOL DEPENDENCE LA English DT Editorial Material DE COCAINE; HIV RISK BEHAVIOR; SUBSTANCE ABUSE AB This journal issue includes seven articles (six plus this introduction) from the ''cocaine workgroup'' of the National Institute on Drug Abuse (NIDA) treatment demonstration grants. In this introduction, results of the first attempts to compare data from seven disparate demonstration grant sites are summarized: Overall, rates of recent cocaine use were high in all locations, injection drug use was common, age of first drug use was between 14 and 17 years with age of first cocaine use between 20 and 25 years, arrests were common at all sites especially among cocaine injectors, and polydrug use was the norm. Interestingly, both gender and ethnic status were significantly associated with polydrug use and marijuana use among the cocaine users. These results indicated that it is possible to define variables precisely for analysis across sites and laid the groundwork for the next set of analyses in which the common theme of human immunodeficiency virus (HIV) risk behaviors among cocaine abusers was agreed upon. This next set of analyses are included in the following six papers. Overall, these reports confirm recent data about the association of cocaine use with HIV risk behaviors. They extend considerably the literature on the association of cocaine with HIV risk behaviors, and the report from New York in which therapeutic community treatment was shown to be feasible and possibly useful to methadone clients represents an interesting and new finding. In conclusion, cross-site collaborations can take different forms and this collection of papers represents one successful approach C1 MED COLL PENN,DEPT MENTAL HLTH SCI,PHILADELPHIA,PA 19129. HAHNEMANN UNIV,PHILADELPHIA,PA 19102. NIDA,ROCKVILLE,MD. RP COMPTON, WM (reprint author), WASHINGTON UNIV,SCH MED,DEPT PSYCHIAT,ST LOUIS,MO 63110, USA. NR 16 TC 13 Z9 14 U1 0 U2 1 PU ELSEVIER SCI PUBL IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0376-8716 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD JAN PY 1995 VL 37 IS 1 BP 1 EP 6 DI 10.1016/0376-8716(94)01061-O PG 6 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA QC705 UT WOS:A1995QC70500001 PM 7882868 ER PT J AU GILLETTE, JR AF GILLETTE, JR TI KEYNOTE ADDRESS - MAN, MICE, MICROSOMES, METABOLITES, AND MATHEMATICS 40 YEARS AFTER THE REVOLUTION SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium on Drug Metabolism as a Cause of Drug Toxicity, Honoring the Research Contributions of Dr James R Gillette CY OCT 14-15, 1993 CL LITTLE ROCK, AR SP DOROTHY SNIDER FDN ID INDUCED HEPATIC NECROSIS; CHEMICALLY REACTIVE METABOLITES; RAT-LIVER MICROSOMES; HALOTHANE-INDUCED HEPATOTOXICITY; COVALENT BINDING; CARBON-TETRACHLORIDE; GLUTATHIONE DEPLETION; ORTHO-BROMOPHENOL; PROTECTIVE ROLE; TESTICULAR CYTOCHROME-P-450 RP GILLETTE, JR (reprint author), NHLBI,CHEM PHARMACOL LAB,BLDG 10,ROOM 8 N 117,BETHESDA,MD 20892, USA. NR 247 TC 9 Z9 9 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1995 VL 27 IS 1-2 BP 1 EP 44 DI 10.3109/03602539509029813 PG 44 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA RB667 UT WOS:A1995RB66700001 PM 7641571 ER PT J AU KORZEKWA, KR GILLETTE, JR TRAGER, WF AF KORZEKWA, KR GILLETTE, JR TRAGER, WF TI ISOTOPE EFFECT STUDIES ON THE CYTOCHROME-P450 ENZYMES SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium on Drug Metabolism as a Cause of Drug Toxicity, Honoring the Research Contributions of Dr James R Gillette CY OCT 14-15, 1993 CL LITTLE ROCK, AR SP DOROTHY SNIDER FDN ID CATALYZED HYDROXYLATION; ALIPHATIC HYDROXYLATION; TESTOSTERONE; DEMETHYLATION; METABOLITE; MECHANISMS; OXIDATION; PROTEINS; SYSTEMS; ANISOLE C1 NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. UNIV WASHINGTON,DEPT MED CHEM,SEATTLE,WA 98195. RP KORZEKWA, KR (reprint author), NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 26 TC 17 Z9 17 U1 0 U2 3 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1995 VL 27 IS 1-2 BP 45 EP 59 DI 10.3109/03602539509029814 PG 15 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA RB667 UT WOS:A1995RB66700002 PM 7641584 ER PT J AU OSAWA, Y DAVILA, JC NAKATSUKA, M MEYER, CA DARBYSHIRE, JF AF OSAWA, Y DAVILA, JC NAKATSUKA, M MEYER, CA DARBYSHIRE, JF TI INHIBITION OF P450 CYTOCHROMES BY REACTIVE INTERMEDIATES SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium on Drug Metabolism as a Cause of Drug Toxicity, Honoring the Research Contributions of Dr James R Gillette CY OCT 14-15, 1993 CL LITTLE ROCK, AR SP DOROTHY SNIDER FDN ID NITRIC-OXIDE SYNTHASE; CARBON-TETRACHLORIDE; COVALENT BINDING; PROSTHETIC HEME; IMINIUM ION; METABOLISM; PHENCYCLIDINE; INACTIVATION; BRCCL3; LIVER RP OSAWA, Y (reprint author), NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892, USA. NR 43 TC 20 Z9 20 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1995 VL 27 IS 1-2 BP 61 EP 72 DI 10.3109/03602539509029815 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA RB667 UT WOS:A1995RB66700003 PM 7641585 ER PT J AU MARTIN, JL MEINWALD, J RADFORD, P LIU, Z GRAF, MLM POHL, LR AF MARTIN, JL MEINWALD, J RADFORD, P LIU, Z GRAF, MLM POHL, LR TI STEREOSELECTIVE METABOLISM OF HALOTHANE ENANTIOMERS TO TRIFLUOROACETYLATED LIVER PROTEINS SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium on Drug Metabolism as a Cause of Drug Toxicity, Honoring the Research Contributions of Dr James R Gillette CY OCT 14-15, 1993 CL LITTLE ROCK, AR SP DOROTHY SNIDER FDN ID ISOFLURANE ANESTHESIA; HEPATITIS PATIENTS; SERUM ANTIBODIES; ENFLURANE; RAT; BIOTRANSFORMATION; HEPATOTOXICITY; STEREOISOMERS; CHILDREN; ANTIGENS C1 JOHNS HOPKINS MED INST,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21287. CORNELL UNIV,DEPT CHEM,ITHACA,NY 14853. RP MARTIN, JL (reprint author), NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892, USA. FU NIGMS NIH HHS [GM 48088A] NR 61 TC 13 Z9 13 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1995 VL 27 IS 1-2 BP 179 EP 189 DI 10.3109/03602539509029822 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA RB667 UT WOS:A1995RB66700009 PM 7641575 ER PT J AU PARDHASARADHI, K KUTTY, RK BERTOLOTTI, R KRISHNA, G AF PARDHASARADHI, K KUTTY, RK BERTOLOTTI, R KRISHNA, G TI EXPRESSION OF MESSENGER-RNA FOR ATRIAL-NATRIURETIC-PEPTIDE RECEPTOR-A IN HUMAN LIVER - DETECTION USING RT-PCR SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium on Drug Metabolism as a Cause of Drug Toxicity, Honoring the Research Contributions of Dr James R Gillette CY OCT 14-15, 1993 CL LITTLE ROCK, AR SP DOROTHY SNIDER FDN ID GUANYLATE-CYCLASE; VASORELAXANT ACTIVITY; TISSUES C1 NHLBI,CHEM PHARMACOL LAB,DRUG TISSUE INTERACT SECT,BETHESDA,MD 20892. NR 19 TC 4 Z9 4 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1995 VL 27 IS 1-2 BP 231 EP 239 DI 10.3109/03602539509029824 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA RB667 UT WOS:A1995RB66700011 PM 7641577 ER PT J AU RAVINDRANATH, V BOYD, MR AF RAVINDRANATH, V BOYD, MR TI XENOBIOTIC METABOLISM IN BRAIN SO DRUG METABOLISM REVIEWS LA English DT Review ID FLAVIN-CONTAINING MONOOXYGENASE; FUNCTION OXIDASE SYSTEM; ARYL-HYDROCARBON HYDROXYLASE; AMINOPYRINE N-DEMETHYLASE; SEX-RELATED DIFFERENCE; CENTRAL-NERVOUS-SYSTEM; RAT-BRAIN; REGIONAL DISTRIBUTION; SUBCELLULAR-FRACTIONS; PARKINSONS-DISEASE C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,DRUG DIS RES & DEV LAB,FREDERICK,MD 21702. RP RAVINDRANATH, V (reprint author), NATL INST MENTAL HLTH & NEUROSCI,DEPT NEUROCHEM,HOSUR RD,BANGALORE 560029,KARNATAKA,INDIA. NR 117 TC 47 Z9 47 U1 1 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1995 VL 27 IS 3 BP 419 EP 448 DI 10.3109/03602539508998330 PG 30 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA RT291 UT WOS:A1995RT29100002 PM 8521749 ER PT J AU SINHA, BK AF SINHA, BK TI TOPOISOMERASE INHIBITORS - A REVIEW OF THEIR THERAPEUTIC POTENTIAL IN CANCER SO DRUGS LA English DT Review ID DNA STRAND BREAKS; FREE-RADICALS; LUNG-CANCER; CELL LINES; PHASE-II; CAMPTOTHECIN; CYTOTOXICITY; ETOPOSIDE; RESISTANCE; MECHANISM AB The nuclear enzymes topoisomerase I and II are critical for DNA function and cell survival, and recent studies have identified these enzymes as cellular targets for several clinically active anticancer drugs. Topoisomerase II inhibitors (anthracyclines, epipodophyllotoxins, etc.) are active against several types of tumours. However, treatment with these drugs often results in the development of the multi-drug resistance. Because topoisomerase II-active drugs have several different modes of action, different mechanisms of resistance, including decreased activation and increased detoxification by glutathione-dependent enzymes, have also been implicated. Unlike topoisomerase II, topoisomerase I is not a cell cycle-dependent enzyme and, therefore, it is a more desirable cellular target for anticancer drug development. Topoisomerase I inhibitors, such as camptothecin and its derivatives, have shown significant activity against a broad range of tumours and, in general, are not substrates for either the multi-drug-resistance P-170 glycoprotein or the multi-drug-resistance-associated protein. Because of manageable toxicity and encouraging activity against solid tumours, topoisomerase I-active drugs offer promise in the clinical management of human tumours. RP SINHA, BK (reprint author), NCI,CLIN PHARMACOL BRANCH,BIOCHEM & MOLEC PHARMACOL SECT,BLDG 10,ROOM 6N-119,BETHESDA,MD 20892, USA. NR 53 TC 137 Z9 146 U1 0 U2 9 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 0012-6667 J9 DRUGS JI Drugs PD JAN PY 1995 VL 49 IS 1 BP 11 EP 19 PG 9 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA QB443 UT WOS:A1995QB44300002 PM 7705211 ER PT J AU DOMANSKI, MJ COLLERAN, JA CUNNION, RE NANDA, NC AF DOMANSKI, MJ COLLERAN, JA CUNNION, RE NANDA, NC TI CORRELATION OF ECHOCARDIOGRAPHIC NORMALIZED PEAK RATE OF LEFT-VENTRICULAR AREA EXPANSION WITH RADIONUCLIDE PEAK FILLING RATE SO ECHOCARDIOGRAPHY-A JOURNAL OF CARDIOVASCULAR ULTRASOUND AND ALLIED TECHNIQUES LA English DT Article DE CARDIAC IMAGING; ECHOCARDIOGRAPHY; DIASTOLIC FUNCTION; PEAK FILLING RATE AB The purpose of this study was to determine whether normalized peak rate of left ventricular area expansion during diastole, as obtained from echocardiography using the parasternal short-axis view, correlates well with left ventricular diastolic peak filling rate, as determined from radionuclide ventriculography. Normalized peak rate of area expansion, readily calculated from tracings of the ventricular endocardium on sequential echocardiographic image frames, can be measured rapidly, non-invasively, repeatedly, and without radiation exposure. The advent of automated edge detection systems that permit continuous, on line display of ventricular areas may further enhance the utility of this technique. Twenty-four patients with and without regional wall-motion abnormalities who had both echocardiography and radionuclide ventriculography as part of their clinical care were analyzed. Comparing normalized peak rate of area expansion with peak filling rate, the correlation coefficient was 0.86 (P < 0.001). These findings suggest that echocardiographically derived normalized peak area expansion measured in the parasternal short-axis view is an excellent measure of global diastolic function. RP DOMANSKI, MJ (reprint author), NHLBI,CLIN TRIALS BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 0742-2822 J9 ECHOCARDIOGR-J CARD JI Echocardiogr.-J. Cardiovasc. Ultrasound Allied Techn. PD JAN PY 1995 VL 12 IS 1 BP 23 EP 27 DI 10.1111/j.1540-8175.1995.tb00517.x PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QC372 UT WOS:A1995QC37200003 ER PT J AU GALANIS, DJ CHINHONG, PV MCGARVEY, ST MESSER, E PARKINSON, D AF GALANIS, DJ CHINHONG, PV MCGARVEY, ST MESSER, E PARKINSON, D TI DIETARY-INTAKE CHANGES ASSOCIATED WITH POST-CYCLONE FOOD AID IN WESTERN-SAMOA SO ECOLOGY OF FOOD AND NUTRITION LA English DT Article DE WESTERN SAMOA; FOOD AID; RELIEF PROGRAMS; DIETARY INTAKE; NATURAL DISASTERS ID CHILDREN AB This study examines dietary intake responses to a food aid program in Western Samoa, which consisted primarily of rice and flour supplements. Using a semi-quantitative food frequency questionnaire, intake estimates were made for 147 Samoans (72 men, 75 women), 5 months before and 8 months after a tropical cyclone. Study participants were from urban Apia (n = 34) and three rural, more traditional villages (n = 113). For the total sample, consumption of rice and pancakes more than doubled, and the contribution of these foods to total carbohydrate and kilocalorie intake increased approximately three-fold (p < 0.0001, for paired t-tests). Significant decreases were noted for the nutrient contribution from breadfruit and coconut products. These dietary changes were significantly less in the urban sub-sample. These results indicate the food aid may have accelerated an existing modernizing trend in the diet of Samoans. The nutritional and economic implications are discussed within the context of Western Samoa. C1 BROWN UNIV,MIRIAM HOSP,PROGRAM GEOG MED,PROVIDENCE,RI 02906. BROWN UNIV,WORLD HUNGER PROGRAM,PROVIDENCE,RI 02912. WHO,APIA,WESTERN SAMOA. RP GALANIS, DJ (reprint author), NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,7201 WISCONSIN AVE,GATEWAY BLDG,SUITE 3C-309,BETHESDA,MD 20892, USA. RI McGarvey, Stephen/I-1788-2014 NR 25 TC 6 Z9 6 U1 0 U2 3 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0367-0244 J9 ECOL FOOD NUTR JI Ecol. Food Nutr. PY 1995 VL 34 IS 2 BP 137 EP 147 PG 11 WC Nutrition & Dietetics SC Nutrition & Dietetics GA TD566 UT WOS:A1995TD56600005 ER PT B AU HENNINGFIELD, JE SCHUH, LM HEISHMAN, SJ AF HENNINGFIELD, JE SCHUH, LM HEISHMAN, SJ BE Clarke, PBS Quik, M Adlkofer, F Thurau, K TI Pharmacological determinants of cigarette smoking SO EFFECTS OF NICOTINE ON BIOLOGICAL SYSTEMS II SE ADVANCES IN PHARMACOLOGICAL SCIENCES LA English DT Proceedings Paper CT Satellite Symposium on The Effects of Nicotine on Biological Systems II, at the Congress of the International-Union-of-Pharmacology CY JUL 21-24, 1994 CL SAINTE ADELE, CANADA SP INT UNION PHARM, VERUM FDN RP NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIRKHAUSER VERLAG PI BASEL PA PO BOX 133, CH-4010 BASEL, SWITZERLAND BN 3-7643-5083-0 J9 ADV PHAR SC PY 1995 BP 247 EP 256 PG 10 WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy GA BC71W UT WOS:A1995BC71W00032 ER PT S AU LONG, LR BERMAN, LE THOMA, GR AF LONG, LR BERMAN, LE THOMA, GR GP IEEE TI Client/server design for fast retrieval of large images on the internet SO EIGHTH IEEE SYMPOSIUM ON COMPUTER-BASED MEDICAL SYSTEMS SE COMPUTER-BASED MEDICAL SYSTEMS : PROCEEDINGS OF THE ANNUAL IEEE SYMPOSIUM LA English DT Proceedings Paper CT 8th IEEE Symposium on Computer-Based Medical Systems CY JUN 09-10, 1995 CL LUBBOCK, TX SP IEEE Comp Soc Tech Comm Computat Med, IEEE S Plains Sect, SPIE Int Soc Opt Engn C1 NATL LIB MED,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU I E E E, COMPUTER SOC PRESS PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, LOS ALAMITOS, CA 90720 SN 1063-7125 BN 0-8186-7117-3 J9 COMP MED SY PY 1995 BP 284 EP 291 DI 10.1109/CBMS.1995.465414 PG 8 WC Computer Science, Interdisciplinary Applications; Engineering, Biomedical SC Computer Science; Engineering GA BD65R UT WOS:A1995BD65R00041 ER PT J AU PASH, JM DELANY, AM ADAMO, ML ROBERTS, CT LEROITH, D CANALIS, E AF PASH, JM DELANY, AM ADAMO, ML ROBERTS, CT LEROITH, D CANALIS, E TI REGULATION OF INSULIN-LIKE GROWTH-FACTOR-I TRANSCRIPTION BY PROSTAGLANDIN E(2) IN OSTEOBLAST CELLS SO ENDOCRINOLOGY LA English DT Article ID GENE PROMOTER; LEADER EXONS; CULTURES; BONE; EXPRESSION; ACID AB Insulin-like growth factor I (IGF-I) is a widely expressed abundant autocrine and paracrine factor that regulates the proliferation and differentiation of a variety of cell types. Prostaglandin E(2) (PGE(2)) is a potent stimulator of IGF-I synthesis in bone. We examined the regulation of IGF-I synthesis by PGE(2) in osteoblast-enriched (Ob) cells from fetal rat calvaria. PGE(2) treatment of Ob cells at 1 mu M for 2 h resulted in a 5-fold increase in heterogeneous nuclear RNA levels, as measured by a reverse transcriptase-polymerase chain reaction assay, suggesting an increase in IGF-I gene transcription. RNase protection analysis was used to map the transcriptional start sites in the IGF-I gene that are used in Ob cells. Consistent with other extrahepatic tissues, initiation of transcription occurs primarily at three sites within the 5'-regions of exon 1 of the IGF-I gene. PGE(2) treatment did not alter start site usage. The regions upstream of these transcriptional start sites were analyzed by transiently transfecting Ob cells with putative rat IGF-I promoter sequences ligated to a luciferase reporter gene. Constructs containing 1.4 kilobases of the 5'-regions of exons 1 and 2 had significant promoter activity. PGE(2) treatment of transfected Ob cells increased luciferase activity 5-fold when a 1.4-kilobase exon 1 promoter fragment was tested. This increase in luciferase activity was time and dose dependent. Smaller regions of the exon 1 promoter sequence gave higher basal activity and were less responsive to PGE(2). We conclude that regions involved in IGF-I regulation by PGE(2) are contained within the EGF-I promoter. C1 ST FRANCIS HOSP & MED CTR, DEPT MED, HARTFORD, CT 06105 USA. UNIV CONNECTICUT, SCH MED, FARMINGTON, CT 06030 USA. UNIV TEXAS, HLTH SCI CTR, DEPT BIOCHEM, SAN ANTONIO, TX 78284 USA. NIDDKD, DIABET BRANCH, MOLECULAR & CELLULAR PHYSIOL SECT, BETHESDA, MD 20892 USA. RP PASH, JM (reprint author), ST FRANCIS HOSP & MED CTR, DEPT RES, 114 WOODLAND ST, HARTFORD, CT 06105 USA. FU NIDDK NIH HHS [DK-42424, DK-45277] NR 20 TC 43 Z9 42 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1995 VL 136 IS 1 BP 33 EP 38 DI 10.1210/en.136.1.33 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QD584 UT WOS:A1995QD58400006 PM 7828549 ER PT J AU CROWLEY, RS INSEL, TR OKEEFE, JA KIM, NB AMICO, JA AF CROWLEY, RS INSEL, TR OKEEFE, JA KIM, NB AMICO, JA TI INCREASED ACCUMULATION OF OXYTOCIN MESSENGER-RIBONUCLEIC-ACID IN THE HYPOTHALAMUS OF THE FEMALE RAT - INDUCTION BY LONG-TERM ESTRADIOL AND PROGESTERONE ADMINISTRATION AND SUBSEQUENT PROGESTERONE WITHDRAWAL SO ENDOCRINOLOGY LA English DT Article ID VASOPRESSIN GENE-EXPRESSION; INSITU HYBRIDIZATION; MATERNAL-BEHAVIOR; STRIA TERMINALIS; BED NUCLEUS; PARAVENTRICULAR NUCLEUS; RECEPTOR-BINDING; ESTROUS-CYCLE; HUMAN-PLASMA; RNA AB To examine a possible role for gonadal steroid hormones in the enhanced accumulation of hypothalamic oxytocin (OT) messenger RNA (mRNA) and peptide in late pregnancy, we used an established model (22) in which sequential administration of estradiol (E(2)) and progesterone (P) SILASTIC capsules to ovariectomized rats is followed by removal of P. Long term and sustained E(2) combined with abrupt P withdrawal mimics the gonadal steroid hormone pattern of late gestation in the rat (22). Using this paradigm, we demonstrate that OT mRNA is increased in the rat hypothalamus after long term P treatment, but only in the presence of E(2) and only when P capsules are removed 48 h before killing. Furthermore, we show that P replacement in primiparous rats during late pregnancy blunts the increase in OT mRNA normally observed at the end of gestation. Our results support a role for E(2) priming and P withdrawal in the enhanced accumulation of OT mRNA in the hypothalamus of the female rat. C1 UNIV PITTSBURGH, SCH MED, DEPT MED, PITTSBURGH, PA 15261 USA. DEPT VET AFFAIRS MED CTR, PITTSBURGH, PA 15261 USA. NIMH, NEUROPHYSIOL LAB, POOLESVILLE, MD 20837 USA. FU NIDDK NIH HHS [FT32-DK-0752] NR 47 TC 82 Z9 82 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1995 VL 136 IS 1 BP 224 EP 231 DI 10.1210/en.136.1.224 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QD584 UT WOS:A1995QD58400030 PM 7828535 ER PT J AU PFLUG, BR DIONNE, C KAPLAN, DR LYNCH, J DJAKIEW, D AF PFLUG, BR DIONNE, C KAPLAN, DR LYNCH, J DJAKIEW, D TI EXPRESSION OF A TRK HIGH-AFFINITY NERVE GROWTH-FACTOR RECEPTOR IN THE HUMAN PROSTATE SO ENDOCRINOLOGY LA English DT Article ID FACTOR-LIKE PROTEIN; NEUROTROPHIC FACTOR; EPITHELIAL-CELLS; BINDING; NGF; ADENOCARCINOMA; LOCALIZATION; ANDROGEN; LIGANDS; FAMILY AB Nerve growth factor-beta (NGF beta) and a NGF beta-immunoreactive protein derived from human prostatic stromal cell secretory protein (hPS) have been shown to stimulate the growth of prostate epithelial cells. An NGF beta-immunoreactive protein has been localized to the stroma of human prostate tissues, and a low affinity NGF receptor (gp75(NGFR)) has been localized to the adjacent epithelia, consistent with the paracrine regulation of prostate growth. Interestingly, gp75(NGFR) is progressively lost during neoplastic progression of the human prostate. In this report we have characterized the expression of the signal-transducing component of the NGF receptor, the Trk tyrosine receptor kinase, in prostate epithelial cells that bind exogenous NGF beta and an endogenous NGF beta-immunoreactive protein in hPS. In this context, a pan-Trk antibody that recognizes all of the members of the Trk receptor family (TrkA, TrkB, and TrkC) specifically localized expression of the Trk receptor to the epithelial component of normal prostate tissue, benign prostatic hyperplasia, and adenocarcinoma tissue. The binding of [I-125]NGF beta to the surface of primary cultures of human prostate epithelia and the TSU-pr1 human metastatic prostate tumor cell line was displaced with either excess cold NGF beta or hPS, whereas binding was not displaced by epidermal growth factor or platelet-derived growth factor. Scatchard plot analysis of [I-125]NGF beta binding to these cells identified a low affinity binding site (K-d = 1.9 X 10(-9) M) and a high affinity binding site (K-d = 1.8 X 10(-11) M) on the primary prostate epithelia, whereas only a high affinity binding site (K-d = 1.3 x 10(-11) M) was observed on the TSU-pr1 tumor cells. Stimulation of TSU-pr1 cells with either NGF beta or hPS induced tyrosine phosphorylation of Trk proteins, whereas no phosphorylation was evident in untreated cells, cells treated with hPS immunoprecipitated with anti-NGF beta antibody, or brain-derived neurotrophic factor- and neurotrophin-3-treated cells. The Trk protein was also observed in these cells by immunoblot analysis with pan-Trk antibody. These results demonstrate a functional Trk receptor in the epithelia of the human prostate that is responsive to-exogenous NGF beta and an endogenous NGF beta-immunoreactive protein in hPS, thereby supporting the concept of the paracrine regulation of growth in the human prostate via a stromal neurotrophin-epithelial Trk receptor interaction. C1 GEORGETOWN UNIV, MED CTR, DEPT SURG, DIV UROL, WASHINGTON, DC 20007 USA. CEPHALON INC, W CHESTER, PA 19380 USA. NCI, FREDERICK CANC RES & DEV CTR, EUKARYOT SIGNAL TRANSDUCT GRP, FREDERICK, MD 21702 USA. RP PFLUG, BR (reprint author), GEORGETOWN UNIV, MED CTR, DEPT CELL BIOL, 3900 RESERVOIR RD NW, WASHINGTON, DC 20007 USA. FU NIDDK NIH HHS [K04-DK-02233, R01-DK-46051, R01-DK-47508] NR 31 TC 89 Z9 89 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1995 VL 136 IS 1 BP 262 EP 268 DI 10.1210/en.136.1.262 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QD584 UT WOS:A1995QD58400034 PM 7828539 ER PT J AU OHMORI, M SHIMURA, H SHIMURA, Y IKUYAMA, S KOHN, LD AF OHMORI, M SHIMURA, H SHIMURA, Y IKUYAMA, S KOHN, LD TI CHARACTERIZATION OF AN UP-STREAM THYROID TRANSCRIPTION FACTOR-I BINDING-SITE IN THE THYROTROPIN RECEPTOR PROMOTER SO ENDOCRINOLOGY LA English DT Article ID TISSUE-SPECIFIC EXPRESSION; DNA-BINDING SPECIFICITY; TRANS-ACTING FACTOR; THYROGLOBULIN PROMOTER; CONTAINING PROTEIN; RESPONSE ELEMENT; GENE-EXPRESSION; HOMEODOMAIN; CELLS; MECHANISMS AB A thyroid transcription factor-1 (TTF-1)-binding element in the rat TSH receptor (TSHR) promoter, between -189 and -175 basepairs (bp), is important for both thyroid-specific expression and thyroid-specific TSH/cAMP autoregulation of the TSHR. The identification of an up-stream TTF-1-binding site and its relationship to the function of the down-stream TTF-1 element are the subjects of this report. Sequence analysis identifies a potential TTF-1 site at -878 bp; deoxyribonuclease-I footprinting shows that the -881 to -866 bp region is protected by recombinant TTF-1 protein and by nuclear extracts from FRTL-5 thyroid cells that contain TTF-1, but not by extracts from nonfunctioning FRT thyroid or Buffalo rat liver (BRL) cells, which have no TTF-1, or by Pax-8. FRTL-5, but not FRT or BRL cell nuclear extracts, form a specific protein-DNA complex with this region in gel mobility shift analyses; its formation is prevented by TTF-1-binding elements from the thyroglobulin promoter. The upstream TTF-1 site acts as an enhancer when coupled to a heterologous simian virus-40 promoter-chloramphenical acetyltransferase (CAT) chimera and transfected into FRTL-5 thyroid cells. There is a greater increase, 3- vs. 2-fold (P < 0.05), when TSHR promoter-CAT chimeras, which contain the up-stream TTF-1 element, pTRCAT5'-907 or pTRCAT5'-886, as opposed to those in which it is deleted, pTRCAT5'-907 Delta USTTF-1, are transfected into FRTL-5 cells or cotransfected with a TTF-1 expression vector into BRL cells, which have no endogenous TTF-1. The TTF-1-dependent activity of pTRCAT5'-907 Delta USTTF-1 is the same as that of the minimal promoter, -220 to -39 bp, containing only the down-stream TTF-I site in both cells. Transfection of chimeric TSHR-CAT plasmids with the down- and/or up-stream TTF-1 site deleted reveals that the down-stream TTF-1 element functions in the absence of the up-stream element, but function of the up-stream site requires the down-stream TTF-1 element. Like the down-stream TSHR TTF-1-binding site, the up-stream TTF-1 site is different from TTF-1 sites in the thyroglobulin and thyroid peroxidase promoter, in that it does not interact with Pax-8. Like the down-stream TSHR TTF-1-binding site, as evidenced by mutual competition, the same single strand binding site exists on the noncoding strand, contiguous with and 5' to the TTF-1 double strand site; the single strand DNA-binding site functions conjointly with TTF-1 and is necessary for full expression of the TSHR gene. Like the down-stream TSHR TTF-1 site, formation of the up-stream TTF-1-DNA complex increases within the first 2 h after TSH is added to FRTL-5 cells, and the increase can be mimicked by treating nuclear extracts with protein kinase-A. Like the down-stream TSHR TTF-1 site, TSH treatment causes a decrease in the formation of the upstream TTF-1-DNA complex after 2 h; the decrease parallels a decrease in formation of the down-stream TTF-1-DNA complex and is associated with a simultaneous TSH/cAMP-induced decrease in TTF-1 messenger RNA levels. The sum of these data indicate that there is an up-stream TTF-1 element in the TSHR promoter, -881 to -866 bp. It functions as an enhancer of the activity of the downstream TTF-1 site, but requires its presence for that function; otherwise, it behaves in all respects like the down-stream TTF-1 element with respect to thyroid-specific expression and cAMP autoregulation of the TSHR gene. C1 NIDDKD, CELL REGULAT SECT, BIOCHEM & METAB LAB, BETHESDA, MD 20892 USA. NR 31 TC 34 Z9 34 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1995 VL 136 IS 1 BP 269 EP 282 DI 10.1210/en.136.1.269 PG 14 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QD584 UT WOS:A1995QD58400035 PM 7828540 ER PT J AU LEE, YC PARK, CS KOMATSU, K KWACK, J STROTT, CA AF LEE, YC PARK, CS KOMATSU, K KWACK, J STROTT, CA TI ADRENOCORTICAL PREGNENOLONE BINDING-ACTIVITY RESIDES WITH ESTROGEN SULFOTRANSFERASE SO ENDOCRINOLOGY LA English DT Note ID PIG ADRENAL-CORTEX; HEAT-STABLE FACTOR; PROTEIN-ACTIVITY; PHOSPHORYLATION DEPHOSPHORYLATION; SOLUBLE FRACTION; PURIFICATION AB Cytosol prepared from Chinese hamster ovary (CHO)-K1 cells transfected with guinea pig estrogen sulfotransferase (EST) cDNA demonstrated high affinity binding activity for pregnenolone as well as 17 beta-estradiol but failed to bind dehydroepiandrosterone or testosterone. In contrast, cytosol prepared from nontransfected CHO-K1 cells did not demonstrate steroid binding activity. Additionally, the binding activity for pregnenolone and 17 beta-estradiol was dependent on the presence of the cofactor adenosine-3',5'-diphosphate. Pregnenolone and 17 beta-estradiol effectively competed with each other for binding. On the other hand, pregnenolone, which was not sulfonated, did not inhibit the sulfonation of 17 beta-estradiol by expressed EST. RP LEE, YC (reprint author), NICHHD, ENDOCRINOL & REPROD RES BRANCH, STEROID REG SECT, BETHESDA, MD 20892 USA. NR 11 TC 8 Z9 8 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1995 VL 136 IS 1 BP 361 EP 364 DI 10.1210/en.136.1.361 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QD584 UT WOS:A1995QD58400046 PM 7828553 ER PT J AU Parsegian, VA Rand, RP Rau, DC AF Parsegian, VA Rand, RP Rau, DC TI Macromolecules and water: Probing with osmotic stress SO ENERGETICS OF BIOLOGICAL MACROMOLECULES SE METHODS IN ENZYMOLOGY LA English DT Review ID PROTEIN SOLVATION; HYDRATION FORCES; YEAST HEXOKINASE; DNA; ASSOCIATION; COMPLEX; GLUCOSE; BINDING C1 BROCK UNIV,DEPT BIOL SCI,ST CATHARINES,ON L2S 3A1,CANADA. NIDDK,OFF INTRAMURAL RES,NIH,BETHESDA,MD 20892. RP Parsegian, VA (reprint author), NIH,LAB STRUCT BIOL,DCRT,BETHESDA,MD 20892, USA. NR 46 TC 330 Z9 334 U1 1 U2 29 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 259 BP 43 EP 94 PG 50 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA BE40L UT WOS:A1995BE40L00003 PM 8538466 ER PT J AU Lee, B AF Lee, B TI Analyzing solvent reorganization and hydrophobicity SO ENERGETICS OF BIOLOGICAL MACROMOLECULES SE METHODS IN ENZYMOLOGY LA English DT Review ID NONPOLAR SOLUTES; LIQUID WATER; THERMODYNAMICS; SIZE RP Lee, B (reprint author), NCI, MOLEC BIOL LAB, DIV CANC BIOL DIAG & CTR, NIH, BLDG 37, BETHESDA, MD 20892 USA. NR 31 TC 28 Z9 28 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 259 BP 555 EP 576 PG 22 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA BE40L UT WOS:A1995BE40L00025 PM 8538472 ER PT J AU MALLING, HV AF MALLING, HV TI GENETIC-HETEROGENEITY IN MAMMALIAN SPECIFIC-LOCUS MUTATION SYSTEMS SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Editorial Material ID MICE RP MALLING, HV (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 8 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1995 VL 26 IS 3 BP 187 EP 188 DI 10.1002/em.2850260302 PG 2 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA TC855 UT WOS:A1995TC85500001 PM 7588643 ER PT J AU ZEIGER, E AF ZEIGER, E TI UNTITLED SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Editorial Material RP ZEIGER, E (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1995 VL 25 SU 26 BP 1 EP 1 DI 10.1002/em.2850250602 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA RD910 UT WOS:A1995RD91000001 ER PT J AU DELLARCO, VL ERICKSON, RP LEWIS, SE SHELBY, MD AF DELLARCO, VL ERICKSON, RP LEWIS, SE SHELBY, MD TI MUTAGENESIS AND HUMAN GENETIC-DISEASE - AN INTRODUCTION SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article ID HUMAN-SPERM; MOUSE ZYGOTES; MUTATIONS; FREQUENCY; EXPOSURE; CELLS; LOCUS; MICE; RADIOTHERAPY; ABERRATIONS C1 UNIV ARIZONA,DEPT PEDIAT,TUCSON,AZ 85721. NIEHS,CTR LIFE SCI & TOXICOL,RES TRIANGLE PK,NC 27709. NIEHS,ENVIRONM TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. RP DELLARCO, VL (reprint author), US EPA,OFF HLTH & ENVIRONM ASSESSMENT 8602,401 M ST SW,WASHINGTON,DC 20460, USA. NR 44 TC 8 Z9 9 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1995 VL 25 SU 26 BP 2 EP 6 DI 10.1002/em.2850250603 PG 5 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA RD910 UT WOS:A1995RD91000002 PM 7789358 ER PT J AU BURKHART, JG AF BURKHART, JG TI PERSPECTIVES ON MOLECULAR ASSAYS FOR MEASURING MUTATION IN HUMANS AND RODENTS SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Review DE MUTATION DETECTION; HUMAN MUTAGENESIS; MOLECULAR TECHNOLOGY ID GRADIENT GEL-ELECTROPHORESIS; SINGLE BASE SUBSTITUTIONS; FLUORESCENCE INSITU HYBRIDIZATION; POLYMERASE CHAIN-REACTION; ETHYL-N-NITROSOUREA; HUMAN-LYMPHOBLASTOID-CELLS; AQUATICUS DNA-POLYMERASE; ATOMIC-BOMB SURVIVORS; 3 AFFECTED SIBLINGS; WHITE BLOOD-CELLS AB The original idea for this article was to examine the new molecular techniques for detection of mutation directly at the DNA level in exposed individuals or their offspring and to assess their relative advantages and disadvantages for mutation monitoring in humans and rodents. However, on examination of the articles and a comparison of the technology indicated that our constant quests for methods improvement were leading to some loss of insight into the important health-related questions that should be guiding these endeavors. As a result, individual methods are not covered here in great technical detail. Instead, a few molecular methods are presented in a general overview, along with some of the biological issues related to the detection of induced mutations within individuals and populations. Some hypothetical scenarios are also presented because molecular ap proaches will continue to change rapidly, and we must continually adjust our thinking to combine the useful attributes of each current and future technical approach with the most appropriate biological questions. (C) 1995 Wiley-Liss, Inc. RP BURKHART, JG (reprint author), NIEHS, ENVIRONM TOXICOL PROGRAM, POB 12233, RES TRIANGLE PK, NC 27709 USA. NR 132 TC 9 Z9 9 U1 0 U2 1 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1995 VL 25 SU 26 BP 88 EP 101 DI 10.1002/em.2850250613 PG 14 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA RD910 UT WOS:A1995RD91000012 PM 7789367 ER PT J AU PIEGORSCH, WW MARGOLIN, BH SHELBY, MD JOHNSON, A FRENCH, JE TENNANT, RW TINDALL, KR AF PIEGORSCH, WW MARGOLIN, BH SHELBY, MD JOHNSON, A FRENCH, JE TENNANT, RW TINDALL, KR TI STUDY DESIGN AND SAMPLE SIZES FOR A LACL TRANSGENIC MOUSE MUTATION ASSAY SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE EXPERIMENT DESIGN; EXTRA-BINOMIAL VARIABILITY; HIERARCHICAL SAMPLING; MUTAGENICITY; STATISTICAL METHODS; SAMPLE SIZE DETERMINATIONS; SECTORED PLAQUES; TRANSGENE ID MICE AB Design features that adjust and account for excess variation in a transgenic mouse mutation assay based on a loci target transgene from E. coli ore considered. These features include proper identification of plate, packaging reaction, and animal identifier codes throughout the experimental and analysis phases of the study, ''blocking'' of exposed and unexposed animals when preparing and plating multiple packaging reactions from the same genomic DNA sample, separating sectored mutant plaques and complete mutant plaques before performing any quantitative analyses, and testing for sources of excess variation attributable to features of the experimental protocol-such as plate-to-plate (within packaging reactions), packaging reaction-to-packaging reaction (within animals), and animal-to-animal (within study). Control and ethylnitrosourea-treated animal data are presented from a fully designed study in the lad assay. The study design incorporates many of these experimental principles. Statistical methods to identify excess variability are noted, and the designed study data are used to illustrate the types of variability encountered in practice. A standard statistical test for two-sample testing is highlighted, from which recommendations are made for sample size selection in future studies. (C) 1995 Wiley-Liss, Inc. C1 UNIV N CAROLINA,CHAPEL HILL,NC. NIEHS,RES TRIANGLE PK,NC 27709. RP PIEGORSCH, WW (reprint author), UNIV S CAROLINA,DEPT STAT,COLUMBIA,SC 29208, USA. OI Piegorsch, Walter/0000-0003-2725-5604 NR 21 TC 58 Z9 58 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1995 VL 25 IS 3 BP 231 EP 245 DI 10.1002/em.2850250310 PG 15 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA QV949 UT WOS:A1995QV94900009 PM 7737141 ER PT J AU SHELBY, MD WITT, KL AF SHELBY, MD WITT, KL TI COMPARISON OF RESULTS FROM MOUSE BONE-MARROW CHROMOSOME ABERRATION AND MICRONUCLEUS TESTS SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE GENETIC TOXICOLOGY; IN VIVO; CYTOGENETICS ID CELLS; MICE AB Tests for the induction of chromosomal aberrations (ABS) and micronuclei (MN) in bone marrow cells of mice have been conducted on 65 chemicals. Although these tests were not conducted with the purpose of-comparing the outcomes of these two in vivo genetic toxicity endpoints, the availability of these test results permits such a comparison. Based on studies to date, results from the 2 tests agree for more than 80% of the chemicals; 17 gave positive results in both tests, and 36 gave negative results in both. Seven chemicals were positive only for ABS and 5 were positive only for MN. Three chemicals that were originally concluded to be positive for ABS but not for MN were found to induce MN when the MN protocol was modified to more closely reflect the ABS protocol. Among the 12 chemicals for which there are discrepant results, there are only 2 for which the difference is convincing. One of these, selenium sulfide (MN negative, ABS positive) remains an enigma; further studies are being conducted. The second, isoprene (MN positive, ABS negative) will be difficult to pursue because the studies reported here were done by inhalation exposure. Based on the outcomes of these comparisons, protocol factors, rather than endpoint specificity, appear to be the major source of discrepant test results. Thus, these results do not support a recommendation that both tests be conducted in a primary testing scheme for genetic toxicity.* (C) 1995 Wiley-Liss, Inc.* C1 OAK RIDGE INST SCI & EDUC,DIV MED SCI,OAK RIDGE,TN. RP SHELBY, MD (reprint author), NIEHS,ENVIRONM TOXICOL PROGRAM,A2-03,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU NIEHS NIH HHS [Y01-ES-20098, Y01-ES-20100, N01-ES-15789] NR 11 TC 36 Z9 37 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1995 VL 25 IS 4 BP 302 EP 313 DI 10.1002/em.2850250407 PG 12 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA RG036 UT WOS:A1995RG03600006 PM 7607185 ER PT J AU BERGERON, J CREWS, D MCLACHLAN, JA AF BERGERON, J CREWS, D MCLACHLAN, JA TI ESTROGENICITY OF ENVIRONMENTAL PCBS - RESPONSE SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Letter C1 NIEHS,RES TRIANGLE PK,NC. RP BERGERON, J (reprint author), UNIV TEXAS,INST REPROD BIOL,AUSTIN,TX 78712, USA. NR 4 TC 1 Z9 1 U1 0 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1995 VL 103 IS 1 BP 12 EP 13 PG 2 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA RF753 UT WOS:A1995RF75300003 ER PT B AU Bouville, A Dreicer, M AF Bouville, A Dreicer, M GP IAEA TI Assessment of thyroid doses due to I-131 from atmospheric nuclear weapons tests in Nevada SO ENVIRONMENTAL IMPACT OF RADIOACTIVE RELEASES SE INTERNATIONAL ATOMIC ENERGY AGENCY PROCEEDINGS SERIES 2 : NUCLEAR SAFETY AND ENVIRONMENTAL PROTECTION LA English DT Proceedings Paper CT International Symposium on Environmental Impact of Radioactive Releases CY MAY 08-12, 1995 CL VIENNA, AUSTRIA SP Int Atom Energy Agcy C1 NCI,RADIAT EFFECTS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT ATOMIC ENERGY AGENCY PI VIENNA PA WAGRAMERSTRASSE 5, PO BOX 100, A-1400 VIENNA, AUSTRIA BN 92-0-104495-X J9 INT AEAPS 2 PY 1995 BP 421 EP 433 PG 13 WC Environmental Sciences; Nuclear Science & Technology SC Environmental Sciences & Ecology; Nuclear Science & Technology GA BG16L UT WOS:A1995BG16L00036 ER PT S AU VASILIOU, V REUTER, SF KOZAK, CA NEBERT, DW AF VASILIOU, V REUTER, SF KOZAK, CA NEBERT, DW BE Weiner, H Holmes, RS Wermuth, B TI Mouse class 3 aldehyde dehydrogenases SO ENZYMOLOGY AND MOLECULAR BIOLOGY OF CARBONYL METABOLISM 5 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 7th International Workshop on Enzymology and Molecular Biology of Carbonyl Metabolism CY JUL 03-07, 1994 CL PALMERSTON NORTH, NEW ZEALAND ID CDNA; CLONING; LIVER; GENE; RAT; EXPRESSION; EUKARYOTES C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RP UNIV CINCINNATI,MED CTR,DEPT ENVIRONM HLTH,POB 670056,CINCINNATI,OH 45267, USA. FU NIA NIH HHS [R01 AG09235]; NIEHS NIH HHS [P30 ES06096] NR 25 TC 10 Z9 10 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44989-7 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 372 BP 151 EP 158 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD26P UT WOS:A1995BD26P00020 PM 7484373 ER PT S AU SATO, S OLD, S CARPER, D KADOR, PF AF SATO, S OLD, S CARPER, D KADOR, PF BE Weiner, H Holmes, RS Wermuth, B TI Purification and characterization of recombinant human placental and rat lens aldose reductases expressed in Escherichia coli SO ENZYMOLOGY AND MOLECULAR BIOLOGY OF CARBONYL METABOLISM 5 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 7th International Workshop on Enzymology and Molecular Biology of Carbonyl Metabolism CY JUL 03-07, 1994 CL PALMERSTON NORTH, NEW ZEALAND ID SITE-DIRECTED MUTAGENESIS; ALDEHYDE REDUCTASE; DIABETIC COMPLICATIONS; CRYSTAL-STRUCTURE; CLONING; SEQUENCE; INHIBITION; BINDING; DOMAIN; KIDNEY C1 NEI,MECHANISM OCULAR DIS LAB,BETHESDA,MD 20892. RP NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892, USA. NR 34 TC 7 Z9 7 U1 0 U2 2 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44989-7 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 372 BP 259 EP 268 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD26P UT WOS:A1995BD26P00032 PM 7484387 ER PT S AU IWATA, T CARPER, D AF IWATA, T CARPER, D BE Weiner, H Holmes, RS Wermuth, B TI Human sorbitol dehydrogenase gene - cDNA sequence and expression SO ENZYMOLOGY AND MOLECULAR BIOLOGY OF CARBONYL METABOLISM 5 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 7th International Workshop on Enzymology and Molecular Biology of Carbonyl Metabolism CY JUL 03-07, 1994 CL PALMERSTON NORTH, NEW ZEALAND ID ALDOSE REDUCTASE; MESSENGER-RNA; ALCOHOL-DEHYDROGENASE; PROTEIN; CLONING; FAMILY; LENS; COMPLICATIONS; PATHWAY; ENZYME RP NEI,MECHANISMS OCULAR DIS LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 26 TC 2 Z9 2 U1 0 U2 1 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44989-7 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 372 BP 373 EP 381 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD26P UT WOS:A1995BD26P00044 PM 7484401 ER PT J AU GIOVINO, GA HENNINGFIELD, JE TOMAR, SL ESCOBEDO, LG SLADE, J AF GIOVINO, GA HENNINGFIELD, JE TOMAR, SL ESCOBEDO, LG SLADE, J TI EPIDEMIOLOGY OF TOBACCO USE AND DEPENDENCE SO EPIDEMIOLOGIC REVIEWS LA English DT Review ID RACIAL ETHNIC-DIFFERENCES; ILLICIT DRUG-USE; CIGARETTE-SMOKING; UNITED-STATES; NICOTINE DEPENDENCE; MAJOR DEPRESSION; SMOKELESS TOBACCO; YOUNG-ADULTS; WITHDRAWAL SYMPTOMS; LUNG-CANCER C1 NIDA,ADDICT RES CTR,CLIN PHARMACOL BRANCH,BALTIMORE,MD 21224. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,ST PETERS MED CTR,DEPT MED,NEW BRUNSWICK,NJ 08903. RP GIOVINO, GA (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,OFF SMOKING & HLTH,ATLANTA,GA 30341, USA. NR 191 TC 198 Z9 203 U1 7 U2 17 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1995 VL 17 IS 1 BP 48 EP 65 PG 18 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA RU555 UT WOS:A1995RU55500007 PM 8521946 ER PT J AU Inskip, PD Linet, MS Heineman, EF AF Inskip, PD Linet, MS Heineman, EF TI Etiology of brain tumors in adults SO EPIDEMIOLOGIC REVIEWS LA English DT Review ID CENTRAL-NERVOUS-SYSTEM; N-NITROSO COMPOUNDS; LOS-ANGELES COUNTY; CENTRAL NEUROEPITHELIAL TUMORS; OCCUPATIONAL RISK-FACTORS; VONHIPPEL-LINDAU DISEASE; PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; PRIMITIVE NEUROECTODERMAL TUMORS; SERUM-CHOLESTEROL CONCENTRATION; PRIMARY INTRACRANIAL NEOPLASMS C1 NCI, EPIDEMIOL & BIOSTAT PROGRAM, DIV CANC EPIDEMIOL & GENET, BETHESDA, MD USA. NR 452 TC 189 Z9 194 U1 0 U2 7 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1995 VL 17 IS 2 BP 382 EP 414 PG 33 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UB036 UT WOS:A1995UB03600009 PM 8654518 ER PT J AU ROWLAND, AS AF ROWLAND, AS TI PESTICIDES AND BIRTH-DEFECTS SO EPIDEMIOLOGY LA English DT Editorial Material RP ROWLAND, AS (reprint author), NIEHS,EPIDEMIOL BRANCH,POB 12233,MD A3-05,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 9 Z9 10 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 1995 VL 6 IS 1 BP 6 EP 7 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA PY488 UT WOS:A1995PY48800003 PM 7888447 ER PT S AU AMERY, AKP BEAGLEHOLE, R BOEDHIDARMOJO, R BROCK, DB DAVIES, AM DODU, SRA FEHER, J FLETCHER, AE HIGGINS, M NAJEEB, MA OMAE, T SCHROLL, M STRASSER, T KINGMA, M CHIGAN, EN GYARFAS, I AF AMERY, AKP BEAGLEHOLE, R BOEDHIDARMOJO, R BROCK, DB DAVIES, AM DODU, SRA FEHER, J FLETCHER, AE HIGGINS, M NAJEEB, MA OMAE, T SCHROLL, M STRASSER, T KINGMA, M CHIGAN, EN GYARFAS, I GP WHO WHO WHO TI EPIDEMIOLOGY AND PREVENTION OF CARDIOVASCULAR-DISEASES IN ELDERLY PEOPLE SO EPIDEMIOLOGY AND PREVENTION OF CARDIOVASCULAR DISEASES IN ELDERLY PEOPLE: REPORT OF A WHO STUDY GROUP SE WHO Technical Report Series LA English DT Review ID CORONARY HEART-DISEASE; SOCIETY CONSENSUS CONFERENCE; ACTIVE LIFE EXPECTANCY; HIGH BLOOD-PRESSURE; RISK-FACTORS; PHYSICAL-ACTIVITY; CHOLESTEROL CONCENTRATION; CARDIAC REHABILITATION; MYOCARDIAL-INFARCTION; COST-EFFECTIVENESS AB The remarkable growth seen this century in the elderly populations of developed countries is likely to be mirrored in developing countries in the coming decades. One of the results will be a greatly increased prevalence of cardiovascular diseases, which become more common with increasing age and which are already the leading cause of death among adults. This report of a WHO Study Group examines the implications of the projected trends for the health policies and strategies of both developing and developed countries. Starting from a consideration of demographic and disease patterns, the report discusses the importance of prevention activities aimed at whole populations as well as at individuals at high risk. While acknowledging that more research is needed, particularly among the ''oldest old'' - those over 80 years of age - the report highlights the need for governments to act now to reduce the burden of disease among the elderly. Policies need to be developed to promote better nutrition, discourage smoking, and raise awareness among the general population of the risk factors for cardiovascular disease, and of the possibilities for their control. C1 UNIV AUCKLAND, SCH MED, DEPT COMMUNITY HLTH, AUCKLAND, NEW ZEALAND. DIPONEGORO UNIV, RES INST, DEPT PENDIDIKAN KEBUDAYAAN, SEMARANG, INDONESIA. NIA, EPIDEMIOL DEMOG & BIOMETRY PROGRAM, BETHESDA, MD USA. HEBREW UNIV JERUSALEM, SCH PUBL HLTH & COMMUNITY MED, JERUSALEM, ISRAEL. UNIV GHANA, SCH MED, DEPT MED & THERAPEUT, ACCRA, GHANA. HOSP ISRAELITA ALBERT EINSTEIN, MORUMBI, SP, BRAZIL. UNIV LONDON LONDON SCH HYG & TROP MED, DEPT EPIDEMIOL & POPULAT SCI, LONDON WC1E 7HT, ENGLAND. NHLBI, DIV EPIDEMIOL & CLIN APPLICAT, BETHESDA, MD 20892 USA. ARMED FORCES MED COLL, AF INST CARDIOL, LAHORE, PAKISTAN. NATL CARDIOVASC CTR, SUITA, OSAKA, JAPAN. COPENHAGEN CITY HOSP, DEPT GERIATR, COPENHAGEN, DENMARK. RP AMERY, AKP (reprint author), UNIV HOSP LEUVEN, UNIV ZIEKENHUIS ST RAFAEL GASTHUISBERG, HYPERTENS UNIT, LOUVAIN, BELGIUM. NR 158 TC 1 Z9 1 U1 0 U2 1 PU WORLD HEALTH ORGANIZATION PI GENEVA PA DISTRIBUTION & SALES SERVICE, 1211 27 GENEVA, SWITZERLAND SN 0512-3054 BN 92-4-120853-8 J9 WHO TECH REP SER JI WHO Tech. Rep. Ser. PY 1995 VL 853 BP 1 EP + PG 0 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA BD89L UT WOS:A1995BD89L00001 ER PT J AU BURGESS, RC EBERSOLE, JS MEADOR, KJ THEODORE, WH AF BURGESS, RC EBERSOLE, JS MEADOR, KJ THEODORE, WH TI QUANTITATIVE EEG - DEUS-EX-MACHINA OR GENIE IN THE BOTTLE SO EPILEPSIA LA English DT Meeting Abstract C1 CLEVELAND CLIN,CLEVELAND,OH 44106. YALE UNIV,NEW HAVEN,CT 06520. MED COLL GEORGIA,AUGUSTA,GA 30912. NIH,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 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 4 BP 2 EP 2 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA TD347 UT WOS:A1995TD34700005 ER PT J AU WEINBERGER, DR GOLD, J HERMANN, BP AF WEINBERGER, DR GOLD, J HERMANN, BP TI PSYCHOSIS IN EPILEPSY AND IN SCHIZOPHRENIA - CONTRASTS AND PARALLELS SO EPILEPSIA LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD. UNIV TENNESSEE,KNOXVILLE,TN 37996. 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 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 4 BP 137 EP 137 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA TD347 UT WOS:A1995TD34700543 ER PT J AU GAILLARD, WD CONRY, J WEINSTEIN, S FAZILAT, S KOLODGIE, M REEVES, P DECARLI, C VEZINA, LG THEODORE, WH AF GAILLARD, WD CONRY, J WEINSTEIN, S FAZILAT, S KOLODGIE, M REEVES, P DECARLI, C VEZINA, LG THEODORE, WH TI FDG-PET IN CHILDREN WITH NEW-ONSET PARTIAL SEIZURES SO EPILEPSIA LA English DT Meeting Abstract C1 CHILDRENS NATL MED CTR,DEPT NEUROL,WASHINGTON,DC 20010. NIH,NINDS,EPILEPSY RES UNIT,BETHESDA,MD 20892. RI DeCarli, Charles/B-5541-2009 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 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 4 BP 653 EP 653 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA TD347 UT WOS:A1995TD34700648 ER PT J AU SWANSON, SJ GRAFMAN, J SALAZAR, AM SCHWAB, K PRIDGEN, AW AF SWANSON, SJ GRAFMAN, J SALAZAR, AM SCHWAB, K PRIDGEN, AW TI THE INTERACTIVE EFFECTS OF SEIZURES AND LESION LOCATION ON MOOD SO EPILEPSIA LA English DT Meeting Abstract C1 MED COLL WISCONSIN,DEPT NEUROL,MILWAUKEE,WI 53226. UNIFORMED SERV UNIV HLTH SCI,NINDS,COGNIT NEUROSCI SECT,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT NEUROL,DEF & VET HEAD INJURY PROGRAM,BETHESDA,MD 20814. 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 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 4 BP K3 EP K3 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA TD347 UT WOS:A1995TD34700574 ER PT J AU MONTPIED, P WINSKY, L DAILEY, JW JOBE, PC JACOBOWITZ, DM AF MONTPIED, P WINSKY, L DAILEY, JW JOBE, PC JACOBOWITZ, DM TI ALTERATION IN THE LEVELS OF EXPRESSION OF BRAIN CALBINDIN D-28K AND CALRETININ MESSENGER-RNAS IN GENETICALLY EPILEPSY-PRONE RATS SO EPILEPSIA LA English DT Meeting Abstract C1 CNRS,INSERM,EXPTL MED LAB,F-34033 MONTPELLIER,FRANCE. NIMH,CLIN SCI 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 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 3 BP S54 EP S54 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA RQ685 UT WOS:A1995RQ68500255 ER PT J AU THEODORE, WH AF THEODORE, WH TI FUNCTIONAL NEUROIMAGING FOR EPILEPSY WITH PET SO EPILEPSIA LA English DT Meeting Abstract C1 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 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 3 BP S166 EP S166 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA RQ685 UT WOS:A1995RQ68500803 ER PT J AU THEODORE, WH SATO, S KUFTA, C AF THEODORE, WH SATO, S KUFTA, C TI [F-18] 2-DEOXYGLUCOSE PET IN PATIENTS WITH NONLOCALIZED SURFACE EEG SO EPILEPSIA LA English DT Meeting Abstract C1 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 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 3 BP S139 EP S139 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA RQ685 UT WOS:A1995RQ68500669 ER PT S AU Levine, PH Lin, A Tucker, MA AF Levine, PH Lin, A Tucker, MA BE Jarrett, RF TI What can we learn about the aetiology of Hodgkin's disease from family studies? SO ETIOLOGY OF HODGKIN'S DISEASE SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES A, LIFE SCIENCES LA English DT Proceedings Paper CT NATO Advanced Research Workshop on the Etiology of Hodgkins Disease CY MAY 02-05, 1994 CL LOCH LOMOND, SCOTLAND SP NATO C1 NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. RI Tucker, Margaret/B-4297-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0258-1213 BN 0-306-45205-7 J9 NATO ADV SCI INST SE PY 1995 VL 280 BP 27 EP 32 PG 6 WC Oncology; Virology SC Oncology; Virology GA BE86R UT WOS:A1995BE86R00003 ER PT S AU Levine, PH Manak, M Jagodzinski, L AF Levine, PH Manak, M Jagodzinski, L BE Jarrett, RF TI Hodgkin's disease and human herpesvirus-6: A model for studies of new aetiological agents SO ETIOLOGY OF HODGKIN'S DISEASE SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES A, LIFE SCIENCES LA English DT Proceedings Paper CT NATO Advanced Research Workshop on the Etiology of Hodgkins Disease CY MAY 02-05, 1994 CL LOCH LOMOND, SCOTLAND SP NATO C1 NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0258-1213 BN 0-306-45205-7 J9 NATO ADV SCI INST SE PY 1995 VL 280 BP 99 EP 107 PG 9 WC Oncology; Virology SC Oncology; Virology GA BE86R UT WOS:A1995BE86R00009 ER PT J AU BLAGOSKLONNY, MV NECKERS, LM AF BLAGOSKLONNY, MV NECKERS, LM TI THE ROLE OF BCL-2 PROTEIN AND AUTOCRINE GROWTH-FACTORS IN A HUMAN FOLLICULAR LYMPHOMA-DERIVED B-CELL LINE SO EUROPEAN CYTOKINE NETWORK LA English DT Article DE LYMPHOMA; BCL-2; ANTISENSE; AUTOCRINE SECRETION; PROLIFERATION; SURVIVAL ID MALIGNANT LYMPHOCYTES-B; TUMOR-NECROSIS-FACTOR; EPSTEIN-BARR VIRUS; C-MYC; EXPRESSION; GENE; SURVIVAL; INHIBITION; ANTISENSE; LEUKEMIA AB We have shown that the ability of the human follicular lymphoma-derived cell line SU-DHL-6 to proliferate and survive in vitro depends on both Bcl-2 expression and multiple autocrine growth factors. Treatment with Bcl-2 antisense (AS Bcl-2) decreased Bcl-2 protein levels, However, a cytotoxic effect was seen only at very restricted cell densities. Below such densities cells underwent spontaneous death without any treatment, while above these cell densities no cytotoxic effect of AS Bcl-2 could be seen. The conditioned medium of SU-DHL cells supported the survival and growth of these cells cultivated at low cell densities and partially reversed the cytotoxicity associated with Bcl-2 depletion, RT/PCR analysis revealed autocrine expression of IL-1 beta, IL-2, IL-5 and TNF-beta in SU-DHL cells. Neutralizing antibodies against these cytokines inhibited SU-DHL proliferation, Thus, development of autocrine GF secretion may be the second step in the pathogenesis of follicular lymphomas, RP BLAGOSKLONNY, MV (reprint author), NCI,CLIN PHARMACOL BRANCH,BLDG 10,12N226,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 32 TC 4 Z9 4 U1 0 U2 0 PU JOHN LIBBEY EUROTEXT LTD PI MONTROUGE PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE SN 1148-5493 J9 EUR CYTOKINE NETW JI Eur. Cytokine Netw. PD JAN-FEB PY 1995 VL 6 IS 1 BP 21 EP 27 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA QR954 UT WOS:A1995QR95400002 PM 7795171 ER PT J AU HILDESHEIM, A HERRERO, R JOHNSON, J BRATTI, C BHATIA, K MAGRATH, IT FRAUMENI, JF AF HILDESHEIM, A HERRERO, R JOHNSON, J BRATTI, C BHATIA, K MAGRATH, IT FRAUMENI, JF TI ELEVATED LEVELS OF P53 PROTEIN IN ADRENOCORTICAL CARCINOMAS FROM COSTA-RICA SO EUROPEAN JOURNAL OF CANCER LA English DT Letter ID LI-FRAUMENI SYNDROME; MUTATIONS; CANCER; FAMILIES C1 NCI,DIV CANC TREATMENT,BETHESDA,MD 20892. NATL TUMOUR REGISTRY,SAN JOSE,COSTA RICA. RP HILDESHEIM, A (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892, USA. NR 9 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 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1995 VL 31A IS 1 BP 125 EP 125 DI 10.1016/0959-8049(94)00465-H PG 1 WC Oncology SC Oncology GA QG869 UT WOS:A1995QG86900025 PM 7695963 ER PT J AU TERRIER, P HENRYAMAR, M TRICHE, TJ HOROWITZ, ME TERRIERLACOMBE, MJ MISER, JS KINSELLA, TJ CONTESSO, G LLOMBARTBOSCH, A AF TERRIER, P HENRYAMAR, M TRICHE, TJ HOROWITZ, ME TERRIERLACOMBE, MJ MISER, JS KINSELLA, TJ CONTESSO, G LLOMBARTBOSCH, A TI IS NEURO-ECTODERMAL DIFFERENTIATION OF EWINGS-SARCOMA OF BONE ASSOCIATED WITH AN UNFAVORABLE PROGNOSIS SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE EWINGS SARCOMA; BONE; NEURO-ECTODERMAL DIFFERENTIATION; PROGNOSIS ID PERIPHERAL NEUROECTODERMAL TUMORS; COMBINED MODALITY THERAPY; ROUND-CELL SARCOMAS; TERM FOLLOW-UP; INITIAL CHEMOTHERAPY; YOUNG-ADULTS; SOFT-TISSUE; DIAGNOSIS; NEUROEPITHELIOMA; CHILDREN AB Among Ewing's sarcoma (ES) of bone and related entities are tumours with neuro-ectodermal features that could represent a biologically distinct type. In order to assess the prognostic significance of the various forms of ES, a retrospective joint study involving three cancer centres in Europe and the U.S.A. was initiated. The material from 315 primary ES was reviewed by a panel of five pathologists and classified as typical ES (220 cases), atypical ES (48 cases) or ES with neuro-ectodermal features (47 cases). Prognostic factor analysis on treatment failure-free survival was performed using the Cox model. It included histopathological classification, initial patient characteristics, clinical presentation and treatment type. After multivariate analysis, in addition to treatment type (P < 0.001), metastases (P = 0.003) and proximal tumour location (P = 0.006), two histopathological parameters correlated with poor treatment failure-free survival, the presence of filigree pattern (P = 0.044) and dark cells (P = 0.043). We conclude that ES with neuro-ectodermal features does not appear to have a different outcome to the other subtypes. C1 INST GUSTAVE ROUSSY,DEPT PATHOL,VILLEJUIF,FRANCE. INST GUSTAVE ROUSSY,DEPT BIOSTAT & EPIDEMIOL,VILLEJUIF,FRANCE. NCI,DEPT PATHOL,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. UNIV VALENCIA,SCH MED,DEPT PATHOL,E-46100 VALENCIA,SPAIN. RP TERRIER, P (reprint author), INST GUSTAVE ROUSSY,DEPT PATHOL ANAT,39-53 CAMILLE DESMOULINS,F-94805 VILLEJUIF,FRANCE. NR 44 TC 54 Z9 54 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1995 VL 31A IS 3 BP 307 EP 314 DI 10.1016/0959-8049(94)00417-4 PG 8 WC Oncology SC Oncology GA QP937 UT WOS:A1995QP93700006 PM 7786593 ER PT J AU GALSKI, H LAZAROVICI, P GOTTESMAN, MM MURAKATA, C MATSUDA, Y HOCHMAN, J AF GALSKI, H LAZAROVICI, P GOTTESMAN, MM MURAKATA, C MATSUDA, Y HOCHMAN, J TI KT-5720 REVERSES MULTIDRUG-RESISTANCE IN VARIANT S49 MOUSE LYMPHOMA-CELLS TRANSDUCED WITH THE HUMAN MDR1 CDNA AND IN HUMAN MULTIDRUG-RESISTANT CARCINOMA-CELLS SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE CHEMOSENSITIZERS; K-252A DERIVATIVES; KT-5720; MDR1; MULTIDRUG RESISTANCE; P-GLYCOPROTEIN; PROTEIN KINASES; PROTEIN KINASE INHIBITORS ID PROTEIN-KINASE-C; P-GLYCOPROTEIN; DRUG ACCUMULATION; TRANSGENIC MICE; BONE-MARROW; CROSS-RESISTANCE; PLASMA-MEMBRANE; TUMOR-CELLS; STAUROSPORINE; PHOSPHORYLATION AB T-25-Adh cells, cell variants derived from S49 mouse lymphoma, were transduced with a retrovirus containing the human MDR1 cDNA. The resultant cells (HU-1) are cross-resistant to colchicine, doxorubicin, vinblastine and actinomycin D, and their resistance to colchicine is reversed by verapamil. HU-1 cells were used to screen several protein kinase modulators for their ability to reverse multidrug resistance. Among the tested indole carbazole (K-252a) family of protein kinase inhibitors, only the antibiotic alkaloid KT-5720 (9-n-hexyl derivative of K-252a) could overcome the multidrug resistance of HU-1 cells and KB-V1 human carcinoma cells. Since other protein kinase A, C and G modulators did not reverse multidrug resistance in the tested multidrug-resistant cells, the chemosensitising activity of KT-5720 on these cells is apparently independent of its kinase inhibitory effects. Since KT-5720 fully reversed multidrug resistance at non-toxic concentrations, it might be a candidate for clinical chemosensitisation in combination chemotherapy. C1 HEBREW UNIV JERUSALEM,INST LIFE SCI,DEPT CELL & ANIM BIOL,IL-91904 JERUSALEM,ISRAEL. HADASSAH UNIV HOSP,MOLEC BIOL & GENET ENGN UNIT,IL-91240 JERUSALEM,ISRAEL. HEBREW UNIV JERUSALEM,SCH PHARM,DEPT PHARMACOL & EXPTL THERAPEUT,IL-91120 JERUSALEM,ISRAEL. NCI,CELL BIOL LAB,BETHESDA,MD 20892. KYOWA HAKKO KOGYO CO LTD,TOKYO 194,JAPAN. FU NCI NIH HHS [CA-48146] NR 32 TC 11 Z9 11 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1995 VL 31A IS 3 BP 380 EP 388 DI 10.1016/0959-8049(94)00511-3 PG 9 WC Oncology SC Oncology GA QP937 UT WOS:A1995QP93700021 PM 7786606 ER PT J AU GAETANO, C MANNI, I BOSSI, G PIAGGIO, G SODDU, S FARINA, A HELMAN, LJ SACCHI, A AF GAETANO, C MANNI, I BOSSI, G PIAGGIO, G SODDU, S FARINA, A HELMAN, LJ SACCHI, A TI RETINOIC ACID AND CAMP DIFFERENTIALLY REGULATE HUMAN CHROMOGRANIN-A PROMOTER ACTIVITY DURING DIFFERENTIATION OF NEUROBLASTOMA-CELLS SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE CHROMOGRANIN; NEUROBLASTOMA; PROMOTER; E-BOX; DIFFERENTIATION; NEUROENDOCRINE; CHROMAFFIN ID HUMAN NEURO-BLASTOMA; EXPRESSION; GENE; INVITRO; SYSTEM; LINES AB We report the first evidence that differential transcriptional regulation of human chromogranin A (CHGA) gene expression occurs during in vitro treatment of tumorigenic neuroblastoma (NB) cells with retinoic acid (5 mu M) and/or dibutyryl-cAMP (1 mM). The CHGA gene encodes a tissue specific protein restricted to cells of the diffuse neuroendocrine system, but also widely expressed among NE tumours. We previously reported that CHGA as well as other neuroendocrine markers are modulated during NE differentiation in vitro. To investigate, at the molecular level, the mechanisms leading to NE tumour cell differentiation during the treatment with biologically active compounds, we sequenced and functionally characterised 2169 bp of a genomic DNA clone encompassing the 5' flanking region of the human CHGA gene. Computer-assisted analysis of the sequence revealed the presence of a cAMP responsive element at positions -56 to -49, and Spl binding sites at positions -181 to -176 and -216 to -210. Two novel 9 bp motifs, located at position -462 to -454 and -91 to -83 of the CHGA promoter were identified in the regulatory regions of two other neuroendocrine genes encoding for tyrosine hydroxylase and neuropeptide Y. In addition, in the first 1000 bp of the untranslated 5' region, we found the presence of several putative DNA binding sites of bHLH molecules, a protein family regulating tissue specific differentiation. Transient transfection experiments of chloramphenicol acetyltransferase (CAT) deletion constructs, showed the presence of an active promoter within the first 455 bp upstream from the start site. This region conferred tissue specific expression to a CA Treporter gene. In addition, the transcriptional activity of this fragment was modulated during the induction of differentiation of NE cells treated by retinoic acid and/or dibutyryl-cAMP. These observations provide preliminary data regarding CHGA transcriptional regulation in NE cells, and indicate that retinoic acid and cAMP activate distinct, apparently competitive, transcriptional pathways during NE cell differentiation. The molecular characterisation of the mechanisms regulating CHGA expression in tumour and normal neuroendocrine tissue could lead to the identification of novel molecules potentially relevant for future gene therapy of NE tumours. C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. RP GAETANO, C (reprint author), IST REGINA ELENA,CTR RIC SPERIMENTALE,ONCOGENESI MOLEC LAB,VIA DELLE MESS DORO 156,I-00158 ROME,ITALY. RI Bossi, Gianluca/G-8375-2016; OI Bossi, Gianluca/0000-0002-2947-1063; Gaetano, Carlo/0000-0002-5238-1832; piaggio, giulia/0000-0003-2114-1892 NR 27 TC 12 Z9 12 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1995 VL 31A IS 4 BP 447 EP 452 DI 10.1016/0959-8049(95)00038-K PG 6 WC Oncology SC Oncology GA QY180 UT WOS:A1995QY18000006 PM 7576943 ER PT J AU GROVES, FD LINET, MS DEVESA, SS AF GROVES, FD LINET, MS DEVESA, SS TI PATTERNS OF OCCURRENCE OF THE LEUKEMIAS SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE LEUKEMIA; MYELOID; LYMPHOID; INCIDENCE; MORTALITY; SURVIVAL; TRENDS ID ACUTE LYMPHOBLASTIC-LEUKEMIA; CHILDHOOD; EPIDEMIOLOGY; SUBTYPES; REGISTRY; CANCER AB Despite a proliferation of epidemiological studies during the past two decades, aetiologies of the leukaemias remain poorly understood, and characterisation of descriptive patterns has been limited. Recent publications of international mortality and incidence data, along with the expanding U.S. database, make a comprehensive assessment of leukaemia patterns particularly timely. Total leukaemia mortality has dramatically declined among children and increased among the elderly, while incidence has declined somewhat (for Caucasian and African-American females) or remained stable (for African-American males) during the past two decades in the United States. Population-based 5-year relative survival for total leukaemia has risen substantially among children since the mid-1970s, and improved slightly among other age groups in the U.S., where survival is consistently higher among Caucasians than African-Americans, but differs little by gender. In a detailed assessment by leukaemia subtype, some important differences in geographic, racial/ethnic, age and trend patterns are identified, suggesting that the subtypes may have different aetiologic factors. Proven and suspected risk factors cannot explain more than a small fraction of the observed geographic and temporal variation in incidence. Several noteworthy subtype-specific characteristics or trends warrant further investigation: for acute lymphoid leukaemia (ALL), increasing incidence, with higher rates in Spanish and Latino populations; for chronic lymphoid leukaemia (CLL), declining incidence, with dramatically low rates among Asians; for acute myeloid leukaemia (AML), increasing incidence among African-American males; and for chronic myeloid leukaemia (CML), declining rates among Caucasian but not among African-Americans. RP GROVES, FD (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,ANALYT STUDIES BIOSTAT BRANCH,EXECUT PLAZA N,BETHESDA,MD 20892, USA. NR 29 TC 53 Z9 55 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1995 VL 31A IS 6 BP 941 EP 949 DI 10.1016/0959-8049(95)00024-0 PG 9 WC Oncology SC Oncology GA RG476 UT WOS:A1995RG47600022 PM 7646927 ER PT J AU CASASCO, A CASASCO, M REGUZZONI, M CALLIGARO, A TATEO, S STETLERSTEVENSON, WG LIOTTA, LA AF CASASCO, A CASASCO, M REGUZZONI, M CALLIGARO, A TATEO, S STETLERSTEVENSON, WG LIOTTA, LA TI OCCURRENCE AND DISTRIBUTION OF MATRIX METALLOPROTEINASE-2-IMMUNOREACTIVITY IN HUMAN EMBRYONIC-TISSUES SO EUROPEAN JOURNAL OF HISTOCHEMISTRY LA English DT Article DE COLLAGENASE; EXTRACELLULAR MATRIX; DEVELOPMENT; IMMUNOCYTOCHEMISTRY ID BASEMENT-MEMBRANE COLLAGEN; EXTRACELLULAR-MATRIX; DEGRADING METALLOPROTEINASES; PLASMINOGEN-ACTIVATOR; TOOTH DEVELOPMENT; IV COLLAGENASES; TUMOR INVASION; CELLS; EXPRESSION; GROWTH AB Tissue development and structure is controlled by dynamic and interactive relationships between cells and the extra-cellular matrix (ECM) which they secrete. We have investigated the occurrence and distribution of metalloproteinase-2 (MMP-2), an enzyme involved in the catabolism of ECM components, in human embryonic tissues by immunocytochemistry. Cells displaying MMP-2 immunoreactivity showed a widespread distribution in human embryonic tissues and organs. Cytoplasmic staining was detected in cells deriving from all three embryonic layers. Although further studies are needed to clarify the possible substrates of MMP-2 in developing tissues, these morphological data lend support to the hypothesis that ECM remodelling and degradation may represent a physiological counterpart of ECM deposition that occur during development. C1 SAN MATTEO HOSP, IRCCS, OBSTET & GYNECOL CLIN, PAVIA, ITALY. NCI, PATHOL LAB, TUMOR INVAS & METASTASIS SECT, BETHESDA, MD 20892 USA. RP CASASCO, A (reprint author), UNIV PAVIA, INST HISTOL & EMBRYOL, VIA PALESTRO 3, I-27100 PAVIA, ITALY. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 54 TC 10 Z9 10 U1 0 U2 0 PU LUIGI PONZIO E FIGLIO PI PAVIA PA VIA D DA CATALOGNA 1/3, 27100 PAVIA, ITALY SN 1121-760X J9 EUR J HISTOCHEM JI Eur. J. Histochem. PY 1995 VL 39 IS 1 BP 31 EP 38 PG 8 WC Cell Biology SC Cell Biology GA QN217 UT WOS:A1995QN21700004 PM 7612955 ER PT J AU CASASCO, A FRATTINI, P CASASCO, M SANTAGOSTINO, G SPRINGALL, DR KUHN, DM POLAK, JM AF CASASCO, A FRATTINI, P CASASCO, M SANTAGOSTINO, G SPRINGALL, DR KUHN, DM POLAK, JM TI CATECHOLAMINES IN HUMAN DENTAL-PULP - A COMBINED IMMUNOHISTOCHEMICAL AND CHROMATOGRAPHIC STUDY SO EUROPEAN JOURNAL OF HISTOCHEMISTRY LA English DT Article DE HUMAN DENTAL PULP; INNERVATION; CATECHOLAMINES; IMMUNOHISTOCHEMISTRY; HIGH PERFORMANCE LIQUID CHROMATOGRAPHY ID BLOOD-FLOW; ELECTRICAL-STIMULATION; INHIBITORY INFLUENCE; PEPTIDERGIC NERVES; SYMPATHETIC FIBERS; NEUROPEPTIDE-Y; RAT; TOOTH; IMMUNOREACTIVITY; ENDOTHELIN AB Pharmacological studies have suggested that nerve-released catecholamines may play an important role in the regulation of vascular tone and in the modulation of sensory nerve activity in animal teeth. We have used tyrosine hydroxylase-immunohistochemistry to detect catecholamine-producing cells in human dental pulp and high performance liquid chromatography to identify and quantitate catecholamines in this tissue. Tyrosine hydroxylase-immunoreactivity was confined to a sub-population of nerve fibres that were mainly localized around blood vessels. Considerable concentrations of norepinephrine (17.8 +/- 3.75 pg/mg tissue) and much lower concentrations of dopamine and epinephrine (0.27 +/- 0.10 and 0.19 +/- 0.11 pg/mg, respectively) were measured in all samples examined. It is suggested that catecholamines in human dental pulp are exclusively contained in nervous structures that are mainly associated with blood vessels and that norepinephrine is the candidate neurotransmitter of these nerve fibres. These data provide the basis to further studies addressed to clarify the possible functions of catecholamines in human dental pulp during physiological as well as inflammatory situations. C1 UNIV PAVIA,INST PHARMACOL,I-27100 PAVIA,ITALY. UNIV LONDON,HAMMERSMITH HOSP,ROYAL POSTGRAD MED SCH,HISTOCHEM UNIT,LONDON W12 0NN,ENGLAND. NHLBI,BIOCHEM PHARMACOL SECT,BETHESDA,MD 20205. RP CASASCO, A (reprint author), UNIV PAVIA,INST HISTOL & EMBRIOL,VIA FORLANINI 10,I-27100 PAVIA,ITALY. NR 27 TC 11 Z9 11 U1 0 U2 0 PU LUIGI PONZIO E FIGLIO PI PAVIA PA VIA D DA CATALOGNA 1/3, 27100 PAVIA, ITALY SN 1121-760X J9 EUR J HISTOCHEM JI Eur. J. Histochem. PY 1995 VL 39 IS 2 BP 133 EP 140 PG 8 WC Cell Biology SC Cell Biology GA RC186 UT WOS:A1995RC18600007 PM 7549016 ER PT J AU PANTALEO, G DEMAREST, JF VACCAREZZA, M GRAZIOSI, C BANSAL, GP KOENIG, S FAUCI, AS AF PANTALEO, G DEMAREST, JF VACCAREZZA, M GRAZIOSI, C BANSAL, GP KOENIG, S FAUCI, AS TI EFFECT OF ANTI-V3 ANTIBODIES ON CELL-FREE AND CELL-TO-CELL HUMAN-IMMUNODEFICIENCY-VIRUS TRANSMISSION SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS TYPE 1; ANTI-V3; VIRAL TRANSMISSION ID PRINCIPAL NEUTRALIZING DETERMINANT; ENVELOPE GLYCOPROTEIN; LYMPHOCYTES-T; MONOCLONAL-ANTIBODIES; MATERNAL ANTIBODIES; HIV-INFECTION; HOST RANGE; HTLV-III; V3 LOOP; CYTOPATHIC PROPERTIES AB The present study was undertaken to compare the effects of a type-specific (HIV-1 MN) anti-V3 antibody on in vitro human immunodeficiency virus (HIV) infection of peripheral blood mononuclear cells in systems of cell-free versus cell-to-cell transmission of virus. Anti-V3 antibody completely prevented HIV-1 infection when cell-free virus was the sole mechanism of infection. A significant reduction of the neutralizing activity of the anti-V3 antibody was observed when infectivity was dependent on both cell-free and cell-to-cell mechanisms of infection. Furthermore, when cell-to-cell transfer of virions was the primary mechanism of HIV-1 infection, inhibition of HIV-1 infection was not observed. Therefore, a potent neutralizing antibody with a single epitope specificity failed to effectively control dissemination of a persistent HIV-1 infection in a system characterized predominantly by cell-to-cell transfer of virus. C1 MEDIMMUNE INC,GAITHERSBURG,MD 20878. RP PANTALEO, G (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B-13,BETHESDA,MD 20892, USA. RI Pantaleo, Giuseppe/K-6163-2016; OI VACCAREZZA, Mauro/0000-0003-3060-318X NR 61 TC 23 Z9 24 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 1995 VL 25 IS 1 BP 226 EP 231 DI 10.1002/eji.1830250137 PG 6 WC Immunology SC Immunology GA QQ478 UT WOS:A1995QQ47800036 PM 7843235 ER PT J AU EPLINGBURNETTE, PK WEI, S LIU, JH PERICLE, F USSERY, DW RUSSELL, SM LEONARD, WJ DJEU, JY AF EPLINGBURNETTE, PK WEI, S LIU, JH PERICLE, F USSERY, DW RUSSELL, SM LEONARD, WJ DJEU, JY TI EXPRESSION OF INTERLEUKIN-2 RECEPTOR-GAMMA ON HUMAN MONOCYTES - CHARACTERIZATION OF LINEAGE-SPECIFIC POSTTRANSLATIONAL MODIFICATIONS SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Note DE INTERLEUKIN-2 RECEPTOR; MONOCYTE; GLYCOSYLATION ID IL-2 RECEPTOR; BETA-CHAIN; FUNCTIONAL COMPONENT; CLONING; GENE; P64; INVIVO; CDNAS AB Functional interleukin-2 receptors (IL-2R) on lymphocytes contain both IL-2R beta P and gamma chains. Whereas constitutive expression of IL-2R beta has been found on monocytes, the expression of IL-2R gamma on these phagocytes has not been examined. We performed reverse-transcription-polymerase chain reaction with Southern blot analysis on RNA derived from purified human monocytes and discovered that they constitutively produce IL-2R gamma mRNA. Western immunoblotting revealed 58- and 64-kDa forms of IL-2R gamma on YT-1 and human monocytes, whereas 58-, 64-, and 69-kDa bands were detected using peripheral blood mononuclear cells and non-adherent lymphocytes. These different forms resulted from variable N-linked glycosylation since culture of the cells in tunicamycin resulted in detection of a single 39-kDa band which corresponds to the molecular weight predicted from the deduced amino acid sequence. By co-immunoprecipitation, the IL-2R beta subunit associates with only the 64-kDa IL-2R gamma protein band in monocytes. C1 UNIV S FLORIDA,COLL MED,DEPT MED MICROBIOL,TAMPA,FL. UNIV S FLORIDA,COLL MED,DEPT BIOCHEM,TAMPA,FL. NHLBI,PULM & MOLEC IMMUNOL SECT,BETHESDA,MD. RP EPLINGBURNETTE, PK (reprint author), H LEE MOFFIT CANC CTR & RES INST,IMMUNOL RES PROGRAM,12902 MAGNOLIA DR,TAMPA,FL 33612, USA. RI Russell, Sarah/B-9341-2009 OI Russell, Sarah/0000-0001-5826-9641 FU NCI NIH HHS [CA-46820] NR 25 TC 16 Z9 16 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 1995 VL 25 IS 1 BP 291 EP 294 DI 10.1002/eji.1830250148 PG 4 WC Immunology SC Immunology GA QQ478 UT WOS:A1995QQ47800047 PM 7843245 ER PT J AU ZHANG, W LIU, R HUANG, Q ZHANG, P KOEHLER, KF HARRIS, B SKOLNICK, P COOK, JM AF ZHANG, W LIU, R HUANG, Q ZHANG, P KOEHLER, KF HARRIS, B SKOLNICK, P COOK, JM TI SYNTHESES OF 5-THIENYL-SUBSTITUTED AND 5-FURYL-SUBSTITUTED BENZODIAZEPINES - PROBES OF THE PHARMACOPHORE FOR BENZODIAZEPINE RECEPTOR AGONISTS SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article DE BENZODIAZEPINE RECEPTOR; AGONIST PHARMACOPHORE; 5-FURYLBENZODIAZEPINE; 5-THIENYLBENZODIAZEPINE; STRUCTURE-ACTIVITY RELATIONSHIP ID BINDING-SITE; MOLECULAR MECHANICS; BETA-CARBOLINES; ANTAGONIST; PROTEINS; STEREOCHEMISTRY; DIRECTIONALITY; DIAZEPAM; LIGANDS; SYSTEM AB The synthesis of 5-thienyl- and 5-furyl-substituted benzodiazepines is described. These compounds were employed to probe the lipophilic pocket (L(3)) of the benzodiazepine receptor (BzR) and to determine the effect of occupation of L(3) on biological activity. Of the new analogs synthesized, the 5-(2-thienyl)-benzodiazepines 6a and 7a displayed high affinity for the BzR (IC50 28 and 18 nM, respectively) and exhibited both anticonvulsant (ED(50) approximate to 9 and 3 mg/kg) and muscle relaxant (ED(50) approximate to 10 and 7 mg/kg) activity. The 5-(3-thienyl)benzodiazepines 6d and 7d displayed only moderate affinity for the BzR (IC50 140 and 110 nM) and exhibited no biological activity (no anticonvulsant or muscle relaxant activity) at doses up to 40 mg/kg. The 5-(2-furyl)benzodiazepines (6b, 7b, 19b and 20b) exhibit low affinities for the BzR. These in vitro and in vivo findings are consistent with our model suggesting that pocket L(3) is very sensitive to lipophilic effects. Thus, decreasing the lipophilicity of functional groups which occupy this region decreases ligand affinity at BzR. The 2'-halogen (F or Cl) substituent of the 5-phenylbenzodiazepines increases ligand affinity in vitro because the active conformation of the phenyl N(4)=C(5)-C(1')=C(2') moiety is syn rather than anti. The syn conformation permits the 2'-halogen (F or Cl) atom to interact at the hydrogen bonding site H-2 and form a stable three-centered hydrogen bond in the proposed ligand binding cleft. The 3-thienyl and 2-furyl groups decrease the lipophilicity of the substituent which occupies L(3) but do not form a hydrogen bond at H-2, thus resulting in a diminished affinity at BzR. C1 UNIV WISCONSIN,DEPT CHEM,MILWAUKEE,WI 53201. IST RIC BIOL MOLEC P ANGELETTI,I-00040 POMEZIA,ITALY. NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. NR 59 TC 12 Z9 12 U1 3 U2 3 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0223-5234 J9 EUR J MED CHEM JI Eur. J. Med. Chem. PY 1995 VL 30 IS 6 BP 483 EP 496 DI 10.1016/0223-5234(96)88259-6 PG 14 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA RF745 UT WOS:A1995RF74500004 ER PT J AU NEWLING, DWW ROBINSON, MRG SMITH, PH BYAR, D LOCKWOOD, R STEVENS, I DEPAUW, M SYLVESTER, R AF NEWLING, DWW ROBINSON, MRG SMITH, PH BYAR, D LOCKWOOD, R STEVENS, I DEPAUW, M SYLVESTER, R TI TRYPTOPHAN-METABOLITES, PYRIDOXINE (VITAMIN-B-6) AND THEIR INFLUENCE ON THE RECURRENCE RATE OF SUPERFICIAL BLADDER-CANCER SO EUROPEAN UROLOGY LA English DT Article DE PYRIDOXINE; SUPERFICIAL BLADDER CANCER; TRYPTOPHAN METABOLITES AB This double-blind randomised phase III trial was designed to assess the effect of pyridoxine administration on the recurrence of Ta and Tl transitional cell tumours of the bladder. The trial accrued 291 patients and showed no significant difference between the pyridoxine and placebo treatment groups with respect to the time to first recurrence or the recurrence rate. Adjustment for the main prognostic factors, namely the recurrence rate prior to entry, the number of tumours at entry, the G grade and the levels of the tryptophan metabolites kynurenine plus acetyl kynurenine at entry do not change the overall conclusions. C1 ST JAMES UNIV HOSP,LEEDS LS9 7TF,W YORKSHIRE,ENGLAND. PONTEFRACT DIST GEN HOSP,PONTEFRACT,ENGLAND. NCI,BETHESDA,MD 20892. EORTC DATA CTR,BRUSSELS,BELGIUM. RP NEWLING, DWW (reprint author), FREE UNIV AMSTERDAM HOSP,DEPT UROL,POB 7057,1007 MB AMSTERDAM,NETHERLANDS. FU NCI NIH HHS [5R10CA11488-11, 2U10CA1488-13, 5R10CA11488-12] NR 8 TC 31 Z9 31 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0302-2838 J9 EUR UROL JI Eur. Urol. PY 1995 VL 27 IS 2 BP 110 EP 116 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA QJ590 UT WOS:A1995QJ59000005 PM 7744151 ER PT J AU ABIOLA, FA APPELGREN, LE ARNOLD, D BOISSEAU, J CUERPO, L ELLIS, R FURROW, RD MCLEAN, JG PINTER, A PUGH, DM RICO, A SINHASENI, P WELLS, R YNDESTAD, M CHAMBERLAIN, P FUCHS, R HEITZMAN, RJ HERRMAN, JL KIDD, ARM LIVINGSTON, RC MAHLER, J MILLER, M MITSUMORI, K PAAKKANEN, J RITTER, L ROBERTS, G ROSTELPETERS, B VANLEEUWEN, FXR WILKINS, TD WOODWARD, K YONG, MS AF ABIOLA, FA APPELGREN, LE ARNOLD, D BOISSEAU, J CUERPO, L ELLIS, R FURROW, RD MCLEAN, JG PINTER, A PUGH, DM RICO, A SINHASENI, P WELLS, R YNDESTAD, M CHAMBERLAIN, P FUCHS, R HEITZMAN, RJ HERRMAN, JL KIDD, ARM LIVINGSTON, RC MAHLER, J MILLER, M MITSUMORI, K PAAKKANEN, J RITTER, L ROBERTS, G ROSTELPETERS, B VANLEEUWEN, FXR WILKINS, TD WOODWARD, K YONG, MS TI EVALUATION OF CERTAIN VETERINARY DRUG RESIDUES IN FOOD SO EVALUATION OF CERTAIN VETERINARY DRUG RESIDUES IN FOOD SE WHO TECHNICAL REPORT SERIES LA English DT Review AB This report presents the conclusions of a Joint FAO/WHO Expert Committee convened to evaluate the safety of residues of certain veterinary drugs in edible animal products, with a view to promoting human food safety and harmonization in international trade. In the first part of the report, principles for evaluating the safety of residues of veterinary drugs in food and for establishing Acceptable Daily Intakes and Maximum Residue Limits for such residues are elaborated. In particular, risk assessment procedures use by the Committee, the application of safety factors, the assessment of microbiological risk due to residues of antimicrobial drugs in food, and the problem of residues at the injection site are discussed. The information required by the Committee in investigating the human food safety of residues of veterinary drugs is also listed. A summary follows of the Committee's evaluations and toxicological and residue data on an anthelminthic (levamisole), five antimicrobial agents (chloramphenicol, flumequine, olaquindox, spectinomycin and sulfadimidine), an antiprotozoal agent (ronidazole), a glucocorticosteroid (dexamethasone) and a trypanocide (diminazene). For each drug, an Acceptable Daily Intake and Maximum Residue Limits for certain edible animal products are recommended, as appropriate, or deficiencies in the available data are identified and requirements for further information specified. C1 SWEDISH UNIV AGR SCI,CTR BIOMED,FAC VET MED,DEPT PHARMACOL & TOXICOL,UPPSALA,SWEDEN. CTR SURVEILLANCE & HLTH EVALUAT ENVIRONM CRISIS,BERLIN,GERMANY. NATL CTR VET & FOOD STUDIES,VET DRUGS LAB,FOUGERES,FRANCE. NATL INST AGR TECHNOL,DEPT MEAT TECHNOL,VET SCI RES CTR,BUENOS AIRES,DF,ARGENTINA. US FOOD SAFETY & INSPECT SERV,DIV CHEM,WASHINGTON,DC 20250. SWINEBURNE UNIV TECHNOL,HAWTHORN,VIC,AUSTRALIA. NATL INST HYG,BUDAPEST,HUNGARY. UNIV COLL BALLSBRIDGE,FAC VET MED,DEPT SMALL ANIM CLIN STUDIES,BALLSBRIDGE,IRELAND. NATL VET SCH,INRA,BIOCHEM TOXICOL PHYSIOPATHOL & EXPTL TOXICOL LAB,TOULOUSE,FRANCE. CHULALONGKORN UNIV,DEPT PHARMACOL,BANGKOK,THAILAND. AUSTRALIAN GOVT ANALYT LABS,PYMBLE,NSW,AUSTRALIA. NORWEGIAN COLL VET MED,DEPT FOOD HYG,OSLO,NORWAY. MINIST SCI,ZAGREB,CROATIA. WHO,INT PROGRAMME CHEM SAFETY,GENEVA,SWITZERLAND. NIEHS,ENVIRONM CARCINOGENESIS PROGRAM,EXPTL PATHOL LAB,RES TRIANGLE PK,NC 27709. US FDA,CTR VET MED,OFF NEW ANIM DRUG EVALUAT,DIV TOXICOL & ENVIRONM SCI,ROCKVILLE,MD 20857. NATL INST HYG SCI,DIV PATHOL,BIOL SAFETY RES CTR,TOKYO,JAPAN. FAO,FOOD QUAL SERV,ROME,ITALY. FAO,STAND SERV,ROME,ITALY. UNIV GUELPH,CANADIAN NETWORK TOXICOL CTR,GUELPH,ON,CANADA. DEPT HLTH HOUSING LOCAL GOVT & COMMUNITY SERV,CHEM SAFETY UNIT,TOXICOL EVALUAT SECT,CANBERRA,ACT,AUSTRALIA. COMMISS EUROPEAN COMMUNITIES,DIRECTORATE GEN IIIE3,COMM VET MED PROD WORKING GRP SAFETY RESIDUES,BRUSSELS,BELGIUM. MAFF,VET MED DIRECTORATE,ADDLESTONE,SURREY,ENGLAND. HLTH CANADA,HLTH PROTECT BRANCH,BUR VET DRUGS,DIV HUMAN SAFETY,OTTAWA,ON,CANADA. VIRGINIA POLYTECH INST & STATE UNIV,DEPT ANAEROB MICROBIOL,BLACKSBURG,VA 24061. NATL INST PUBL HLTH & ENVIRONM PROTECT,CTR TOXICOL ADVISORY,BILTHOVEN,NETHERLANDS. RP ABIOLA, FA (reprint author), INTERSTATE SCH VET SCI & MED,DEPT PHARM & TOXICOL,DAKAR,SENEGAL. NR 144 TC 2 Z9 2 U1 4 U2 8 PU WORLD HEALTH ORGANIZATION PI GENEVA PA 1211 27 GENEVA, SWITZERLAND SN 0512-3054 J9 WHO TECH REP SER PY 1995 VL 851 BP 1 EP & PG 0 WC Food Science & Technology; Toxicology; Veterinary Sciences SC Food Science & Technology; Toxicology; Veterinary Sciences GA BD93B UT WOS:A1995BD93B00001 ER PT J AU SEI, Y TAKEMURA, M GUSOVSKY, F SKOLNICK, P BASILE, A AF SEI, Y TAKEMURA, M GUSOVSKY, F SKOLNICK, P BASILE, A TI DISTINCT MECHANISMS FOR CA2+ ENTRY INDUCED BY OKT3 AND CA2+ DEPLETION IN JURKAT T-CELLS SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID MEDIATED CALCIUM ENTRY; ATPASE INHIBITOR THAPSIGARGIN; T3-ANTIGEN RECEPTOR COMPLEX; CYTOPLASMIC FREE CALCIUM; HUMAN LYMPHOCYTE-T; PROTEIN-KINASE-C; ANTIGEN RECEPTOR; PLASMA-MEMBRANE; INOSITOL 1,4,5-TRISPHOSPHATE; INTRACELLULAR CA2+ AB Ca2+ influx triggered by antigen binding to T cell receptors (TCR) is an early event in T cell activation. An additional Ca2+ influx induced by depletion of intracellular Ca2+ (CDCI) has been characterized in human Jurkat T cells that is both temporally and mechanistically distinct from TCR-mediated Ca2+ influx (TCRCI). Both TCRCI and CDCI were insensitive to voltage-gated Ca2+ channel antagonists (e.g., nifedipine, verapamil, and omega-conotoxin G) and pertussis toxin, yet were voltage-sensitive and inhibited by SKF 96365 (a receptor-gated Ca2+ channel blocker) and cholera toxin. However, TCRCI but not CDCI was associated with a significant increase in inositol phosphate (IPx) levels and inhibited by phorbol ester, while CDCI but not TCRCI was inhibited by Sr2+, forskolin (FSK), and 1,9-dideoxy FSK in a cAMP-independent fashion. Moreover, TCR stimulation did not deplete thapsigargin-sensitive Ca2+ stores, suggesting that TCRCI is not merely a consequence of Ca2+ depletion. These results indicate that Ca2+ entry following the depletion of intracellular Ca2+ stores or TCR stimulation occur through distinct cellular mechanisms coexisting in Jurkat T cells. (C) 1995 Academic Press, Inc. C1 NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD 20892. RP SEI, Y (reprint author), NIDDK,NEUROSCI LAB,BLDG 8,ROOM 111,BETHESDA,MD 20892, USA. NR 59 TC 20 Z9 20 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD JAN PY 1995 VL 216 IS 1 BP 222 EP 231 DI 10.1006/excr.1995.1028 PG 10 WC Oncology; Cell Biology SC Oncology; Cell Biology GA QB473 UT WOS:A1995QB47300028 PM 7813624 ER PT J AU NEY, PA FARINA, SF BODINE, DM ANDREWS, NC ORKIN, SH NIENHUIS, AW AF NEY, PA FARINA, SF BODINE, DM ANDREWS, NC ORKIN, SH NIENHUIS, AW TI MICROCYTIC ANEMIA IN MK/MK MICE IS NOT CORRECTED BY RETROVIRAL-MEDIATED GENE-TRANSFER OF WILD-TYPE P45 NF-E2 SO EXPERIMENTAL HEMATOLOGY LA English DT Note DE NF-E2; RETROVIRUS; ANEMIA; MK MUTATION ID PORPHOBILINOGEN DEAMINASE GENE; TRANSCRIPTION FACTOR NF-E2; DOMINANT CONTROL REGION; LEUCINE ZIPPER PROTEIN; LOCUS-CONTROL REGION; ERYTHROID PROMOTER; GLOBIN GENE; ENHANCER; ORGANIZATION; BINDING AB Mice homozygous for the mk mutation have a severe hypochromic, microcytic anemia that is characterized by a decreased mean-corpuscular hemoglobin concentration and balanced alpha- and beta-globin-chain synthesis. Transplantation studies have shown that the defect in homozygous mk/mk mice is intrinsic to both the hematopoietic system and the gut. The gene for the hematopoietic-specific transcription factor, p45 NF-E2, has been found to cosegregate with the mk phenotype and contain a point mutation in mk/mk mice that results in an amino acid substitution (V-173-->A). In order to test the hypothesis that this amino acid substitution is responsible for the mk phenotype, we have used recombinant retroviruses to introduce wild-type p45 NF-E2 into the bone marrow of mk/mk mice. Despite gene transfer and expression of p45 NF-E2 in erythroid cells, we found no evidence for correction of the phenotype in mk/mk mice. These results indicate that the ink mutation cannot be corrected by enforced expression of wild-type p45 NF-E2 and suggest that the V-173-->A mutation of the p45 NF-E2 gene is not the cause of anemia in mk/mk mice. C1 ST JUDE CHILDRENS RES HOSP, DEPT EXPTL HEMATOL, MEMPHIS, TN 38101 USA. NIH, NATL CTR HUMAN GENOME RES, GENE TRANSFER LAB, HEMATOPOIESIS SECT, BETHESDA, MD 20892 USA. CHILDRENS HOSP, DEPT PEDIAT, DIV HEMATOL ONCOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. HOWARD HUGHES MED INST, BOSTON, MA 02115 USA. RP NEY, PA (reprint author), ST JUDE CHILDRENS RES HOSP, DEPT BIOCHEM, 332 N LAUDERDALE ST, MEMPHIS, TN 38101 USA. OI Andrews, Nancy/0000-0003-0243-4462 FU NCI NIH HHS [P30 CA21765] NR 38 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JAN PY 1995 VL 23 IS 1 BP 74 EP 80 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA PY648 UT WOS:A1995PY64800013 PM 7995373 ER PT S AU Trickett, EJ AF Trickett, EJ BE Hobfoll, SE deVries, MW TI The community context of disaster and traumatic stress: An ecological perspective from community psychology SO EXTREME STRESS AND COMMUNITIES: IMPACT AND INTERVENTION SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES D, BEHAVIORAL AND SOCIAL SCIENCES LA English DT Proceedings Paper CT NATO Advanced Research Workshop on Stress and Communities CY JUN 14-18, 1994 CL CHATEAU DE BONAS, FRANCE SP NATO C1 NIMH,ROCKVILLE,MD 20857. NR 0 TC 5 Z9 5 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0258-123X BN 0-7923-3468-X J9 NATO ADV SCI INST SE PY 1995 VL 80 BP 11 EP 25 PG 15 WC Psychology, Clinical; Psychiatry; Psychology, Social SC Psychology; Psychiatry GA BE42B UT WOS:A1995BE42B00002 ER PT J AU VIVINO, MA MAHURKAR, A TRUS, B LOPEZ, ML DATILES, M AF VIVINO, MA MAHURKAR, A TRUS, B LOPEZ, ML DATILES, M TI QUANTITATIVE-ANALYSIS OF RETROILLUMINATION IMAGES SO EYE LA English DT Article ID LENS OPACITIES; CATARACT; PHOTOGRAPHY AB We have developed a semi-automated image processing system for analysis and evaluation of retroillumination images. This paper describes methods used to compensate for illumination variations in the images, separation of data into cataractous and non-cataractous portions, how quantitative measurements are made and how they assess the pathological condition. In addition to the traditional area measurement, this system computes the net integral of density and several measurements involving the location of the opacity in relation to the pupillary margin, The computer measures of area, integral of density, area centrality, weighted area, density centrality and weighted density provide more data than previously described systems. Data produced by this interactive and automated system can be used in studies of posterior subcapsular and cortical cataracts, and to study the effect of these opacities on vision. C1 US DEPT HHS,NEI,OPHTHALM GENET & CLIN SERV BRANCH,CATARACT & CORNEA SECT,BETHESDA,MD 20892. US DEPT HHS,NEI,DIV COMP RES & TECHNOL,COMPUTAT BIOSCI & ENGN LAB,BETHESDA,MD 20892. OI Datiles, Manuel III B./0000-0003-4660-1664 NR 22 TC 4 Z9 4 U1 0 U2 0 PU ROYAL COLL OPHTHALMOLOGISTS PI LONDON PA 17 CORNWALL TERRACE, LONDON, ENGLAND NW1 4QW SN 0950-222X J9 EYE JI Eye PY 1995 VL 9 BP 77 EP 84 PN 1 PG 8 WC Ophthalmology SC Ophthalmology GA QK628 UT WOS:A1995QK62800012 PM 7713254 ER PT B AU MILES, FA AF MILES, FA BE Findlay, JM Walker, R Kentridge, RW TI The sensing of optic flow by the primate optokinetic system SO EYE MOVEMENT RESEARCH: MECHANISMS, PROCESSES AND APPLICATIONS SE STUDIES IN VISUAL INFORMATION PROCESSING LA English DT Proceedings Paper CT 7th European Conference on Eye Movements CY SEP, 1993 CL DURHAM, ENGLAND DE OPTIC FLOW; OPTOKINETIC RESPONSE; VESTIBULE OCULAR REFLEX; TRANSLATION; ROTATION C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. NR 0 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-444-81473-6 J9 STUD VIS INFORM PROC PY 1995 VL 6 BP 47 EP 62 PG 16 WC Neurosciences SC Neurosciences & Neurology GA BD54U UT WOS:A1995BD54U00003 ER PT J AU DAVIES, DR WLODAWER, A AF DAVIES, DR WLODAWER, A TI CYTOKINES AND THEIR RECEPTOR COMPLEXES SO FASEB JOURNAL LA English DT Review DE GROWTH FACTORS; 3-DIMENSIONAL STRUCTURES; SUPER-FAMILIES; SIGNAL TRANSDUCTION ID COLONY-STIMULATING FACTOR; TUMOR NECROSIS FACTOR; NERVE GROWTH-FACTOR; HUMAN TRANSFORMING GROWTH-FACTOR-BETA-2; REFINED CRYSTAL-STRUCTURE; 3-DIMENSIONAL STRUCTURE; ANGSTROM RESOLUTION; INTERLEUKIN 1-ALPHA; 2.6-A RESOLUTION; 2.7-A RESOLUTION AB The 3-dimensional structures resulted from X-ray diffraction and nuclear magnetic resonance analyses of a variety of cytokines are reviewed. These proteins form distinct, well-defined superfamilies based on the structures of their monomers, even in the absence of significant sequence homology. However, in several cases, where the active form of a cytokine is a dimer or higher oligomer, these similar monomers adopt very different modes of dimerization. Two examples of complexes of cytokines with receptor molecules are described and the implications for signal transduction are discussed. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOLEC STRUCT LAB,FREDERICK,MD 21702. RP DAVIES, DR (reprint author), NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. FU NCI NIH HHS [N01-CO-74101] NR 61 TC 43 Z9 43 U1 0 U2 1 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 JAN PY 1995 VL 9 IS 1 BP 50 EP 56 PG 7 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QD202 UT WOS:A1995QD20200009 PM 7821759 ER PT J AU CLORE, GM GRONENBORN, AM AF CLORE, GM GRONENBORN, AM TI 3-DIMENSIONAL STRUCTURES OF ALPHA-CHEMOKINES AND BETA-CHEMOKINES SO FASEB JOURNAL LA English DT Review DE TERTIARY STRUCTURE; QUATERNARY STRUCTURE; NMR; X-RAY CRYSTALLOGRAPHY ID 3-DIMENSIONAL STRUCTURE; FUNCTIONAL EXPRESSION; RECEPTOR-BINDING; CYTOKINE FAMILY; INTERLEUKIN-8; BIOLOGY AB Members of the chemokine family of proteins play a key role in the orchestration of the immune response. This family has been further divided into two subfamilies, alpha and beta, based on sequence, function, and chromosomal location. To date, the three-dimensional structures of two members of the alpha subfamily, interleukin-8 (IL-8) and platelet factor 4, and one member of the beta subfamily, human macrophage inflammatory protein-1 beta (hMIP-1 beta), have been solved by either NMR or X-ray crystallography. In this review, we discuss their three-dimensional structures and their possible relationship to function. The structures of the monomers are very similar, as expected from the significant degree of sequence identity between these proteins. The quaternary structures of the alpha and beta chemokines, however, are entirely distinct and the dimer interface is formed by a completely different set of residues. Whereas the IL-8 dimer is globular, the hMIP-1 beta dimer is elongated and cylindrical. Platelet factor 4 is a tetramer comprising a dimer of dimers of the IL-8 type. The IL-8 dimer comprises a six stranded anti-parallel beta-sheet, three strands contributed by each subunit, on top of which lie two antiparallel helices separated by approximately 14 Angstrom, and the symmetry axis is located between residues 26 and 26' (equivalent to residue 29 of hMIP-1 beta) at the center of strands beta(1) and beta(1)'. In contrast, in the hMIP-1 beta dimer the symmetry axis is located between residues 10 and 10' which are part of an additional mini-antiparallel beta-sheet formed by strands beta(0) and beta(0)'; the two helices are 46 Angstrom apart on opposite sides of the molecule; and strands beta(1) and beta(1)' are about 30 Angstrom apart and located on the exterior of the protein. Calculation of the solvation free energies of dimerization and analysis of hydrophobic clusters strongly suggests that the formation and stabilization of the two different types of dimers arise from the burial of hydrophobic residues, and that the distinct quaternary structures are preserved throughout the two subfamilies. The implications with regard to receptor recognition and the absence of cross-binding between the two subfamilies are discussed. RP CLORE, GM (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 5,BETHESDA,MD 20892, USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 26 TC 98 Z9 100 U1 1 U2 3 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 JAN PY 1995 VL 9 IS 1 BP 57 EP 62 PG 6 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QD202 UT WOS:A1995QD20200010 PM 7821760 ER PT J AU PADLAN, EA ABERGEL, C TIPPER, JP AF PADLAN, EA ABERGEL, C TIPPER, JP TI IDENTIFICATION OF SPECIFICITY-DETERMINING RESIDUES IN ANTIBODIES SO FASEB JOURNAL LA English DT Article DE COMPLEMENTARITY-DETERMINING REGIONS; HUMANIZATION ID 3-DIMENSIONAL STRUCTURE; CRYSTAL-STRUCTURE; ANTIGEN COMPLEX; BINDING-SITE; LIGHT-CHAINS; COMPLEMENTARITY; PROTEIN; MOUSE; NEURAMINIDASE; RESOLUTION AB The successful identification of the residues that contact ligand has important implications, especially in view of the increasing use of antibodies in various medical and industrial applications. Analysis of the crystallographically derived, three-dimensional Structures of five antibody-antigen complexes and of the available amino acid sequence data on antibody variable regions reveals that the residues that contact antigen are in the main also the most variable. It is proposed that a good first guess of the identity of the specificity-determining residues can be made from an examination of the variability values at sequence positions. New boundaries for the complementarity-determining regions are proposed. RP PADLAN, EA (reprint author), NIDDKD,MOLEC BIOL LAB,BLDG 5,ROOM 303,BETHESDA,MD 20892, USA. NR 31 TC 99 Z9 100 U1 0 U2 1 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 JAN PY 1995 VL 9 IS 1 BP 133 EP 139 PG 7 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QD202 UT WOS:A1995QD20200021 PM 7821752 ER PT J AU HEIDARAN, MA MAHADEVAN, D LAROCHELLE, WJ AF HEIDARAN, MA MAHADEVAN, D LAROCHELLE, WJ TI BETA-PDGFR-IGG CHIMERA DEMONSTRATES THAT HUMAN BETA-PDGFR IG-LIKE DOMAIN-1 TO DOMAIN-3 ARE SUFFICIENT FOR HIGH-AFFINITY PDGF-BB BINDING SO FASEB JOURNAL LA English DT Article DE FUSION PROTEINS; PLATELET-DERIVED GROWTH FACTOR RECEPTOR; SURAMIN ID GROWTH-FACTOR RECEPTORS; SIMIAN SARCOMA-VIRUS; MONOCLONAL-ANTIBODY; HUMAN-ALPHA; EXTRACELLULAR DOMAIN; FUSION PROTEINS; LIGAND-BINDING; V-SIS; EXPRESSION; INHIBITION AB To localize human beta PDGFR binding determinants, we constructed a fusion protein comprising beta PDGFR Ig-like domains 1 to 3 and an IgG(1) Fc domain (beta PDGFR-HFc). beta PDGFR-HFc was expressed as a 200 kDa dimeric molecule and contained Fc epitopes as demonstrated by anti-mouse Fc antibody recognition. Scatchard analysis revealed that PDGF BB possessed a dissociation constant of 1.5 nM for beta PDGFR-HFc. Thus, beta PDGFR Ig-like domains 1 to 3 are sufficient for high affinity PDGF BB binding. We exploited this fusion protein technology to identify and characterize beta PDGFR antagonists using a sensitive beta PDGFR immunosorbent assay. In this assay, beta PDGFR-HFc half-maximally bound to PDGF BB with an affinity of around 150 pM. Suramin, as well as bacterially expressed and refolded human alpha PDGFR domains 1-3, inhibited beta PDGFR-HFc binding to PDGF BB half-maximally at 25 mu M and 10 nM respectively. Therefore, alpha PDGFR D1-3, like beta PDGFR D1-3, are sufficient for high affinity PDGF BB binding. Furthermore, the beta PDGFR-HFc immunosorbent assay will be useful to identify beta PDGFR antagonists as well as to study alpha and beta PDGFR substitution mutants which further map receptor binding determinants. C1 NCI,BETHESDA,MD 20892. NR 45 TC 21 Z9 22 U1 0 U2 1 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 JAN PY 1995 VL 9 IS 1 BP 140 EP 145 PG 6 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QD202 UT WOS:A1995QD20200022 PM 7821753 ER PT J AU Agarwal, R Mustafa, J Gupta, A Osman, SM AF Agarwal, R Mustafa, J Gupta, A Osman, SM TI Oil rich euphorbiaceae seeds with high contents of linoleic acid SO FETT WISSENSCHAFT TECHNOLOGIE-FAT SCIENCE TECHNOLOGY LA English DT Article AB Seed oils of Aleurites molucanna and Aleurites montance of Euphorbiaceae family have been studied and their fatty acid composition was determined using chromatographic and spectroscopic techniques, Both the seeds contain high percentage (46.3%: 48%) of oils. The chief components of both oils were palmitic (41.7%; 27.9%) and linoleic (45%; 65.5%) acids. C1 NCI,FREDERICK CANC RES & DEV CTR,BASIC RES PROGRAM,ABL,FREDERICK,MD 21702. NR 3 TC 2 Z9 2 U1 2 U2 2 PU KONRADIN INDUSTRIEVERLAG GMBH PI LEINFELDEN-ECHTERDINGEN PA ERNST-MEY-STR 8, 70771 LEINFELDEN-ECHTERDINGEN, GERMANY SN 0931-5985 J9 FETT WISS TECHNOL JI Fett Wiss. Technol.-Fat Sci. Technol. PY 1995 VL 97 SI 2 BP 526 EP 527 PG 2 WC Chemistry, Applied; Food Science & Technology SC Chemistry; Food Science & Technology GA TP005 UT WOS:A1995TP00500004 ER PT J AU Agarwal, R Ansari, MH Ahmad, M AF Agarwal, R Ansari, MH Ahmad, M TI Physico-chemical screening of minor seed oils SO FETT WISSENSCHAFT TECHNOLOGIE-FAT SCIENCE TECHNOLOGY LA English DT Article AB Six seed oils were analysed for their fatty acid composition by physico-chemical methods. These seed oils, belonging to three different families, are interesting in having more than 50 - 80% of unsaturated acids. Seeds from Antirrlinum majus and Solanum saforthianum contain oil which on the basis of chromatographic analyses, appears to be a suitable source for oleic and linoleic acids, respectively. C1 ABL,BASIC RES PROGRAM,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 6 TC 1 Z9 1 U1 0 U2 0 PU KONRADIN INDUSTRIEVERLAG GMBH PI LEINFELDEN-ECHTERDINGEN PA ERNST-MEY-STR 8, 70771 LEINFELDEN-ECHTERDINGEN, GERMANY SN 0931-5985 J9 FETT WISS TECHNOL JI Fett Wiss. Technol.-Fat Sci. Technol. PY 1995 VL 97 SI 2 BP 548 EP 549 PG 2 WC Chemistry, Applied; Food Science & Technology SC Chemistry; Food Science & Technology GA TP005 UT WOS:A1995TP00500010 ER PT J AU Westergaard, GC Suomi, SJ AF Westergaard, GC Suomi, SJ TI Stone-throwing by capuchins (Cebus apella): A model of throwing capabilities in Homo habilis SO FOLIA PRIMATOLOGICA LA English DT Article DE capuchin; Cebus apella; hominid; Homo habilis; stone tools; throwing ID HAND PREFERENCE; MONKEYS; TOOLS; AGE RP Westergaard, GC (reprint author), NICHHD,ANIM CTR,COMPARAT ETHOL LAB,POB 529,POOLESVILLE,MD 20837, USA. NR 17 TC 2 Z9 2 U1 2 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 1995 VL 65 IS 4 BP 234 EP 238 PG 5 WC Zoology SC Zoology GA VG097 UT WOS:A1995VG09700008 PM 8810051 ER PT J AU CAO, GH CUTLER, RG AF CAO, GH CUTLER, RG TI THE DEFINITION AND MEASUREMENT OF ANTIOXIDANTS IN BIOLOGICAL-SYSTEMS - REPLY SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Letter C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. RP CAO, GH (reprint author), TUFTS UNIV,HUMAN NUTR RES CTR AGING,USDA ARS,711 WASHINGTON ST,BOSTON,MA 02111, USA. NR 4 TC 1 Z9 1 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD JAN PY 1995 VL 18 IS 1 BP 126 EP 126 DI 10.1016/0891-5849(95)90077-2 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA PZ979 UT WOS:A1995PZ97900016 ER PT J AU CHAMULITRAT, W PARKER, CE TOMER, KB MASON, RP AF CHAMULITRAT, W PARKER, CE TOMER, KB MASON, RP TI PHENYL N-TERT-BUTYL NITRONE FORMS NITRIC-OXIDE AS A RESULT OF ITS FE(III)-CATALYZED HYDROLYSIS OR HYDROXYL RADICAL ADDUCT FORMATION SO FREE RADICAL RESEARCH LA English DT Article; Proceedings Paper CT 4th International Symposium on Spin Trapping and Organic EPR Spectroscopy with Applications in Chemistry, Biology and Medicine CY OCT 24-28, 1993 CL OKLAHOMA MED RES FDN, OKLAHOMA CITY, OK HO OKLAHOMA MED RES FDN DE SPIN TRAPS; NITRIC OXIDE; EPR; NITROSYL IRON COMPLEXES; NITRONES; HYDROXYLAMINES ID SPIN-TRAPPING AGENTS; TRANSDUCTION MECHANISM; ISCHEMIA-REPERFUSION; OXIDATIVE DAMAGE; L-ARGININE; PBN; BUTYLNITRONE; GENERATION; BRAIN; COMMUNICATION AB Phenyl N-tert-butyl nitrone (PEN) is commonly employed in spin-trapping studies. We report here evidence that PEN in aqueous solutions is decomposed by two pathways leading to the generation of nitric oxide ((NO)-N-.). The first pathway is by hydrolysis of PEN, which is strongly catalyzed by ferric iron. The second pathway is via PBN-hydroxyl radical adduct formation. (NO)-N-. was trapped in the presence of cysteine and ferrous iron to form a [(cys)(2)Fe(NO)(2)](-3) complex, which was measured by use of electron paramagnetic resonance (EPR) spectroscopy. A concomitant metabolite, benzaldehyde, was detected from both reaction mixtures. We propose that PEN is hydrolyzed by Fe3+ or attacked by hydroxyl radical, leading eventually to a common transient species, tert-butyl hydronitroxide [t-BuN(O-.)H], which is further oxidized to a (NO)-N-. source, t-BuNO. Our data imply that PEN may decompose to (NO)-N-. when used in biological models with oxidative stress conditions. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RI Tomer, Kenneth/E-8018-2013 NR 31 TC 23 Z9 23 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 1995 VL 23 IS 1 BP 1 EP 14 DI 10.3109/10715769509064014 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QW910 UT WOS:A1995QW91000002 PM 7647915 ER PT J AU MILES, AM GIBSON, MF KIRSHNA, M PACELLI, R WINK, D COOK, JC GRISHAM, MB AF MILES, AM GIBSON, MF KIRSHNA, M PACELLI, R WINK, D COOK, JC GRISHAM, MB TI EFFECTS OF SUPEROXIDE ON NITRIC OXIDE-DEPENDENT N-NITROSATION REACTIONS SO FREE RADICAL RESEARCH LA English DT Article DE NITRIC OXIDE; SUPEROXIDE; N-NITROSATION; POLYMORPHONUCLEAR LEUKOCYTES ID DNA DAMAGE; MACROPHAGES; KINETICS; PEROXYNITRITE; INHIBITORS; SYNTHASE; NITRATE; AGENTS; CELLS AB Recent studies have demonstrated that nitric oxide (NO) in the presence of superoxide (O-2(-)) may mediate mutagenesis via the N-nitrosation of DNA bases followed by nitrosative deamination to yield their hydroxylated derivatives. We have found that phorbol myristate acetate (PMA)-activated extravasated rat neutrophils (PMNs) will N-nitrosate 2,3-diaminonaphthalene (DAN) to yield its highly fluorescent nitrosation product 2,3- naphthotriazole (triazole) via the L-arginine dependent formation of NO. Addition of SOD enhanced triazole formation suggesting that O-2(-) production may inhibit the N-nitrosating activity and thus the mutagenic activity of inflammatory PMNs. The objective of this study was to assess the role of superoxide as a modulator of NO-dependent N-nitrosation reactions using PMA-activated PMNs as well as a chemically defined-system that generates both NO and superoxide. We found that PMA-activation of PMNs reduced the amount of N-nitrosation of DAN by approximately 64% when compared to non- stimulated cells (450 vs. 1250 nM). Addition of SOD but not inactivated SOD or catalase to PMA-activated PMNs enhanced the formation of triazole by approximately 4-fold (1950 nM). In addition, we found that the NO-releasing spermine/NO adduct (Sp/NO; 50 mu M) which produces approximately 1.0 nmol NO/min generated approximately 8000 nM of triazole whereas the combination of Sp/NO and a superoxide generator (hypoxanthine/xanthine oxidase) that produces approximately 1.0 nmol O-2(-)/min reduced triazole formation by 90% (790 nM). Addition of SOD but not catalase restored the N-nitrosating activity. We conclude that equimolar fluxes of superoxide react rapidly with NO to generate products that have only limited ability to N-nitrosate aromatic amino compounds and thus may have limited ability to promote mutagenesis via the nitrosative deamination of DNA bases. C1 LOUISIANA STATE UNIV,MED CTR,DEPT PHYSIOL & BIOPHYS,SHREVEPORT,LA 71130. NCI,RADIAT BIOL BRANCH,RADIOBIOL SECT,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,CHEM SECT,FREDERICK,MD 21702. FU NCI NIH HHS [CA63641]; NIDDK NIH HHS [DK47663] NR 38 TC 27 Z9 27 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 1995 VL 23 IS 4 BP 379 EP 390 DI 10.3109/10715769509065259 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RN642 UT WOS:A1995RN64200008 PM 7493044 ER PT J AU SELGRADE, MJK COOPER, KD DEVLIN, RB VANLOVEREN, H BIAGINI, RE LUSTER, MI AF SELGRADE, MJK COOPER, KD DEVLIN, RB VANLOVEREN, H BIAGINI, RE LUSTER, MI TI IMMUNOTOXICITY-BRIDGING THE GAP BETWEEN ANIMAL RESEARCH AND HUMAN HEALTH-EFFECTS SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Editorial Material ID ULTRAVIOLET-RADIATION; CONTACT HYPERSENSITIVITY; INDUCED SUPPRESSION; RISK ASSESSMENT; SKIN-CANCER; EXPOSURE; IMMUNE; INDUCTION; INVIVO; TESTS C1 UNIV MICHIGAN,DEPT DERMATOL,ANN ARBOR,MI 48109. NATL INST PUBL HLTH & ENVIRONM PROTECT,PATHOL LAB,3720 BA BILTHOVEN,NETHERLANDS. NIOSH,CINCINNATI,OH 45226. NIEHS,ENVIRONM IMMUNOL & NEUROBIOL SECT,RES TRIANGLE PK,NC 27709. RP SELGRADE, MJK (reprint author), US EPA,HLTH EFFECTS RES LAB,RES TRIANGLE PK,NC 27711, USA. NR 28 TC 27 Z9 29 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1995 VL 24 IS 1 BP 13 EP 21 DI 10.1006/faat.1995.1003 PG 9 WC Toxicology SC Toxicology GA QC921 UT WOS:A1995QC92100003 PM 7713335 ER PT J AU VOSS, KA CHAMBERLAIN, WJ BACON, CW HERBERT, RA WALTERS, DB NORRED, WP AF VOSS, KA CHAMBERLAIN, WJ BACON, CW HERBERT, RA WALTERS, DB NORRED, WP TI SUBCHRONIC FEEDING STUDY OF THE MYCOTOXIN FUMONISIN B1 IN B6C3F1 MICE AND FISCHER-344 RATS SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID FUSARIUM-MONILIFORME; ESOPHAGEAL CANCER; EQUINE LEUKOENCEPHALOMALACIA; NATURAL OCCURRENCE; CORN; TOXICITY; TRANSKEI; CONTAMINATION; CYTOTOXICITY; SPHINGANINE AB Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium moniliforme, a common fungus which occurs naturally on corn, and other Fusarium species. FB1 and other fumonisins are now recognized as having potentially important animal and human health implications. However, few toxicological data are currently available. Male and female B6C3F1 mice and Fischer 344 rats were fed diets containing O, 1, 3, 9, 27, or 81 ppm FB1 (greater than or equal to 98% purity) for 13 weeks. No differences in behavior or appearance, body weight or food consumption between control and FB1-fed groups were found. In mice, hepatopathy and altered serum chemical profiles indicative of hepatotoxicity were found in females fed the 81 ppm diet. No adverse effects were found in female mice fed less than or equal to 27 ppm FB1 or in male mice at any dietary level studied. In rats, nephrosis involving the outer medulla was found in males fed greater than or equal to 9 ppm and, to a lesser degree, in females fed 81 ppm FB1, while decreased kidney weight was found in both sexes at dietary levels greater than or equal to 9 ppm FB1. Although the liver is a target organ of FB1 in rats, hepatotoxicity was not found in rats fed diets containing up to 81 ppm FB 1 for 90 days. Thus, FB1 was toxic to both species following subchronic oral exposure, although significant interspecies differences in the no observed effect levels and organ-specific responses were found. (C) 1995 Society of Toxicology. C1 NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. RP VOSS, KA (reprint author), USDA ARS,RICHARD B RUSSELL AGR RES CTR,TOXICOL & MYCOTOXIN RES UNIT,POB 5677,ATHENS,GA 30613, USA. FU PHS HHS [58-6612-M-016] NR 48 TC 90 Z9 92 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1995 VL 24 IS 1 BP 102 EP 110 DI 10.1006/faat.1995.1012 PG 9 WC Toxicology SC Toxicology GA QC921 UT WOS:A1995QC92100012 PM 7713333 ER PT J AU GRIZZLE, TB GEORGE, JD FAIL, PA HEINDEL, JJ AF GRIZZLE, TB GEORGE, JD FAIL, PA HEINDEL, JJ TI CARISOPRODOL - REPRODUCTIVE ASSESSMENT BY CONTINUOUS BREEDING IN SWISS MICE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID TOXICOLOGY; RATS AB Carisoprodol (CARI), a commonly prescribed neuromuscular relaxant, was evaluated for reproductive toxicity in Swiss CD-1 mice using the Reproductive Assessment by Continuous Breeding (RACE) protocol. Male and female mice were given CARI in corn oil suspension by daily gavage at doses of 0, 300, 750, and 1200 mg/kg body wt/day. Clinical signs of general toxicity in F-0 animals included sedation, primarily in the high-dose group during the first week of exposure, and reduced body weight in high-dose females. CARI administration for 14 weeks did not affect the ability of the F-0 animals to produce litters. However, decreases in proportion of pups born alive (4%) and absolute (5%) and adjusted live pup weight (7%) were observed at 1200 mg/kg CARI when compared to controls. In a crossover mating trial to determine the affected sex, there were no significant differences in the measured reproductive parameters. CARI at the high dose increased the proportion of time spent in proestrus and estrus, but cycle length was unaffected. At F-0 nec ropsy (Week 27 of treatment), all sperm parameters were normal. Right epididymis and liver weights, relative to body weight, were increased (12 and 23%, respectively) over the control group for high-dose males. A mating trial to determine the fertility and reproductive competence of the F-1 generation showed no effect of CARI on indices of mating, pregnancy, or fertility, the proportion of F-2 pups born alive, the sex ratio of live F-2 pups, live F-2 pup weight, or gestation length. However, decreases in the number of F-2 pups per litter (22%) and adjusted live F-2 pup weight (8%) were observed in the high-dose group. Indications of generalized toxicity in the F-1 generation included decreased survival through Postnatal Day 21 at 750 (5%) and 1200 (9%) mg/kg CARI, and transiently decreased body weights during postnatal development and as adults for males and females at all dose levels. At necropsy, there was no effect of treatment on the relative weight of any male or female reproductive organs; testicular spermatid concentration was reduced at all levels of CARI. Relative liver weight was increased for females at 300 mg/kg and for males and females at both 750 and 1200 mg/kg. In summary, CARI produced generalized toxicity and moderate effects on the reproductive processes of F-0 and F-1 generation Swiss mice during chronic exposures of up to 1200 mg/kg/day. (C) 1995 Society of Toxicology. C1 NIEHS,NATL TOXICOL PROGRAM,DEV & REPROD TOXICOL GRP,RES TRIANGLE PK,NC 27709. RP GRIZZLE, TB (reprint author), RES TRIANGLE INST,CTR LIFE SCI & TOXICOL,DIV CHEM & LIFE SCI,POB 12194,RES TRIANGLE PK,NC 27709, USA. FU NIEHS NIH HHS [N01-ES-65141] NR 30 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1995 VL 24 IS 1 BP 132 EP 139 DI 10.1006/faat.1995.1014 PG 8 WC Toxicology SC Toxicology GA QC921 UT WOS:A1995QC92100014 PM 7713336 ER PT J AU LE, SY SONENBERG, N MAIZEL, JV AF LE, SY SONENBERG, N MAIZEL, JV TI UNUSUAL FOLDING REGIONS AND RIBOSOME LANDING PAD WITHIN HEPATITIS-C VIRUS AND PESTIVIRUS RNAS SO GENE LA English DT Article DE MESSENGER-RNA TRANSLATION; INTERNAL INITIATION; PSEUDOKNOT ID 5' NONTRANSLATED REGION; SECONDARY STRUCTURE; UNTRANSLATED REGION; FUNCTIONAL-ANALYSIS; PICORNAVIRUS RNA; INITIATION SITE; TRANSLATION; ELEMENTS; SEQUENCE; MECHANISM AB A statistically significant folding region is identified in the 5' untranslated region (5'-UTR) of hepatitis C virus (HCV), bovine viral diarrhea virus and hog cholera virus. This unusual folding region (UFR) detected in HCV encompasses 199 nucleotides (nt) and coincides with the reported internal ribosome entry site or ribosome landing pad (RLP), as determined by the 5' and 3' deletions [Tsukiyama-Kohara et al., J. Virol. 66 (1992) 1476-1483], The RNA structure predicted in the UFR of HCV consists of a large stem-loop and a pseudoknot. The proposed structural model is consistent with RNase sensitivity studies [Brown et al., Nucleic Acids Res. 20 (1992) 5041-5045]. Moreover, the structure is highly conserved among these divergent HCV and pestivirus RNAs. The covariation of paired bases in the helical regions offers support for the proposed structural models, The pseudoknot predicted in these UFR shares a similar structural feature to those proposed in the RLP of cardioviruses, aphthoviruses and hepatitis A virus. Based on the common structural motif, a putative base-pairing model between HCV RNA and 18S rRNA, as well as pestiviral RNAs and 18S rRNA are suggested, Intriguingly, the proposed base-pairing models in this study are comparable to those proposed in picornaviruses in terms of their folded shape and location of the predicted complementary sequences between viral RNAs and 18S rRNA. Taken together, we suggest that the common base-pairing model between the UFR detected in the 5'-UTR of pestivirus and HCV and 18S rRNA have a general function in the internal initiation of cap-independent translation. C1 MCGILL UNIV,DEPT BIOCHEM,MONTREAL,PQ H3G 1Y6,CANADA. MCGILL UNIV,MCGILL CANC CTR,MONTREAL,PQ H3G 1Y6,CANADA. RP LE, SY (reprint author), NCI,DCBDC,MATH BIOL LAB,BLDG 469,ROOM 151,FREDERICK,MD 21702, USA. NR 23 TC 40 Z9 43 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PY 1995 VL 154 IS 2 BP 137 EP 143 DI 10.1016/0378-1119(94)00859-Q PG 7 WC Genetics & Heredity SC Genetics & Heredity GA QN064 UT WOS:A1995QN06400001 PM 7890155 ER PT J AU PARIKH, H SHAH, S HILT, D PETERKOFSKY, A AF PARIKH, H SHAH, S HILT, D PETERKOFSKY, A TI ORGANIZATION, SEQUENCE AND REGULATION OF EXPRESSION OF THE MURINE HOXA-7 GENE SO GENE LA English DT Note DE CAT FUSION; PRIMER EXTENSION; RT-PCR ID PROMOTER; ELEMENTS AB The genomic sequence of Hoxa-7 (encoding the HOXa-7 homeobox protein), including the coding region (0.7 kb), flanked by a 5'-upstream region (2.8 kb), a 3'-downstream region (1 kb) and interrupted by an intron (995 bp), was determined, Northern blot analysis indicated the transcript size of Hoxa-7 to be 2.1-2.4 kb. Reverse transcription-PCR and primer extension analysis established the 5'-boundary of the mRNA to be in the region 1166 nt upstream from the start codon. Transient transfection of various Hoxa-7::cat constructs in NIH 3T3 cells was used to characterize the transcriptional activity of the 5'-flanking region of the gene, Constructs containing 544, 274 and 71 bp of the region upstream from the transcription start point (tsp) exhibited 78, 203 and 407%, respectively, of the activity shown by a control construct containing 739 bp of the upstream region. These data suggested the presence of negative regulatory elements in the region from 544 to 71 bp upstream from the tsp. C1 NHLBI,BIOCHIM GENET LAB,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DEPT NEUROL,BALTIMORE,MD 21201. NR 19 TC 12 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PY 1995 VL 154 IS 2 BP 237 EP 242 DI 10.1016/0378-1119(94)00850-R PG 6 WC Genetics & Heredity SC Genetics & Heredity GA QN064 UT WOS:A1995QN06400018 PM 7890170 ER PT S AU Pennypacker, KR Hong, JS AF Pennypacker, KR Hong, JS BE Yu, ACH Eng, LF McMahan, UJ Schulman, H Shooter, EM Stadlin, A TI Kainate-induced changes in gene expression in the rat hippocampus SO GENE EXPRESSION IN THE CENTRAL NERVOUS SYSTEM SE PROGRESS IN BRAIN RESEARCH LA English DT Article; Proceedings Paper CT 2nd Stanford International Neuroscience Symposium CY OCT 19-22, 1993 CL BEIJING, PEOPLES R CHINA SP Stanford Univ, Sch Med, Beijing Med Univ, Chinese Univ Hong Kong, Fac Med, N Amer Med Assoc Fdn, Hong Kong ID PROENKEPHALIN MESSENGER-RNA; ACID-INDUCED SEIZURES; DNA-BINDING ACTIVITY; KAINIC ACID; KAPPA-B; GLUCOCORTICOID REGULATION; INDUCIBLE ENHANCER; PROTEIN-KINASE; CYCLIC AMP; FOS RP Pennypacker, KR (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,NEUROPHARMACOL SECT,RES TRIANGLE PK,NC 27709, USA. RI Pennypacker, Keith/I-5092-2012 NR 64 TC 3 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 BN 0-444-81852-9 J9 PROG BRAIN RES PY 1995 VL 105 BP 105 EP 116 PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Cell Biology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BE39G UT WOS:A1995BE39G00010 PM 7568869 ER PT J AU LACORAZZA, HD JENDOUBI, M AF LACORAZZA, HD JENDOUBI, M TI CORRECTION OF ORNITHINE-DELTA-AMINOTRANSFERASE DEFICIENCY IN A CHINESE-HAMSTER OVARY CELL-LINE MEDIATED BY RETROVIRUS GENE-TRANSFER SO GENE THERAPY LA English DT Article DE ORNITHINE-DELTA-AMINOTRANSFERASE; RETROVIRUS; GENE TRANSFER; DEFICIENCY TRANSFECTION; VIRAL TRANSDUCTION ID GYRATE ATROPHY; EXPRESSION; HEPATOCYTES; THERAPY; MOUSE; HYPERCHOLESTEROLEMIA; VECTORS; RETINA; DNA AB Gyrate atrophy (GA) of the choroid and retina is an autosomal recessive chorioretinal degeneration, caused by deficiency of the mitochondrial matrix enzyme ornithine- delta-aminotransferase (OAT). This deficiency results in the accumulation of ornithine in the body fluids and leads to hyperornithinemia. Although the clinical phenotype is largely confined to the eye, OAT deficiency is a systemic disorder. With the final goal of applying gene therapy to this human genetic disease, we have established an in vitro model to test the correction of OAT enzymatic deficiency in mammalian cells, using OAT recombinant retroviruses. We report the construction of several Moloney murine leukemia virus (MoMLV)-based recombinant retrovirus vectors, in which the human OAT cDNA was placed under the transcriptional control of the mouse phosphoglycerate kinase (PGK) promoter or under the enhancer-promoter regulatory element derived from the MoMLV long terminal repeat (LTR). The retrovirus constructs were packaged in the PG13-GALV cell line and used to transduce C9, an OAT deficient cell line derived from Chinese hamster ovary cells (CHO-K1). We show that the recombinant retrovirus transfers the human OAT (hOAT) gene into C9. Expression of the hOAT gene in the transduced C9 deficient cell line exceeded the OAT mRNA level and enzymatic activity of endogenous human fibroblasts. C1 NEI,IMMUNOL LAB,GENET & MOLEC IMMUNOL SECT,BETHESDA,MD 20892. NR 30 TC 7 Z9 7 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0969-7128 J9 GENE THER JI Gene Ther. PD JAN PY 1995 VL 2 IS 1 BP 22 EP 28 PG 7 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA QD783 UT WOS:A1995QD78300004 PM 7712330 ER PT J AU CARREJO, MH SHARRETT, AR PATSCH, W BOERWINKLE, E AF CARREJO, MH SHARRETT, AR PATSCH, W BOERWINKLE, E TI NO ASSOCIATION OF APOLIPOPROTEIN A-IV CODON-347 AND CODON-360 VARIATION WITH ATHEROSCLEROSIS AND LIPID TRANSPORT IN A SAMPLE OF MIXED HYPERLIPIDEMICS SO GENETIC EPIDEMIOLOGY LA English DT Article DE APOLIPOPROTEIN A-IV; COMBINED HYPERLIPIDEMIA; HYPERTRIGLYCERIDEMIA ID DENSITY-LIPOPROTEIN CHOLESTEROL; IMPROVED LIPOLYTIC EFFICIENCY; ENZYMATIC DETERMINATION; BLOOD COLLECTION; PLASMA; PRECIPITATION; POLYMORPHISM; QUANTITATION; REAGENT; GENES AB Genetic variation at the apolipoprotein (ape) A-I/C-III/A-IV gene cluster on chromosome 11 has been associated with differences in occurrence of atherosclerosis and with variability in lipid levels among hypercholesterolemic-hypertriglyceridemic individuals. The functional cause of the association is not known, but polymorphisms of the apo A-IV gene are of interest because apo A-IV is involved in both triglyceride and cholesterol metabolism. Two mutations in the apo A-IV gene, 347T-->S and 360Q-->H, are known to cause amino acid substitutions in the mature protein. These polymorphisms were typed in a sample of 119 subjects with high cholesterol and high triglycerides in whom carotid artery wall thickness was previously shown to be strongly associated with silent polymorphic variation in the A-I/C-III/A-IV gene cluster. The relative allele frequencies were 0.83 and 0.17 for codon 347T-->S, and 0.95 and 0.05 for codon 360Q-->H. These polymorphisms did not show a statistically significant relationship with prevalent hypertension, diabetes, or cardiovascular disease or with plasma lipid levels. Most importantly, these amino acid substitutions in apo A-IV were not associated with carotid artery wall thickness. Therefore, the genetic cause of disease variability in a sample of mixed hyperlipidemics is not amino acid substitutions in codons 347 or 360 of the apolipoprotein A-IV gene. (C) 1995 Wiley-Liss, Inc. C1 UNIV TEXAS,HLTH SCI CTR,CTR HUMAN GENET,HOUSTON,TX 77225. BAYLOR COLL MED,DEPT INTERNAL MED,HOUSTON,TX 77030. NHLBI,BETHESDA,MD 20892. FU NHLBI NIH HHS [HL-40613, HL-27341, N01-HC55015] NR 32 TC 10 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1995 VL 12 IS 4 BP 371 EP 380 DI 10.1002/gepi.1370120405 PG 10 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA RT125 UT WOS:A1995RT12500004 PM 8536954 ER PT J AU Goldin, LR Chase, GA King, TM Badner, JA Gershon, ES AF Goldin, LR Chase, GA King, TM Badner, JA Gershon, ES TI Use of exact and adjusted liability scores to detect genes affecting common traits SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT Genetic Analysis Workshop 9 - Analysis of Complex Oligogenic Traits (GAW9) CY OCT 16-18, 1994 CL VAL MORIN, CANADA DE sib-pair test; genome screening; liability traits ID LINKAGE AB We used the Haseman-Elston sib-pair test to screen for linkage of markers to genes for disease susceptibility in the simulated data as given in Problem 2 of GAW9. We applied the analysis to the underlying quantitative liability trait (Q1), other covariates of Q1 (Q2-Q4), and the dichotomous affection status trait. In addition, we analyzed the residual Q1 after adjusting for the covariates. Using the sib-pair linkage test, we identified a large region of chromosome 5 affecting the residual value of Q1, a region of chromosome 2 affecting Q3, and a region of chromosome 1 possibly affecting Q2. The analysis of the dichotomous traits did not reveal any regions to be significant. This is likely to be due to lack of information since the families were not selected through affected probands. (C) 1995 Wiley-Liss, Inc. C1 GEORGETOWN UNIV,MED CTR,OFF CONSULTING BIOSTAT,WASHINGTON,DC 20007. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT EPIDEMIOL,HOUSTON,TX. RP Goldin, LR (reprint author), NIMH,CNG,CLIN NEUROGENET BRANCH,BLDG 10,RM 3N218,10 CTR DR,MSC 1274,BETHESDA,MD 20814, USA. FU NCRR NIH HHS [RR03655] NR 7 TC 5 Z9 5 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1995 VL 12 IS 6 BP 765 EP 769 DI 10.1002/gepi.1370120639 PG 5 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA TP137 UT WOS:A1995TP13700037 PM 8788006 ER PT J AU Goldin, LR Bishop, DT Meyers, DA Morgan, K Rice, JP MacCluer, JW AF Goldin, LR Bishop, DT Meyers, DA Morgan, K Rice, JP MacCluer, JW TI Genetic Analysis Workshop 9 - Analysis of Complex Oligogenic Traits - Preface SO GENETIC EPIDEMIOLOGY LA English DT Editorial Material C1 IMPERIAL CANC RES FUND,GENET EPIDEMIOL LAB,LEEDS LS2 9LU,W YORKSHIRE,ENGLAND. JOHNS HOPKINS UNIV HOSP,CTR GENET MED,BALTIMORE,MD 21205. MONTREAL GEN HOSP,DIV MED GENET,MONTREAL,PQ H3G 1A4,CANADA. WASHINGTON UNIV,SCH MED,DEPT PSYCHIAT,ST LOUIS,MO 63110. SW FDN BIOMED RES,DEPT GENET,SAN ANTONIO,TX 78228. RP Goldin, LR (reprint author), NIMH,CLIN NEUROGENET BRANCH,BLDG 10,ROOM 3N218,10 CTR DR,MSC 1274,BETHESDA,MD 20814, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1995 VL 12 IS 6 BP R19 EP R20 PG 2 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA TP137 UT WOS:A1995TP13700001 ER PT B AU KASPRZAK, KS AF KASPRZAK, KS BE Sarkar, B TI OXIDATIVE MECHANISMS OF NICKEL(II) AND COBALT(II) GENOTOXICITY SO GENETIC RESPONSE TO METALS LA English DT Proceedings Paper CT 1st International Symposium on Metals and Genetics - Genetic Response to Metals CY MAY 24-27, 1994 CL TORONTO, CANADA SP Hosp Sick Children, Toronto, Canada, Int Assoc Environm Anal Chem, Basel, Switzerland C1 FREDERICK CANC RES & DEV,DEPT HUMAN HLTH,FREDERICK,MD 21702. NR 0 TC 3 Z9 3 U1 0 U2 0 PU MARCEL DEKKER PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 BN 0-8247-9615-2 PY 1995 BP 69 EP 85 PG 17 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD32B UT WOS:A1995BD32B00005 ER PT B AU KALER, SG AF KALER, SG BE Sarkar, B TI COPPER-HISTIDINE THERAPY IN MENKES DISEASE - CLINICAL, BIOCHEMICAL, AND MOLECULAR ASPECTS SO GENETIC RESPONSE TO METALS LA English DT Proceedings Paper CT 1st International Symposium on Metals and Genetics - Genetic Response to Metals CY MAY 24-27, 1994 CL TORONTO, CANADA SP Hosp Sick Children, Toronto, Canada, Int Assoc Environm Anal Chem, Basel, Switzerland C1 NICHHD,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARCEL DEKKER PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 BN 0-8247-9615-2 PY 1995 BP 317 EP 321 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD32B UT WOS:A1995BD32B00020 ER PT J AU KOZMAN, HM KEITH, TP DONISKELLER, H WHITE, RL WEISSENBACH, J DEAN, M VERGNAUD, G KIDD, K GUSELLA, J ROYLE, NJ SUTHERLAND, GR MULLEY, JC AF KOZMAN, HM KEITH, TP DONISKELLER, H WHITE, RL WEISSENBACH, J DEAN, M VERGNAUD, G KIDD, K GUSELLA, J ROYLE, NJ SUTHERLAND, GR MULLEY, JC TI THE CEPH CONSORTIUM LINKAGE MAP OF HUMAN-CHROMOSOME-16 SO GENOMICS LA English DT Article ID HUMAN GENOME; LENGTH POLYMORPHISM; DISEASE LOCUS; MARKERS; CLN3 AB A Centre d'Etude du Polymorphisme Humain (CEPH) consortium map of human chromosome 16 has been constructed. The map contains 158 loci defined by 191 different probe/restriction enzyme combinations or primer pairs. The marker genotypes, contributed by 9 collaborating laboratories, originated from the CEPH families DNA. A total of 60 loci, with an average heterozygosity of 68%, have been placed on the framework genetic map. The genetic map contains 7 genes. The length of the sex-averaged map is 165 cM, with a mean genetic distance between loci of 2.8 cM; the median distance between markers is 2.0 cM. The male map length is 136 cM, and the female map length is 197 cM. The map covers virtually the entire chromosome, from D16S85, within 170 to 430 kb of the 16p telomere, to D16S303 at 16qter. The markers included in the linkage map have been physically mapped on a partial human chromosome 16 somatic cell hybrid panel, thus anchoring the genetic map to the cytogenetic-based physical map. (C) 1995 Academic Press, Inc. C1 WOMENS & CHILDRENS HOSP,CTR MED GENET,DEPT CYTOGENET & MOLEC GENET,ADELAIDE,SA 5006,AUSTRALIA. UNIV ADELAIDE,DEPT PAEDIAT,ADELAIDE,SA,AUSTRALIA. COLLABORAT RES INC,DEPT HUMAN & MOLEC GENET,WALTHAM,MA. WASHINGTON UNIV,SCH MED,DEPT SURG,ST LOUIS,MO 63110. UNIV UTAH,HOWARD HUGHES MED INST,SALT LAKE CITY,UT. INST PASTEUR,PARIS,FRANCE. NCI,FREDERICK CANC RES FACIL,FREDERICK,MD. CTR ETUD BOUCHET,NANTES,FRANCE. INST BIOL,NANTES,FRANCE. YALE UNIV,SCH MED,DEPT HUMAN GENET,NEW HAVEN,CT 06510. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV LEICESTER,DEPT GENET,LEICESTER LE1 7RH,LEICS,ENGLAND. RI Sutherland, Grant/D-2606-2012; Vergnaud, Gilles/P-1304-2015; OI Vergnaud, Gilles/0000-0003-0913-194X; Dean, Michael/0000-0003-2234-0631 NR 38 TC 21 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 44 EP 58 DI 10.1016/0888-7543(95)80108-X PG 15 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400006 PM 7774955 ER PT J AU KOZAK, CA GATIGNOL, A GRAHAM, K JEANG, KT MCBRIDE, OW AF KOZAK, CA GATIGNOL, A GRAHAM, K JEANG, KT MCBRIDE, OW TI GENETIC-MAPPING IN HUMAN AND MOUSE OF THE LOCUS ENCODING TRBP, A PROTEIN THAT BINDS THE TAR REGION OF THE HUMAN-IMMUNODEFICIENCY-VIRUS (HIV-1) SO GENOMICS LA English DT Article ID RNA-BINDING; HUMAN CHROMOSOME-12; TRANS-ACTIVATION; SPECIFICALLY BINDS; NUCLEAR-PROTEIN; RODENT CELLS; TYPE-1; LOCALIZATION; LOOP; IDENTIFICATION AB Productive infection with HIV-1, the virus responsible for AIDS, requires the involvement of host cell factors for completion of the replicative cycle, but the identification of these factors and elucidation of their specific functions has been difficult. A human cDNA, TRBP, was recently cloned and characterized as a positive regulator of gene expression that binds to the TAR region of the HIV-1 genome. Here we demonstrate that this factor is encoded by a gene, TARBP2, that maps to human chromosome 12 and mouse chromosome 15, and we also identify and map one human pseudogene (TARBP2P) and two mouse TRBP-related sequences (Tarbp2-rs1, Tarbp2-rs2). The map location of the expressed gene identifies it as a candidate for the previously identified factor encoded on human chromosome 12 that has been shown to be important for expression of HIV-1 genes. Western blotting indicates that despite high sequence conservation in human and mouse, the TARBP2 protein differs in apparent size in primate and rodent cells. (C) 1995 Academic Press, Inc. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. RP KOZAK, CA (reprint author), NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892, USA. RI Jeang, Kuan-Teh/A-2424-2008 NR 40 TC 26 Z9 28 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 66 EP 72 DI 10.1016/0888-7543(95)80110-8 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400008 PM 7774957 ER PT J AU PAPPAS, GJ POLYMEROPOULOS, MH BOYLE, JM TRENT, JM AF PAPPAS, GJ POLYMEROPOULOS, MH BOYLE, JM TRENT, JM TI REGIONAL ASSIGNMENT BY HYBRID MAPPING OF 36 EXPRESSED SEQUENCE TAGS (ESTS) ON HUMAN-CHROMOSOME-6 SO GENOMICS LA English DT Article ID HUMAN-MALIGNANT MELANOMA; HUMAN GENOME; LONG ARM; GENE; IDENTIFICATION; LOCALIZATION AB We have determined the regional chromosome assignment of 36 cDNAs from infant brain libraries by assessing the concordant segregation of PCR products using a human-rodent hybrid mapping panel that subdivides chromosome 6 into 15 regions. These mapped sequences serve as markers for the physical and expression maps of chromosome 6, as well as candidate genes for various disease loci. Sequence analysis has identified putative functions and motifs for some of these genes. C1 UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. CHRISTIE HOSP & HOLT RADIUM INST,CANC RES CAMPAIGN,RES CTR,PATERSON INST CANC RES,MANCHESTER M20 9BX,LANCS,ENGLAND. RP PAPPAS, GJ (reprint author), NIH,NATL CTR HUMAN GENOME RES,BLDG 49,ROOM 4A22,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 25 TC 20 Z9 20 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 124 EP 129 DI 10.1016/0888-7543(95)80117-5 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400015 PM 7774909 ER PT J AU VALENZUELA, DM ROJAS, E LEBEAU, MM ESPINOSA, R BRANNAN, CI MCCLAIN, J MASIAKOWSKI, P IP, NY COPELAND, NG JENKINS, NA YANCOPOULOS, GD AF VALENZUELA, DM ROJAS, E LEBEAU, MM ESPINOSA, R BRANNAN, CI MCCLAIN, J MASIAKOWSKI, P IP, NY COPELAND, NG JENKINS, NA YANCOPOULOS, GD TI GENOMIC ORGANIZATION AND CHROMOSOMAL LOCALIZATION OF THE HUMAN AND MOUSE GENES ENCODING THE ALPHA-RECEPTOR COMPONENT FOR CILIARY NEUROTROPHIC FACTOR SO GENOMICS LA English DT Article ID CNTF RECEPTOR; LINKAGE MAP; CYTOKINES; LEUKEMIA AB Ciliary neurotrophic factor (CNTF) has recently been found to share receptor components with, and to be structurally related to, a family of broadly acting cytokines, including interleukin-6, leukemia inhibitory factor, and oncostatin M. However, the CNTF receptor complex also includes a CNTF-specific component known as CNTF receptor alpha (CNTFR alpha). Here we describe the molecular cloning of the human and mouse genes encoding CNTFR. We report that the human and mouse genes have an identical intron-exon structure that correlates well with the domain structure of CNTFR alpha. That is, the signal peptide and the immunoglobulin-like domain are each encoded by single exons, the cytokine receptor-like domain is distributed among 4 exons, and the C-terminal glycosyl phosphatidylinositol recognition domain is encoded by the final coding exon. The position of the introns within the cytokine receptor-like domain corresponds to those found in other members of the cytokine receptor superfamily. Confirming a recent study using radiation hybrids, we have also mapped the human CNTFR gene to chromosome band 9p13 and the mouse gene to a syntenic region of chromosome 4. (C) 1995 Academic Press, Inc. C1 UNIV CHICAGO,DEPT MED,HEMATOL ONCOL SECT,CHICAGO,IL 60637. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP VALENZUELA, DM (reprint author), REGENERON PHARMACEUT INC,777 OLD SAW RIVER RD,TARRYTOWN,NY 10591, USA. FU NCI NIH HHS [CA40046, N01-CO-74101] NR 24 TC 20 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 157 EP 163 DI 10.1016/0888-7543(95)80121-2 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400019 PM 7774913 ER PT J AU BRODY, LC ABEL, KJ CASTILLA, LH COUCH, FJ MCKINLEY, DR YIN, GY HO, PP MERAJVER, S CHANDRASEKHARAPPA, SC XU, JZ COLE, JL STRUEWING, JP VALDES, JM COLLINS, FS WEBER, BL AF BRODY, LC ABEL, KJ CASTILLA, LH COUCH, FJ MCKINLEY, DR YIN, GY HO, PP MERAJVER, S CHANDRASEKHARAPPA, SC XU, JZ COLE, JL STRUEWING, JP VALDES, JM COLLINS, FS WEBER, BL TI CONSTRUCTION OF A TRANSCRIPTION MAP SURROUNDING THE BRCA1 LOCUS OF HUMAN-CHROMOSOME-17 SO GENOMICS LA English DT Article ID PROTEIN-CODING REGIONS; HUMAN GENOME PROJECT; OVARIAN-CANCER; FAMILIAL BREAST; MULTIGENE FAMILY; BINDING-PROTEIN; DNA-SEQUENCE; GENE; CDNA; IDENTIFICATION AB We have used a combination of methods (exon amplification, direct selection, direct screening, evolutionary conservation, island rescue-PCR, and direct sequence analysis) to survey approximately 600 kb of genomic DNA surrounding the BRCA1 gene for transcribed sequences. We have cloned a set of fragments representing at least 26 genes. The DNA sequence of these clones reveals that 5 are previously cloned genes; the precise chromosomal location of 2 was previously unknown, and 3 have been cloned and mapped by others to this interval. Three other genes, including BRCA1 itself, have recently been mapped independently to this region. Sequences from 11 genes are similar but not identical matches to known genes; 5 of these appear to be the human homologues of genes cloned from other species. Another 7 genes have no similarity with known genes. In addition, 39 putative exons and 14 expressed sequence tags have been identified and mapped to individual cosmids. This transcript map provides a detailed description of gene organization for this region of the genome. (C) 1995 Academic Press, Inc. C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892. UNIV MICHIGAN,DEPT MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,CTR HUMAN GENOME,ANN ARBOR,MI 48109. UNIV PENN,DEPT INTERNAL MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT GENET,PHILADELPHIA,PA 19104. RI Struewing, Jeffery/C-3221-2008; Struewing, Jeffery/I-7502-2013 OI Struewing, Jeffery/0000-0002-4848-3334 FU NCI NIH HHS [CA-57601] NR 64 TC 52 Z9 53 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 238 EP 247 DI 10.1016/0888-7543(95)80131-5 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400029 PM 7774924 ER PT J AU OSBORNELAWRENCE, S WELCSH, PL SPILLMAN, M CHANDRASEKHARAPPA, SC GALLARDO, TD LOVETT, M BOWCOCK, AM AF OSBORNELAWRENCE, S WELCSH, PL SPILLMAN, M CHANDRASEKHARAPPA, SC GALLARDO, TD LOVETT, M BOWCOCK, AM TI DIRECT SELECTION OF EXPRESSED SEQUENCES WITHIN A 1-MB REGION FLANKING BRCA1 ON HUMAN-CHROMOSOME 17Q21 SO GENOMICS LA English DT Article ID OVARIAN-CANCER; FAMILIAL BREAST; TRANSCRIBED SEQUENCES; CDNA SELECTION; DNA; PROTEIN; GENES; FRAGMENTS; INTERVAL; STRATEGY AB Direct selection of genes within the interval of chromosome 17q21 containing BRCA1 was performed, YAC and cosmid contigs spanning the BRCA1 region were used to select cDNA clones from pools of cDNAs derived from human placenta, HeLa cells, activated T cells, and fetal head. A minimum set of 48 fragments of nonoverlapping cDNAs that unequivocally mapped within a 1-Mb region was identified, although it is not yet known how many of these are derived from the same transcript. DNA sequence analyses revealed that 4 of these cDNAs were derived from known genes (EDH17B2, glucose-6-phosphatase, IAI.3B, and E1AF), 1 is a member of a previously described gene family (HMG-17), and 7 share substantial identity with previously described genes from human or other species. The remainder showed no significant homology to known genes. Limited PCR-based expression profiles of a set of 13 of the genes were performed, and all gave positive results with at least some cDNA sources supporting the contention that they truly represent transcribed sequences, A comparison between genes obtained from this region by direct selection with those obtained by direct screening or exon trapping (see accompanying papers, this issue) revealed that over 90% of the genes identified by exon trapping were represented in the selected material and that at least two additional genes that appear to represent low abundance transcripts with restricted expression profiles were identified by selection but not by other means. (C) 1995 Academic Press, Inc. C1 MCDERMOTT CTR HUMAN GROWTH & DEV,DALLAS,TX 75235. UNIV TEXAS,SW MED CTR,DEPT PEDIAT,DALLAS,TX 75235. UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. FU NCI NIH HHS [CA60650]; NHGRI NIH HHS [HG00368, HG00882] NR 39 TC 24 Z9 24 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 248 EP 255 DI 10.1016/0888-7543(95)80132-6 PG 8 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400030 PM 7774925 ER PT J AU COUCH, FJ CASTILLA, LH XU, JZ ABEL, KJ WELCSH, P KING, SE WONG, LH HO, PP MERAJVER, S BRODY, LC YIN, GY HAYES, ST GIESER, LM FLEJTER, WL GLOVER, TW FRIEDMAN, LS LYNCH, ED MEZA, JE KING, MC LAW, DJ DEAVEN, L BOWCOCK, AM COLLINS, FS WEBER, BL CHANDRASEKHARAPPA, SC AF COUCH, FJ CASTILLA, LH XU, JZ ABEL, KJ WELCSH, P KING, SE WONG, LH HO, PP MERAJVER, S BRODY, LC YIN, GY HAYES, ST GIESER, LM FLEJTER, WL GLOVER, TW FRIEDMAN, LS LYNCH, ED MEZA, JE KING, MC LAW, DJ DEAVEN, L BOWCOCK, AM COLLINS, FS WEBER, BL CHANDRASEKHARAPPA, SC TI A YAC-BASED, P1-BASED, AND COSMID-BASED PHYSICAL MAP OF THE BRCA1 REGION ON CHROMOSOME-17Q21 SO GENOMICS LA English DT Article ID FAMILIAL BREAST; OVARIAN-CANCER; GENETIC-ANALYSIS; YEAST; LINKAGE; DNA AB A familial early-onset breast cancer gene (BRCA1) has been localized to chromosome 17q21. To characterize this region and to aid in the identification of the BRCA1 gene, a physical map of a region of 1.0-1.5 Mb between the EDH17B1 and the PPY loci on chromosome 17q21 was generated. The physical map is composed of a yeast artificial chromosome (YAC) and P1 phage contig with one gap. The majority of the interval has also been converted to a cosmid contig. Twenty-three PCR-based sequence-tagged sites (STSs) were mapped to these contigs, thereby confirming the order and overlap of individual clones. This complex physical map of the BRCA1 region was used to isolate genes by a number of gene identification techniques and to generate transcript maps of the region, as presented in the three accompanying manuscripts of Brody et al. (1995), Osborne-Lawrence et al. (1995), and Friedman et al. (1995). (C) 1995 Academic Press, Inc. C1 NCHGR,GENE TRANSFER LAB,BETHESDA,MD 20892. UNIV PENN,SCH MED,DEPT INTERNAL MED,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT GENET,PHILADELPHIA,PA 19104. UNIV MICHIGAN,SCH MED,CTR HUMAN GENOME,ANN ARBOR,MI 48109. SW UNIV,DEPT PEDIAT,DALLAS,TX 75235. SW UNIV,MCDERMOTT CTR,DALLAS,TX 75235. UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,BERKELEY,CA 94720. UNIV CALIF BERKELEY,SCH PUBL HLTH,BERKELEY,CA 94720. LOS ALAMOS NATL LAB,LOS ALAMOS,NM. FU NCI NIH HHS [R01 CA-61231, R01 CA-57601, R01 CA-60650] NR 32 TC 17 Z9 17 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 264 EP 273 DI 10.1016/0888-7543(95)80134-8 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400032 PM 7774927 ER PT J AU AUTIERI, MV KOZAK, CA COHEN, JA PRYSTOWSKY, MB AF AUTIERI, MV KOZAK, CA COHEN, JA PRYSTOWSKY, MB TI GENOMIC ORGANIZATION AND GENETIC-MAPPING OF THE NEUROIMMUNE GENE I2RF5 TO MOUSE CHROMOSOME-4 SO GENOMICS LA English DT Note ID EXPRESSION; NEURONS AB The nervous and immune systems share many functional and molecular similarities, including shared surface antigens, secretions of soluble factors, and cross-modulatory effects. We have identified previously a novel mRNA termed F5, which is expressed only in activated T lymphocytes and mature, postmitotic neurons. Tissue specificity and sequence conservation suggest an important function for F5 in T-lymphocyte proliferation and neuronal maturation. The F5 gene product is an evolutionarily conserved, cytoskeletal-associated phosphoprotein. A full-length mouse genomic clone has been isolated. The protein coding region of the F5 gene is approximately 16 kb in length and is composed of 13 coding exons. The gene encoding F5, termed I2rf5, was mapped using interspecies mouse crosses in close proximity to a number of genes associated with neuronal defects on distal chromosome 4. (C) 1995 Academic Press, Inc. C1 ALBERT EINSTEIN COLL MED,MONTEFIORE MED CTR,DEPT PATHOL,BRONX,NY 10467. SMITHKLINE BEECHAM PHARMACEUT,DEPT CARDIOVASC PHARM,KING OF PRUSSIA,PA 19406. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. CLEVELAND CLIN FDN,MELLEN CTR MULTIPLE SCLEROSIS TREATMENT & RES,CLEVELAND,OH 44195. FU NCI NIH HHS [CA09140-19]; NIGMS NIH HHS [GM-41226]; PHS HHS [9-526-0522] NR 14 TC 2 Z9 2 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 282 EP 284 DI 10.1016/0888-7543(95)80137-B PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400035 PM 7774930 ER PT J AU PATEL, A ROCHELLE, JM JONES, JM SUMEGI, J UHL, GR SELDIN, MF MEISLER, MH GREGOR, P AF PATEL, A ROCHELLE, JM JONES, JM SUMEGI, J UHL, GR SELDIN, MF MEISLER, MH GREGOR, P TI MAPPING OF THE TAURINE TRANSPORTER GENE TO MOUSE CHROMOSOME-6 AND TO THE SHORT ARM OF HUMAN-CHROMOSOME-3 SO GENOMICS LA English DT Note ID INTERSPECIFIC CROSS; CONSERVED LINKAGE; RAT-BRAIN; EXPRESSION; CLONING; LOCALIZATION; MUTATION; LOCUS; CELLS; MICE AB Transport proteins have essential functions in the uptake of neurotransmitters and neuromodulators. We have mapped the gene encoding the taurine transporter, Taut, to the central region of mouse chromosome 6. Analysis of a cross segregating the neurological mutant mnd2 excluded Taut as a candidate gene for this closely linked mutation, To map the human taurine transporter gene, TAUT, a sequence-tagged site (STS) corresponding to the 3' untranslated region of the human cDNA was developed, TAUT was assigned to human chromosome 3 by typing this STS on a panel of somatic cell hybrids. Further analysis of a hybrid panel containing defined deletions of chromosome 3 suggested that TAUT maps to 3p21-p25, These data extend a conserved linkage group on mouse chromosome 6 and human chromosome 3p, Deletion of TAUT might contribute to some phenotypic features Of the 3p(-) syndrome. (C) 1995 Academic Press, Inc. C1 NIDA,INTRAMURAL RES PROGRAM,NEUROSCI BRANCH,BALTIMORE,MD 21224. NIDA,INTRAMURAL RES PROGRAM,MOLEC NEUROBIOL BRANCH,BALTIMORE,MD 21224. DUKE UNIV,DEPT MED,DURHAM,NC 27710. DUKE UNIV,DEPT MICROBIOL,DURHAM,NC 27710. UNIV MICHIGAN,SCH MED,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV NEBRASKA,MED CTR,DEPT PATHOL & MICROBIOL,OMAHA,NE 68198. FU NHGRI NIH HHS [HG00734] NR 32 TC 6 Z9 7 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 314 EP 317 DI 10.1016/0888-7543(95)80146-D PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400044 PM 7774940 ER PT J AU GREGOR, P NASH, SR CARON, MG SELDIN, MF WARREN, ST AF GREGOR, P NASH, SR CARON, MG SELDIN, MF WARREN, ST TI ASSIGNMENT OF THE CREATINE TRANSPORTER GENE (SLC6A8) TO HUMAN-CHROMOSOME XQ28 TELOMERIC TO G6PD SO GENOMICS LA English DT Note ID BARTH SYNDROME; LOCUS C1 NIDA,MOLEC NEUROBIOL BRANCH,BALTIMORE,MD 21224. DUKE UNIV,HOWARD HUGHES MED INST,DEPT CELL BIOL,DURHAM,NC 27710. DUKE UNIV,HOWARD HUGHES MED INST,DEPT MED,DURHAM,NC 27710. DUKE UNIV,HOWARD HUGHES MED INST,DEPT MICROBIOL,DURHAM,NC 27710. EMORY UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT BIOCHEM,ATLANTA,GA 30322. EMORY UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT PEDIAT,ATLANTA,GA 30322. RI Warren, Stephen/A-2498-2012 FU NHGRI NIH HHS [HG00734] NR 12 TC 37 Z9 38 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1995 VL 25 IS 1 BP 332 EP 333 DI 10.1016/0888-7543(95)80155-F PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QE734 UT WOS:A1995QE73400053 PM 7774949 ER PT B AU Fauci, AS AF Fauci, AS BE Shiokawa, Y Kitamura, T TI Host factors in the immunopathogenesis of HIV disease SO GLOBAL CHALLENGE OF AIDS - TEN YEARS OF HIV/AIDS RESEARCH LA English DT Proceedings Paper CT 10th International Conference on AIDS/International Conference on STD CY AUG 07-12, 1994 CL YOKOHAMA, JAPAN SP WHO, Minist Hlth & Welfare Japan RP Fauci, AS (reprint author), NIAID,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND BN 3-8055-6222-5 PY 1995 BP 49 EP 56 PG 8 WC Public, Environmental & Occupational Health; Infectious Diseases; Pharmacology & Pharmacy SC Public, Environmental & Occupational Health; Infectious Diseases; Pharmacology & Pharmacy GA BE40K UT WOS:A1995BE40K00006 ER PT B AU Paul, WE AF Paul, WE BE Shiokawa, Y Kitamura, T TI A turning point in AIDS research: The search for new frontiers SO GLOBAL CHALLENGE OF AIDS - TEN YEARS OF HIV/AIDS RESEARCH LA English DT Proceedings Paper CT 10th International Conference on AIDS/International Conference on STD CY AUG 07-12, 1994 CL YOKOHAMA, JAPAN SP WHO, Minist Hlth & Welfare Japan RP Paul, WE (reprint author), NIH,OFF AIDS RES,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND BN 3-8055-6222-5 PY 1995 BP 57 EP 63 PG 7 WC Public, Environmental & Occupational Health; Infectious Diseases; Pharmacology & Pharmacy SC Public, Environmental & Occupational Health; Infectious Diseases; Pharmacology & Pharmacy GA BE40K UT WOS:A1995BE40K00007 ER PT B AU Gallo, RC AF Gallo, RC BE Shiokawa, Y Kitamura, T TI AIDS research towards the future SO GLOBAL CHALLENGE OF AIDS - TEN YEARS OF HIV/AIDS RESEARCH LA English DT Proceedings Paper CT 10th International Conference on AIDS/International Conference on STD CY AUG 07-12, 1994 CL YOKOHAMA, JAPAN SP WHO, Minist Hlth & Welfare Japan RP Gallo, RC (reprint author), NCI,TUMOR CELL BIOL LAB,BLDG 37,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND BN 3-8055-6222-5 PY 1995 BP 263 EP 273 PG 11 WC Public, Environmental & Occupational Health; Infectious Diseases; Pharmacology & Pharmacy SC Public, Environmental & Occupational Health; Infectious Diseases; Pharmacology & Pharmacy GA BE40K UT WOS:A1995BE40K00028 ER PT J AU LINNEKIN, D KELLER, JR FERRIS, DK MOU, SM BROUDY, V LONGO, DL AF LINNEKIN, D KELLER, JR FERRIS, DK MOU, SM BROUDY, V LONGO, DL TI STEM-CELL FACTOR INDUCES PHOSPHORYLATION OF A 200 KDA PROTEIN WHICH ASSOCIATES WITH C-KIT SO GROWTH FACTORS LA English DT Article DE STEM CELL FACTOR; GM-CSF; SIGNAL TRANSDUCTION; TYROSINE PHOSPHORYLATION; C-KIT ID COLONY-STIMULATING FACTOR; TYROSINE KINASE-ACTIVITY; FACTOR GM-CSF; GROWTH-FACTOR; SIGNAL TRANSDUCTION; PROTOONCOGENE PRODUCT; EXPRESSION CLONING; MOLECULAR-CLONING; PROGENITOR CELLS; RECEPTOR KINASE AB Stem cell factor (SCF) promotes limited proliferation and differentiation of hematopoietic progenitor cells and is potently synergistic in combination with growth factors such as granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin 3 (IL-3) or erythropoietin (Epo). We have examined tyrosine phosphorylation induced by SCF in the megakaryoblastic cell line Mo7e and found phosphorylation of proteins of 200, 145, 120, 58 and 55 KDa. The dominant phosphotyrosylproteins in SCF treated cells were 200 and 145 kDa. Our studies indicated that the 145 kDa protein was c-kit, the receptor for SCF. Subsequent work was directed towards further characterizing the 200 kDa protein. Surface labeling of Mo7e cells suggested that p200 had an extracellular domain and could be induced to associate with c-kit after stimulation with SCF. The rapid phosphorylation of p200 and its immediate association with c-kit suggest that p200 is potentially a component of the SCF signal transduction pathway. C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURSES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. UNIV WASHINGTON,DEPT MED,DIV HEMATOL,SEATTLE,WA 98195. RP LINNEKIN, D (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702, USA. NR 44 TC 7 Z9 7 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 1995 VL 12 IS 1 BP 57 EP 67 DI 10.3109/08977199509003214 PG 11 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA RN617 UT WOS:A1995RN61700007 PM 8527164 ER PT J AU CUNNINGHAM, NS JENKINS, NA GILBERT, DJ COPELAND, NG REDDI, AH LEE, SJ AF CUNNINGHAM, NS JENKINS, NA GILBERT, DJ COPELAND, NG REDDI, AH LEE, SJ TI GROWTH-DIFFERENTIATION FACTOR-10 - A NEW MEMBER OF THE TRANSFORMING GROWTH-FACTOR-BETA SUPERFAMILY RELATED TO BONE MORPHOGENETIC PROTEIN-3 SO GROWTH FACTORS LA English DT Article DE GROWTH DIFFERENTIATION FACTOR; BONE MORPHOGENETIC PROTEIN-3 ID COMPLEMENTARY-DNA; GENE FAMILY; EMBRYONIC-DEVELOPMENT; FOLLICULAR-FLUID; CELLS; MOUSE; IDENTIFICATION; EXPRESSION; INHIBIN; BOVINE AB We have identified a new member of the transforming growth factor-beta (TGF-beta) superfamily, growth/differentiation factor-10 (GDF-10), which is highly related to bone morphogenetic protein-3 (BMP-3). The nucleotide sequence of GDF-10 encodes a predicted protein of 476 amino acids with a molecular weight of approximately 52,000. The GDF-10 polypeptide contains a potential signal sequence for secretion, a putative RXXR proteolytic processing site, and a carboxy-terminal domain with considerable homology to other known members of the TGF-beta superfamily. In the mature carboxy-terminal domain GDF-10 is more homologous to BMP-3 (83% amino acid sequence identity) than to any other previously identified TGF-beta family member. GDF-10 also shows significant homology to BMP-3 (approximately 30% amino acid sequence identity) in the pro- region of the molecule. Based on these sequence comparisons, GDF-10 and BMP-3 define a new subgroup within the larger TGF-beta superfamily. By Northern analysis, GDF-10 mRNA was detected primarily in murine uterus, adipose tissue, and brain and to a lesser extent in liver and spleen. In addition, GDF-10 mRNA was present in both neonatal and adult bone samples, with higher levels being detected in calvaria than in long bone. These results suggest that GDF10 may play multiple roles in regulating cell differentiation events, including those involved in skeletal morphogenesis. Gdf10 was mapped to the proximal region of mouse chromosome 14 close to a region known to contain a spontaneous recessive mutation that is associated with a craniofacial defect. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT ORTHOPAED SURG,MUSCULOSKELETAL CELL BIOL LAB,BALTIMORE,MD 21205. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. FU NCI NIH HHS [CA-58236, N01-CO-74101]; NICHD NIH HHS [R01 HD30740] NR 50 TC 73 Z9 78 U1 1 U2 3 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 1995 VL 12 IS 2 BP 99 EP 109 DI 10.3109/08977199509028956 PG 11 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA RV835 UT WOS:A1995RV83500002 PM 8679252 ER PT B AU HSIEH, RKC GAMBOA, CA CID, V AF HSIEH, RKC GAMBOA, CA CID, V BE Lacroix, EM TI BITNIS project helping health scientists in Latin America access NLM databases through Grateful Med SO HEALTH INFORMATION FOR THE GLOBAL VILLAGE LA English DT Proceedings Paper CT 7th International Congress on Medical Librarianship - Health Information for the Global Village CY MAY 10-12, 1995 CL WASHINGTON, DC C1 NATL LIB MED,INT PROGRAMS,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MEDICAL LIBRARY ASSOC PI CHICAGO PA 919 N MICHIGAN AVE, SUITE 3208, CHICAGO, IL 60611 PY 1995 BP 87 EP 89 PG 3 WC Computer Science, Information Systems; Information Science & Library Science SC Computer Science; Information Science & Library Science GA BD71S UT WOS:A1995BD71S00017 ER PT B AU COLAIANNI, LA AF COLAIANNI, LA BE McSean, T vanLoo, J Coutinho, E TI Looking toward the future while working in the present SO HEALTH INFORMATION - NEW POSSIBILITIES LA English DT Proceedings Paper CT 1994 Conference of the European-Association-for-Health-Information-and-Libraries on Health Information - New Possibilities CY 1994 CL OSLO, NORWAY SP European Assoc Hlth Informat & Libs C1 NATL LIB MED,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-3584-8 PY 1995 BP 18 EP 20 PG 3 WC Health Policy & Services; Information Science & Library Science SC Health Care Sciences & Services; Information Science & Library Science GA BD84M UT WOS:A1995BD84M00006 ER PT J AU HOOFNAGLE, JH CARITHERS, RL SHAPIRO, C ASCHER, N AF HOOFNAGLE, JH CARITHERS, RL SHAPIRO, C ASCHER, N TI FULMINANT HEPATIC-FAILURE - SUMMARY OF A WORKSHOP SO HEPATOLOGY LA English DT Article ID ORTHOTOPIC LIVER-TRANSPLANTATION; B VIRUS-DNA; MICROCARRIER-ATTACHED HEPATOCYTES; PROSPECTIVE CONTROLLED TRIAL; VIRAL-HEPATITIS; CEREBRAL EDEMA; INTRACRANIAL-PRESSURE; UNITED-STATES; ASSIST DEVICE; RATS AB Fulminant hepatic failure (FHF) is defined by the appearance of severe Liver injury with hepatic encephalopathy in a previously healthy person. There are an estimated 2,000 cases of FHF in the United States yearly, representing 0.1% of all deaths and, perhaps, 6% of liver-related deaths. The causes of FHF are many, the chief ones in the United States being hepatitis A; B; non-A, non-B and drug induced liver disease. There are no specific therapies for FHF, however, liver transplantation is recommended for situations in which spontaneous recovery appears unlikely, Factors that are valuable in assessing the likelihood of spontaneous recovery are static features such as patient age and etiology of FHF and dynamic features including encephalopathy grade, prothrombin time, and serum bilirubin. Presently, approximately 7% of all liver transplants are done for FHF and the 1-year patient survival rates average 63%, somewhat less than survival rates for nonfulminant liver disease, averaging 78%. The management of patients with FHF is challenging, particularly important being monitoring and early treatment of infections, hemodynamic abnormalities, and brain edema. Innovative approaches to management and therapy include use of cytoprotective or antiviral medications, hepatic support systems, extracorporeal liver support, hepatocyte transplantaauxiliary liver transplantation, and xenotransplantation. None of these are of proven benefit, but many are promising as a means to support the patient with FHF until spontaneous recovery occurs or a suitable liver graft is available for transplantation. C1 UNIV WASHINGTON,MED CTR,DEPT MED,SEATTLE,WA 98195. CTR DIS CONTROL & PREVENT,HEPATITIS BRANCH,ATLANTA,GA 30341. UNIV CALIF SAN FRANCISCO,LIVER TRANSPLANT SERV,SAN FRANCISCO,CA. RP HOOFNAGLE, JH (reprint author), NIDDKD,DIV DIGEST DIS & NUTR,BLDG 31,ROOM 9A23,BETHESDA,MD 20892, USA. NR 74 TC 404 Z9 419 U1 2 U2 17 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD JAN PY 1995 VL 21 IS 1 BP 240 EP 252 DI 10.1016/0270-9139(95)90434-4 PG 13 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA RB788 UT WOS:A1995RB78800036 PM 7806160 ER PT J AU NAKAMURA, T AF NAKAMURA, T TI GENETIC-MARKERS AND ANIMAL-MODELS OF NEUROCRISTOPATHY SO HISTOLOGY AND HISTOPATHOLOGY LA English DT Review DE NEURAL CREST; NEUROCRISTOPATHY; TUMOR SUPPRESSOR; PROTOONCOGENE; ANIMAL MODEL ID NEUROFIBROMATOSIS TYPE-1 GENE; GTPASE-ACTIVATING PROTEIN; DYSPLASTIC NEVUS SYNDROME; NEUROBLASTOMA CELL-LINES; TRANSGENIC MOUSE MODEL; NITROSO-N-ETHYLUREA; BILATERAL ACOUSTIC NEUROFIBROMATOSIS; ENDOCRINE NEOPLASIA TYPE-2A; VONHIPPEL-LINDAU DISEASE; HUMAN-MALIGNANT MELANOMA AB Neurocristopathy is the disorder in which the series of cell and tissue derived from the neural crest are affected, A variety of neural crest tumors, and systemic neurocristopathies such as neurofibromatosis type 1 (NF1) and type 2 (NF2), multiple endocrine neoplasia type 2 (MEN2) and dysplastic nevus syndrome are included in this category. Genetic abnormalities of specific proto-oncogenes and tumor suppressor genes have been discovered in the neurocristopathies. The NF1 gene has GTP-ase activating protein activity, regulates ras pathway and acts as a potential tumor suppressor. The NF2 gene, which is also considered as a tumor suppressor of Schwann cell and meningocyte, has a unique character that it is a linker between adhesion molecule and cytoskeletal protein. Ret proto-oncogene has been proven to be the responsible gene not only of MEN2A but also of MEN2B, familial medullary carcinoma and Hirschsprung disease, Recent progress of positional cloning technique further revealed that p16 gene which is an inhibitor of cycline-dependent kinase is the gene for some of familial malignant melanoma/dysplastic nevus syndrome and sporadic melanoma. ENU-induced rodent model for human Schwann cell tumor and fish model for malignant melanoma have provided useful insights to molecular mechanisms of neural crest tumors. Moreover, introduction of transgenic and gene targeted mouse models for neurocristopathies has made great progress in understanding of the genetic functions in tumoriginesis. C1 UNIV TOKYO,FAC MED,DEPT PATHOL,TOKYO 113,JAPAN. RP NAKAMURA, T (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,POB B,FREDERICK,MD 21702, USA. NR 144 TC 12 Z9 12 U1 0 U2 0 PU F HERNANDEZ PI MURCIA PA PLAZA FUENSANTA 2-7 C, 30008 MURCIA, SPAIN SN 0213-3911 J9 HISTOL HISTOPATHOL JI Histol. Histopath. PY 1995 VL 10 IS 3 BP 747 EP 759 PG 13 WC Cell Biology; Pathology SC Cell Biology; Pathology GA RP979 UT WOS:A1995RP97900026 PM 7579825 ER PT S AU Brightman, MW Ishihara, S Chang, L AF Brightman, MW Ishihara, S Chang, L BE Oldstone, MB Vitkovic, L TI Penetration of solutes, viruses, and cells across the blood-brain barrier SO HIV AND DEMENTIA SE Current Topics in Microbiology and Immunology LA English DT Review CT Conference on Pathogenesis of HIV Infection of the Brain - Impact on Function and Behavior CY APR 04-07, 1994 CL CHANTILLY, VA SP NIMH ID CENTRAL-NERVOUS-SYSTEM; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; TUMOR-NECROSIS-FACTOR; CEREBROSPINAL-FLUID; IMMUNE-RESPONSE; SERUM-PROTEINS; RAT; PEROXIDASE; TRANSPORT; NEURONS RP Brightman, MW (reprint author), NIH, NEUROBIOL LAB, BLDG 36, RM 2A-21, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 56 TC 15 Z9 15 U1 0 U2 1 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0070-217X BN 3-540-59117-6 J9 CURR TOP MICROBIOL JI Curr.Top.Microbiol.Immunol. PY 1995 VL 202 BP 63 EP 78 PG 16 WC Infectious Diseases; Clinical Neurology; Neurosciences SC Infectious Diseases; Neurosciences & Neurology GA BE60P UT WOS:A1995BE60P00005 PM 7587371 ER PT S AU Power, C McArthur, JC Johnson, RT Griffin, DE Glass, JD Dewey, R Chesebro, B AF Power, C McArthur, JC Johnson, RT Griffin, DE Glass, JD Dewey, R Chesebro, B BE Oldstone, MB Vitkovic, L TI Distinct HIV-1 env sequences are associated with neurotropism and neurovirulence SO HIV AND DEMENTIA SE CURRENT TOPICS IN MICROBIOLOGY AND IMMUNOLOGY LA English DT Article; Proceedings Paper CT Conference on Pathogenesis of HIV Infection of the Brain - Impact on Function and Behavior CY APR 04-07, 1994 CL CHANTILLY, VA SP NIMH ID MURINE LEUKEMIA-VIRUS; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; CENTRAL NERVOUS-SYSTEM; AIDS DEMENTIA COMPLEX; BLOOD-BRAIN-BARRIER; CELL TROPISM; MOLECULAR CHARACTERIZATION; NEUROLOGIC MANIFESTATIONS; PRODUCTIVE INFECTION; CEREBROSPINAL-FLUID C1 JOHNS HOPKINS UNIV,DEPT EPIDEMIOL,BALTIMORE,MD 21287. JOHNS HOPKINS UNIV,DEPT MED,BALTIMORE,MD 21287. JOHNS HOPKINS UNIV,DEPT PATHOL,BALTIMORE,MD 21287. ST PATRICKS HOSP,DEPT NEUROSURG,MISSOULA,MT 59801. NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. JOHNS HOPKINS UNIV,DEPT NEUROL,BALTIMORE,MD 21287. RI Power, Christopher/C-7181-2013; OI Power, Christopher/0000-0002-5131-9711 FU NCRR NIH HHS [RR 00722]; NIAID NIH HHS [AI 767234]; NINDS NIH HHS [NS 26643] NR 66 TC 61 Z9 62 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN 33 PA HEIDELBERGER PLATZ 3, W-1000 BERLIN 33, GERMANY SN 0070-217X BN 3-540-59117-6 J9 CURR TOP MICROBIOL JI Curr.Top.Microbiol.Immunol. PY 1995 VL 202 BP 89 EP 104 PG 16 WC Infectious Diseases; Clinical Neurology; Neurosciences SC Infectious Diseases; Neurosciences & Neurology GA BE60P UT WOS:A1995BE60P00007 PM 7587373 ER PT S AU Vitkovic, L daCunha, A AF Vitkovic, L daCunha, A BE Oldstone, MB Vitkovic, L TI Role for astrocytosis in HIV-1-associated dementia SO HIV AND DEMENTIA SE Current Topics in Microbiology and Immunology LA English DT Review CT Conference on Pathogenesis of HIV Infection of the Brain - Impact on Function and Behavior CY APR 04-07, 1994 CL CHANTILLY, VA SP NIMH ID TRANSFORMING GROWTH FACTOR-BETA-1; IMMUNODEFICIENCY-VIRUS HIV; SUBACUTE AIDS ENCEPHALITIS; DEFICIENCY-SYNDROME AIDS; NERVOUS-SYSTEM; CALCIUM WAVES; NEUROPATHOLOGICAL CHANGES; GLUTAMINE-SYNTHETASE; CULTURED ASTROCYTES; CEREBRAL-CORTEX C1 NIMH, NIH, CELL BIOL LAB, BETHESDA, MD 20892 USA. RP Vitkovic, L (reprint author), NIMH, NIH, DIV NEUROSCI & BEHAV SCI, 5600 FISHERS LANE, ROOM 11C-06, ROCKVILLE, MD 20857 USA. NR 48 TC 30 Z9 30 U1 0 U2 1 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0070-217X BN 3-540-59117-6 J9 CURR TOP MICROBIOL JI Curr.Top.Microbiol.Immunol. PY 1995 VL 202 BP 105 EP 116 PG 12 WC Infectious Diseases; Clinical Neurology; Neurosciences SC Infectious Diseases; Neurosciences & Neurology GA BE60P UT WOS:A1995BE60P00008 PM 7587357 ER PT B AU Hadley, EC AF Hadley, EC BE Leung, EMF Chi, I Ho, S Lee, JJ TI Interventions to reduce physical frailty among older persons SO HONG KONG JOURNAL OF GERONTOLOGY, VOL 10, SUPPLEMENT 1996: PROCEEDINGS OF 5TH ASIA/OCEANIA REGIONAL CONGRESS OF GERONTOLOGY - TOTAL CARE OF THE ELDERLY: A MULTIDISCIPLINARY APPROACH LA English DT Proceedings Paper CT 5th Asia/Oceania Regional Congress of Gerontology - Total Care of the Elderly: A Multidisciplinary Approach CY NOV 19-23, 1995 CL HONG KONG, HONG KONG SP Hong Kong Assoc Gerontol RP Hadley, EC (reprint author), NIA,GERIATR PROGRAM,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HONG KONG ASSOCIATION GERONTOLOGY PI HONG KONG PA GPO BOX 10020, HONG KONG, HONG KONG PY 1995 BP 209 EP 211 PG 3 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA BH17L UT WOS:A1995BH17L00050 ER PT J AU SCHARENBERG, AM KINET, JP AF SCHARENBERG, AM KINET, JP TI EARLY EVENTS IN MAST-CELL SIGNAL-TRANSDUCTION SO HUMAN BASOPHILS AND MAST CELLS: BIOLOGICAL ASPECTS SE CHEMICAL IMMUNOLOGY LA English DT Review ID BASOPHILIC LEUKEMIA-CELLS; PROTEIN-KINASE-C; HIGH-AFFINITY RECEPTOR; RAT RBL-2H3 CELLS; IGE-RECEPTOR; IMMUNOGLOBULIN-E; TYROSINE PHOSPHORYLATION; HISTAMINE-RELEASE; PHOSPHOLIPASE C-GAMMA-1; FC-RECEPTORS C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. NR 76 TC 31 Z9 33 U1 0 U2 1 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 1015-0145 J9 CHEM IMMUNOL JI Chem.Immunol. PY 1995 VL 61 BP 72 EP 87 PG 16 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BD55N UT WOS:A1995BD55N00004 PM 7662147 ER PT J AU Haxby, JV Ungerleider, LG Horwitz, B Rapoport, SI Grady, CL AF Haxby, JV Ungerleider, LG Horwitz, B Rapoport, SI Grady, CL TI Hemispheric differences in neural systems for face working memory: A PET-rCBF study SO HUMAN BRAIN MAPPING LA English DT Article DE human brain; memory; cognition; faces; cerebral blood flow; positron emission tomography ID FRONTAL-LOBE; IMAGES; OBJECT; CORTEX AB Neural systems that participate in working memory for faces were investigated in an experiment designed to distinguish face perception areas from working memory areas. Regional cerebral blood flow (rCBF) was measured using positron emission tomography (PET) while subjects performed a sensorimotor control task, a face perception control task, and five working memory tasks with parametrically varied retention intervals, ranging from 1 to 21 sec. Striate and ventral occipitotemporal extrastriate areas demonstrated a simple negative correlation between rCBF and retention delay, indicating that these areas participate principally in perceptual operations performed during visual stimulation. By contrast, right and left frontal areas demonstrated rCBF increases that were significantly more sustained across delays than were increases in ventral extrastriate areas, but the relation between rCBF and retention interval differed significantly by hemisphere. Whereas right frontal rCBF showed a nonsignificant tendency to diminish at longer delays, left inferior frontal, middle frontal, and anterior cingulate cortex, as well as left parietal and inferior temporal cortex, demonstrated their largest rCBF increases at the longest delays. These results indicate that right frontal and left frontal, parietal, and temporal areas all participate in face working memory, but that left hemisphere areas are associated with a more durable working memory representation or strategy that subjects rely on increasingly with longer retention intervals. One possible explanation for this hemispheric difference is that left hemisphere activity is associated with a face representation that embodies the results of more analysis and elaboration, whereas right frontal activity is associated with a simpler, icon-like image of a face that is harder to maintain in working memory. (C) 1995 Wiley-Liss, Inc.* C1 NIA,BETHESDA,MD 20892. RP Haxby, JV (reprint author), NIMH,LPP,SECT FUNCT BRAIN IMAGING,BLDG 10,ROOM 4C110,BETHESDA,MD 20892, USA. NR 33 TC 185 Z9 185 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 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PY 1995 VL 3 IS 2 BP 68 EP 82 DI 10.1002/hbm.460030204 PG 15 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA TU288 UT WOS:A1995TU28800002 ER PT J AU Leonardo, M Fieldman, J Sadato, N Campbell, G Ibanez, V Cohen, L Deiber, MP Jezzard, P Pons, T Turner, R LeBihan, D Hallett, M AF Leonardo, M Fieldman, J Sadato, N Campbell, G Ibanez, V Cohen, L Deiber, MP Jezzard, P Pons, T Turner, R LeBihan, D Hallett, M TI A functional magnetic resonance imaging study of cortical regions associated with motor task execution and motor ideation in humans SO HUMAN BRAIN MAPPING LA English DT Article DE magnetic resonance imaging; cerebral blood flow; motor cortex; brain mapping; movement control ID POSITRON EMISSION TOMOGRAPHY; HUMAN BRAIN; SENSORY STIMULATION; INFERIOR AREA-6; VISUAL-CORTEX; ORGANIZATION; PERFORMANCE; MOVEMENTS; ACTIVATION AB Although motor performance may be enhanced through mental practice, the neurophysiological substrate of mental stimulation (ideation) of a motor task is not well established. We used blood oxygen level-dependent contrast echo planar imaging at 1.5 T to identify regions of increased neural activity during the performance and ideation of a motor task. Five subjects performed a sequential finger-to-thumb opposition task and also imagined themselves performing the task in the absence of actual muscle movement. In all subjects, the left primary sensorimotor cortex showed more activation with actual movement than with motor ideation, but two subjects had significant activation with motor ideation. The left premotor area showed comparable activation with both actual and imagined performance in three subjects. These findings support the involvement of the primary motor area as well as the premotor area in motor ideation. (C) 1995 Wiley-Liss, Inc* C1 NINCDS,NIH,HUMAN MOTOR CONTROL SECT,MED NEUROL BRANCH,BETHESDA,MD 20892. NINCDS,NIH,BIOMETRY & FIELD STUDIES BRANCH,BETHESDA,MD 20892. NHLBI,NIH,CARDIAC ENERGET LAB,BETHESDA,MD. NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. NIMH,NIH,CTR CLIN,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. HOWARD HUGHES MED INST,BETHESDA,MD 20817. RI Turner, Robert/C-1820-2008; Deiber, Marie-Pierre/M-5949-2014; OI Jezzard, Peter/0000-0001-7912-2251 NR 41 TC 90 Z9 93 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 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PY 1995 VL 3 IS 2 BP 83 EP 92 DI 10.1002/hbm.460030205 PG 10 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA TU288 UT WOS:A1995TU28800003 ER PT J AU Bookheimer, SY Zeffiro, IA Blaxton, T Gaillard, W Theodore, W AF Bookheimer, SY Zeffiro, IA Blaxton, T Gaillard, W Theodore, W TI Regional cerebral blood flow during object naming and word reading SO HUMAN BRAIN MAPPING LA English DT Article DE PET; language; brain activation; speech ID POSITRON EMISSION TOMOGRAPHY; TEMPORAL LANGUAGE AREA; BY-LETTER READER; INTRAVENOUS (H2O)-O-15; PHONOLOGICAL ALEXIA; HUMAN-BRAIN; PET IMAGES; LOCALIZATION; ANATOMY AB By several accounts, reading single words may be accomplished either by sequentially transcribing orthographic units into their corresponding sounds (an indirect route), or by directly associating a visual word form to the semantic or articulatory representation (a direct route). By contrast, the similar task of naming objects must rely only on a direct route, since objects cannot be ''sounded out.'' To study the localization of cognitive processes specific to reading, we used positron emission tomography (PET) to measure regional cerebral blood flow while subjects named words and pictures of objects silently or aloud. Group averages of blood now changes were obtained for experimental vs. control tasks. Object and word presentations elicited similar blood now increases in extra-striate visual cortices compared with a visual noise control. Silent reading invoked a neural network very similar to that seen when subjects named objects silently, consistent with a ''direct'' route. Naming objects aloud produced the addition of motor output regions to this network By contrast, oral reading produced a markedly different pattern of activated regions, suggesting reliance on a separate phonological pathway. These results provide support for the dual coding hypothesis in reading and challenge the use of strict hierarchical models of cognitive operations in PET activation studies. (C) 1995 Wiley-Liss, Inc* C1 NIA,NIH,NEUROSCI LAB,BETHESDA,MD 20892. NINCDS,NIH,EPILEPSY RES BRANCH,BETHESDA,MD 20892. NR 46 TC 308 Z9 315 U1 0 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PY 1995 VL 3 IS 2 BP 93 EP 106 DI 10.1002/hbm.460030206 PG 14 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA TU288 UT WOS:A1995TU28800004 ER PT J AU WILLIAMS, RC JACOBSSON, LTH KNOWLER, WC DELPUENTE, A KOSTYU, D MCAULEY, JE BENNETT, PH PETTITT, DJ AF WILLIAMS, RC JACOBSSON, LTH KNOWLER, WC DELPUENTE, A KOSTYU, D MCAULEY, JE BENNETT, PH PETTITT, DJ TI METAANALYSIS REVEALS ASSOCIATION BETWEEN MOST COMMON CLASS-II HAPLOTYPE IN FULL-HERITAGE NATIVE-AMERICANS AND RHEUMATOID-ARTHRITIS SO HUMAN IMMUNOLOGY LA English DT Note ID SHARED-EPITOPE HYPOTHESIS; RIVER-INDIAN-COMMUNITY; PIMA-INDIANS; DIABETES-MELLITUS; ADMIXTURE; SEQUENCE; ARIZONA; PREVALENCE; GENETICS; ALLELES AB The association of RA with the alleles at the HLA system was tested among Pima and Tohono O'odham Indians (Pimans) of the Gila River Indian Community of Arizona. Serologic class I (HLA-A, -B, and -C) alleles were typed in 51 individuals with RA and in 302 without RA. Serologic class II (HLA-DR, DQ; DR52 DR53) alleles were typed in a subset of 47 with RA and 147 without RA. Molecular subtypes of DR3Xb, DRB1(*)1402, and (*)1406 were determined in 29 individuals, 16 with RA and 13 without RA. Among the cases with RA, 46 of 47 had the serologic antigen HLA-DR3X6, as did 140 of 147 of those without the disease. However, this association was not statistically significant because of the high prevalence of the antigen in the controls. Data from Pimans were analyzed with similar results from the Tlingit and Yakima Indians. A meta-analysis employing the Mantel-Haenszel procedure, stratified by tribe, revealed a statistically significant association between the most common haplotype, DRB1(*)1402 DQA1(*)0501 DQB1(*)0301 DRB3(*)0101, and RA (summary odds ratio = 2.63, 95% confidence interval = 1.08, 6.46). There was also a statistically significant difference in the genotype distributions of one class I locus, HLA-C, between those with and without RA(chi(2) = 12.4, 5 df, p = 0.03). It is concluded that the association with the most common class II haplotype in full-heritage Native Americans might help explain their high prevalence of RA. C1 ARIZONA STATE UNIV,DEPT ANTHROPOL,TEMPE,AZ 85287. NIAMSD,PHOENIX,AZ. NIDDKD,DIABET ARTHRIT EPIDEMIOL SECT,PHOENIX,AZ. UNIV NAPLES,DEPT RHEUMATOL,NAPLES,ITALY. DUKE UNIV,MED CTR,DEPT IMMUNOL,DURHAM,NC. RP WILLIAMS, RC (reprint author), BLOOD SYST INC,HISTOCOMPATIBIL LAB,6220 E OAK ST,SCOTTSDALE,AZ 85257, USA. FU NCRR NIH HHS [2 S07 RR07112] NR 25 TC 43 Z9 45 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD JAN PY 1995 VL 42 IS 1 BP 90 EP 94 DI 10.1016/0198-8859(94)00079-6 PG 5 WC Immunology SC Immunology GA QE583 UT WOS:A1995QE58300012 PM 7751165 ER PT J AU LEDBETTER, DH ENGEL, E AF LEDBETTER, DH ENGEL, E TI UNIPARENTAL DISOMY IN HUMANS - DEVELOPMENT OF AN IMPRINTING MAP AND ITS IMPLICATIONS FOR PRENATAL-DIAGNOSIS SO HUMAN MOLECULAR GENETICS LA English DT Review ID PRADER-WILLI-SYNDROME; INTRAUTERINE GROWTH-RETARDATION; FAMILIAL ANGELMAN SYNDROME; FLUID CELL-CULTURES; MOLECULAR DIAGNOSIS; LINKAGE ANALYSIS; NORMAL PHENOTYPE; PATERNAL DISOMY; NORMAL DAUGHTER; SHORT STATURE AB Uniparental disomy (UPD) in humans is caused primarily by meiotic nondisjunction events, followed by trisomy or monosomy 'rescue'. The majority of cases appear to be associated with advanced maternal age, and may be initially detected as mosaic trisomies during routine prenatal diagnosis by chorionic villus sampling or amniocentesis. In addition, structural abnormalities including Robertsonian translocations, reciprocal translocations and supernumerary marker chromosomes appear to be associated with an increased risk of UPD. Predicting the phenotypic effects of UPD is complex, as three independent factors are involved: (i) effects of trisomy on the placenta or the fetus; (ii) autosomal recessive disease due to reduction to homozygosity; and (iii) imprinted gene effects for some chromosomes. To date, UPD in humans has been reported for 25 of the 47 possible uniparental types. Imprinting effects have been established with certainty for four human chromosomes that have homology to mouse chromosomes which have been shown to have significant phenotypic effects in uniparental animals. A normal phenotype has been reported for 14 other UPD types. Thus, collection of data on UPD cases in humans is providing an imprinting map analogous to the experimentally derived imprinting map in mouse. This human imprinting map has important clinical implications, particularly in the area of prenatal diagnosis. C1 UNIV GENEVA,DEPT GENET & MICROBIOL,DIV MED GENET,GENEVA,SWITZERLAND. RP LEDBETTER, DH (reprint author), NIH,NATL CTR HUMAN GENOME RES,DIAGNOST DEV BRANCH,BETHESDA,MD 20892, USA. NR 100 TC 277 Z9 278 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PY 1995 VL 4 SI SI BP 1757 EP 1764 PG 8 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA TC033 UT WOS:A1995TC03300010 PM 8541876 ER PT J AU RABEN, N SHERMAN, JB AF RABEN, N SHERMAN, JB TI MUTATIONS IN MUSCLE PHOSPHOFRUCTOKINASE GENE SO HUMAN MUTATION LA English DT Article DE GLYCOGENOSIS; TARUI DISEASE; EXERTIONAL MYOPATHY ID GLYCOGEN-STORAGE-DISEASE; 5' UNTRANSLATED REGION; SOMATIC-CELL HYBRIDS; DEFICIENCY; RNA; EXPRESSION; ASSIGNMENT; ISOENZYMES; ANTIBODY; CLONING AB Mutations in the muscle phosphofructokinase gene (PFK-M) result in a metabolic myopathy characterized by exercise intolerance and compensated hemolysis. PFK deficiency, glycogenosis type VII (Tarui disease) is a rare, autosomal, recessively inherited disorder. Multiple mutations, including splicing defects, frameshifts, and missense mutations, have recently been identified in patients from six different ethnic backgrounds establishing genetic heterogeneity of the disease. There is no obvious correlation between the genotype and phenotypic expression of the disease. PFK-M deficiency appears to be prevalent among people of Ashkenazi Jewish descent. Molecular diagnosis is now feasible for Ashkenazi patients who share two common mutations in the gene; the more frequent is an exon 5 splicing defect, which accounts for similar to 68% of mutant alleles in this population. (C) 1995 Wiley-Liss, Inc.(+) RP RABEN, N (reprint author), NIAMS,ARTHRITIS & RHEUMATISM BRANCH,BETHESDA,MD 20892, USA. NR 39 TC 21 Z9 22 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 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1995 VL 6 IS 1 BP 1 EP 6 DI 10.1002/humu.1380060102 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA RG503 UT WOS:A1995RG50300001 PM 7550225 ER PT J AU HONE, J ACCILI, D PSIACHOU, H ALGHBANDZADEH, J MITTON, S WERTHEIMER, E SINCLAIR, L TAYLOR, SI AF HONE, J ACCILI, D PSIACHOU, H ALGHBANDZADEH, J MITTON, S WERTHEIMER, E SINCLAIR, L TAYLOR, SI TI HOMOZYGOSITY FOR A NULL ALLELE OF THE INSULIN-RECEPTOR GENE IN A PATIENT WITH LEPRECHAUNISM SO HUMAN MUTATION LA English DT Article DE DIABETES MELLITUS; INSULIN RECEPTOR; INSULIN RESISTANCE; LEPRECHAUNISM; PREMATURE CHAIN TERMINATION MUTATION ID POLYMERASE CHAIN-REACTION; NONSENSE MUTATION; MESSENGER-RNA; PROLINE MUTATION; DECREASED LEVELS; MUTANT ALLELES; RESISTANCE; MECHANISMS; TRANSPORT; DISEASE AB Mutations in the insulin receptor gene can cause genetic syndromes associated with extreme insulin resistance, We have investigated a patient with leprechaunism (leprechaun/Qatar-1) born of a con sanguineous marriage. Postnatally, the proband had episodes of severe hypoglycemia and hyperinsu-linernia, with blood glucose levels ranging from 0.9 to 9.9 mmol/L. The C peptide concentration with 1880 nmol/L, and the total insulin concentration was 1409 mU/L. The patient died outside the hospital at the age of four months, All 22 exons of the patient's insulin reseptor gene were screened for mutations using denaturing gradient gel electrophoresis, Thereafter, the nucleotide sequences of selected exons were determined directly. The patient was homozygous for a mutation in exon 13; thirteen base pairs were deleted and replaced by a 5 b.p. sequence. This mutation shifts the reading frame and introduces a premature chain termination codon downstream in exon 13. Thus, the mutant allele is predicted to be a null allele that encodes a truncated receptor lacking both transmembrane and tyrosine kinase domains. (C) 1995 Wiley Liss, Inc. C1 NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. CHARING CROSS & WESTMINSTER MED SCH,ENDOCRINE LAB,LONDON W6 8RF,ENGLAND. WESTMINISTER CHILDRENS HOSP,DEPT PEDIAT,LONDON,ENGLAND. NR 26 TC 25 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 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1995 VL 6 IS 1 BP 17 EP 22 DI 10.1002/humu.1380060105 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA RG503 UT WOS:A1995RG50300004 PM 7550226 ER PT J AU HAHN, SH KRASNEWICH, D BRANTLY, M KVITTINGEN, EA GAHL, WA AF HAHN, SH KRASNEWICH, D BRANTLY, M KVITTINGEN, EA GAHL, WA TI HETEROZYGOSITY FOR AN EXON-12 SPLICING MUTATION AND A W234G MISSENSE MUTATION IN AN AMERICAN CHILD WITH CHRONIC TYROSINEMIA TYPE-1 SO HUMAN MUTATION LA English DT Article DE TYROSINEMIA; FUMARYLACETOACETATE HYDROLASE; SPLICING; MISSENSE; TRANSFECTION ID HUMAN FUMARYLACETOACETATE HYDROLASE; HEREDITARY TYROSINEMIA; GENE; IDENTIFICATION; EXPRESSION; DEFICIENT; QUEBEC; ENZYME; LIVER AB Hereditary tyrosinemia type 1, an autosomal recessive disorder caused by deficiency of fumarylacetoacetate hydrolase (FAH), manifests in either an acute or a chronic form, We used reverse transcription and the polymerase chain reaction to amplify the FAH cDNA of a 12-year-old American boy with chronic tyrosinemia type 1. The patient is a compound heterozygote for mutations in the FAH gene. One allele contains a missense mutation in codon 234 changing a tryptophan to a glycine; this allele was of maternal origin. Mutagenesis and transfection into COS cells demonstrated that the W234G mutation abolishes FAH activity. The patient's paternally derived allele is a splicing mutation in the + 5 position of intron 12, causing either insertion of a 105 bp fragment due to a cryptic splice site, or skipping of exon 12, or skipping of both exons 12 and 13. The chronic phenotype of tyrosinemia type 1 in this patient may be due to some residual, correct splicing by the allele with the splicing mutation. (C) 1995 Wiley-Liss, Inc. C1 NICHHD,HUMAN GENET BRANCH,HUMAN BIOCHEM GENET SECT,BETHESDA,MD 20892. UNIV OSLO,INST CLIN BIOCHEM,OSLO,NORWAY. NR 26 TC 8 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1995 VL 6 IS 1 BP 66 EP 73 DI 10.1002/humu.1380060113 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA RG503 UT WOS:A1995RG50300012 PM 7550234 ER PT J AU ROGAN, PK SCHNEIDER, TD AF ROGAN, PK SCHNEIDER, TD TI USING INFORMATION-CONTENT AND BASE FREQUENCIES TO DISTINGUISH MUTATIONS FROM GENETIC POLYMORPHISMS IN SPLICE JUNCTION RECOGNITION SITES SO HUMAN MUTATION LA English DT Article DE INFORMATION THEORY; HUMAN SPLICE SITES; DNA SEQUENCING; MUTATION; POLYMORPHISM ID SEQUENCES; HOMOLOG; CANCER AB Predicting the effects of nucleotide substitutions in human splice sites has been based on analysis of consensus sequences. We used a graphic representation of sequence conservation and base frequency, the sequence logo, to demonstrate that a change in a splice acceptor of hMSH2 (a gene associated with familial nonpolyposis colon cancer) probably does not reduce splicing efficiency. This confirms a population genetic study that suggested that this substitution is a genetic polymorphism. The information theory based sequence logo is quantitative and more sensitive than the corresponding splice acceptor consensus sequence for detection of true mutations, Information analysis may potentially be used to distinguish polymorphisms from mutations in other types of transcriptional, translational, or protein coding motifs. (C) 1995 Wiley-Liss, Inc. C1 PENN STATE UNIV,MILTON S HERSHEY MED CTR,DEPT PEDIAT,DIV GENET,HERSHEY,PA 17033. NCI,FREDERICK CANC RES & DEV CTR,MATH BIOL LAB,FREDERICK,MD 21702. RI Rogan, Peter/B-9845-2017; OI Rogan, Peter/0000-0003-2070-5254; Schneider, Thomas/0000-0002-9841-1531 NR 14 TC 33 Z9 34 U1 1 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1995 VL 6 IS 1 BP 74 EP 76 DI 10.1002/humu.1380060114 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA RG503 UT WOS:A1995RG50300013 PM 7550236 ER PT J AU GRACE, MB BUZARD, GS WEINTRAUB, BD AF GRACE, MB BUZARD, GS WEINTRAUB, BD TI ALLELE-SPECIFIC ASSOCIATED POLYMORPHISM ANALYSIS - NOVEL MODIFICATION OF SSCP FOR MUTATION DETECTION IN HETEROZYGOUS ALLELES USING THE PARADIGM OF RESISTANCE TO THYROID-HORMONE SO HUMAN MUTATION LA English DT Article DE MUTATIONAL ANALYSIS; COLD-SINGLE CONFORMATION POLYMORPHISM (COLD-SSCP); ALLELE-SPECIFIC ASSOCIATED POLYMORPHISM (ASAP); RESISTANCE TO THYROID HORMONE (RTH); HUMAN THYROID HORMONE RECEPTOR-BETA (HTR-BETA); DNA TESTING; POLYMERASE CHAIN REACTION (PCR) ID STRAND CONFORMATION POLYMORPHISM; POLYMERASE CHAIN-REACTION; ERBA-BETA GENE; GENERALIZED RESISTANCE; POINT MUTATIONS; PCR-SSCP; KINDREDS; AMPLIFICATION; RECEPTOR; BINDING AB Allele specific polymorphism (ASAP) analysis is a modification of single strand conformation polymorphism (SSCP) mutation screening under optimized temperature conditions in a minigel format with ethidium bromide detection. ASAP analysis was used to screen for and identify mutations within the human thryoid hormone receptor-beta (hTR-beta) gene, These mutations are the underlying cause of resistance to thyroid hormone (RTH). Eleven dissimilar known hTR-beta mutations and six previously uncharacterized mutations were accurately identified, ASAP screening extends to unique ASAP-DNA fingerprinting as an identifying signature for each novel hTR-beta mutation detected thus far. Gel plugs from the SSCP gels containing polymorphic single stranded DNA alleles were used without elution to prepare solid-phase sequencing templates for mutant allele PCR and sequencing (MAPS). The coupling of ASAP analysis with MAPS has eliminated many of the interpretative and technical problems associated with the sequencing of heterozygous alleles. Together, this convenient screening and sequencing methodology offers accuracy, reproducibility, speed, and the potential elimination of all radioactivity, providing a general strategy for future automated detection and characterization of genetic mutations. (C) 1995 Wiley Liss, Inc. C1 NIDDK, MOLEC & CELLULAR ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. GEORGE WASHINGTON UNIV, DEPT GENET, WASHINGTON, DC 20052 USA. NCI, FREDERICK CANC RES & DEV CTR, SAIC FREDERICK, BIOL CARCINOGENESIS & DEV PROGRAM, FREDERICK, MD 21701 USA. NR 32 TC 5 Z9 5 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1059-7794 EI 1098-1004 J9 HUM MUTAT JI Hum. Mutat. PY 1995 VL 6 IS 3 BP 232 EP 242 DI 10.1002/humu.1380060306 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA RX124 UT WOS:A1995RX12400005 PM 8535442 ER PT J AU GLAVAC, D DEAN, M AF GLAVAC, D DEAN, M TI APPLICATIONS OF HETERODUPLEX ANALYSIS FOR MUTATION DETECTION IN DISEASE GENES SO HUMAN MUTATION LA English DT Review DE CYSTIC FIBROSIS; HLA TYPING ID CYSTIC-FIBROSIS GENE; POLYMERASE CHAIN-REACTION; FAMILIAL ADENOMATOUS POLYPOSIS; SINGLE BASE SUBSTITUTIONS; DNA HETERODUPLEXES; GEL-ELECTROPHORESIS; POINT MUTATIONS; DYSTROPHIN GENE; RAPID DETECTION; HYDROLINK GELS AB Double-stranded heteroduplex molecules that form between a mutant and wild-type DNA strand are often distinguished from homoduplex molecules upon gel electrophoresis. This method, heteroduplex analysis (HA), can be performed rapidly without radioisotopes or specialized equipment. Modifications and enhancements of the HA method have been developed that increase the sensitivity of detection of single base pair alterations. (dagger)(C) 1995 Wiley-Liss, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NATL INST CHEM,LJUBLJANA,SLOVENIA. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 NR 75 TC 35 Z9 35 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1995 VL 6 IS 4 BP 281 EP 287 DI 10.1002/humu.1380060402 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA TH400 UT WOS:A1995TH40000001 PM 8680402 ER PT J AU CHEN, F KISHIDA, T YAO, M HUSTAD, T GLAVAC, D DEAN, M GNARRA, JR ORCUTT, ML DUH, FM GLENN, G GREEN, J HSIA, YE LAMIELL, J LI, H WEI, MH SCHMIDT, L TORY, K KUZMIN, I STACKHOUSE, T LATIF, F LINEHAN, WM LERMAN, M ZBAR, B AF CHEN, F KISHIDA, T YAO, M HUSTAD, T GLAVAC, D DEAN, M GNARRA, JR ORCUTT, ML DUH, FM GLENN, G GREEN, J HSIA, YE LAMIELL, J LI, H WEI, MH SCHMIDT, L TORY, K KUZMIN, I STACKHOUSE, T LATIF, F LINEHAN, WM LERMAN, M ZBAR, B TI GERMLINE MUTATIONS IN THE VONHIPPEL-LINDAU DISEASE TUMOR-SUPPRESSOR GENE - CORRELATIONS WITH PHENOTYPE SO HUMAN MUTATION LA English DT Article DE VON HIPPEL-LINDAU DISEASE; GERMLINE MUTATION; PHEOCHROMOCYTOMA; RENAL CELL CARCINOMA ID POINT MUTATIONS; REGION; CHROMOSOME-3; LOCUS AB von Hippel-Lindau disease (VHL) is an inherited neoplastic disease characterized by a predisposition to develop retinal angiomas, central nervous system hemangioblastomas, renal cell carcinomas, pancreatic cysts, and pheochromocytomas. The VHL gene was recently isolated by positional cloning. The cDNA encodes 852 nucleotides in 3 exons. The VHL gene is unrelated to any known gene families. We identified germline mutations in 85/114 (75%) of VHL families. Clinical heterogeneity is a well known feature of VHL. VHL families were classified into 2 types based on the presence or absence of pheochromocytoma. The types of mutations responsible for VHL without pheochromocytoma (VHL type 1) differed from those responsible for VHL with pheochromocytoma (VHL type 2). Fifty-six % of the mutations responsible for VHL type 1 were microdeletions/insertions, nonsense mutations, or deletions; 96% of the mutations responsible for VHL type 2 were missense mutations, Specific mutations in codon 238 accounted for 43% of the mutations responsible for VHL type 2, The mutations identified in these families will be useful in presymptomatic diagnosis. The identification of mutations associated with phenotypes contributes to the understanding of fundamental genetic mech anisms of VHL disease. (C) 1995 Wiley Liss, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK,MD 21702. NCI,SURG BRANCH,BETHESDA,MD 20892. NCI,CANC DIAGNOSIS BRANCH,BETHESDA,MD 20892. MEM UNIV NEWFOUNDLAND,DIV COMMUNITY MED,ST JOHNS,NF A1B 3V6,CANADA. UNIV HAWAII,JOHN A BURNS SCH MED,HONOLULU,HI 96826. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 NR 16 TC 385 Z9 391 U1 0 U2 6 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1995 VL 5 IS 1 BP 66 EP 75 DI 10.1002/humu.1380050109 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA QC244 UT WOS:A1995QC24400008 PM 7728151 ER PT J AU MCINTOSH, I ABBOTT, MH FRANCOMANO, CA AF MCINTOSH, I ABBOTT, MH FRANCOMANO, CA TI CONCENTRATION OF MUTATIONS CAUSING SCHMID METAPHYSEAL CHONDRODYSPLASIA IN THE C-TERMINAL NONCOLLAGENOUS DOMAIN OF TYPE-X COLLAGEN SO HUMAN MUTATION LA English DT Article DE TYPE X COLLAGEN; MUTATIONS; NC1 DOMAIN; SCHMID METAPHYSEAL CHONDRODYSPLASIA ID GENE; SSCP; DISEASES; SEQUENCE AB Schmid metaphyseal chondrodysplasia (SMCD) has previously been shown to be the result of mutations in the type X collagen gene, COL1OA1. A further three mutations have been identified, including two nonsense mutations (Y268X, W651X) and a frameshift mutation (1856delCC). Each of the 10 SMCD mutations identified to date is within the C-terminal noncollagenous domain of type X collagen and three of five deletions initiated around the same nucleotide. This domain is believed to be involved in the initiation of collagen trimerization. The concentration of mutations within this domain is consistent with the hypothesis that the phenotype is the result of a reduction in the level of mature type X collagen due to the mutant polypeptide's inability to participate in trimer formation, although a dominant negative mechanism cannot be discounted, on the basis of current evidence. (C) 1995 Wiley-Liss, Inc. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21287. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21287. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. RP MCINTOSH, I (reprint author), JOHNS HOPKINS UNIV,SCH MED,CTR GENET MED,DEPT MED,BALTIMORE,MD 21287, USA. NR 19 TC 38 Z9 39 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 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1995 VL 5 IS 2 BP 121 EP 125 DI 10.1002/humu.1380050204 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA QH627 UT WOS:A1995QH62700003 PM 7749409 ER PT J AU TORRONI, A BROWN, MD LOTT, MT NEWMAN, NJ WALLACE, DC AF TORRONI, A BROWN, MD LOTT, MT NEWMAN, NJ WALLACE, DC TI AFRICAN, NATIVE-AMERICAN, AND EUROPEAN MITOCHONDRIAL DNAS IN CUBANS FROM PINAR-DEL-RIO PROVINCE AND IMPLICATIONS FOR THE RECENT EPIDEMIC NEUROPATHY IN CUBA SO HUMAN MUTATION LA English DT Article DE MTDNA VARIATION IN CUBA; ETHNIC-SPECIFIC MTDNA POLYMORPHISMS; CUBAN OPTIC NEUROPATHY ID ENDONUCLEASE CLEAVAGE PATTERNS; BASE PAIR RECOGNITION; RESTRICTION ENZYMES; POLYMORPHISMS; POPULATIONS; NEPAL; MIGRATIONS; AFFINITIES; RADIATION; SEQUENCE AB Genetic predisposition, particularly specific mitochondrial DNA (mtDNA) backgrounds, has been proposed as a contributing factor in the expression of an epidemic of bilateral optic neuropathy that has affected residents of Cuba since 1991. To substantiate or refute the possibility that specific subsets of mtDNAs could participate in disease expression, we took advantage of the heterogeneous ethnic origin of the Cuban population and the recent identification of a number of mtDNA polymorphisms that appear to be specific for Africans, Native Americans, and Europeans. The screening of both carefully selected people with epidemic neuropathy and control subjects from the Pinar del Rio Province for these polymorphisms revealed that African, Native American, and European mtDNA haplotypes were equally represented among case and control subjects, and suggested that similar to 50% of Cuban mtDNAs originated from Europeans, 46% from Africans, and 4% from Native Americans. These findings demonstrate that mutations arising in specific mtDNAs are unlikely to play a role in the epidemic neuropathy and indicate that analysis of mtDNA haplotypes can be a valuable tool for assessing the relative maternal contribution of Africans, Native Americans, and Europeans in a mixed population. (C) 1995 Wiley-Liss, Inc. C1 EMORY UNIV,SCH MED,DEPT GENET & MOLEC MED,ATLANTA,GA 30332. EMORY UNIV,SCH MED,DEPT OPHTHALMOL,ATLANTA,GA 30332. EMORY UNIV,SCH MED,DEPT NEUROL,ATLANTA,GA 30332. EMORY UNIV,SCH MED,DEPT NEUROSURG,ATLANTA,GA 30332. UNIV ROMA LA SAPIENZA,DEPT GENET & MOLEC BIOL,ROME,ITALY. CUBAN MINIST PUBL HLTH,HAVANA,CUBA. CTR DIS CONTROL & PREVENT,ATLANTA,GA. PAN AMER HLTH ORG,WASHINGTON,DC 20090. NIH,BETHESDA,MD 20514. US FDA,WASHINGTON,DC 20204. RI Torroni, Antonio/E-1557-2011 OI Torroni, Antonio/0000-0002-4163-4478 FU NEI NIH HHS [P30 EY06360]; NIGMS NIH HHS [GM 46915]; NINDS NIH HHS [NS21328] NR 49 TC 18 Z9 19 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1995 VL 5 IS 4 BP 310 EP 317 DI 10.1002/humu.1380050407 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA QZ864 UT WOS:A1995QZ86400006 PM 7627185 ER PT J AU FUKUDA, Y BASSET, F FERRANS, VJ YAMANAKA, N AF FUKUDA, Y BASSET, F FERRANS, VJ YAMANAKA, N TI SIGNIFICANCE OF EARLY INTRAALVEOLAR FIBROTIC LESIONS AND INTEGRIN EXPRESSION IN LUNG-BIOPSY SPECIMENS FROM PATIENTS WITH IDIOPATHIC PULMONARY FIBROSIS SO HUMAN PATHOLOGY LA English DT Article DE IDIOPATHIC PULMONARY FIBROSIS; INTEGRIN; ALPHA-5-BETA-1; VINCULIN; INTRAALVEOLAR FIBROSIS; CYTOPLASMIC HYALINE ID LOWER RESPIRATORY-TRACT; INTERSTITIAL PNEUMONIA; INTRAALVEOLAR FIBROSIS; INTRALUMINAL FIBROSIS; CHRONIC INFLAMMATION; UNKNOWN CAUSE; FIBRONECTIN; PATHOGENESIS; DISORDERS; FIBERS AB To study the pulmonary structural remodeling in idiopathic pulmonary fibrosis (IPF), ultrastructural, immunohistochemical, and light microscopic molphometric observations were made on 11 pulmonary biopsy specimens from patients with IPF. The morphometric study was done using sequentially cut tissue sections stained for keratin-alcian blue periodic acid-Schiff (PAS), fibronectin, and type IV collagen-alcian blue PAS. Most of the early fibrotic lesions, which were alcian blue- and fibronectin-positive, were intra-alveolar in location. Intra-alveolar fibrosis is considered to be essential for the fusion of alveolar walls in IPF. A strong reaction for integrin alpha 5 beta 1 and vinculin was found in epithelial cells and mesenchymal cells in areas of intra-alveolar fibrosis. These finding show that these cells are active in adhesion to fibronectin in areas of early intra-alveolar fibrosis. Some of the epithelial cells, including cytoplasmic hyaline-laden cells, showed evidence of inadequate adhesion to the extracellular matrix, and this may constitute one of the mechanisms of progression of fibrosis in IPF. HUM PATHOL 26:53-61. Copyright (C) 1995 by W.B. Saunders Company C1 FAC XAVIER BICHAT,INSERM,U82,F-75018 PARIS,FRANCE. NHLBI,PATHOL BRANCH,BETHESDA,MD 20892. RP FUKUDA, Y (reprint author), NIPPON MED COLL,DEPT PATHOL,BUNKYO KU,1-1-5 SENDAGI,TOKYO 113,JAPAN. NR 29 TC 53 Z9 55 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JAN PY 1995 VL 26 IS 1 BP 53 EP 61 DI 10.1016/0046-8177(95)90114-0 PG 9 WC Pathology SC Pathology GA QB220 UT WOS:A1995QB22000008 PM 7529742 ER PT S AU DOUGLAS, T BULTE, JWM DICKSON, DPE FRANKEL, RB PANKHURST, QA MOSKOWITZ, BM MANN, S AF DOUGLAS, T BULTE, JWM DICKSON, DPE FRANKEL, RB PANKHURST, QA MOSKOWITZ, BM MANN, S BE Mark, JE Lee, CYC Bianconi, PA TI INORGANIC-PROTEIN INTERACTIONS IN THE SYNTHESIS OF A FERRIMAGNETIC NANOCOMPOSITE SO HYBRID ORGANIC-INORGANIC COMPOSITES SE ACS SYMPOSIUM SERIES LA English DT Article; Proceedings Paper CT Symposium on Hybrid Organic-Inorganic Composites, at the 207th National Meeting of the American-Chemical-Society CY MAR 13-17, 1994 CL SAN DIEGO, CA SP Amer Chem Soc, Div Polym Mat Sci & Engn Inc ID FERRITIN AB The iron-storage protein ferritin provides a spatially constrained reaction environment within a catalytically active bio-polymer. These properties have facilitated the synthesis of a ferrimagnetic iron oxide-protein composite, formed by tailoring conditions for the synthesis of magnetite. The controlled partial oxidation of Fe(II), at high pH and elevated temperature, in the presence of apo-ferritin resulted in the formation of a colloidal composite with a narrow particle size distribution. This material combines characteristics of both the protein and the inorganic phase. Direct magnetic measurements indicated 13,100 Bohr magnetons per particle. Electron and x-ray diffraction data indicated the presence of a cubic iron oxide mineral phase but could not distinguish between magnetite and maghemite. Data from Mossbauer spectroscopy, measured both in the presence and absence of an applied field as well as at low temperature, suggested that the predominant mineral phase was maghemite rather than magnetite. C1 NATL INST HLTH,BETHESDA,MD 20892. UNIV LIVERPOOL,DEPT PHYS,LIVERPOOL L69 3BX,MERSEYSIDE,ENGLAND. CALIF POLYTECH STATE UNIV SAN LUIS OBISPO,DEPT PHYS,SAN LUIS OBISPO,CA 93407. UNIV MINNESOTA,DEPT GEOL & GEOPHYS,MINNEAPOLIS,MN 55455. UNIV BATH,SCH CHEM,BATH BA2 7AY,AVON,ENGLAND. RI Bulte, Jeff/A-3240-2008; Mann, Stephen/D-1332-2012; Douglas, Trevor/F-2748-2011 OI Bulte, Jeff/0000-0003-1202-1610; Mann, Stephen/0000-0003-3012-8964; NR 13 TC 3 Z9 3 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 SN 0097-6156 BN 0-8412-3148-6 J9 ACS SYM SER PY 1995 VL 585 BP 19 EP 28 PG 10 WC Materials Science, Composites; Polymer Science SC Materials Science; Polymer Science GA BD31A UT WOS:A1995BD31A00003 ER PT J AU TOTH, M KUKOR, Z ROMERO, R HERTELENDY, F AF TOTH, M KUKOR, Z ROMERO, R HERTELENDY, F TI NITRIC-OXIDE SYNTHASE IN FIRST-TRIMESTER HUMAN PLACENTA - CHARACTERIZATION AND SUBCELLULAR-DISTRIBUTION SO HYPERTENSION IN PREGNANCY LA English DT Article DE ARGININE; CITRULLINE; NITRIC OXIDE SYNTHASE; PLACENTA ID AMINOGUANIDINE; PREECLAMPSIA; INHIBITION; EXPRESSION; PREGNANCY; 1ST AB Objectives: To characterize the activity and subcellular distribution of nitric oxide synthase (NOS) in primordial human placenta. Methods: Enzyme activity was assayed in chorion frondosum homogenate and subcellular fractions by measuring the conversion of radiolabeled L-arginine to L-citrulline in the presence or absence of EGTA, NAME (a NOS inhibitor), and NADPH. Main Outcome Measures: Analysis of NOS activity in first-trimester human placental tissue, in terms of citrulline production that is generated in 1:1 ratio with nitric oxide, a potent vasodilator. Results: Both Ca2+-dependent and -independent NOS activities were detected in whole homogenate, as well as in subcellular fractions. Specific activity of NOS was highest in the microsomal fraction, where the enzyme exhibited an absolute requirement for NADPH. Unexpectedly, both Ca2+-activated and Ca2+-independent activities were insensitive to the calmodulin antagonist chlorpromazine, while aminoguanidine, a selective inhibitor of the inducible NOS, effectively suppressed Ca2+-dependent generation of citrulline. Conclusion: Some of the properties of the NO-generating enzyme in the primordial placenta. described here for the first time, differ in several respects from those reported for the term placenta. A coordinated local interaction of NO with the immune system of the developing placenta and the prostaglandin-generating mechanism is suggested, ensuring proper implantation, which may be compromised in hypertensive pregnancies associated with impaired NO synthesis. C1 ST LOUIS UNIV,HLTH SCI CTR,SCH MED,DEPT OBSTET & GYNECOL,ST LOUIS,MO 63110. SEMMELWEIS UNIV MED,INST BIOCHEM 1,H-1085 BUDAPEST,HUNGARY. WAYNE STATE UNIV,DEPT OBSTET & GYNECOL,DETROIT,MI. NICHHD,PERINATOL RES BRANCH,BETHESDA,MD. ST LOUIS UNIV,SCH MED,DEPT PHARMACOL & PHYSIOL SCI,ST LOUIS,MO 63110. NR 30 TC 12 Z9 12 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1064-1955 J9 HYPERTENS PREGNANCY JI Hypertens. Pregnancy PY 1995 VL 14 IS 3 BP 287 EP 300 DI 10.3109/10641959509015675 PG 14 WC Obstetrics & Gynecology; Physiology; Peripheral Vascular Disease SC Obstetrics & Gynecology; Physiology; Cardiovascular System & Cardiology GA TB393 UT WOS:A1995TB39300003 ER PT B AU LEVIN, RL DOUGLAS, MA AF LEVIN, RL DOUGLAS, MA BE Costianes, PJ TI MRIPS/MEDX, A SYSTEM FOR MEDICAL IMAGE PROCESSING SO IMAGE AND INFORMATION SYSTEMS: APPLICATIONS AND OPPORTUNITIES: 23RD AIPR WORKSHOP SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT 23rd AIPR Workshop on Image and Information Systems - Applications and Opportunities CY OCT 12-14, 1994 CL WASHINGTON, DC SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS, AIPR EXECUT COMM DE IMAGE PROCESSING; VISUALIZATION; BIOMEDICAL COMPUTING; PACS C1 NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1710-6 J9 P SOC PHOTO-OPT INS PY 1995 VL 2368 BP 143 EP 148 DI 10.1117/12.200791 PG 6 WC Computer Science, Artificial Intelligence; Optics SC Computer Science; Optics GA BC33L UT WOS:A1995BC33L00014 ER PT B AU BERMAN, LE LONG, R THOMA, GR AF BERMAN, LE LONG, R THOMA, GR BE Costianes, PJ TI CHALLENGES IN PROVIDING GENERAL ACCESS TO DIGITIZED XRAYS OVER THE INTERNET SO IMAGE AND INFORMATION SYSTEMS: APPLICATIONS AND OPPORTUNITIES: 23RD AIPR WORKSHOP SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT 23rd AIPR Workshop on Image and Information Systems - Applications and Opportunities CY OCT 12-14, 1994 CL WASHINGTON, DC SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS, AIPR EXECUT COMM C1 LISTER HILL NATL CTR BIOMED COMMUN,NATL LIB MED,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1710-6 J9 P SOC PHOTO-OPT INS PY 1995 VL 2368 BP 183 EP 193 DI 10.1117/12.200797 PG 11 WC Computer Science, Artificial Intelligence; Optics SC Computer Science; Optics GA BC33L UT WOS:A1995BC33L00019 ER PT J AU CASTELLINO, F GERMAIN, RN AF CASTELLINO, F GERMAIN, RN TI EXTENSIVE TRAFFICKING OF MHC CLASS II-INVARIANT CHAIN COMPLEXES IN THE ENDOCYTIC PATHWAY AND APPEARANCE OF PEPTIDE-LOADED CLASS-II IN MULTIPLE COMPARTMENTS SO IMMUNITY LA English DT Article ID LYSOSOMAL MEMBRANE-GLYCOPROTEINS; RECEPTOR-MEDIATED ENDOCYTOSIS; INTRACELLULAR-TRANSPORT; SURFACE EXPRESSION; PLASMA-MEMBRANE; HLA ANTIGENS; CELL-SURFACE; MOLECULES; BINDING; IDENTIFICATION AB Major histocompatibility complex class II molecules bind and present to T cells fragments of protein antigens entering the endocytic pathway. Using normal B lymphoblasts, we have combined metabolic pulse-chase labeling, high resolution organelle fractionation, and immunoprecipitation to examine class II trafficking and antigen loading in a physiological model system. Most newly synthesized class II-invariant chain complexes first entered early endosomes, then accessed multiple discrete endocytic subcompartments cofractionating with late endosomes and immature lysosomes. Invariant chain was removed and peptide-loaded class II molecules appeared in each of these latter distinct organelles. These findings suggest that class II molecules traffic through much of the endocytic pathway, permitting capture of distinct determinants made available under differing conditions of pH and proteolytic activity. RP CASTELLINO, F (reprint author), NIAID,LYMPHOCYTE BIOL SECT,IMMUNOL LAB,BETHESDA,MD 20892, USA. NR 84 TC 165 Z9 166 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD JAN PY 1995 VL 2 IS 1 BP 73 EP 88 DI 10.1016/1074-7613(95)90080-2 PG 16 WC Immunology SC Immunology GA QC593 UT WOS:A1995QC59300007 PM 7600303 ER PT S AU McFarland, HI Critchfield, JM Racke, MK Mueller, JP Nye, SH Boehme, SA Lenardo, MJ AF McFarland, HI Critchfield, JM Racke, MK Mueller, JP Nye, SH Boehme, SA Lenardo, MJ BE Atassi, MZ Bixler, GS TI Amelioration of autoimmune reactions by antigen-induced apoptosis of T cells SO IMMUNOBIOLOGY OF PROTEINS AND PEPTIDES III: MANIPULATION OR MODULATION OF THE IMMUNE RESPONSE SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 8th International Symposium on the Immunobiology of Proteins and Peptides CY NOV 16-20, 1994 CL PIO RICO, AZ SP Inivax Biologics Inc, Amgen, Smith Kline ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; LYMPHOCYTES-T; MICE; CLONES; ALPHA C1 UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. WASHINGTON UNIV,SCH MED,DEPT NEUROL,ST LOUIS,MO 63110. ALEX PHARMACEUT INC,NEW HAVEN,CT 06511. RP McFarland, HI (reprint author), NIAID,IMMUNOL LAB,BLDG 10,BETHESDA,MD 20892, USA. RI McFarland, Hugh/K-1503-2016 OI McFarland, Hugh/0000-0002-3322-038X NR 17 TC 13 Z9 13 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45125-5 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 383 BP 157 EP 166 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA BE37X UT WOS:A1995BE37X00018 PM 8644500 ER PT S AU Loftus, DJ Kubo, RT Sakaguchi, K Celis, E Sette, A Appella, E AF Loftus, DJ Kubo, RT Sakaguchi, K Celis, E Sette, A Appella, E BE Atassi, MZ Bixler, GS TI Analysis of MHC-specific peptide motifs - Applications in immunotherapy SO IMMUNOBIOLOGY OF PROTEINS AND PEPTIDES III: MANIPULATION OR MODULATION OF THE IMMUNE RESPONSE SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 8th International Symposium on the Immunobiology of Proteins and Peptides CY NOV 16-20, 1994 CL PIO RICO, AZ SP Inivax Biologics Inc, Amgen, Smith Kline ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-I MOLECULES; T-CELL EPITOPES; 3-DIMENSIONAL STRUCTURE; ENDOGENOUS PEPTIDES; BINDING PEPTIDES; VIRAL PEPTIDES; LYMPHOCYTES-T; HLA; ANTIGEN C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. CYTEL CORP,SAN DIEGO,CA 92121. RP Appella, E (reprint author), NCI,CELL BIOL LAB,BLDG 37,BETHESDA,MD 20892, USA. NR 72 TC 6 Z9 6 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45125-5 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 383 BP 201 EP 210 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA BE37X UT WOS:A1995BE37X00021 PM 8644503 ER PT B AU FAMILARI, M DEAN, J AF FAMILARI, M DEAN, J BE Nilsson, O Mattsson, R TI Molecular genetics of the zona pellucida SO IMMUNOCONTRACEPTION SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT International Symposium on Immunocontraception CY JUN 30-JUL 01, 1994 CL UPPSALA, SWEDEN SP ARES SERONO SYMPOSIA RP NIDDK,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-21-X J9 FRONT ENDOCRINOL PY 1995 VL 12 BP 183 EP 195 PG 13 WC Electrochemistry; Immunology; Reproductive Biology SC Electrochemistry; Immunology; Reproductive Biology GA BC87A UT WOS:A1995BC87A00018 ER PT J AU THIA, KYT JENKINS, NA GILBERT, DJ COPELAND, NG SMYTH, MJ AF THIA, KYT JENKINS, NA GILBERT, DJ COPELAND, NG SMYTH, MJ TI THE NATURAL-KILLER-CELL SERINE-PROTEASE GENE LMET1 MAPS TO MOUSE CHROMOSOME-10 SO IMMUNOGENETICS LA English DT Note ID LYMPHOCYTE-T; LINKAGE MAP; GRANZYME-A; LEUKEMIA; LOCUS; PURIFICATION; APOPTOSIS; GRANULES; CLONING; FAMILY C1 AUSTIN HOSP,AUSTIN RES INST,CELLULAR CYTOTOXIC LAB,HEIDELBERG,VIC 3084,AUSTRALIA. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. RI Smyth, Mark/H-8709-2014 OI Smyth, Mark/0000-0001-7098-7240 FU NCI NIH HHS [N01-CO-74101] NR 24 TC 8 Z9 8 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 JAN PY 1995 VL 41 IS 1 BP 47 EP 49 DI 10.1007/BF00188433 PG 3 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA PV360 UT WOS:A1995PV36000007 PM 7806275 ER PT J AU NAGATA, T WEISS, EH ABE, K KITAGAWA, K ANDO, A YARAKIKUTI, Y SELDIN, MF OZATO, K INOKO, H TAKETO, M AF NAGATA, T WEISS, EH ABE, K KITAGAWA, K ANDO, A YARAKIKUTI, Y SELDIN, MF OZATO, K INOKO, H TAKETO, M TI PHYSICAL MAPPING OF THE RETINOID-X RECEPTOR B-GENE IN MOUSE AND HUMAN SO IMMUNOGENETICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; NUCLEAR HORMONE RECEPTOR; EMBRYONAL CARCINOMA-CELLS; THYROID-HORMONE; ACID RECEPTORS; RXR-BETA; SIGNALING PATHWAYS; CLOSE LINKAGE; H-2K REGION; RAR-BETA AB Retinoid X receptors (RXRs) are zinc finger-containing nuclear transcription factors. They belong to the nuclear receptor superfamily that contains retinoid receptors, vitamin D receptors, thyroid hormone receptors, and steroid hormone receptors as well as the so-called orphan receptors. We previously mapped all three RXR genes on mouse chromosomes, using a panel of Mus spretus-Mus musculus interspecific backcross mice: Namely, the RXRA-gene (Rxra) on Chr 2 near the centromere, the RXRB gene (Rxrb) on Chr 17 in the H2 region, and the RXRG gene (Rxrg) on distal Chr 1. Using cosmid clones that cover the major histocompatibility complex (MHC) region, we determined the precise physical map positions of the gene encoding mouse and human RXRB, respectively. The mouse gene (Rxrb) maps between H2-Ke4 and H2-Ke5: namely, immediately telomeric to H2-Ke4 which encodes a histidine-rich transmembrane protein, and 12 kilobases centromeric to H2-Ke5 which is expressed in lymphoid tissues. Rxrb and H2-Ke4 are transcribed into opposite directions from a CpG-rich promoter of about 250 base pairs. This gene organization is well conserved also in the human genome at the HLA-DP subregion of Chr 6p, underscoring the strong conservation of the gene organization in the MHC region between the two mammals. C1 BANYU TSUKUBA RES INST MERCK,TSUKUBA,IBARAKI 30033,JAPAN. UNIV MUNICH,INST ANTHROPOL & HUMAN GENET,D-80333 MUNICH,GERMANY. KUMAMOTO UNIV,SCH MED,INST MOLEC EMBRYOL & GENET,KUMAMOTO 862,JAPAN. TOKAI UNIV,SCH MED,DEPT GENET INFORMAT,DIV MOLEC LIFE SCI,ISEHARA,KANAGAWA 25911,JAPAN. DUKE UNIV,MED CTR,DEPT MED & MICROBIOL,DURHAM,NC 27710. NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. FU NHGRI NIH HHS [HG00734] NR 54 TC 20 Z9 20 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JAN PY 1995 VL 41 IS 2-3 BP 83 EP 90 PG 8 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA PZ789 UT WOS:A1995PZ78900004 PM 7806300 ER PT S AU Braden, BC Cauerhff, A DallAcqua, W Fields, BA Goldbaum, FA Malchiodi, EL Mariuzza, RA Poljak, RJ Schwarz, FP Ysern, X Bhat, TN AF Braden, BC Cauerhff, A DallAcqua, W Fields, BA Goldbaum, FA Malchiodi, EL Mariuzza, RA Poljak, RJ Schwarz, FP Ysern, X Bhat, TN BE Casali, P Silberstein, LE TI Structure and thermodynamics of antigen recognition by antibodies SO IMMUNOGLOBULIN GENE EXPRESSION IN DEVELOPMENT AND DISEASE SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Immunoglobulin Gene Expression in Development and Disease CY JUL 13-17, 1994 CL MONTREAL, CANADA SP New York Acad Sci ID X-RAY DIFFRACTION; 3-DIMENSIONAL STRUCTURE; CRYSTAL-STRUCTURE; PROTEIN ANTIGEN; SERINE PROTEASE; COMPLEX; LYSOZYME; RESOLUTION; REFINEMENT; WATER C1 UNIV MARYLAND,CTR ADV RES BIOTECHNOL,INST BIOTECHNOL,ROCKVILLE,MD 20850. NATL INST STAND & TECHNOL,ROCKVILLE,MD 20850. US FDA,CTR DRUG EVALUAT & RES,ROCKVILLE,MD 20857. NCI,FREDERICK CANC RES & DEV CTR,BIOMED SUPERCOMP CTR,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21202. OI Malchiodi, Emilio/0000-0001-7501-3330 NR 36 TC 10 Z9 10 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-933-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 764 BP 315 EP 327 PG 13 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Immunology GA BE39E UT WOS:A1995BE39E00046 PM 7486542 ER PT J AU PARKER, KC SHIELDS, M DIBRINO, M COLIGAN, JE AF PARKER, KC SHIELDS, M DIBRINO, M COLIGAN, JE TI PEPTIDE BINDING TO MHC CLASS-I MOLECULES - IMPLICATIONS FOR ANTIGENIC PEPTIDE PREDICTION SO IMMUNOLOGIC RESEARCH LA English DT Review DE BETA-2-MICROGLOBULIN; ANTIGENIC PEPTIDES; ANCHOR RESIDUES ID T-CELL RECEPTOR; TOXIC LYMPHOCYTES-T; HISTOCOMPATIBILITY COMPLEX-MOLECULES; VIRUS MATRIX PROTEIN; DROSOPHILA-MELANOGASTER CELLS; ALLELE-SPECIFIC MOTIFS; HLA-B27 HEAVY-CHAIN; ENDOGENOUS PEPTIDES; VIRAL PEPTIDES; HIV-1 PROTEINS AB The human mayor histocompatibility complex class I molecule HLA-A2 preferentially binds peptides that contain Leu at P2 and Val or Leu at the C terminus. The other amino acids in the peptide also contribute to binding positively or negatively. It is possible to estimate the binding stability of HLA-A2 complexes containing particular peptides by applying coefficients, deduced from a large amount of binding data, that quantify the relative contribution of each amino acid at each position. In this review, we describe the molecular basis for these coefficients and demonstrate that estimates of binding stability based on the coefficients are generally concordant with experimental measurements of binding affinities. Peptides that contained cysteine were predicted less well, possibly because of complications resulting from peptide dimerization and oxidation. Apparently, peptide binding affinity is largely controlled by the rate of dissociation of the HLA/peptide/beta(2)-microglobulin complex, whereas the rate of formation of the complex has less impact on peptide affinity. Although peptides that bind tightly to HLA-A2, including many antigenic peptides bind much more weakly. Therefore, a full understanding of why certain peptides are immunodominant will require further research. RP PARKER, KC (reprint author), NIAID,MOLEC STRUCT LAB,TWINBROOK 2,ROOM 103,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. OI Parker, Kenneth/0000-0002-6282-2478 NR 129 TC 76 Z9 78 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1995 VL 14 IS 1 BP 34 EP 57 DI 10.1007/BF02918496 PG 24 WC Immunology SC Immunology GA RN124 UT WOS:A1995RN12400003 PM 7561340 ER PT J AU PUCILLO, CEM PALMER, LD HODES, RJ AF PUCILLO, CEM PALMER, LD HODES, RJ TI SUPERANTIGENIC CHARACTERISTICS OF MOUSE MAMMARY-TUMOR VIRUSES PLAY A CRITICAL ROLE IN SUSCEPTIBILITY TO INFECTION IN MICE SO IMMUNOLOGIC RESEARCH LA English DT Article DE MOUSE MAMMARY TUMOR VIRUS; SUPERANTIGEN; MHC CLASS II; T-CELL RECEPTOR; TRANSGENE ID T-CELL-RECEPTOR; STAPHYLOCOCCAL ENTEROTOXIN-A; LONG TERMINAL REPEAT; ANTIGEN RECEPTOR; MYCOPLASMA-ARTHRITIDIS; RETROVIRAL SUPERANTIGENS; BETA-CHAIN; HLA-DR; EXPRESSION; RECOGNITION AB Mouse mammary tumor viruses (MMTV) are retroviruses that induce mammary carcinomas. An interesting feature of these viruses is the superantigen (SAg) encoded in an open reading frame within the 3' long terminal repeat. The mechanism by which ingestion of milk-borne virus results in infection of the host mammary tissue remains incompletely understood. However, a working model has been proposed in which the interaction between viral SAg, T-cell receptor and MHC class III-E facilitates viral replication and hence infectivity. In this review we summarize current studies demonstrating the role of SAg stimulation in susceptibility to MMTV infection. C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NIA,BETHESDA,MD 20892. RI Pucillo, Carlo/A-5515-2008; OI Pucillo, Carlo/0000-0002-4872-6156 NR 62 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1995 VL 14 IS 1 BP 58 EP 68 DI 10.1007/BF02918497 PG 11 WC Immunology SC Immunology GA RN124 UT WOS:A1995RN12400004 PM 7561341 ER PT J AU KLEIN, HG AF KLEIN, HG TI NOVEL CELLULAR THERAPIES SO IMMUNOLOGICAL INVESTIGATIONS LA English DT Article; Proceedings Paper CT 12th International Convocation on Immunology - Transfusion Immunology and Medicine CY MAY 14-18, 1994 CL BUFFALO, NY SP ERNEST WITEBSKY CTR IMMUNOL, SUNY BUFFALO, SCH MED ID TUMOR-INFILTRATING LYMPHOCYTES; BONE-MARROW TRANSPLANTATION; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PERIPHERAL-BLOOD LYMPHOCYTES; CHRONIC MYELOGENOUS LEUKEMIA; ACTIVATED KILLER CELLS; ADOPTIVE IMMUNOTHERAPY; METASTATIC MELANOMA; GENE-THERAPY; CANCER RP KLEIN, HG (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892, USA. NR 29 TC 2 Z9 2 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0882-0139 J9 IMMUNOL INVEST JI Immunol. Invest. PY 1995 VL 24 IS 1-2 BP 411 EP 420 DI 10.3109/08820139509062789 PG 10 WC Immunology SC Immunology GA QE096 UT WOS:A1995QE09600031 PM 7713600 ER PT J AU DAVEY, RJ AF DAVEY, RJ TI TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE AND THE IRRADIATION OF BLOOD COMPONENTS SO IMMUNOLOGICAL INVESTIGATIONS LA English DT Article; Proceedings Paper CT 12th International Convocation on Immunology - Transfusion Immunology and Medicine CY MAY 14-18, 1994 CL BUFFALO, NY SP ERNEST WITEBSKY CTR IMMUNOL, SUNY BUFFALO, SCH MED ID RED-CELLS; STORAGE; PLASMA AB Transfusion-associated graft-versus-host disease (TA-GVHD) is a rare but lethal disorder caused when viable donor lymphocytes engraft and proliferate in a susceptible transfusion recipient, Patients with immune deficiency disorders, hematologic malignancies and bone marrow transplants are at risk to TA-GVHD, as are premature newborns and transfusion recipients who are HLA heterozygous for an HLA-haplotype that is shared with an HLA homozygous donor. Irradiation of blood components with 2500 cGy will inactivate donor lymphocytes and prevent TA-GVHD. Platelets and granulocytes are not functionally impaired by this radiation dose, but red cells sustain detectible damage. Red cell units irradiated and stored for 42 days have significantly higher supernatant recovery of chromium-51 labeled cells is sub-optimal. Based on these data, the maximum permissible storage time for irradiated red cells has been reduced to 28 days. RP DAVEY, RJ (reprint author), NIH,BLDG 10,BETHESDA,MD 20892, USA. NR 15 TC 10 Z9 10 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0882-0139 J9 IMMUNOL INVEST JI Immunol. Invest. PY 1995 VL 24 IS 1-2 BP 431 EP 434 DI 10.3109/08820139509062791 PG 4 WC Immunology SC Immunology GA QE096 UT WOS:A1995QE09600033 PM 7713602 ER PT J AU ROVEECOLLIER, C BOLLER, K AF ROVEECOLLIER, C BOLLER, K TI CURRENT THEORY AND RESEARCH ON INFANT LEARNING AND MEMORY - APPLICATION TO EARLY INTERVENTION SO INFANTS AND YOUNG CHILDREN LA English DT Article DE INFANTS; LEARNING; MEMORY; REACTIVATION; TIME WINDOW; TRANSFER OF TRAINING ID RETRIEVAL; RETENTION; CATEGORIZATION AB Young infants remember their prior experiences for relatively long periods with surprising specificity. This specificity can be overridden, however, to facilitate transfer to new situations. Even seemingly forgotten memories can often be reactivated, and multiple reactivations can further protract retention. Individuals who plan interventions with infants and young children can program these events in ways that optimize cumulative learning and retention. The principles on which such interventions should be based are embodied in the time-window construct. C1 NICHHD,HUMAN LEARNING & BEHAV BRANCH,BALTIMORE,MD 21224. RP ROVEECOLLIER, C (reprint author), RUTGERS STATE UNIV,DEPT PSYCHOL,BUSCH CAMPUS,NEW BRUNSWICK,NJ 08903, USA. NR 43 TC 4 Z9 4 U1 0 U2 0 PU ASPEN PUBL INC PI FREDERICK PA 7201 MCKINNEY CIRCLE, FREDERICK, MD 21701 SN 0896-3746 J9 INFANT YOUNG CHILD JI Infants Young Child. PD JAN PY 1995 VL 7 IS 3 BP 1 EP 12 PG 12 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA QE348 UT WOS:A1995QE34800003 ER PT J AU MCCARDLE, P KIM, J GRUBE, C RANDALL, V AF MCCARDLE, P KIM, J GRUBE, C RANDALL, V TI AN APPROACH TO BILINGUALISM IN EARLY INTERVENTION SO INFANTS AND YOUNG CHILDREN LA English DT Article DE BICULTURALISM; BILINGUALISM; BILINGUAL LANGUAGE DEVELOPMENT; COGNITIVE EFFECTS; KOREAN-AMERICAN CHILDREN; LANGUAGE DEVELOPMENT ID WHOLE LANGUAGE; COGNITIVE-DEVELOPMENT; EDUCATION AB A growing number of persons in the United States speak languages other than English, and there has been confusion about approaches to language teaching/intervention and to education in general among this heterogeneous group. While early research indicated that bilingualism might have possible deleterious effects on child development, in later studies, bilingualism has been associated with cognitive advantages. This article discusses the concepts, principles, and practical application of serving children who live in bicultural households; explores possible reasons for the delays identified in these children; and offers a population-based approach to intervention with them, using a case study example. Developmental screening of children who are military dependents living in South Korea, many of whose parents speak two different languages (one Korean and one American English), revealed a high prevalence of risk for language delay. A solution is proposed that addresses both language and cultural identity and that does not isolate children or promote ethocentrism. C1 NIH,DIV RES GRANTS,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT PREVENT MED & BIOMETR,BETHESDA,MD 20814. UNIFORMED SERV UNIV HLTH SCI,DEPT PEDIAT,BETHESDA,MD 20814. DEPT ARMY,MED COMMAND 18,SEOUL,SOUTH KOREA. USA,OFF SURGEON GEN,SPECIAL EDUC LIAISON SERV,FALLS CHURCH,VA. USA,OFF SURGEON GEN,MED CORPS,FALLS CHURCH,VA. NR 67 TC 4 Z9 4 U1 3 U2 9 PU ASPEN PUBL INC PI FREDERICK PA 7201 MCKINNEY CIRCLE, FREDERICK, MD 21701 SN 0896-3746 J9 INFANT YOUNG CHILD JI Infants Young Child. PD JAN PY 1995 VL 7 IS 3 BP 63 EP 73 PG 11 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA QE348 UT WOS:A1995QE34800008 ER PT J AU GORDON, VM KLIMPEL, KR ARORA, N HENDERSON, MA LEPPLA, SH AF GORDON, VM KLIMPEL, KR ARORA, N HENDERSON, MA LEPPLA, SH TI PROTEOLYTIC ACTIVATION OF BACTERIAL TOXINS BY EUKARYOTIC CELLS IS PERFORMED BY FURIN AND BY ADDITIONAL CELLULAR PROTEASES SO INFECTION AND IMMUNITY LA English DT Article ID PSEUDOMONAS EXOTOXIN-A; ANTHRAX TOXIN; DIPHTHERIA-TOXIN; PROTECTIVE ANTIGEN; KEX2-LIKE ENDOPROTEASE; LETHAL FACTOR; SEQUENCE; CLEAVAGE; CYTOSOL; FRAGMENT AB Before intoxication can occur, anthrax toxin protective antigen (PA), Pseudomonas exotoxin A (PE), and diphtheria toxin (DT) must be activated by proteolytic cleavage at specific amino acid sequences. Previously, it was shown that PA and DT can be activated by furin. In Chinese hamster ovary (CHO) cells, wild-type (RKKR) and cleavage site mutants of PA, each administered with a modified form of anthrax toxin lethal factor (the N terminus of lethal factor fused to PE domain III), had the following potencies: RKKR (wild type) (concentration causing 50% cell death [EC(50)]= 12 ng/ml) greater than or equal to RAAR (EC(50) = 18 ng/ml) > FTKR (EC(50) = 24 ng/ml) > STRR (EC(50) = 49 ng/ml). In vitro cleavage of PA and cleavage site mutants of PA by furin demonstrated that native PA (RKKR) and PA with the cleavage sequence RAAR are substrates for furin. To characterize eukaryotic proteases that play a role in activating bacterial toxins, furin deficient CHO cells were selected after chemical mutagenesis. Furin-deficient cells were resistant to PE, whose cleavage site, RQPR, constitutes a furin recognition site and to all PA cleavage site mutants, but were sensitive to DT (EC(50) = 2.9 ng/ml) and PA (EC(50) = 23 ng/ml), whose respective cleavage sites, RKKR and RVRR, contain additional basic residues. Furin-deficient cells that were transfected with the furin gene regained sensitivity to PE and PA cleavage site mutants. These studies provide evidence that furin can activate the three toxins and that one or more additional proteases contribute to the activation of DT and PA. C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. NR 42 TC 185 Z9 187 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1995 VL 63 IS 1 BP 82 EP 87 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA PY400 UT WOS:A1995PY40000011 PM 7806387 ER PT J AU MYERS, KR BEINING, P BETTS, M SNIPPE, H INMAN, J GOLDING, B AF MYERS, KR BEINING, P BETTS, M SNIPPE, H INMAN, J GOLDING, B TI MONOPHOSPHORYL LIPID-A BEHAVES AS A T-CELL-INDEPENDENT TYPE-1 CARRIER FOR HAPTEN-SPECIFIC ANTIBODY-RESPONSES IN MICE SO INFECTION AND IMMUNITY LA English DT Article ID MALARIA CIRCUMSPOROZOITE PROTEIN; BRUCELLA-ABORTUS; PHASE-I; ADJUVANT; LIPOPOLYSACCHARIDE; ANTIGENS; VACCINE; PEPTIDE; INVIVO; COVALENT AB It is known that the lipopolysaccharide (LPS) of gram-negative bacteria, in addition to being a potent adjuvant, is an effective carrier for covalently associated haptens. However, the toxic nature of most forms of LPS precludes their use as adjuvants or carriers for human vaccines, 4'-Monophosphoryl lipid A (MLA), a derivative of LPS with attenuated toxicity, is currently being tested in humans as an immunological adjuvant. In this study,MLA was tested for its ability to function as a carrier for a small hapten, the trinitrophenyl group (TNP). MW was first modified by addition of 6-aminocaproic acid to the 6' position of the disaccharide backbone (Cap-MLA). TNP was then attached to Cap-MLA via the free amino group, yielding TNP-Cap-MLA. Immunization of normal mice with TNP-Cap-MLA resulted in high-titer anti-TNP responses of immunoglobulin hi and all immunoglobulin G subclasses. Furthermore MLA, like other T-cell-independent type 1 (TI I) carriers, induced responses in athymic and X-linked immunodeficient mice. In all cases, immunization with either MLA alone or TNP-Cap plus MLA failed to induce measurable anti-TNP antibodies of any isotype, indicating that covalent association of MLA and hapten was necessary for MLA's carrier activity to be manifested. These properties of MLA make it a potential candidate as a carrier for vaccine subunit components, such as small peptides, especially for situations in which T-cell help is impaired, as occurs following human immunodeficiency virus type 1 infection. C1 US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL,PLASMA DERIVAT LAB,OFF BLOOD,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. UNIV UTRECHT,EIJKMAN WINKLER LAB MED MICROBIOL,UTRECHT,NETHERLANDS. RP MYERS, KR (reprint author), RIBI IMMUNOCHEM RES INC,553 OLD CORVALLIS RD,HAMILTON,MT 59840, USA. NR 40 TC 23 Z9 23 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1995 VL 63 IS 1 BP 168 EP 174 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA PY400 UT WOS:A1995PY40000025 PM 7806354 ER PT J AU BEATTY, WL MORRISON, RP BYRNE, GI AF BEATTY, WL MORRISON, RP BYRNE, GI TI REACTIVATION OF PERSISTENT CHLAMYDIA-TRACHOMATIS INFECTION IN CELL-CULTURE SO INFECTION AND IMMUNITY LA English DT Article ID OUTER-MEMBRANE PROTEIN; PROTECTIVE MONOCLONAL-ANTIBODIES; DEVELOPMENTAL REGULATION; DEOXYRIBONUCLEIC-ACID; INFERTILE WOMEN; PATHOGENESIS; PENICILLIN; RNA; PURIFICATION; PSITTACI AB Gamma interferon induces persistent chlamydial infections in cell culture. These infections are characterized by altered morphologic and biochemical features of the pathogen. These persistent forms are abnormally large and noninfectious and undergo unusual structural and functional changes, including production of a paucity of outer envelope constituents and normal levels of the chlamydial hsp60, an immunopathological antigen. The current investigation evaluates the events that occur during reactivation of infectious Chlamydia trachomatis from persistently infected cell cultures. Transfer of persistent chlamydial organisms to gamma interferon-free medium resulted in recovery of infectivity accompanied by an increase in levels of structural membrane proteins and reorganization of aberrant organisms to morphologically typical elementary bodies. In addition, reactivation of infectious organisms from persistent chlamydiae that were maintained in culture for several weeks was demonstrated. These studies show that persistent C. trachomatis maintains viability for extended periods, illustrate the reversibility of immunologically mediated persistent infections, and characterize reactivation at the ultrastructural and biochemical levels. C1 UNIV WISCONSIN,DEPT MICROBIOL & IMMUNOL,MADISON,WI 53706. NIAID,ROCKY MT LABS,INTRACELLULAR PARASITES LAB,HAMILTON,MT 59840. FU NIAID NIH HHS [AI19782, AI34617, P01 AI034617, R01 AI019782] NR 37 TC 87 Z9 90 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 JAN PY 1995 VL 63 IS 1 BP 199 EP 205 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA PY400 UT WOS:A1995PY40000029 PM 7806358 ER PT B AU PURCELL, RH AF PURCELL, RH BE Roizman, B TI HEPATITIS VIRUSES - CHANGING PATTERNS OF HUMAN DISEASE SO INFECTIOUS DISEASES IN AN AGE OF CHANGE: THE IMPACT OF HUMAN ECOLOGY AND BEHAVIOR ON DISEASE TRANSMISSION LA English DT Proceedings Paper CT Colloquium on Infectious Diseases In An Age of Change - The Impact of Human Ecology and Behavior on Disease Transmission CY SEP 27-28, 1993 CL NATL ACAD SCI, WASHINGTON, DC HO NATL ACAD SCI C1 NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU NATL ACADEMY PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, PO BOX 285, WASHINGTON, DC 20055 BN 0-309-05136-3 PY 1995 BP 59 EP 75 PG 17 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA BC57N UT WOS:A1995BC57N00005 ER PT B AU QUINN, TC AF QUINN, TC BE Roizman, B TI POPULATION MIGRATION AND THE SPREAD OF TYPE-1 AND TYPE-2 HUMAN IMMUNODEFICIENCY VIRUSES SO INFECTIOUS DISEASES IN AN AGE OF CHANGE: THE IMPACT OF HUMAN ECOLOGY AND BEHAVIOR ON DISEASE TRANSMISSION LA English DT Proceedings Paper CT Colloquium on Infectious Diseases In An Age of Change - The Impact of Human Ecology and Behavior on Disease Transmission CY SEP 27-28, 1993 CL NATL ACAD SCI, WASHINGTON, DC HO NATL ACAD SCI C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU NATL ACADEMY PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, PO BOX 285, WASHINGTON, DC 20055 BN 0-309-05136-3 PY 1995 BP 77 EP 97 PG 21 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA BC57N UT WOS:A1995BC57N00006 ER PT B AU MILLER, LH AF MILLER, LH BE Roizman, B TI IMPACT OF MALARIA ON GENETIC POLYMORPHISM AND GENETIC DISEASES IN AFRICANS AND AFRICAN AMERICANS SO INFECTIOUS DISEASES IN AN AGE OF CHANGE: THE IMPACT OF HUMAN ECOLOGY AND BEHAVIOR ON DISEASE TRANSMISSION LA English DT Proceedings Paper CT Colloquium on Infectious Diseases In An Age of Change - The Impact of Human Ecology and Behavior on Disease Transmission CY SEP 27-28, 1993 CL NATL ACAD SCI, WASHINGTON, DC HO NATL ACAD SCI C1 NIAID,MALARIA RES LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 4 U1 0 U2 0 PU NATL ACADEMY PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, PO BOX 285, WASHINGTON, DC 20055 BN 0-309-05136-3 PY 1995 BP 99 EP 111 PG 13 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA BC57N UT WOS:A1995BC57N00007 ER PT B AU LOWY, DR KIRNBAUER, R SCHILLER, JT AF LOWY, DR KIRNBAUER, R SCHILLER, JT BE Roizman, B TI GENITAL HUMAN PAPILLOMAVIRUS INFECTION SO INFECTIOUS DISEASES IN AN AGE OF CHANGE: THE IMPACT OF HUMAN ECOLOGY AND BEHAVIOR ON DISEASE TRANSMISSION LA English DT Proceedings Paper CT Colloquium on Infectious Diseases In An Age of Change - The Impact of Human Ecology and Behavior on Disease Transmission CY SEP 27-28, 1993 CL NATL ACAD SCI, WASHINGTON, DC HO NATL ACAD SCI C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NATL ACADEMY PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, PO BOX 285, WASHINGTON, DC 20055 BN 0-309-05136-3 PY 1995 BP 157 EP 169 PG 13 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA BC57N UT WOS:A1995BC57N00011 ER PT S AU BLUMBERG, PM ACS, G ACS, P ARECES, LB KAZANIETZ, MG LEWIN, NE SZALLASI, Z AF BLUMBERG, PM ACS, G ACS, P ARECES, LB KAZANIETZ, MG LEWIN, NE SZALLASI, Z BE Doherty, NS Weichman, BM Morgan, DW Marshall, LA TI Protein kinase C in cell signaling: Strategies for the development of selective inhibitors SO INFLAMMATION: MECHANISMS AND THERAPEUTICS SE AGENTS AND ACTIONS SUPPLEMENTS LA English DT Proceedings Paper CT 7th International Conference of the Inflammation-Research-Association on Inflammation, Mechanisms and Therapeutics CY SEP 25-29, 1994 CL WHITE HAVEN, PA SP INFLAMMAT RES ASSOC RP NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,MOLEC MECHANISMS TUMOR PROMOT SECT,BETHESDA,MD 20892, USA. NR 0 TC 11 Z9 11 U1 0 U2 1 PU BIRKHAUSER VERLAG PI BASEL PA PO BOX 133, CH-4010 BASEL, SWITZERLAND SN 0379-0363 BN 3-7643-5129-2 J9 AGENT ACTION SUPPL PY 1995 VL 47 BP 87 EP 100 PG 14 WC Immunology SC Immunology GA BD05X UT WOS:A1995BD05X00007 PM 7785505 ER PT B AU LANGE, N AF LANGE, N BE Bizais, Y Barillot, C DiPaola, R TI Nonlinear Fourier analysis of fMRI time series SO INFORMATION PROCESSING IN MEDICAL IMAGING SE COMPUTATIONAL IMAGING AND VISION LA English DT Proceedings Paper CT 14th International Conference on Information Processing in Medical Imaging CY JUN, 1995 CL ILE DE BERDER, FRANCE SP INSERM, Reg Bretagne, Dept Morbihan, Dist Vannes, Univ Nantes, Univ Rennes, Gen Elect Med Syst Europe, Philips Med Syst, Siemens Med Syst, Control Cata, IBM, Sun Microsyst Inc, Canon France, Dome, CIS BIO Mallinkrodt C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-3593-7 J9 COMP IMAG VIS PY 1995 VL 3 BP 357 EP 358 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA BD56U UT WOS:A1995BD56U00034 ER PT S AU Robinson, MA AF Robinson, MA BE Aledort, LM Hoyer, LW Lusher, JM Reisner, HM White, GC TI T-cell receptors in immune responses SO INHIBITORS TO COAGULATION FACTORS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 2nd International Symposium on Inhibitors to Coagulation Factors CY NOV 03-05, 1993 CL CHAPEL HILL, NC SP N Carolina Sch Med, Ctr Thrombosis & Hemostasis, N Carolina Sch Med, Off Continuing Med Educ & Alumni Affairs, Amer Red Cross, Ctr Dis Control & Prevent, NIH, NHLBI, Natl Hemophilia Fdn, Coalit Hemophilia B ID V-BETA GENE; VARIABLE REGION GENES; ANTIGEN RECEPTOR; MULTIPLE-SCLEROSIS; ALLELIC VARIATIONS; CHAIN GENES; SEGMENTS; POLYMORPHISM; REPERTOIRE; ORGANIZATION RP Robinson, MA (reprint author), NIAID,IMMUNOGENET LAB,NIH,ROCKVILLE,MD 20852, USA. NR 37 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45196-4 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 386 BP 121 EP 132 PG 12 WC Biochemistry & Molecular Biology; Hematology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Hematology; Research & Experimental Medicine GA BF02J UT WOS:A1995BF02J00010 PM 8851020 ER PT B AU Ruttimann, UE Ramsey, NF Hommer, DW Thevenaz, P Lee, C Unser, M AF Ruttimann, UE Ramsey, NF Hommer, DW Thevenaz, P Lee, C Unser, M GP IEEE, SIGNAL PROC SOC TI Analysis of functional magnetic resonance images by wavelet decomposition SO INTERNATIONAL CONFERENCE ON IMAGE PROCESSING - PROCEEDINGS, VOLS I-III LA English DT Proceedings Paper CT International Conference on Image Processing CY OCT 23-26, 1995 CL WASHINGTON, DC SP IEEE, Signal Proc Soc C1 NIAAA,SECT BRAIN ELECTROPHYSIOL & IMAGING,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU I E E E, COMPUTER SOC PRESS PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, LOS ALAMITOS, CA 90720 BN 0-7803-3122-2 PY 1995 BP A633 EP A636 PG 4 WC Computer Science, Interdisciplinary Applications; Engineering, Electrical & Electronic; Optics SC Computer Science; Engineering; Optics GA BE52H UT WOS:A1995BE52H00160 ER PT B AU Unser, M AF Unser, M GP IEEE, SIGNAL PROC SOC TI Multigrid adaptive image processing SO INTERNATIONAL CONFERENCE ON IMAGE PROCESSING - PROCEEDINGS, VOLS I-III LA English DT Proceedings Paper CT International Conference on Image Processing CY OCT 23-26, 1995 CL WASHINGTON, DC SP IEEE, Signal Proc Soc C1 NIH,NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU I E E E, COMPUTER SOC PRESS PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, LOS ALAMITOS, CA 90720 BN 0-7803-3122-2 PY 1995 BP A49 EP A52 PG 4 WC Computer Science, Interdisciplinary Applications; Engineering, Electrical & Electronic; Optics SC Computer Science; Engineering; Optics GA BE52H UT WOS:A1995BE52H00013 ER PT B AU Vrhel, M Trus, BL AF Vrhel, M Trus, BL GP IEEE, SIGNAL PROC SOC TI Multi-channel restoration of electron micrographs SO INTERNATIONAL CONFERENCE ON IMAGE PROCESSING - PROCEEDINGS, VOLS I-III LA English DT Proceedings Paper CT International Conference on Image Processing CY OCT 23-26, 1995 CL WASHINGTON, DC SP IEEE, Signal Proc Soc C1 NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU I E E E, COMPUTER SOC PRESS PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, LOS ALAMITOS, CA 90720 BN 0-7803-3122-2 PY 1995 BP B516 EP B519 PG 4 WC Computer Science, Interdisciplinary Applications; Engineering, Electrical & Electronic; Optics SC Computer Science; Engineering; Optics GA BE52H UT WOS:A1995BE52H00295 ER PT B AU Thevenaz, P Ruttimann, UE Unser, M AF Thevenaz, P Ruttimann, UE Unser, M GP IEEE, SIGNAL PROC SOC TI Iterative multi-scale registration without landmarks SO INTERNATIONAL CONFERENCE ON IMAGE PROCESSING - PROCEEDINGS, VOLS I-III LA English DT Proceedings Paper CT International Conference on Image Processing CY OCT 23-26, 1995 CL WASHINGTON, DC SP IEEE, Signal Proc Soc C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU I E E E, COMPUTER SOC PRESS PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, LOS ALAMITOS, CA 90720 BN 0-7803-3122-2 PY 1995 BP C228 EP C231 PG 4 WC Computer Science, Interdisciplinary Applications; Engineering, Electrical & Electronic; Optics SC Computer Science; Engineering; Optics GA BE52H UT WOS:A1995BE52H00387 ER PT J AU DOHERTY, TM MORSE, HC COFFMAN, RL AF DOHERTY, TM MORSE, HC COFFMAN, RL TI MODULATION OF SPECIFIC T-CELL RESPONSES BY CONCURRENT INFECTION WITH LEISHMANIA-MAJOR AND LP-BM5 MURINE LEUKEMIA VIRUSES SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE MURINE ACQUIRED IMMUNODEFICIENCY SYNDROME; LEISHMANIA MAJOR; T HELPER SUBSETS ID RETROVIRUS-INDUCED IMMUNODEFICIENCY; CUTANEOUS LEISHMANIASIS; MONOCLONAL-ANTIBODY; SYNDROME MAIDS; C57BL/6 MICE; RESISTANCE; DISEASE; INDUCTION; MOUSE; AIDS AB C57BL/6 mice infected with a murine leukemia virus (MuLV) mixture designated LP-BM5 develop an immunodeficiency syndrome termed MAIDS, characterized by a variety of T and B cell abnormalities, including elevated levels of IgE, suggesting that IL-4 expression is increased in these animals. It has been suggested that the immunodeficiency associated with MAIDS is caused by a conversion of immune responses normally characterized by T(h)1 development towards a T(h)2-dominated response. Mice of the same strain, infected with Leishmania major, mount a protective T(h)1 response with the induction of high levels of IFN-gamma and undetectable IL-4. We therefore infected mice with L. major at differing time points before and after virus infection and assessed the effects on T cell responsiveness, cytokine production and survival to L. major, as well as the effect on MAIDS-associated pathology. We have also immunized C57BL/6 mice with trinitrophenol-keyhole limpet haemocyanin (TNP-KLH), which leads to a predominantly T(h)2 response, and compared the effects of MAIDS on the response to TNP-KLH with the effect of MAIDS on L. major infection, Our results show that significant immunodeficiency with regard to infection by L. major is only apparent after 8 weeks of LP-BM5 MuLV infection, by which time T and B cell defects are well advanced. Further, we have found that the strongly polarized T(h)1 response stimulated by L. major infection can modulate the effect of MAIDS on T cells, leading to the survival of antigen-specific T cells, Our results suggest that the impairment of immune responses to either TNP-KLH or L. major is due not to an alteration of the balance of T-h/T(h)2 subsets but to a general loss of reactivity in antigen-specific CD4(+) cells. However, prior activation of T(h)1 but not T(h)2 cells can inhibit the development of lymphoproliferation and immunodeficiency caused by MAIDS. C1 NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. RP DOHERTY, TM (reprint author), DNAX RES INST MOLEC & CELLULAR BIOL INC,DEPT IMMUNOL,901 CALIF AVE,PALO ALTO,CA 94304, USA. OI Morse, Herbert/0000-0002-9331-3705 FU NIAID NIH HHS [N01-AI-72622] NR 37 TC 17 Z9 17 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 JAN PY 1995 VL 7 IS 1 BP 131 EP 138 DI 10.1093/intimm/7.1.131 PG 8 WC Immunology SC Immunology GA QD674 UT WOS:A1995QD67400015 PM 7718509 ER PT J AU AZARI, NP PETTIGREW, KD PIETRINI, P MURPHY, DG HORWITZ, B SCHAPIRO, MB AF AZARI, NP PETTIGREW, KD PIETRINI, P MURPHY, DG HORWITZ, B SCHAPIRO, MB TI SEX-DIFFERENCES IN PATTERNS OF HEMISPHERIC CEREBRAL METABOLISM - A MULTIPLE-REGRESSION DISCRIMINANT-ANALYSIS OF POSITRON EMISSION TOMOGRAPHIC DATA SO INTERNATIONAL JOURNAL OF NEUROSCIENCE LA English DT Article DE HUMAN; SEX; POSITRON EMISSION TOMOGRAPHY; DISCRIMINANT ANALYSIS; CEREBRAL METABOLISM; BRAIN ID HUMAN CORPUS-CALLOSUM; OBSESSIVE-COMPULSIVE DISORDER; LEFT-RIGHT ASYMMETRIES; GLUCOSE-UTILIZATION; ALZHEIMERS-DISEASE; HUMAN-BRAIN; ALTERED INTERCORRELATIONS; TRANSMISSION MEASUREMENTS; GENDER DIFFERENCES; SPATIAL ABILITY AB Sex differences in brain hemispheric structure and function have been reported, acid sex-related differences in hemispheric interregional correlations were reported in a prior analysis of resting PET glucose metabolic (rCMRglc) data. To explore further the effect of sex on patterns of hemispheric brain functional interactions, we applied a multiple regression/discriminant analysis to resting rCMRglc PET data from young normal men and women to test two hypotheses: (1) women have stronger between-hemisphere functional interactions; (2) men have stronger within-hemisphere functional interactions. Two separate discriminant functions based on these hypotheses distinguished men and women: the first reflected rCMRglc interdependencies between hemispheres and correctly classified all women and 94% of the men; the second reflected rCMRglc interdependencies within the left hemisphere and correctly classified 82% of the women and 88% of the men. Because the discriminant functions successfully distinguished men and women, these results provide support for both hypotheses. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NIMH,DIV EPIDEMIOL APPL SERV RES,BETHESDA,MD 20892. NR 89 TC 27 Z9 27 U1 0 U2 0 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0020-7454 J9 INT J NEUROSCI JI Int. J. Neurosci. PY 1995 VL 81 IS 1-2 BP 1 EP 20 DI 10.3109/00207459509015294 PG 20 WC Neurosciences SC Neurosciences & Neurology GA QM314 UT WOS:A1995QM31400001 PM 7775064 ER PT J AU RISING, R FONTVIEILLE, AM LARSON, DE SPRAUL, M BOGARDUS, C RAVUSSIN, E AF RISING, R FONTVIEILLE, AM LARSON, DE SPRAUL, M BOGARDUS, C RAVUSSIN, E TI RACIAL DIFFERENCE IN BODY CORE TEMPERATURE BETWEEN PIMA-INDIAN AND CAUCASIAN MEN SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE OBESITY; METABOLIC RATE; BODY TEMPERATURE ID 24-HOUR ENERGY-EXPENDITURE; DIABETES-MELLITUS AB A low body temperature is associated with a low metabolic rate for a given body size and body composition. These two traits might have been assets in the history of a population subjected to cycles of feast and famine, but became part of an obesity-prone syndrome in our westernized society characterized by plenty of food and a sedentary lifestyle, We tested whether Pima Indians have lower body temperatures than Caucasians, a trait which might partly explain the high prevalence of obesity in this population, Twenty-five Pima Indian (28 +/- 6 yrs, 87.8 +/- 22.8 kg, 29 +/- 9% body fat) and 25 Caucasian (30 +/- 5 yrs, 80.7 +/- 18.4 kg, 22 +/- 11% body fat) men had body core temperatures measured by telemetry for 24 h while in a respiratory chamber, Mean daily body core temperature was 36.93 +/- 0.12 and 36.90 +/- 0.22 degrees C in Pima Indians and Caucasians, respectively, Since body core temperature during sleep (SLBCT) correlated with percentage body fat, a subset of 10 Pima Indians and 10 Caucasians were pair-matched for body weight and percentage body fat, In this group, SLBCT was lower in Pima Indians than in Caucasians (36.45 +/- 0.10 vs 36.65 +/- 0.27 degrees C; P < 0.01) and, ethnic group accounted for 20% of the variance in SLBCT (P < 0.01), Surprisingly, the lower SLBCT was not associated with a low metabolic rate and therefore does not seem to play a role in the etiology of obesity in Pima Indians, More studies during cold exposure and/or energy restriction are needed to test whether the maintenance of a lower body temperature might be involved in the pathogenesis of obesity in some populations. C1 NIDDK,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. NR 18 TC 25 Z9 25 U1 1 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD JAN PY 1995 VL 19 IS 1 BP 1 EP 5 PG 5 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA QD770 UT WOS:A1995QD77000001 PM 7719384 ER PT J AU ALGER, S SEAGLE, H RAVUSSIN, E AF ALGER, S SEAGLE, H RAVUSSIN, E TI FOOD-INTAKE AND ENERGY-EXPENDITURE IN OBESE FEMALE BINGERS AND NON-BINGERS SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE EATING BEHAVIOR; DIETARY COMPOSITION; METABOLIC RATE; INDIRECT CALORIMETRY; BODY COMPOSITION ID DEXAMETHASONE SUPPRESSION TEST; EATING DISORDER; BULIMIA NERVOSA; MEAL-FREQUENCY; SCREENING-TEST; BODY-WEIGHT; MULTISITE; SELECTION; SYSTEM AB Since compulsive eating occurs in approximately 30% of obese females and is associated with earlier relapse following weight loss, we compared daily energy intake, dietary composition and energy expenditure among obese binge eaters and obese non-bingers. Nine obese bingers (33 +/- 4 yrs, 95 +/- 6 kg, 39 +/- 1% fat) and nine obese non-bingers (47 +/- 3 yrs, 93 +/- 5 kg, 40 +/- 1% fat) were admitted for 12 days to a metabolic unit. Binge eaters were defined as scoring > 25 on the binge eating scale (BES). During the initial 8 days, subjects ate ad libitum from two computerized vending machines offering a variety of foods and beverages. A weight maintenance diet was then provided for the next 4 days. Twenty-four hour energy expenditure (24EE) and respiratory quotient (24Q) were measured on the last day of both feeding periods in a respiratory chamber. Obese bingers showed a wider range of energy intake compared to non-bingers, but the mean daily energy intake was similar between the two groups (2587 +/- 454 vs 2386 +/- 201 kcal/d) during 8 days of ad libitum intake. 24EE was not different between bingers and non-bingers after 8 days of ad libitum intake (2298 +/- 147 vs 2109 +/- 97 kcal/d, P = 0.3) or 4 days of weight maintenance diet, even more so after adjustment for differences in fat-free mass, fat mass and age. Resting metabolic rate, sleeping metabolic rate, and macronutrient intake and oxidation were also similar between groups. In a controlled experimental environment, obese binge eaters exhibited a greater variability in daily energy intake than non-bingers, but showed no difference in mean daily energy intake, diet composition or metabolic rate compared to obese non-bingers. C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. NR 28 TC 17 Z9 17 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD JAN PY 1995 VL 19 IS 1 BP 11 EP 16 PG 6 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA QD770 UT WOS:A1995QD77000003 PM 7719385 ER PT J AU ROSOLEN, A FRASCELLA, E TORETSKY, J NECKERS, LM AF ROSOLEN, A FRASCELLA, E TORETSKY, J NECKERS, LM TI EPISOME GENERATED C-MYC ANTISENSE RNA INHIBITS GROWTH AND TUMORIGENICITY OF A HUMAN NEUROENDOCRINE TUMOR-CELL LINE SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE MYC ANTISENSE RNA; NEUROENDOCRINE TUMOR ID NEURO-BLASTOMA CELLS; GENE-PRODUCT; EXPRESSION; DIFFERENTIATION; ONCOGENE; MAX AB The neuroepithelioma cell line CHP100 expresses low but detectable amounts of N-myc protein together with large amounts of c-myc protein. We have recently demonstrated that antisense inhibition of N-myc expression in CHP100 cells leads to decreased in vitro growth and alterations in cellular morphology without affecting tumorigenicity in nude mice. In this study we report the construction of an episomally replicating vector designed to generate RNA antisense to part of the human c-myc gene. Such a Vector is able to inhibit c-myc expression in cell lines carrying multiple copies of the gene. Inhibition of c-myc expression leads to a decrease of in vitro growth and cloning efficiency and in vivo tumorigenicity of CHP100 cells. Our findings suggest that N-myc and c-myc subserve different functions in regulating the biology of CHP100 cells. C1 NCI,BETHESDA,MD. RP ROSOLEN, A (reprint author), UNIV PADUA,DIPARTIMENTO PEDIAT,PEDIAT CLIN 2,VIA GIUSTINIANI 3,I-35128 PADUA,ITALY. NR 21 TC 1 Z9 1 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1995 VL 6 IS 1 BP 175 EP 179 PG 5 WC Oncology SC Oncology GA PY335 UT WOS:A1995PY33500028 PM 21556520 ER PT J AU MUELLER, BU AF MUELLER, BU TI ROLE OF CYTOKINES IN CHILDREN WITH HIV-INFECTION SO INTERNATIONAL JOURNAL OF PEDIATRIC HEMATOLOGY/ONCOLOGY LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; COLONY-STIMULATING FACTOR; RECOMBINANT-HUMAN-ERYTHROPOIETIN; AIDS-RELATED COMPLEX; GROWTH FACTOR-I; NECROSIS-FACTOR-ALPHA; HEMATOPOIETIC PROGENITOR CELLS; AVIUM-INTRACELLULARE INFECTION; ZIDOVUDINE-INDUCED NEUTROPENIA; PLACEBO-CONTROLLED TRIAL AB As of June, 1994 over 5700 children in the United States have been diagnosed with the Acquired Immunodeficiency Syndrome (AIDS) caused by infection with the human immunodeficiency virus type-1 (HIV-1).(1) HIV infection in children differs from adults mainly in the early onset of encephalopathy and the often very short period of asymptomatic infection.(2) Hematopoietic growth factors (cytokines) have been used to promote the proliferation and differentiation of stem cells to overcome bone marrow suppression in HIV-infected children and adults. These agents have also been explored for their potential to enhance and support the host immune system,(3) and preliminary results also indicate an important role in the pathogenesis of HIV disease (Table 1).(4,5) The endogenous levels of cytokines and hematopoietic growth factors are often altered by HIV-infection. It is possible that some disease manifestations are directly related to these changes (e.g., increased levels of tumor necrosis factor and the development of wasting syndrome, or increased interleukin-1 levels and encephalopathy). The rate of viral replication is not only influenced by the level of certain cytokines but in turn also induces a cytokine response.(4,5) Because of these multiple interactions it is often complicated to define the therapeutic indications of cytokines and growth factors in HIV-infected patients and benefits have to be balanced carefully against potential disadvantages. RP MUELLER, BU (reprint author), NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 161 TC 0 Z9 0 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1070-2903 J9 INT J PEDIAT HEM ONC JI Int. J. Pediatr. Hematol-Oncol. PY 1995 VL 2 IS 2 BP 151 EP 161 PG 11 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA RJ129 UT WOS:A1995RJ12900009 ER PT J AU CHANOCK, SJ FREIFELD, AG AF CHANOCK, SJ FREIFELD, AG TI CYTOKINES IN THE MANAGEMENT OF INFECTIOUS COMPLICATIONS IN CHILDREN WITH CANCER SO INTERNATIONAL JOURNAL OF PEDIATRIC HEMATOLOGY/ONCOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; BONE-MARROW TRANSPLANTATION; HIGH-DOSE CHEMOTHERAPY; ACUTE LYMPHOBLASTIC-LEUKEMIA; NON-HODGKINS-LYMPHOMA; CELL LUNG-CANCER; BLOOD PROGENITOR CELLS; RECOMBINANT GM-CSF; CONTROLLED TRIAL; INTERFERON-GAMMA AB Children receiving cancer therapy are susceptible to infectious complications that compromise the ability to deliver therapy in a timely manner and may adversely affect outcome. The most significant risk factor is severe neutropenia. The recently discovered myeloid growth factors have the potential to abrogate neutropenia post-intensive therapy and to possibly reduce infectious complications. In addition, these agents can augment effector cell response to established infection. Recently, in various clinical trials, the use of cytokines has been shown to decrease the incidence and severity of infectious complications in pediatric patients, especially those receiving intensive chemotherapy or autologous bone marrow transplant. However, to date, cytokine therapy has not impacted on survival rates. This is an important consideration since these agents are very costly. In an effort to direct the rational use of these agents and to limit the cost, it will be necessary to conduct randomized pediatric studies to examine not only clinical endpoints but also the impact of cytokines on the cost of therapy. RP CHANOCK, SJ (reprint author), NCI,PEDIAT BRANCH,INFECT DIS SECT,10-13N240,BETHESDA,MD 20892, USA. NR 97 TC 8 Z9 8 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1070-2903 J9 INT J PEDIAT HEM ONC JI Int. J. Pediatr. Hematol-Oncol. PY 1995 VL 2 IS 2 BP 173 EP 183 PG 11 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA RJ129 UT WOS:A1995RJ12900011 ER PT J AU SUFFNESS, M CRAGG, GM GREVER, MR GRIFO, FJ JOHNSON, G MEAD, JAR SCHEPARTZ, SA VENDITTI, JM WOLPERT, M AF SUFFNESS, M CRAGG, GM GREVER, MR GRIFO, FJ JOHNSON, G MEAD, JAR SCHEPARTZ, SA VENDITTI, JM WOLPERT, M TI THE NATIONAL-COOPERATIVE-NATURAL-PRODUCTS-DRUG-DISCOVERY-GROUP (NCNPDDG) AND INTERNATIONAL-COOPERATIVE-BIODIVERSITY-GROUP (ICBG) PROGRAMS SO INTERNATIONAL JOURNAL OF PHARMACOGNOSY LA English DT Article; Proceedings Paper CT 3rd Drug Discovery and Development Symposium CY JUL 22-24, 1993 CL SAN DIEGO, CA SP NIH DE DRUG DISCOVERY GROUPS; BIODIVERSITY GROUPS AB The high interest in natural products as sources of pharmaceutical products led to the creation of the National Cooperative Natural Products Drug Discovery Group (NCNPDDG) Program by the National Cancer Institute with the goal of bringing together scientists from academia, industry and government in a focussed effort for discovery of new drugs for cancer treatment. Similarly, the National Institutes of Health, the National Science Foundation, and the U.S. Agency for International Development have joined together to form the International Cooperative Biodiversity Group (ICBG) program To promote the goals of biodiversity conservation, economic development and pharmaceutical discovery. C1 NCI,DIV CANC TREATMENT,GRANTS & CONTRACTS OPERAT BRANCH,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,NAT PROD BRANCH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV HOSP,DIV HEMATOL DIS,BALTIMORE,MD 21287. NIH,FOGARTY INT CTR,INT STUDIES BANCH,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,SCI APPLICAT INT CORP,FREDERICK,MD 21702. NR 2 TC 17 Z9 18 U1 0 U2 0 PU SWETS ZEITLINGER BV PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 0925-1618 J9 INT J PHARMACOGN JI Int. J. Pharmacogn. PY 1995 VL 33 SU S BP 5 EP 16 PG 12 WC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy SC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy GA TH495 UT WOS:A1995TH49500002 ER PT J AU VALERIOTE, F CORBETT, T LORUSSO, P MOORE, RE SCHEUER, P PATTERSON, G PAUL, V GRINDEY, G BONJOUKLIAN, R PEARCE, H SUFFNESS, M AF VALERIOTE, F CORBETT, T LORUSSO, P MOORE, RE SCHEUER, P PATTERSON, G PAUL, V GRINDEY, G BONJOUKLIAN, R PEARCE, H SUFFNESS, M TI DISCOVERY OF ANTICANCER AGENTS FROM NATURAL-PRODUCTS SO INTERNATIONAL JOURNAL OF PHARMACOGNOSY LA English DT Article; Proceedings Paper CT 3rd Drug Discovery and Development Symposium CY JUL 22-24, 1993 CL SAN DIEGO, CA SP NIH DE DRUG DISCOVERY; NATURAL PRODUCTS; IN VITRO ASSAY; CYANOPHYTES; SPONGES AB Cellular, in vitro assays have been both developed and employed by us to search for new, solid tumor specific anticancer agents. Parallel in vivo models are then used to assess the therapeutic efficacy of candidates selected by the in vitro assays. During the past 4 years, extracts as well as pure compounds from natural products have been obtained from collaborators at the University of Hawaii and Lilly Research Laboratories. The samples have been analyzed, the structures identified and a number of lead compounds proposed. C1 WAYNE STATE UNIV,SCH MED,DIV HEMATOL & ONCOL,DETROIT,MI 48201. UNIV HAWAII,DEPT CHEM,HONOLULU,HI 96822. UNIV GUAM,MARINE LAB,MANGILAO,GU 96923. ELI LILLY & CO,LILLY RES LABS,INDIANAPOLIS,IN 46285. NCI,BETHESDA,MD 20892. NR 7 TC 13 Z9 13 U1 1 U2 3 PU SWETS ZEITLINGER BV PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 0925-1618 J9 INT J PHARMACOGN JI Int. J. Pharmacogn. PY 1995 VL 33 SU S BP 59 EP 66 PG 8 WC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy SC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy GA TH495 UT WOS:A1995TH49500007 ER PT J AU TULLY, JG ROSE, DL YUNKER, CE CARLE, P BOVE, JM WILLIAMSON, DL WHITCOMB, RF AF TULLY, JG ROSE, DL YUNKER, CE CARLE, P BOVE, JM WILLIAMSON, DL WHITCOMB, RF TI SPIROPLASMA IXODETIS SP-NOV, A NEW SPECIES FROM IXODES PACIFICUS TICKS COLLECTED IN OREGON SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID CLASS MOLLICUTES; BORRELIA-BURGDORFERI; CLASSIFICATION; GROWTH; MYCOPLASMATALES; OCCIDENTALIS; DEFORMATION; SUBGROUPS; IXODIDAE; TAXONOMY AB Eight strains of mollicutes were isolated from pooled suspensions prepared from western black-legged ticks (Ixodes pacificus) collected in Oregon. Morphologic examination by electron and dark-field microscopic techniques showed that each strain consisted of a mixture of motile, tightly coiled helical cells, small coccoid cells with diameters ranging from 300 to 500 nm, and pleomorphic, straight or branched filamentous forms. All cellular forms were surrounded by a single cytoplasmic membrane, and there was no evidence of a cell wall. The organisms were filterable and fastidious in their growth requirements. The optimum temperature for growth was 30 degrees C, but multiplication occurred at temperatures ranging from 23 to 32 degrees C. The strains catabolized glucose but did not hydrolyze arginine or urea. The genome size of strain Y32(T) (T = type strain) was 2,220 kbp, and the DNA base composition (guanine-plus-cytosine content) of this organism was 25 +/- 1 mol%. The eight isolates were serologically related to each other but were not related to 37 other type or representative strains belonging to the genus Spiroplasma. Strain Y32 (= ATCC 33835) is the type strain of Spiroplasma ixodetis sp. nov. C1 NIAID,ROCKY MT LAB,HAMILTON,MT 59840. INRA,BIOL CELLULAIRE & MOLEC LAB,F-33883 VILLENAVE DORNON,FRANCE. UNIV BORDEAUX 2,F-33883 VILLENAVE DORNON,FRANCE. SUNY STONY BROOK,DEPT ANAT SCI,STONY BROOK,NY 11794. USDA ARS,INSECT PATHOL LAB,BELTSVILLE,MD 20705. RP TULLY, JG (reprint author), NIAID,FREDERICK CANC RES & DEV CTR,FREDERICK CANC RES FACIL,MOLEC MICROBIOL LAB,FREDERICK,MD 21702, USA. NR 53 TC 30 Z9 30 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1995 VL 45 IS 1 BP 23 EP 28 PG 6 WC Microbiology SC Microbiology GA QB873 UT WOS:A1995QB87300004 PM 7857803 ER PT J AU DELGIUDICE, RA ROSE, DL TULLY, JG AF DELGIUDICE, RA ROSE, DL TULLY, JG TI MYCOPLASMA ADLERI SP-NOV, AN ISOLATE FROM A GOAT SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID SHEEP AB Mycoplasma sp. strain G145(T) (T = type strain) was isolated from a goat's abscessed ankle. Strain G145(T) required cholesterol or serum for growth and possessed characteristics similar to those of other members of the genus Mycoplasma. This strain was serologically distinct from previously described Mycoplasma species and from a group of currently unnamed strains thought to belong to the genus Mycoplasma. Strain G145(T) hydrolyzed arginine, but did not hydrolyze urea or ferment glucose. The guanine-plus-cytosine content of the DNA was 29.6 mol%. We propose that strain G145 (= ATCC 27948) is the type strain of a new species, for which we propose the name Mycoplasma adleri. C1 NIAID,MOLEC MICROBIOL LAB,MYCOPLASMA SECT,FREDERICK,MD 21702. RP DELGIUDICE, RA (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,MYCOPLASMA LAB,POB B,FREDERICK,MD 21702, USA. NR 20 TC 3 Z9 4 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1995 VL 45 IS 1 BP 29 EP 31 PG 3 WC Microbiology SC Microbiology GA QB873 UT WOS:A1995QB87300005 PM 7857804 ER PT J AU CARLE, P LAIGRET, F TULLY, JG BOVE, JM AF CARLE, P LAIGRET, F TULLY, JG BOVE, JM TI HETEROGENEITY OF GENOME SIZES WITHIN THE GENUS SPIROPLASMA SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Note ID PULSED-FIELD ELECTROPHORESIS; HOST-PARASITE RELATIONSHIPS; SP-NOV; CLASS MOLLICUTES; MYCOPLASMA-GENITALIUM; GEL-ELECTROPHORESIS; PHYSICAL MAP; CLASSIFICATION; FLOWERS; UREAPLASMAS AB Organisms belonging to the genus Spiroplasma are currently classified into 23 groups, 17 of which have been assigned species epithets. We determined the genome sizes of representatives of 20 groups by using pulsed-field gel electrophoresis. Each genome size was deduced from the mobility of linear nonrestricted DNA, as well as from the sum of the sizes of restriction fragments obtained after digestion with NotI, a restriction endonuclease with a limited number of restriction sites in spiroplasma DNA. The values which we obtained indicated that the genome sizes of members of the genus Spiroplasma range from 940 to 2,220 kbp. C1 INRA,CELLULAR & MOLEC BIOL LAB,F-33883 VILLENAVE DORNON,FRANCE. UNIV BORDEAUX 2,F-33883 VILLENAVE DORNON,FRANCE. NIAID,FREDERICK CANC RES & DEV CTR,MYCOPLASMA SECT,FREDERICK,MD 21702. NR 52 TC 54 Z9 61 U1 1 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1995 VL 45 IS 1 BP 178 EP 181 PG 4 WC Microbiology SC Microbiology GA QB873 UT WOS:A1995QB87300030 PM 7857799 ER PT J AU TULLY, JG WHITCOMB, RF HACKETT, KJ ROSE, DL HENEGAR, RB BOVE, JM CARLE, P WILLIAMSON, DL CLARK, TB AF TULLY, JG WHITCOMB, RF HACKETT, KJ ROSE, DL HENEGAR, RB BOVE, JM CARLE, P WILLIAMSON, DL CLARK, TB TI TAXONOMIC DESCRIPTIONS OF 8 NEW NON-STEROL-REQUIRING MOLLICUTES ASSIGNED TO THE GENUS MESOPLASMA (VOL 44, PG 685, 1994) SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Correction, Addition C1 USDA,INSECT BIOCONTROL LAB,BELTSVILLE,MD 20705. INRA,CELLULAR & MOLEC BIOL LAB,F-33883 VILLENAVE DORNON,FRANCE. UNIV BORDEAUX 2,F-33883 VILLENAVE DORNON,FRANCE. SUNY STONY BROOK,DEPT ANAT SCI,STONY BROOK,NY 11794. RP TULLY, JG (reprint author), NIAID,FREDERICK CANC RES & DEV CTR,MYCOPLASM SECT,FREDERICK,MD 21702, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1995 VL 45 IS 1 BP 201 EP 201 PG 1 WC Microbiology SC Microbiology GA QB873 UT WOS:A1995QB87300035 ER PT J AU GORDIS, E AF GORDIS, E TI CRITICAL ISSUES IN ALCOHOLISM RESEARCH SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Note RP GORDIS, E (reprint author), NIAAA,BETHESDA,MD 20892, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1995 VL 30 IS 4 BP 497 EP 505 PG 9 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA QU158 UT WOS:A1995QU15800009 PM 7607782 ER PT J AU MAIL, PD AF MAIL, PD TI EARLY MODELING OF DRINKING BEHAVIOR BY NATIVE-AMERICAN ELEMENTARY-SCHOOL-CHILDREN PLAYING DRUNK SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Note DE NATIVE AMERICAN; CHILDRENS GAMES; PLAY; PREVENTION STRATEGIES ID ALCOHOL-RELATED EXPECTANCIES; STUDENTS; PATTERNS AB A report of games played by elementary school children on a Native American reservation in the United States illustrates how intoxicated adult behavior is perceived as funny. Only later does one develop an awareness that the consequences of misuse can be injury, illness, and death. Prevention messages targeted at elementary school children need to provide positive alternatives to the humor in drunkenness and may need to be culturally adapted. Examples of some culturally specific approaches are discussed. RP MAIL, PD (reprint author), NIAAA,WILLCO 505,6000 EXECUT BLVD,ROCKVILLE,MD 20892, USA. NR 40 TC 13 Z9 13 U1 2 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1995 VL 30 IS 9 BP 1187 EP 1197 PG 11 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA RL545 UT WOS:A1995RL54500008 PM 7591357 ER PT J AU Borowsky, B Hoffman, BJ AF Borowsky, B Hoffman, BJ TI Neurotransmitter transporters: Molecular biology, function, and regulation SO INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL 38 SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID GAMMA-AMINOBUTYRIC-ACID; PROTEIN-KINASE-C; PLASMA-MEMBRANE VESICLES; BETA-ADRENERGIC-RECEPTOR; LONG-TERM POTENTIATION; HIGH-AFFINITY UPTAKE; FREE FATTY-ACIDS; PLATELET 5-HYDROXYTRYPTAMINE TRANSPORT; CALCIUM-INDEPENDENT RELEASE; HUMAN SEROTONIN TRANSPORTER C1 NIMH,CELL BIOL LAB,UNIT MOLEC PHARMACOL,BETHESDA,MD 20892. NR 231 TC 89 Z9 90 U1 3 U2 5 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0074-7742 J9 INT REV NEUROBIOL PY 1995 VL 38 BP 139 EP 199 PG 61 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BE46F UT WOS:A1995BE46F00004 PM 8537200 ER PT J AU SWAIN, SM PARKER, B WELLSTEIN, A LIPPMAN, ME STEAKLEY, C DELAP, R AF SWAIN, SM PARKER, B WELLSTEIN, A LIPPMAN, ME STEAKLEY, C DELAP, R TI PHASE-I TRIAL OF PENTOSAN POLYSULFATE SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE PENTOSAN POLYSULFATE; ADULT SOLID TUMORS; PHASE I TRIAL ID GROWTH-FACTOR; HEPARIN; ANGIOGENESIS; METABOLISM; INHIBITION; CRITERIA; TOXICITY; INVITRO; CELLS AB Pentosan polysulfate is a semisynthetic pentasaccharide heparinoid derived from beechwood shavings. A total of nineteen patients with various adult solid tumors were treated with three dose levels (15, 22.5, and 30 mg/m(2)/dose) of subcutaneous pentosan polysulfate every 6 hours. The dose limiting toxicities were thrombocytopenia and elevated transaminases at the dose of 30 mg/m(2) every 6 hours. The recommended starting dose for phase II trials is 22.5 mg/m(2) given every 6 hours. There was an increase in anticoagulant activity as measured by activated partial thromboplastin time (aPTT) at the dose of 22.5 mg/m(2) every 6 hours in most patients. There were no objective responses and three patients had stable disease lasting 16, 19 and 76 weeks. C1 NCI,MED ONCOL BRANCH,CLIN ONCOL PROGRAM,WASHINGTON,DC. GEORGETOWN UNIV,LOMBARDI CANC RES CTR,DEPT PHARMACOL,WASHINGTON,DC 20007. GEORGETOWN UNIV,LOMBARDI CANC RES CTR,DEPT MED,WASHINGTON,DC 20007. US FDA,DIV ONCOL & PULM DRUG PROD,ROCKVILLE,MD. OI Wellstein, Anton/0000-0002-0570-4950 NR 20 TC 14 Z9 14 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1995 VL 13 IS 1 BP 55 EP 62 DI 10.1007/BF02614221 PG 8 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA RX433 UT WOS:A1995RX43300008 PM 7499109 ER PT J AU Link, CJ Sarosy, GA Kohn, EC Christian, MC Davis, P Adamo, DO Reed, E AF Link, CJ Sarosy, GA Kohn, EC Christian, MC Davis, P Adamo, DO Reed, E TI Cutaneous manifestations of Taxol(R) therapy SO INVESTIGATIONAL NEW DRUGS LA English DT Article ID PHASE-I AB Taxol(R) is a novel chemotherapeutic agent that has produced substantial responses in early clinical studies [1]. Taxol has excellent activity in a number of malignancies based on recently completed clinical trials, including a 30% response rate in platinum-refractory ovarian cancer patients [2-5]. We are currently conducting trials of dose-intense taxol with granulocyte colony stimulating factor (G-CSF) support in relapsed or refractory ovarian cancer patients. Such dose intensification produces a major response rate in 50% of patients with this disease [6]. Taxol was supplied in 5 mi ampules (6 mg/ml) in polyethoxylated castor oil (Cremophor EL) 50% and dehydrated alcohol and the dose was diluted in either 0.9% sodium chloride or 5% dextrose at concentrations of 0.6 to 1.2 mg/ml. We have noted 3 patients with previously unreported cutaneous manifestations which we believe are taxol related and also report our overall complication rate with the administration of taxol by peripheral intravenous lines. C1 NCI,MED BRANCH,NIH,BETHESDA,MD 20892. NR 9 TC 15 Z9 15 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1995 VL 13 IS 3 BP 261 EP 263 DI 10.1007/BF00873811 PG 3 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA UD850 UT WOS:A1995UD85000014 PM 8729957 ER PT J AU Geyer, JR Balis, FM Krailo, MD Heideman, R Broxson, E Sato, JK Poplack, D Bleyer, WA AF Geyer, JR Balis, FM Krailo, MD Heideman, R Broxson, E Sato, JK Poplack, D Bleyer, WA TI A phase II study of thioTEPA in children with recurrent solid tumor malignancies: A children's cancer group study SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE thioTEPA; alkylating agents; sarcomas; chemotherapy ID CHEMOTHERAPY AB A Phase II study of thioTEPA was performed by the Children's Cancer Group. ThioTEPA was administered intravenously every three weeks, at a dose of 65 mg/m(2). Pediatric patients with recurrent sarcomas were targeted, but patients with other tumor diagnoses were also eligible. Toxicity was primarily hematopoietic, with thrombocytopenia being predominant. ThioTEPA did not demonstrate significant activity in the target tumor groups evaluated. C1 UNIV WASHINGTON, MED CTR, SEATTLE, WA 98195 USA. CHILDRENS HOSP, SEATTLE, WA USA. NCI, NIH, BETHESDA, MD 20892 USA. UNIV SO CALIF, SCH MED, LOS ANGELES, CA USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38105 USA. WRIGHT PATTERSON AFB, DAYTON, OH USA. CHILDRENS HOSP LOS ANGELES, LOS ANGELES, CA 90027 USA. TEXAS CHILDRENS CANC CTR, HOUSTON, TX USA. UNIV TEXAS, MD ANDERSON CANC CTR, HOUSTON, TX USA. NR 11 TC 0 Z9 1 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1995 VL 13 IS 4 BP 337 EP 342 DI 10.1007/BF00873141 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA VB110 UT WOS:A1995VB11000009 ER PT J AU OLD, SE CARPER, DA HOHMAN, TC AF OLD, SE CARPER, DA HOHMAN, TC TI NA,K-ATPASE RESPONSE TO OSMOTIC-STRESS IN PRIMARY DOG LENS EPITHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE NA,K-ATPASE ACTIVITY; NA,K-ATPASE MESSENGER-RNA; HYPERTONIC STRESS; LENS CELL CULTURE ID ATPASE PUMPING ACTIVITY; ALDOSE REDUCTASE; HYPERTONIC STRESS; MOLECULAR-CLONING; GENE-EXPRESSION; RENAL-CELLS; SORBINIL TREATMENT; ORGANIC OSMOLYTES; NA+/K+-ATPASE; MESSENGER-RNA AB Purpose, Na,K-ATPase activity increases in lens cells exposed to hypertonic stress. To test whether the increase in activity involves stimulation of Na,K-ATPase expression, dog lens epithelial cells were subjected to hypertonic stress, and the time course of Na,K-ATPase protein and mRNA response was measured. Methods. Primary cultures of dog lens epithelial cells were maintained in isotonic or hypertonic media over the course of several days. Rubidium-86 uptake measurements, immunoreactive protein, and northern blot analysis were performed. Results, Dog lens epithelial cells exposed to hypertonic stress from culture medium supplemented with 150 mM NaCl or 250 mM cellobiose showed a twofold increase in Na,K-ATPase activity. The increase in activity was blocked by cycloheximide and was reversible when the cells were returned to isotonic medium. This activity was unaffected by the aldose reductase inhibitor, tolrestat. Na,K-ATPase protein and mRNA levels increased in cells exposed to medium containing 150 mM NaCl. Northern blot analysis showed that the alpha-1, and beta-1 mRNA levels increased as early as 6 hours and maximally increased 1.5-fold to twofold by 12 to 24 hours. Conclusions. Elevation of Na,K-ATPase activity in dog lens epithelial cells exposed to hypertonic stress was associated with increased expression of Na,K-ATPase subunit mRNAs and was dependent on protein synthesis. These results suggest that upregulation of the enzyme activity is the result of an induction of Na,K-ATPase. C1 NEI,BETHESDA,MD 20892. WYETH AYERST LAB,PRINCETON,NJ. NR 40 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 1995 VL 36 IS 1 BP 88 EP 94 PG 7 WC Ophthalmology SC Ophthalmology GA QC195 UT WOS:A1995QC19500015 PM 7822162 ER PT B AU WALKER, FL THOMA, GR AF WALKER, FL THOMA, GR BE Cibbarelli, PR Nixon, C TI DOCVIEW - PROVIDING ACCESS TO PRINTED LITERATURE THROUGH THE INTERNET SO IOLS '95 - INTEGRATED ONLINE LIBRARY SYSTEMS, PROCEEDINGS-1995: IOLS IN THE AGE OF NETWORKS LA English DT Proceedings Paper CT 10th Integrated Online Library Systems Meeting CY MAY 03-04, 1995 CL NEW YORK, NY SP Learned Informat Inc C1 NATL LIB MED,BETHESDA,MD 20209. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INFORMATION TODAY INC PI MEDFORD PA 143 OLD MARLTON PIKE, MEDFORD, NJ 08055 BN 1-57387-005-6 PY 1995 BP 165 EP 173 PG 9 WC Information Science & Library Science SC Information Science & Library Science GA BD12G UT WOS:A1995BD12G00018 ER PT B AU GUY, HR DURELL, SR AF GUY, HR DURELL, SR BE Dawson, DC Frizzell, RA TI Structural models of Na+, Ca2+, and K+ channels SO ION CHANNELS AND GENETIC DISEASES SE SOCIETY OF GENERAL PHYSIOLOGISTS SERIES LA English DT Proceedings Paper CT 48th Annual Symposium of the Society-of-General-Physiologists on Ion Channels and Genetic Diseases CY SEP 07-11, 1994 CL MARINE BIOL LAB, WOODS HOLE, MA SP Soc Gen Physiologists HO MARINE BIOL LAB C1 NCI,DIV CANC BIOL DIAG & CTR,MATH BIOL LAB,BETHESDA,MD 20892. NR 0 TC 53 Z9 58 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1230 YORK AVE, NEW YORK, NY 10021 BN 0-87470-057-4 J9 SOC GEN PHY PY 1995 VL 50 BP 1 EP 16 PG 16 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA BD54Q UT WOS:A1995BD54Q00001 PM 7676315 ER PT B AU THOMA, GR BERMAN, LE LONG, LR AF THOMA, GR BERMAN, LE LONG, LR GP SOC IMAGING SCI & TECHNOL TI Digitized medical xrays on the information superhighway SO IS&T'S 48TH ANNUAL CONFERENCE - IMAGING ON THE INFORMATION SUPERHIGHWAY, FINAL PROGRAM AND PROCEEDINGS LA English DT Proceedings Paper CT IS&Ts 48th Annual Conference on Imaging on the Information Superhighway CY MAY 07-11, 1995 CL WASHINGTON, DC SP Soc Imaging Sci & Technol C1 NATL LIB MED,LISTER HILL NATL CTR BIOMED COMMUN,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC IMAGING SCIENCE & TECHNOLOGY PI SPRINGFIELD PA 7003 KILWORTH LANE, SPRINGFIELD, VA 22151 BN 0-89208-184-8 PY 1995 BP 111 EP 113 PG 3 WC Imaging Science & Photographic Technology SC Imaging Science & Photographic Technology GA BD74Y UT WOS:A1995BD74Y00027 ER PT B AU UNSER, M ALDROUBI, A AF UNSER, M ALDROUBI, A GP SOC IMAGING SCI & TECHNOL TI Optimal sampling of non-bandlimited signals with applications to image processing SO IS&T'S 48TH ANNUAL CONFERENCE - IMAGING ON THE INFORMATION SUPERHIGHWAY, FINAL PROGRAM AND PROCEEDINGS LA English DT Proceedings Paper CT IS&Ts 48th Annual Conference on Imaging on the Information Superhighway CY MAY 07-11, 1995 CL WASHINGTON, DC SP Soc Imaging Sci & Technol C1 NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC IMAGING SCIENCE & TECHNOLOGY PI SPRINGFIELD PA 7003 KILWORTH LANE, SPRINGFIELD, VA 22151 BN 0-89208-184-8 PY 1995 BP 370 EP 375 PG 6 WC Imaging Science & Photographic Technology SC Imaging Science & Photographic Technology GA BD74Y UT WOS:A1995BD74Y00104 ER PT J AU Lane, HC AF Lane, HC TI The role of immune-based therapies in the context of conventional anti-retroviral therapy SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,NIH,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1995 VL 10 SU 3 BP 1 EP 1 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UC138 UT WOS:A1995UC13800002 ER PT J AU Boyer, PL Tantillo, C Ding, J Ferris, AL Clark, P Arnold, E Hughes, SH AF Boyer, PL Tantillo, C Ding, J Ferris, AL Clark, P Arnold, E Hughes, SH TI Mechanisms of resistance of HIV-1 reverse transcriptase to nucleoside and non-nucleoside inhibitors SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,ABL BASIC RES PROGRAM,FCRDC,FREDERICK,MD 21701. NCI,SAIC FREDERICK,FCRDC,FREDERICK,MD 21701. CTR ADV BIOTECHNOL & MED,PISCATAWAY,NJ. RUTGERS STATE UNIV,PISCATAWAY,NJ. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1995 VL 10 SU 3 BP 6 EP 6 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UC138 UT WOS:A1995UC13800007 ER PT J AU Arnold, E Das, K Ding, JP Hsiou, Y Tantillo, C Roy, BM Yadav, P Zhang, WY Lentz, K Clark, AD Boyer, PL Hughes, SH Mitsuya, H Mellors, J Kleim, JP Rosner, M Moereels, HR Koymans, L Andries, K Pauwels, R Janssen, PAJ AF Arnold, E Das, K Ding, JP Hsiou, Y Tantillo, C Roy, BM Yadav, P Zhang, WY Lentz, K Clark, AD Boyer, PL Hughes, SH Mitsuya, H Mellors, J Kleim, JP Rosner, M Moereels, HR Koymans, L Andries, K Pauwels, R Janssen, PAJ TI The role of nucleic acid in the resistance of HIV-1 reverse transcriptase to nucleoside and non-nucleoside inhibitors SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 RUTGERS STATE UNIV,CTR ADV BIOTECHNOL & MED,PISCATAWAY,NJ 08854. RUTGERS STATE UNIV,DEPT CHEM,PISCATAWAY,NJ. NCI,ABL BASIC RES PROGRAM,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. NCI,BETHESDA,MD 20892. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,PITTSBURGH,PA. HOECHST AG,GEN PHARMA RES,W-6230 FRANKFURT,GERMANY. JANSSEN RES FDN,B-2340 BEERSE,BELGIUM. TIBOTEC,INST ANTIVIRAL RES,EDEGEM,BELGIUM. UMDNJ,RWJMS,NEWARK,NJ. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1995 VL 10 SU 3 BP 7 EP 7 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UC138 UT WOS:A1995UC13800008 ER PT J AU Reichelderfer, PS Coombs, RW AF Reichelderfer, PS Coombs, RW TI Anti-retroviral drug resistance as a modifier of the interaction between viral load and CD4(+) cell decline SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIH,DIV AIDS,BETHESDA,MD. UNIV WASHINGTON,SEATTLE,WA 98195. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1995 VL 10 SU 3 BP 37 EP 37 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UC138 UT WOS:A1995UC13800038 ER PT J AU Gulnik, SV Suvorov, LI Liu, B Yu, B Anderson, B Mitsuya, H Vaillancourt, M Swanstrom, R Erickson, JW AF Gulnik, SV Suvorov, LI Liu, B Yu, B Anderson, B Mitsuya, H Vaillancourt, M Swanstrom, R Erickson, JW TI Kinetic characterization of HIV-1 protease mutants selected under in vitro drug pressure SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. NCI,NIH,BETHESDA,MD. UNIV N CAROLINA,LINEBERGER COMPREHENS CANC CTR,CHAPEL HILL,NC 27599. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1995 VL 10 SU 3 BP 59 EP 59 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UC138 UT WOS:A1995UC13800060 ER PT J AU Erickson, JW Bhat, TN Munshi, S Gulnik, S AF Erickson, JW Bhat, TN Munshi, S Gulnik, S TI Structural mechanisms of drug resistance for HIV-1 protease mutants SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,STRUCT BIOCHEM PROGRAM,FCRDC,FREDERICK,MD 21701. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1995 VL 10 SU 3 BP 63 EP 63 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UC138 UT WOS:A1995UC13800064 ER PT J AU FLEMING, TR NEATON, JD GOLDMAN, A DEMETS, DL LAUNER, C KORVICK, J ABRAMS, D BEERS, D LOVELESS, K MARTINEZ, N MESARD, CA REVES, RR ROUFF, JA KLEIN, T MCDONALD, R SLOTTEN, R BROSGART, C DREW, L FESSEL, J HUDSON, R LOPEZ, C THOMPSON, S KUMI, JO MASTROPOLAK, D SARAVOLATZ, LD KERKERING, TM HIGGINSON, RA GERNON, L BAR, M MENDEZ, D ERNST, J SCOTT, J FINLEY, B WARD, D WISNIEWSKI, T BRANDON, W WALTER, J CALHOUN, C EBRIGHT, JR SCHUMAN, P BINCSIK, A SWANSON, K WINSLOW, D SHERIDAN, A TAYLOR, V PEREZ, G ELSADR, W GUITY, C JULEAU, J SALVATI, S DOWLING, C SALVADOR, GI BURNS, AJ LAM, SH CHILDRESS, JF DEETS, DL FLEMING, TR MEYER, KH POLLARD, RB OFALLON, JR RAHAL, JJ WALTERS, L WHITNEYWILLIAMS, P WHITLEY, RJ AF FLEMING, TR NEATON, JD GOLDMAN, A DEMETS, DL LAUNER, C KORVICK, J ABRAMS, D BEERS, D LOVELESS, K MARTINEZ, N MESARD, CA REVES, RR ROUFF, JA KLEIN, T MCDONALD, R SLOTTEN, R BROSGART, C DREW, L FESSEL, J HUDSON, R LOPEZ, C THOMPSON, S KUMI, JO MASTROPOLAK, D SARAVOLATZ, LD KERKERING, TM HIGGINSON, RA GERNON, L BAR, M MENDEZ, D ERNST, J SCOTT, J FINLEY, B WARD, D WISNIEWSKI, T BRANDON, W WALTER, J CALHOUN, C EBRIGHT, JR SCHUMAN, P BINCSIK, A SWANSON, K WINSLOW, D SHERIDAN, A TAYLOR, V PEREZ, G ELSADR, W GUITY, C JULEAU, J SALVATI, S DOWLING, C SALVADOR, GI BURNS, AJ LAM, SH CHILDRESS, JF DEETS, DL FLEMING, TR MEYER, KH POLLARD, RB OFALLON, JR RAHAL, JJ WALTERS, L WHITNEYWILLIAMS, P WHITLEY, RJ TI INSIGHTS FROM MONITORING THE CPCRA DIDANOSINE ZALCITABINE TRIAL SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article; Proceedings Paper CT 1st Annual Symposium on Surrogate Markers of HIV - Strategies and Issues for Selection and Use CY OCT 12-14, 1994 CL ARLINGTON, VA SP Cambridge Healthtech Inst DE EQUIVALENCE TRIALS; DATA AND SAFETY MONITORING BOARDS; SURROGATE END POINTS; AIDS PROGRESSION; COVARIATES ID CLINICAL-TRIALS; HIV; THERAPY AB The design, conduct, and analysis of clinical trials that evaluate the safety and efficacy of treatment interventions in patients with HIV infection provide many scientific challenges. A recently completed randomized trial of didanosine (ddI) and zalcitabine (ddC), sponsored by the Terry Beirn Community Programs for Clinical Research on AIDS (CPCRA), is an especially valuable resource for illustrating these challenging issues and for providing insights into how they might be properly addressed. Establishing equivalence of treatment effects on clinical efficacy end points is illustrated through the use of the confidence interval approach. The striking changes in treatment efficacy results that occurred during the course of the CPCRA trial provide important insights into how a data and safety monitoring board can reduce the risk of inappropriate early study termination. The trial also provides valuable insights into how treatment effects should be assessed, revealing inconsistencies between effects on the CD4 surrogate end point and effects on primary clinical efficacy end points and showing the incompleteness of the standardly employed definition of AIDS progression. Finally, the results of this ddI/ddC trial are used to examine the role of covariate adjustment. C1 UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV WISCONSIN,MADISON,WI. NIAID,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. RP FLEMING, TR (reprint author), UNIV WASHINGTON,DEPT BIOSTAT,SC-32,SEATTLE,WA 98195, USA. NR 20 TC 14 Z9 14 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. PY 1995 VL 10 SU 2 BP S9 EP S18 PG 10 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA TD186 UT WOS:A1995TD18600003 PM 7552519 ER PT J AU Pantaleo, G Cohen, OJ Schwartzentruber, DJ Graziosi, C Vaccarezza, M Fauci, AS AF Pantaleo, G Cohen, OJ Schwartzentruber, DJ Graziosi, C Vaccarezza, M Fauci, AS TI Pathogenic insights from studies of lymphoid tissue from HIV-infected individuals SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article; Proceedings Paper CT International Symposium on Combination Antiretroviral Therapy for HIV Infection CY MAR 25-26, 1995 CL BERLIN, GERMANY SP Klin Arbeitsgemeninsch AIDS Deutschland, Wellcome Fdn Ltd DE HIV; lymphoid tissue; immune responses; viral replication ID HUMAN-IMMUNODEFICIENCY-VIRUS; FOLLICULAR DENDRITIC CELLS; TYPE-1 INFECTION; AIDS; LYMPHOCYTES; PLASMA; LYMPHADENOPATHY; PROGRESSION; MECHANISMS; RESERVOIRS AB Studies of lymphoid tissue from HIV-infected individuals have provided critical insights into the pathogenesis of HIV disease. Systemic dissemination of virus via the lymphatic system occurs at a very early stage after infection. Explosive viral replication within lymphoid tissue ensues, before the development of cell-mediated and humoral immune responses. By the time potent immune responses downregulate viral expression, an immense viral reservoir within lymphoid tissue has already been established. During the stage of dichotomy in viral load between lymph node and peripheral blood, the viral reservoir is maintained by the ability of the follicular dendritic cells (FDC) network to efficiently trap extracellular virions, as well as by immunologic and microenvironmental factors favoring infection of susceptible cells and sequestration of cells already infected. Degeneration of the FDC network and wholesale disruption of lymphoid architecture herald late-stage disease. The dysfunctional lymphoid tissue contributes directly to immunodeficiency and to sharp increases in viral burden and replication as mechanical and immune controls are lost. Studies in HIV-infected long-term nonprogressors indicate that these individuals are able to maintain excellent cell-mediated and humoral immune responses against HIV. These immune responses are responsible, at least in part, for the maintenance of intact lymphoid tissue architecture and the low levels of viral burden and replication detected in these individuals. Studies of the effect of antiretroviral therapy on HIV infection in lymphoid tissue show that decreases in plasma viremia are associated with and most likely are caused by decreases in viral replication within lymphoid tissue. Further understanding of the pathogenic mechanisms within lymphoid tissue will have important implications for early intervention aimed at inducing a long-term nonprogressor state (i.e., preventing disruption of lymphoid tissue integrity), and later intervention aimed at arresting or even reversing damage to the lymphoid system. C1 NCI,NIH,DIV CANC THERAPY,BETHESDA,MD 20892. RP Pantaleo, G (reprint author), NIAID,NIH,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B-13,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Pantaleo, Giuseppe/K-6163-2016 NR 59 TC 14 Z9 14 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. PY 1995 VL 10 SU 1 BP S6 EP S14 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA TX998 UT WOS:A1995TX99800003 ER PT J AU REICHELDERFER, PS COOMBS, RW AF REICHELDERFER, PS COOMBS, RW TI VIROLOGICAL PARAMETERS AS SURROGATE MARKERS FOR CLINICAL OUTCOME IN HIV-1 DISEASE - VERIFICATION, VARIATION, AND VALIDATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article; Proceedings Paper CT 1st Annual Symposium on Surrogate Markers of HIV - Strategies and Issues for Selection and Use CY OCT 12-14, 1994 CL ARLINGTON, VA SP Cambridge Healthtech Inst DE VIROLOGICAL MEASUREMENTS; HIV INFECTION; VERIFICATION; VARIATION; VALIDATION ID HUMAN-IMMUNODEFICIENCY-VIRUS AB The criteria used to evaluate which virologic measurements are used to monitor HIV-1 infection should include an assessment of verification, variation, and validation. Rationale for use should first be based on understanding the role of the measurement in the pathogenesis of the disease. Subsequently, the prevalence of the measurement, an understanding of its intrinsic variation, and ease of use will determine the utility of the measure. The usefulness of the measurement will depend on its validation in relation to disease prognosis, antiviral activity, and antiviral efficacy. C1 UNIV WASHINGTON,DEPT LAB MED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT MED,SEATTLE,WA. RP REICHELDERFER, PS (reprint author), NIAID,DIV AIDS,BETHESDA,MD 20892, USA. FU PHS HHS [A1-27664] NR 28 TC 4 Z9 4 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. PY 1995 VL 10 SU 2 BP S19 EP S24 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA TD186 UT WOS:A1995TD18600004 PM 7552509 ER PT J AU PIZZO, PA WILFERT, CM BOROWSKY, W CANOSA, C DEMARTINO, M DEROSSI, A DEBRE, M DELGADO, A EHRNST, A FUNDARO, C GIAQUINTO, C KOUP, R MARCHISIO, P MATHIESON, B MOK, J PAHWA, S PLEBANI, A ROSSI, P RUBINSTEIN, A SCARLATTI, G SCOTT, G STIEHM, R TOVO, PA WALKER, B WARA, D WOLINSKY, S AF PIZZO, PA WILFERT, CM BOROWSKY, W CANOSA, C DEMARTINO, M DEROSSI, A DEBRE, M DELGADO, A EHRNST, A FUNDARO, C GIAQUINTO, C KOUP, R MARCHISIO, P MATHIESON, B MOK, J PAHWA, S PLEBANI, A ROSSI, P RUBINSTEIN, A SCARLATTI, G SCOTT, G STIEHM, R TOVO, PA WALKER, B WARA, D WOLINSKY, S TI REPORT OF A CONSENSUS WORKSHOP, SIENA, ITALY, JUNE 4-6, 1993 - MARKERS AND DETERMINANTS OF DISEASE PROGRESSION IN CHILDREN WITH HIV-INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; PNEUMOCYSTIS-CARINII PNEUMONIA; POLYMERASE CHAIN-REACTION; AVIUM COMPLEX INFECTION; AIDS DEMENTIA COMPLEX; P24 ANTIGEN LEVELS; T-CELL RESPONSES; TYPE-1 INFECTION; REVERSE-TRANSCRIPTASE; BACTERIAL-INFECTIONS C1 NCI,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT PEDIAT,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT MICROBIOL,DURHAM,NC 27710. RI Plebani, Alessandro/C-8593-2011; Wolinsky, Steven/B-2893-2012; rossi, paolo/D-6504-2012; De Rossi, Anita/L-3128-2015; Marchisio, Paola /J-7342-2016; OI De Rossi, Anita/0000-0001-6435-7509; Marchisio, Paola /0000-0002-5691-3920; ROSSI, PAOLO/0000-0003-2620-7918 NR 154 TC 47 Z9 49 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN 1 PY 1995 VL 8 IS 1 BP 30 EP 44 PG 15 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA QA526 UT WOS:A1995QA52600006 PM 8548344 ER PT J AU BLATTNER, WA VOLBERDING, PA HASELTINE, WA AF BLATTNER, WA VOLBERDING, PA HASELTINE, WA TI JAIDS AND HUMAN RETROVIROLOGY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Editorial Material C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,DEPT MED,DIV AIDS ACTIV,SAN FRANCISCO,CA 94110. HUMAN GENOME SCI INC,ROCKVILLE,MD 20850. RP BLATTNER, WA (reprint author), NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 3 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN 1 PY 1995 VL 8 IS 1 BP A25 EP A25 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA QA526 UT WOS:A1995QA52600001 ER PT J AU UMBRICHTSCHNEITER, A MONTOYA, I PRESTON, KL AF UMBRICHTSCHNEITER, A MONTOYA, I PRESTON, KL TI FACTORS ASSOCIATED WITH CLONIDINE USE DURING SHORT INPATIENT DETOXIFICATION WITH BUPRENORPHINE SO JOURNAL OF ADDICTIVE DISEASES LA English DT Meeting Abstract C1 NIDA,IRP,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1995 VL 14 IS 1 BP 154 EP 154 PG 1 WC Substance Abuse SC Substance Abuse GA QW403 UT WOS:A1995QW40300033 ER PT J AU LIBERTO, JG KROISS, SL KEENAN, RM ROLF, D AF LIBERTO, JG KROISS, SL KEENAN, RM ROLF, D TI COTININE IN THE TREATMENT OF CIGARETTE-SMOKING SO JOURNAL OF ADDICTIVE DISEASES LA English DT Meeting Abstract C1 VET ADM MED CTR,DEPT PSYCHIAT,BALTIMORE,MD 21218. NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. LECTEC CORP,MINNETONKA,MN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1995 VL 14 IS 3 BP A11 EP A11 PG 1 WC Substance Abuse SC Substance Abuse GA TC347 UT WOS:A1995TC34700021 ER PT J AU JENKINS, AJ DARWIN, WD HUESTIS, MA CONE, EJ MITCHELL, JM AF JENKINS, AJ DARWIN, WD HUESTIS, MA CONE, EJ MITCHELL, JM TI VALIDITY TESTING OF THE ACCUPINCH(TM) THC TEST SO JOURNAL OF ANALYTICAL TOXICOLOGY LA English DT Article C1 NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. USN,DRUG SCREENING LAB,NAVAL AIR STN,JACKSONVILLE,FL 32212. NR 5 TC 15 Z9 15 U1 1 U2 1 PU PRESTON PUBLICATIONS INC PI NILES PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648 SN 0146-4760 J9 J ANAL TOXICOL JI J. Anal. Toxicol PD JAN-FEB PY 1995 VL 19 IS 1 BP 5 EP 12 PG 8 WC Chemistry, Analytical; Toxicology SC Chemistry; Toxicology GA QB340 UT WOS:A1995QB34000002 PM 7723303 ER PT J AU JOSEPH, R DICKERSON, S WILLIS, R FRANKENFIELD, D CONE, EJ SMITH, DR AF JOSEPH, R DICKERSON, S WILLIS, R FRANKENFIELD, D CONE, EJ SMITH, DR TI INTERFERENCE BY NONSTEROIDAL ANTIINFLAMMATORY DRUGS IN EMIT(R) AND TDX(R) ASSAYS FOR DRUGS OF ABUSE SO JOURNAL OF ANALYTICAL TOXICOLOGY LA English DT Article ID ANTIINFLAMMATORY DRUGS; URINE C1 NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. US DEPT TRANSPORTAT,WASHINGTON,DC. NR 10 TC 17 Z9 17 U1 0 U2 2 PU PRESTON PUBLICATIONS INC PI NILES PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648 SN 0146-4760 J9 J ANAL TOXICOL JI J. Anal. Toxicol PD JAN-FEB PY 1995 VL 19 IS 1 BP 13 EP 17 PG 5 WC Chemistry, Analytical; Toxicology SC Chemistry; Toxicology GA QB340 UT WOS:A1995QB34000003 PM 7723297 ER PT J AU SMITH, ML HUGHES, RO LEVINE, B DICKERSON, S DARWIN, WD CONE, EJ AF SMITH, ML HUGHES, RO LEVINE, B DICKERSON, S DARWIN, WD CONE, EJ TI FORENSIC DRUG-TESTING FOR OPIATES .6. URINE TESTING FOR HYDROMORPHONE, HYDROCODONE, OXYMORPHONE, AND OXYCODONE WITH COMMERCIAL OPIATE IMMUNOASSAYS AND GAS-CHROMATOGRAPHY MASS-SPECTROMETRY SO JOURNAL OF ANALYTICAL TOXICOLOGY LA English DT Article C1 ARMED FORCES INST PATHOL,OFF ARMED FORCES MED EXAMINER,WASHINGTON,DC 20306. NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. NR 14 TC 51 Z9 52 U1 0 U2 9 PU PRESTON PUBLICATIONS INC PI NILES PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648 SN 0146-4760 J9 J ANAL TOXICOL JI J. Anal. Toxicol PD JAN-FEB PY 1995 VL 19 IS 1 BP 18 EP 26 PG 9 WC Chemistry, Analytical; Toxicology SC Chemistry; Toxicology GA QB340 UT WOS:A1995QB34000004 PM 7536861 ER PT J AU ALEXANDER, NJ BIALY, G AF ALEXANDER, NJ BIALY, G TI WHAT ARE THE EXISTING MALE CONTRACEPTIVES AND WHAT IS THE OUTLOOK FOR NEW ONES SO JOURNAL OF ANDROLOGY LA English DT Article ID AGENTS RP ALEXANDER, NJ (reprint author), NICHHD,POPULAT RES CTR,CONTRACEPT DEV BRANCH,6100 EXECUT BLVD,ROOM 8B13,BETHESDA,MD 20892, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC ANDROLOGY, INC PI LAWRENCE PA C/O ALLEN PRESS, INC PO BOX 368, LAWRENCE, KS 66044 SN 0196-3635 J9 J ANDROL JI J. Androl. PY 1995 SU S BP 60 EP 62 PG 3 WC Andrology SC Endocrinology & Metabolism GA RC595 UT WOS:A1995RC59500019 ER PT J AU HARMAN, SM BLACKMAN, MR AF HARMAN, SM BLACKMAN, MR TI IS THERE AN ANDROPAUSE, THE ANALOG TO MENOPAUSE, AND IF SO WHAT TISSUES ARE AFFECTED AND HOW SO JOURNAL OF ANDROLOGY LA English DT Article ID MEN C1 JOHNS HOPKINS UNIV,JOHNS HOPKINS BAYVIEW MED CTR,SCH MED,BALTIMORE,MD 21224. RP HARMAN, SM (reprint author), NIA,GERONTOL RES CTR,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC ANDROLOGY, INC PI LAWRENCE PA C/O ALLEN PRESS, INC PO BOX 368, LAWRENCE, KS 66044 SN 0196-3635 J9 J ANDROL JI J. Androl. PY 1995 SU S BP 72 EP 75 PG 4 WC Andrology SC Endocrinology & Metabolism GA RC595 UT WOS:A1995RC59500023 ER PT J AU RUBENSTEIN, CS ALTEMUS, M PIGOTT, TA HESS, A MURPHY, DL AF RUBENSTEIN, CS ALTEMUS, M PIGOTT, TA HESS, A MURPHY, DL TI SYMPTOM OVERLAP BETWEEN OCD AND BULIMIA-NERVOSA SO JOURNAL OF ANXIETY DISORDERS LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; TERM FOLLOW-UP; ANOREXIA-NERVOSA; EATING DISORDERS; VASOPRESSIN; SECRETION; WOMEN AB There have been several suggestions in the literature that obsessive-compulsive disorder (OCD) and the eating disorders anorexia and bulimia nervosa may be related. The present study compared 50 female OCD patients, 69 normal-weight female bulimia nervosa patients, and 28 normal women without a history of an eating disorder, dieting behavior, or a psychiatric disorder on a variety of psychometric measures of obsessiveness and compulsivity, depression, and anxiety. Statistical analysis confirmed that on the OC subsection of the SCL-90-R and on the Maudsley Obsessive Compulsive Inventory, OCD patients scored higher than both normal volunteers and bulimics, and bulimics scored higher than normal volunteers. On the measure of depression, the depression subscale of the SCL-90-R, bulimic and OCD patients scored similarly to one another, and greater than did normal controls. In the bulimic patients, scores on the bulimia subscale of the EDI correlated with both measures of OC symptomatology. A subgroup of the bulimic patients participated in a six-week supervised inpatient treatment program. After six weeks of enforced abstinence from bingeing and vomiting, patients demonstrated a significant decrease in obsessionality and compulsivity as measured by both the SCL-OC and the MOC, but no change in their Hamilton Depression Rating scores. However, their scores on the SCL-depression subscale did decrease significantly. These results suggest that bulimic patients score significantly greater than controls on ratings of obsessionality (MOC, SCL-90-R-OC), and that obsessionality responds to effective nonpharmacological treatments for bulimia. C1 AMERICAN UNIV,DEPT PSYCHOL,WASHINGTON,DC 20016. GEORGETOWN UNIV,MED CTR,DEPT PSYCHIAT,WASHINGTON,DC 20007. RP RUBENSTEIN, CS (reprint author), NIMH,CLIN SCI LAB,CLIN NEUROPHARMACOL SECT,BLDG 10,ROOM 3D41,BETHESDA,MD 20892, USA. NR 29 TC 16 Z9 16 U1 3 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6185 J9 J ANXIETY DISORD JI J. Anxiety Disord. PD JAN-FEB PY 1995 VL 9 IS 1 BP 1 EP 9 DI 10.1016/0887-6185(95)91551-R PG 9 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA QC768 UT WOS:A1995QC76800001 ER PT J AU NORTON, GR COX, BJ ASMUNDSON, GJG MASER, JD AF NORTON, GR COX, BJ ASMUNDSON, GJG MASER, JD TI THE GROWTH OF RESEARCH ON ANXIETY DISORDERS DURING THE 1980S SO JOURNAL OF ANXIETY DISORDERS LA English DT Review ID DSM-III-R; SOCIAL PHOBIA; PANIC DISORDER; CLASSIFICATION; RELIABILITY AB PsycLIT and Medline, two computerized databases, were used to determine the number of articles on anxiety disorders published each year from 1981-1990. The results showed that the proportion of articles on anxiety disorders listed in PsycLIT and Medline increased dramatically during the 1980s, especially during the last half of the decade. The anxiety disorders most frequently researched were panic disorder, obsessive compulsive disorder, and posttraumatic stress disorder. Far fewer abstracts were associated with generalized anxiety disorder, social phobia, and simple phobia. Factors that might have been instrumental in the increased research activity on anxiety disorders are discussed. C1 CLARKE INST PSYCHIAT,TORONTO,ON M5T 1R8,CANADA. NIMH,BETHESDA,MD 20892. RP NORTON, GR (reprint author), UNIV WINNIPEG,DEPT PSYCHOL,WINNIPEG,MB R3B 2E9,CANADA. RI Asmundson, Gordon/C-8071-2011 NR 28 TC 23 Z9 23 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6185 J9 J ANXIETY DISORD JI J. Anxiety Disord. PD JAN-FEB PY 1995 VL 9 IS 1 BP 75 EP 85 PG 11 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA QC768 UT WOS:A1995QC76800006 ER PT J AU ALTSHULER, JL GENEVRO, JL RUBLE, DN BORNSTEIN, MH AF ALTSHULER, JL GENEVRO, JL RUBLE, DN BORNSTEIN, MH TI CHILDRENS KNOWLEDGE AND USE OF COPING STRATEGIES DURING HOSPITALIZATION FOR ELECTIVE SURGERY SO JOURNAL OF APPLIED DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID DEVELOPMENTAL-CHANGES; COGNITIVE-DEVELOPMENT; YOUNG-CHILDREN; STRESS; DISTRESS; MEMORY; EVENTS; MOOD; SELF AB The questions addressed in this study were: (a) how age relates to differences in children's coping knowledge and coping behaviors while they are hospitalized for elective surgery, (b) how individual differences and development in problem-solving relate to children's coping capacities, and how these factors affect relations between age and coping, and (c) the degree to which coping knowledge and coping behaviors are related. The results indicated that age, in combination with problem-solving skills and gender, predicted children's knowledge of specific coping strategies-behavioral distraction, cognitive distraction, adaptive approach, and escape. Specific coping knowledge, in turn, related to aspects of children's coping behaviors while they were hospitalized for elective surgery. Studies of children's responses to hospitalization and medical treatment provide a valuable opportunity to learn more about children's responses to stressful, uncontrollable situations in which awareness and manipulation of cognitive states are likely to be important. C1 NATL INST CHILD HLTH & HUMAN DEV,CHILD & FAMILY RES,BLDG 31,ROOM B2B15,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NYU,NEW YORK,NY 10003. NR 37 TC 18 Z9 18 U1 0 U2 0 PU ABLEX PUBL CORP PI NORWOOD PA 355 CHESTNUT ST, NORWOOD, NJ 07648 SN 0193-3973 J9 J APPL DEV PSYCHOL JI J. Appl. Dev. Psychol. PD JAN-MAR PY 1995 VL 16 IS 1 BP 53 EP 76 DI 10.1016/0193-3973(95)90016-0 PG 24 WC Psychology, Developmental SC Psychology GA QY737 UT WOS:A1995QY73700004 ER PT J AU ARNESON, DW KUHN, GO JAMESON, CW AF ARNESON, DW KUHN, GO JAMESON, CW TI ANALYSIS OF FEED BLENDS CONTAINING MICROENCAPSULATED 2-ETHYL-1-HEXANOL - VERIFICATION OF HOMOGENEITY AND STABILITY SO JOURNAL OF APPLIED TOXICOLOGY LA English DT Article DE 2-ETHYL-1-HEXANOL; MICROCAPSULES; TOXICITY STUDIES; ANALYSIS; STABILITY; DOSED FEED ID METABOLISM; PHTHALATE; PHARMACOKINETICS; RATS; DEHP AB 2-Ethyl-1-hexanol (2-EH) was nominated for carcinogenicity testing by the National Toxicology Program because it is a high-volume chemical and a major metabolite of di(2-ethylhexyl)phthalate, a known hepatocarcinogen and a known contaminant in blood storage bags. In addition to uses as an intermediate in the manufacture of plasticizers, 2-EH is also used as a solvent, a lubricant and as a finishing compound for paper and textiles. The preferred route of administration for the carcinogenicity studies was oral via the diet. However, feed blends containing neat 2-EH were not sufficiently stable for feed studies. Dosed feed blends prepared with neat 2-EH retained only 86% of the theoretical concentration after blending, and 46% of theoretical after storage for 2 days in a rat cage environment. Feed blends containing microencapsulated 2-EH were sufficiently stable for toxicity studies: no losses of 2-EH were observed after blending, feed blends stored for 7 days in a rat cage retained 99% of the theoretical concentration and blends stored in sealed containers at room temperature for 21 days retained 97% of the theoretical concentration. These studies demonstrate the potential for microencapsulation technology to eliminate dose formulation problems associated with volatile chemicals. C1 NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. RP ARNESON, DW (reprint author), MIDWEST RES INST,425 VOLKER BLVD,KANSAS CITY,MO 64110, USA. FU NIEHS NIH HHS [N01-ES-40560] NR 7 TC 2 Z9 2 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0260-437X J9 J APPL TOXICOL JI J. Appl. Toxicol. PD JAN-FEB PY 1995 VL 15 IS 1 BP 1 EP 4 DI 10.1002/jat.2550150103 PG 4 WC Toxicology SC Toxicology GA QF604 UT WOS:A1995QF60400002 PM 7745219 ER PT J AU WOLLE, JM CWI, J AF WOLLE, JM CWI, J TI PHYSICIANS PREVENTION-RELATED PRACTICE BEHAVIORS IN TREATING ADULT PATIENTS WITH ASTHMA - RESULTS OF A NATIONAL SURVEY SO JOURNAL OF ASTHMA LA English DT Article AB To improve the health outcome of adults with asthma, it is important to understand the current practice behaviors of physicians related to the prevention and treatment of asthma. A national survey was conducted to ascertain the practice behaviors of physicians in five specialty areas: internal medicine, pulmonary, alergy/immunology, occupational health, and family health. Similarities and differences in practice among the specialty areas are indicated. The data provide a basis for recommendations to improve the management of asthma by standardizing history taking, Increasing the use of pulmonary function testing, and using effective counseling and patient education strategies. RP WOLLE, JM (reprint author), NHLBI,DLD,TWO ROCKLEDGE CTR,6701 ROCKLEDGE DR,SUITE 1020,BETHESDA,MD 20817, USA. NR 0 TC 8 Z9 8 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0277-0903 J9 J ASTHMA JI J. Asthma PY 1995 VL 32 IS 2 BP 131 EP 140 DI 10.3109/02770909509083234 PG 10 WC Allergy; Respiratory System SC Allergy; Respiratory System GA RB681 UT WOS:A1995RB68100007 PM 7559263 ER PT J AU WOLLE, JM CWI, J AF WOLLE, JM CWI, J TI PHYSICIANS PREVENTION-RELATED PRACTICE BEHAVIORS IN TREATING ADULT PATIENTS WITH ASTHMA - RESULTS OF A NATIONAL SURVEY (REPRINTED FROM JOURNAL-OF-ASTHMA, VOL 32, PG 131-140, 1995) SO JOURNAL OF ASTHMA LA English DT Reprint AB To improve the health outcome of adults with asthma, it is important to understand the current practice behaviors of physicians related to the prevention and treatment of asthma. A national survey was conducted to ascertain the practice behaviors of physicians in five specialty areas: internal medicine, pulmonary, allergy/immunology, occupational health, and family health. Similarities and differences in practice among the specialty areas are indicated. The data provide a basis for recommendations to improve the management of asthma by standardizing history taking, increasing the use of pulmonary function testing, and using effective counseling and patient education strategies. RP WOLLE, JM (reprint author), NHLBI,DLD,2 ROCKLEDGE CTR,6701 ROCKLEDGE DR,SUITE 1020,BETHESDA,MD 20817, USA. NR 0 TC 13 Z9 13 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0277-0903 J9 J ASTHMA JI J. Asthma PY 1995 VL 32 IS 4 BP 309 EP 318 DI 10.3109/02770909509044839 PG 10 WC Allergy; Respiratory System SC Allergy; Respiratory System GA RM546 UT WOS:A1995RM54600009 PM 7629007 ER PT J AU PEACOCK, J HANKINS, S JONES, T LUTZ, R AF PEACOCK, J HANKINS, S JONES, T LUTZ, R TI FLOW INSTABILITIES INDUCED BY CORONARY-ARTERY STENTS - ASSESSMENT WITH AN IN-VITRO PULSE DUPLICATOR SO JOURNAL OF BIOMECHANICS LA English DT Article ID EXPANDABLE INTRACORONARY STENTS; PULSATILE FLOW; SHEAR-STRESS; BLOOD-FLOW; TURBULENCE; INVITRO; GRAFTS; STEADY; CELLS AB An in vitro pulse duplicator system was used to investigate whether coronary artery stents induce downstream flow instabilities. Hot film or electrochemical probes were used to measure wall shear stress before and after deployment of both single and multiple (overlapping) stents in normal and diseased coronary geometries. Left main coronary diameters ranged from 4 to 5 mm, whereas left anterior descending (LAD) and left circumflex (LCX) diameters ranged from 2 to 4 mm. Under resting conditions, all coronary Bow waveforms remained laminar, even after stent placement. However, disturbances were found downstream from a stent placed in the proximal LAD under mild exercise conditions. These disturbances were found 5 mm distal to the stent, in both the LAD and the proximal LCX. Turbulence intensities of order 5% were induced by a single slotted stent in a normal LAD geometry. In cases of distal disease, the turbulence intensity was 9% with one stent and 11% with tandem stents. In cases of proximal disease, these values were 19 and 25%, respectively. The shear stress from these disturbances (20-200 dynes cm(-2)) is sufficient to delay re-endothelialization and promote restenosis. Therefore, the disturbances could contribute to the increased incidence of restenosis reported with multiple stents, and with stents used in cases of diffuse coronary disease. RP PEACOCK, J (reprint author), NIH,BLDG 13,ROOM 3N17,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 31 TC 48 Z9 48 U1 1 U2 8 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0021-9290 J9 J BIOMECH JI J. Biomech. PD JAN PY 1995 VL 28 IS 1 BP 17 EP 26 DI 10.1016/0021-9290(94)E0039-6 PG 10 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA PT627 UT WOS:A1995PT62700003 PM 7852438 ER PT J AU HOLDEN, JP GROOD, ES CUMMINGS, JF AF HOLDEN, JP GROOD, ES CUMMINGS, JF TI FACTORS AFFECTING SENSITIVITY, OF A TRANSDUCER FOR MEASURING ANTERIOR CRUCIATE LIGAMENT FORCE SO JOURNAL OF BIOMECHANICS LA English DT Note AB In order to determine the measurements and calibration methods necessary to accurately measure in vivo forces in the anterior cruciate ligament (ACL) of the goat, an in vitro study was conducted to evaluate the effect of several factors that could influence the sensitivity of a transducer implanted within the ligament. Four factors were studied in six specimens: flexion angle [0 degrees, 10 degrees, 30 degrees, 50 degrees, and 70 degrees from full extension (FFE)]; tibial rotation (0 degrees and 10 degrees of internal rotation at 30 degrees, 50 degrees, and 70 degrees flexion FFE); loading rate (cycling frequencies of 0.2, 0.5, 1.0, and 2.0 Hz); and temperature (22 degrees C and 37 degrees C). Anteroposterior tibial displacements were applied to the specimens following tissue resection to isolate the ACL. The resultant ACL force magnitude was measured with a multi-component load cell, and transducer sensitivity was calculated as the slope of the output vs force curve in the linear response region. Transducer sensitivity varied with joint position in each specimen, but there was no consistent trend from specimen to specimen in how the sensitivity changed. As a result, there were no statistically significant mean differences (p>0.05). There were no significant differences and little variation in sensitivity due to changes in either loading rate or tissue temperature, although the latter produced a voltage offset. The results show that the transducer output with zero force on the ligament must be determined in vivo, after which in vitro calibrations may be conducted at room temperature. The variation in sensitivity suggests that the transducer is best calibrated on a specimen by specimen basis and at multiple joint positions. C1 UNIV CINCINNATI,NOYES GIANNESTRAS BIOMECH LABS,CINCINNATI,OH. RP HOLDEN, JP (reprint author), NIAMS,BIOMECH LAB,BLDG 10,ROOM 6S-235,BETHESDA,MD 20892, USA. FU NIAMS NIH HHS [AR39703] NR 10 TC 14 Z9 15 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0021-9290 J9 J BIOMECH JI J. Biomech. PD JAN PY 1995 VL 28 IS 1 BP 99 EP 102 DI 10.1016/0021-9290(94)E0045-5 PG 4 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA PT627 UT WOS:A1995PT62700011 PM 7852447 ER PT J AU CUNNINGHAM, ML SPENCER, DL CASPARY, WJ STOPPER, H PHILLIPS, A AF CUNNINGHAM, ML SPENCER, DL CASPARY, WJ STOPPER, H PHILLIPS, A TI DETERMINATION OF 5-METHYLCYTOSINE CONTENT IN DNA FROM CELLS IN CULTURE BY MICELLAR ELECTRO-KINETIC CAPILLARY CHROMATOGRAPHY SO JOURNAL OF CAPILLARY ELECTROPHORESIS LA English DT Article DE 5-METHYLCYTOSINE; CAPILLARY ELECTROPHORESIS; AS52 CELLS ID METHYLATION; DIFFERENTIATION; INACTIVATION; SEPARATION AB An assay for the determination of 5-methylcytosine (5-MeC) from DNA isolated from whole animals and cells in culture has been developed using capillary electrophoresis. DNA samples were obtained from whole animals or cultured cells and hydrolyzed in formic acid to remove nucleobases from the phosphate-sugar backbone. Samples were concentrated by lyophilization and redissolved in distilled water prior to analysis by micellar electrokinetic capillary electrophoresis. The calibration curve was linear with a correlation coefficient r(2) = 0.997 to as low as 1% 5-MeC/Cyt (cytosine) ratio and r(2) = 0.952 to as low as 0.1% 5-MeC/Cyt ratio. The limit of detection for 5-methylcytosine in this system is 350 fmol (signal-to-noise ratio=2). C1 NIEHS,CHEM BRANCH,RES TRIANGLE PK,NC 27709. UNIV WURZBURG,NATL INST ENVIRONM HLTH SCI,EXPTL CARCINOGENESIS & MUTAGENESIS LAB,W-8700 WURZBURG,GERMANY. UNIV WURZBURG,INST TOXICOL,W-8700 WURZBURG,GERMANY. NR 25 TC 4 Z9 4 U1 0 U2 0 PU I S C TECHNICAL PUBLICATIONS, INC PI SHELTON PA 30 CONTROLS DR, BOX 828, SHELTON, CT 06484-0828 SN 1079-5383 J9 J CAPILLARY ELECTROP JI J. Capillary Electrophor. PD JAN-FEB PY 1995 VL 2 IS 1 BP 30 EP 33 PG 4 WC Biochemistry & Molecular Biology; Electrochemistry SC Biochemistry & Molecular Biology; Electrochemistry GA TF372 UT WOS:A1995TF37200005 ER PT J AU HIRSCH, J PETRAKOVA, E FEATHER, MS AF HIRSCH, J PETRAKOVA, E FEATHER, MS TI REACTION OF SOME 1-DEOXY-2,3-DICARBONYL HEXOSE DERIVATIVES WITH AMINOGUANIDINE (GUANYLHYDRAZINE) SO JOURNAL OF CARBOHYDRATE CHEMISTRY LA English DT Article AB The reaction of 4-O-acetyl-1-deoxy-5,6-O-isopropylidene-2,3-D-erythro and (D-threo)-hexodiulose with aminoguanidine (guanylhydrazine) was investigated at pH 7.0 and 37 degrees C. The two dicarbonyl compounds reacted rapidly to give 6-methyl-5-substituted triazine derivatives, which were fully characterized. The compounds were deblocked in a stepwise manner to give, first the de-O-acetylated compounds and then (by removal of the isopropylidene groups) the free triazine derivatives which were fully characterized (GLC/MS, NMR and elemental analyses). C1 UNIV MISSOURI,DEPT BIOCHEM,COLUMBIA,MO 65211. NIDDKD,BETHESDA,MD 20892. NR 18 TC 3 Z9 3 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0732-8303 J9 J CARBOHYD CHEM JI J. Carbohydr. Chem. PY 1995 VL 14 IS 8 BP 1179 EP 1186 DI 10.1080/07328309508005403 PG 8 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA TB796 UT WOS:A1995TB79600008 ER PT J AU CHEN, P VUKICEVIC, S SAMPATH, TK LUYTEN, FP AF CHEN, P VUKICEVIC, S SAMPATH, TK LUYTEN, FP TI OSTEOGENIC PROTEIN-1 PROMOTES GROWTH AND MATURATION OF CHICK STERNAL CHONDROCYTES IN SERUM-FREE CULTURES SO JOURNAL OF CELL SCIENCE LA English DT Article DE OSTEOGENIC PROTEIN-1; TRANSFORMING GROWTH FACTOR-BETA(1); RETINOIC ACID; CHONDROCYTE DIFFERENTIATION; SERUM-FREE CULTURE ID BONE MORPHOGENETIC PROTEIN-2B; X COLLAGEN GENE; FACTOR-BETA SUPERFAMILY; OSTEOBLAST-LIKE CELLS; DIFFERENTIATION INVITRO; ARTICULAR-CARTILAGE; MESSENGER-RNA; EXPRESSION; PROLIFERATION; STIMULATION AB We examined the effect of recombinant human osteogenic protein-1 (OP-1, or bone morphogenetie protein-7), a member of the bone morphogenetic protein family, on growth and maturation of day 11, 15 and 17 chick sternal chondrocytes in high density monolayers, suspension and agarose cultures for up to 5 weeks. OP-1 dose-dependently (10-50 ng/ml) promoted chondrocyte maturation associated with enhanced alkaline phosphatase activity, and increased mRNA levels and protein synthesis of type X collagen in both the presence and absence of serum, in serum-free conditions, OP-1 promoted cell proliferation and chondrocyte maturation, without requiring either thyroid hormone or insulin, agents known to support chick chondrocyte differentiation in vitro. When grown in agarose under the same conditions, TGF-beta 1 and retinoic acid neither initiated nor promoted chondrocyte differentiation. The results demonstrate that OP-1, as the sole medium supplement, supports the maturation of embryonic chick sternal chondrocytes in vitro. C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. CREAT BIOMOLECULES INC,HOPKINTON,MA 01748. MED SCH ZAGREB,DEPT ANAT,ZAGREB,CROATIA. NR 47 TC 63 Z9 65 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD JAN PY 1995 VL 108 BP 105 EP 114 PN 1 PG 10 WC Cell Biology SC Cell Biology GA QG255 UT WOS:A1995QG25500011 PM 7738088 ER PT J AU Kelloff, GJ Boone, CW Crowell, JA Nayfield, SG Hawk, E Steele, VE Lubet, RA Sigman, CC AF Kelloff, GJ Boone, CW Crowell, JA Nayfield, SG Hawk, E Steele, VE Lubet, RA Sigman, CC TI Strategies for phase II cancer chemoprevention trials: Cervix, endometrium, and ovary SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT Conference on Prospects for Chemoprevention of Cancers of the Cervix, Endometrium and Ovary - Surrogate Endpoints and Design of Clinical Trials CY FEB 01-05, 1995 CL OXNARD, CA SP NCI, Div Canc Prevent & Control DE cervical cancer; cervical intraepithelial neoplasia (CIN); chemoprevention; computer-assisted image analysis; endometrial cancer; intermediate biomarkers; ovarian cancer; Phase II trials ID FOLIC-ACID; NEOPLASIA; THERAPY AB Well-designed and conducted Phase II clinical trials are very important to cancer chemoprevention drug development. Three critical aspects govern the design and conduct of these trials-well characterized agents, suitable cohorts, and reliable biomarkers for measuring efficacy that can serve as surrogate endpoints for cancer incidence. Requirements for the agent are experimental or epidemiological data showing chemopreventive efficacy, safety on chronic administration, and a mechanistic rationale for the chemopreventive activity observed. Agents that meet these criteria for chemoprevention of cervical cancer include antiproliferative drugs (e.g., 2-difluoromethylornithine), retinoids, folic acid, antioxidant vitamins and other agents that prevent cellular oxidative damage. Because of the significant cervical cancer risk associated with human papilloma virus (HPV) infection, agents that interfere with the activity of HPV products may also prove to be effective chemopreventives. In endometrium, unopposed estrogen exposure has been associated with cancer incidence. Thus, pure antiestrogens and progestins may be chemopreventive in this tissue. Ovarian cancer risk is correlated to ovulation frequency; therefore, oral contraceptives are potentially chemopreventive in the ovary. Recent clinical observations also suggest that retinoids, particularly all-trans-N-4-hydroxyphenylretinamide, may be chemopreventive in this tissue. The cohort should be suitable for measuring the chemopreventive activity of the agent and the intermediate biomarkers chosen. In the cervix, patients with cervical intraepithelial neoplasia (GIN) and in endometrium, patients with atypical hyperplasia, fit these criteria. Defining a cohort for a Phase II trial in the ovary is more difficult. This tissue is less accessible for biopsy; consequently, the presence of precancerous lesions is more difficult to confirm. The criteria for biomarkers are that they fit expected biological mechanisms (i.e., differential expression in normal and high-risk tissue, on or closely linked to the causal pathway for the cancer, modulated by chemopreventive agents, and short latency compared with cancer), may be assayed reliably and quantitatively, measured easily, and correlate to decreased cancer incidence. They must occur in sufficient incidence to allow their biological and statistical evaluation relevant to cancer. Since carcinogenesis is a multipath process, single biomarkers are difficult to validate as surrogate endpoints, perhaps appearing on only one or a few of the many possible causal pathways. Panels of biomarkers, particularly those representing the range of carcinogenesis pathways, may prove more useful as surrogate endpoints. It is important to avoid relying solely on biomarkers that do not describe cancer but represent isolated events that may or may not be on the causal pathway or otherwise associated with carcinogenesis. These include markers of normal cellular processes that may be increased or expressed during carcinogenesis. Chemoprevention trials should be designed to evaluate fully the two or three biomarkers that appear to be the best models of the cancer. additional biomarkers should be considered only if they can be analyzed efficiently and the sample size allows more important biomarkers to be evaluated completely. Two types of biomarkers that stand out regarding their high correlation to cancer and their ability to be quantified are measures of intraepithelial neoplasia and indicators of cellular proliferation. Measurements made by computer-assisted image analysis that are potentially useful as surrogate endpoint biomarkers include nuclear polymorphism comprising nuclear size, shape (roundness), and texture (DNa distribution patterns); nucleolar size and number of nucleoli/nuclei; DNA ploidy; and proliferation biomarkers such as S-phase fraction and PCNA. CIN and atypical endometrial hyperplasia are both examples of intraepithelial neoplasia that meet the biomarker criteria and are the basis for quantifiable surrogate endpoints for Phase II chemoprevention trials. (C) 1995 Wiley-Liss, Inc.* C1 CCS ASSOCIATES,MT VIEW,CA 94043. RP Kelloff, GJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT BRANCH,BETHESDA,MD 20892, USA. NR 49 TC 7 Z9 7 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1995 SU 23 BP 1 EP 9 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TQ519 UT WOS:A1995TQ51900002 ER PT J AU NAYFIELD, SG AF NAYFIELD, SG TI TAMOXIFENS ROLE IN CHEMOPREVENTION OF BREAST-CANCER - AN UPDATE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT Conference on Cancer Chemopreventive Agents - Drug Development Status and Future Prospects CY OCT 18-22, 1994 CL PRINCETON, NJ SP NCI DE BREAST CANCER; BONE METABOLISM; CHEMOPREVENTION; COLORECTAL CANCER; DNA ADDUCTS ID POSTMENOPAUSAL WOMEN; ADJUVANT TAMOXIFEN; ENDOMETRIAL CHANGES; PREVENTION; TRIAL; MORBIDITY; DENSITY; THERAPY AB Tamoxifen is an oral antiestrogen first used in metastatic breast cancer in the early 1970s. Large clinical trials were initiated in the late 1970s and early 1980s to test the drug's role as adjuvant therapy in early stage breast cancer. Observations of marked decreases in the development of contralateral breast cancer among tamoxifen recipients suggested potential for the drug in chemoprevention of breast cancer, and a large clinical trial to test the efficacy of tamoxifen in prevention of invasive breast cancer among women at increased risk was implemented in the United States in 1992. This paper reviews the rational for the clinical studies of tamoxifen as a chemopreventive agent for breast cancer and summarizes new information that has contributed to our understanding of tamoxifen's actions at the molecular and clinical levels. Current knowledge about the drug's mechanism of estrogenic and antiestrogenic action and its beneficial effects on blood Lipids and bone metabolism will be presented. Recent research findings about DNA adduct formation and hepatic lesions, tamoxifen-associated gynecologic conditions, and the occurrence of second primary cancers in other organ systems will also be discussed. (C) 1995 Wiley-Liss, Inc. RP NAYFIELD, SG (reprint author), NCI,DIV CANC PREVENT & CONTROL,COMMUNITY ONCOL & REHABIL BRANCH,EXECUT PLAZA N,SUITE 300,BETHESDA,MD 20892, USA. NR 64 TC 4 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1995 SU 22 BP 42 EP 50 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA RQ210 UT WOS:A1995RQ21000007 ER PT J AU ANDERSON, L STEELE, VK KELLOFF, GJ SHARMA, S AF ANDERSON, L STEELE, VK KELLOFF, GJ SHARMA, S TI EFFECTS OF OLTIPRAZ AND RELATED CHEMOPREVENTION COMPOUNDS ON GENE-EXPRESSION IN RAT-LIVER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT Conference on Cancer Chemopreventive Agents - Drug Development Status and Future Prospects CY OCT 18-22, 1994 CL PRINCETON, NJ SP NCI DE 2-D GEL ELECTROPHORESIS; AFLATOXIN B-1; ALDEHYDE REDUCTASE; GENE EXPRESSION; OLTIPRAZ; PIROXICAM ID 5-(2-PYRAZINYL)-4-METHYL-1,2-DITHIOL-3-THIONE OLTIPRAZ; 2-DIMENSIONAL ELECTROPHORESIS; MOUSE-LIVER; PROTEINS; DITHIOLTHIONES; HEPATOTOXICITY; TUMORIGENESIS; ETHOXYQUIN; MICE AB One promising approach to cancer chemoprevention involves the induction of phase II xenobiotic metabolism enzymes. Since this approach requires drugs specifically intended to alter tissue gene expression patterns over long periods, it will be important to determine experimentally which proteins are increased or decreased by treatment, and how such alterations may (or may not) be related to the postulated chemopreventive mechanism. We have employed two-dimensional electrophoresis to detect and quantitate gene expression effects of-candidate chemoprevention compounds in the livers of treated rats. Oltipraz, an inducer of several phase II enzymes, affected a series of at least 26 proteins, most of which were slightly decreased by treatment. Several proteins were increased, the prime example being rat liver spot 693, which was induced more than 7-fold by oltipraz. This protein was excised from multiple 2-D gels and subjected to in situ tryptic digestion followed by microchemical sequence analysis. The resulting multiple peptide sequences match perfectly with the cDNA-derived sequence of rat aflatoxin B-1 aldehyde reductase (AFAR). Using quantitative measurements of AFAR from 2-D gels, we compared a series of dose regimens. Oltipraz administration by gavage or in diet appeared equally effective, while recovery studies indicated a half-time of 5.5 days for disappearance of the AFAR protein. Oltipraz analogs anethole trithione (ANTT), 1,2-dithiole-3-thione (1,2-DT-3-T) and 1,3-dithiole-2-thione (1,3-DT-3-T) were examined with respect to ability to increase liver AFAR levels: ANTT appeared approximately equipotent with oltipraz, 1,2-DT-3-T appeared more than 10 times as potent, and 1,3-DT-2-T did not significantly induce AFAR, while nevertheless causing significant changes in a distinct set of proteins. This latter set was shown, by multivariate statistical comparison with an extended set of chemoprevention compounds, to closely resemble the effects of piroxicam at high dose. (C) 1995 Wiley-Liss, Inc. C1 NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT BRANCH,BETHESDA,MD 20892. MANTECH ENVIRONM TECHNOL INC,RES TRIANGLE PK,NC 27709. RP ANDERSON, L (reprint author), LARGE SCALE BIOL CORP,9620 MED CTR DR,SUITE 201,ROCKVILLE,MD 20850, USA. NR 20 TC 6 Z9 6 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1995 SU 22 BP 108 EP 116 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA RQ210 UT WOS:A1995RQ21000014 ER PT J AU Sherman, ME Sturgeon, S Brinton, L Kurman, RJ AF Sherman, ME Sturgeon, S Brinton, L Kurman, RJ TI Endometrial cancer chemoprevention: Implications of diverse pathways of carcinogenesis SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT Conference on Prospects for Chemoprevention of Cancers of the Cervix, Endometrium and Ovary - Surrogate Endpoints and Design of Clinical Trials CY FEB 01-05, 1995 CL OXNARD, CA SP NCI, Div Canc Prevent & Control DE carcinogenesis; carcinoma; endometrioid; hyperplasia; intraepithelial; p53; serous ID PAPILLARY SEROUS CARCINOMA; HYPERPLASIA; MUTATIONS; ONCOGENE AB Endometrial cancers may be divided into two groups, reflecting differences in clinical behavior and pathogenesis. Endometrioid adenocarcinoma, which accounts for the majority of endometrial cancers, typifies the group of endometrial carcinomas that develop from atypical endometrial hyperplasia in the setting of excess estrogenic stimulation. In contrast, serous carcinomas are representative of endometrial tumors that occur in older women who have endometrial atrophy and lack the typical endometrial cancer risk factors reflecting unopposed estrogen exposure. Serous carcinomas are frequently associated with p53 abnormalities and appear to develop from a surface lesion termed endometrial intraepithelial carcinoma. Although serous carcinomas are rare, these highly aggressive tumors account for a disproportionate number of endometrial cancer deaths. Further delineation of the estrogen-dependent and estrogen-independent pathways of endometrial carcinogenesis may be useful in developing comprehensive chemopreventive approaches for endometrial cancer. (C) 1995 Wiley-Liss, Inc. C1 NCI,ENVIRONM EPIDEMIOL BRANCH,ROCKVILLE,MD 20852. JOHNS HOPKINS MED INST,DEPT PATHOL,BALTIMORE,MD 21287. RP Sherman, ME (reprint author), GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,2300 EYE ST NW,WASHINGTON,DC 20037, USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 26 TC 9 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1995 SU 23 BP 160 EP 164 PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TQ519 UT WOS:A1995TQ51900021 ER PT J AU MULSHINE, JL AF MULSHINE, JL TI FOSTERING CHEMOPREVENTIVE AGENT DEVELOPMENT - HOW TO PROCEED SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT Conference on Cancer Chemopreventive Agents - Drug Development Status and Future Prospects CY OCT 18-22, 1994 CL PRINCETON, NJ SP NCI DE BREAST CANCER; CHEMOPREVENTION; INTERVENTION; LUNG CANCER; PROMOTION ID CANCER AB Improved molecular-based detection of early epithelial cancer creates an opportunity for selective pharmacologic agents to arrest the development of emerging cancers. Developing a successful prevention approach to cancer control could eventually lead to a significant decline in cancer mortality rates; progress depends on the amount of resources committed to this area. Most major prevention trials are federally supported due to their size, duration, and cost. Much of the initial developmental cost for advanced cancer treatment agents was supported by the pharmaceutical industry. Developing a cancer treatment agent is perceived as more clearly defined and achievable than for prevention agents. Preliminary discussions with representatives of-the pharmaceutical and biotech industry have identified a number of barriers to chemoprevention product development. Researchers agree that a number of promising agents are being passed over for expeditious development due to the uncertainty associated with chemoprevention drug development. The major factors affecting this circumstance are considered, including cost of clinical trials, absence of a positive model, and inability to project liability exposure. Similar problems were encountered in the area of childhood vaccine development. Insights from that process may have applicability to prevention drug development. Resolving these problems now can have a significant effect on the rate of progress in this promising new approach to cancer control. (C) 1995 Wiley-Liss, Inc.* RP MULSHINE, JL (reprint author), NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT & COMMUNITY ONCOL PROGRAM,ROCKVILLE,MD 20850, USA. NR 16 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1995 SU 22 BP 254 EP 259 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA RQ210 UT WOS:A1995RQ21000032 ER PT J AU KELLOFF, GJ AF KELLOFF, GJ TI CANCER CHEMOPREVENTIVE AGENTS - DRUG DEVELOPMENT STATUS AND FUTURE-PROSPECTS - FOREWORD SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Editorial Material RP KELLOFF, GJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1995 SU 22 BP U3 EP U3 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA RQ210 UT WOS:A1995RQ21000001 ER PT J AU BARNES, DM SYKES, DB SHECHTER, Y MILLER, DS AF BARNES, DM SYKES, DB SHECHTER, Y MILLER, DS TI MULTIPLE SITES OF VANADATE AND PEROXOVANADATE ACTION IN XENOPUS OOCYTES SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID PROTEIN TYROSINE PHOSPHORYLATION; INSULIN-RECEPTOR KINASE; RAT ADIPOCYTES; GLUCOSE-UPTAKE; BLOOD-GLUCOSE; STIMULATION; VANADIUM; H2O2; PEROXIDE(S); ACTIVATION AB In Xenopus laevis oocytes, the insulin mimics, vanadate and peroxovanadates (PV), stimulated the uptake of H-3-2-deoxyglucose and incorporation of S-35- methionine into protein. For both hexose transport and protein synthesis, peroxovanadates (produced by reacting vanadate and H2O2) were at least as patent as vanadate. Microinjection of peroxovanadates into the oocytes stimulated 2-deoxyglucose uptake. However, methionine incorporation was not stimulated by microinjection of peroxovanadate or vanadate solutions. Consistent with these results and with the possibility that vanadate and peroxovanadates enter the cell on a phosphate transporter, raising the medium phosphate concentration from 1 mM to 10 mM blocked vanadate-stimulated hexose transport and partially reduced peroxovanadates stimulation of hexose transport. Increased medium phosphate did not reduce stimulation of protein synthesis by either effector. Taken together, these data indicate that vanadate/peroxovanadates act at both intracellular and extracellular sites. Action at the former stimulates hexose uptake and action at the latter, protein synthesis. (C) 1995 Wiley-Liss, Inc.(**) C1 WEIZMANN INST SCI,DEPT HORMONE RES,IL-76100 REHOVOT,ISRAEL. RP BARNES, DM (reprint author), NIEHS,CELLULAR & MOLEC PHARMACOL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 33 TC 8 Z9 8 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD JAN PY 1995 VL 162 IS 1 BP 154 EP 161 DI 10.1002/jcp.1041620119 PG 8 WC Cell Biology; Physiology SC Cell Biology; Physiology GA QF856 UT WOS:A1995QF85600018 PM 7814448 ER PT J AU ADACHI, K CRUZ, NF SOKOLOFF, L DIENEL, GA AF ADACHI, K CRUZ, NF SOKOLOFF, L DIENEL, GA TI LABELING OF METABOLIC POOLS BY [6-C-14]GLUCOSE DURING K+-INDUCED STIMULATION OF GLUCOSE-UTILIZATION IN RAT-BRAIN SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE GLUCOSE UTILIZATION; LACTATE; SPREADING DEPRESSION ID CORTICAL SPREADING DEPRESSION; DEOXYGLUCOSE METHOD; ENERGY-METABOLISM; CULTURED ASTROCYTES; AMINO-ACIDS; LACTIC-ACID; BLOOD-FLOW; LACTATE; TRANSPORT; RELEASE AB [6-C-14]Glucose is the tracer sometimes recommended to assay cerebral glucose utilization (CMR(glc)) during transient or brief functional activations, but when used to study visual stimulation and seizures in other laboratories, it underestimated CMR(glc). The metabolic fate of [6-C-14]glucose during functional activation of cerebral metabolism is not known, and increased labeling of diffusible metabolites might explain underestimation of CMR(glc), and also reveal trafficking of metabolites. In the current studies cerebral cortex in conscious rats was unilaterally activated metabolically by KCI application, and CMR(glc) was determined in activated and contralateral control cortex with [6-C-14]glucose or 2-[C-14]deoxyglucose ([C-14]DG) over a 5- to 7-min interval. Local C-14 concentrations were determined by quantitative autoradiography. Labeled precursor and products were measured bilaterally in paired cortical samples from funnel-frozen brains. Left-right differences in C-14 contents were small with [6-C-14]glucose but strikingly obvious in [C-14]DG autoradiographs. CMR(glc) determined with [6-C-14]glucose was slightly increased in activated cortex but 40-80% below values obtained with [C-14]DG. [C-14]Lactate was a major metabolite of [6-C-14]glucose in activated but not control cortex and increased proportionately with unlabeled lactate. These results demonstrate significant loss of labeled products of [6-C-14]glucose from metabolically activated brain tissue and indicate that [C-14]DG is the preferred tracer even during brief functional activations of brain. C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 59 TC 38 Z9 38 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1995 VL 15 IS 1 BP 97 EP 110 PG 14 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA PY344 UT WOS:A1995PY34400011 PM 7798343 ER PT J AU TAKAHASHI, S CRANE, AM JEHLE, J COOK, M KENNEDY, C SOKOLOFF, L AF TAKAHASHI, S CRANE, AM JEHLE, J COOK, M KENNEDY, C SOKOLOFF, L TI ROLE OF THE CEREBELLAR FASTIGIAL NUCLEUS IN THE PHYSIOLOGICAL REGULATION OF CEREBRAL BLOOD-FLOW SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE AUTOREGULATION; CEREBRAL CIRCULATION; CEREBRAL METABOLISM; DEOXYGLUCOSE; [C-14] IODOANTIPYRINE; NEUROGENIC CONTROL ID ELECTRICAL-STIMULATION; GLUCOSE-UTILIZATION; NEURAL MECHANISMS; AUTO-REGULATION; CONSCIOUS RAT; BRAIN; VASODILATION; METABOLISM; AMPHETAMINE; LESIONS AB Local cerebral blood flow (ICBF) was measured with [C-14]iodoantipyrine in conscious, unrestrained rats during electrical stimulation of the fastigial nucleus (FN). Electrode position in the FN was determined by blood pressure (MABP) responses to stimulation under anesthesia. In nine rats in which MABP responses had been variable under anesthesia, bipolar stimulation (50 Hz, 0.5 ms, 1 s on/1 a off) with currents of 30-100 mu A after recovery from anesthesia produced stereotypic behavior but little effect on MABP and ICBF. In seven other conscious rats currents could be raised to 75-200 mu A without inducing seizures, resulting in sustained MABP elevations during the ICBF measurement and significantly increased ICBF in the sensory-motor (+45%), parietal (+31%), and frontal cortices (+56%) and the caudate-putamen (+27%) above control values (n = 9). Glucose utilization, measured with [C-14]deoxyglucose, in rats similarly stimulated was significantly increased in six structures, including some of the above, indicating increases in ICBF due to metabolic activation. Unilateral or bilateral electrolytic lesions of the FN, placed 6-7 days before ICBF measurement, had negligible effects on resting ICBF and on autoregulation in conscious rats. These results fail to support a specific role for the FN in physiological regulation of cerebral blood flow in unanesthetized rats. C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. RI Takahashi, Shinichi/L-3454-2013 NR 66 TC 5 Z9 12 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1995 VL 15 IS 1 BP 128 EP 142 PG 15 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA PY344 UT WOS:A1995PY34400015 PM 7798331 ER PT J AU LYON, GR AF LYON, GR TI RESEARCH INITIATIVES IN LEARNING-DISABILITIES - CONTRIBUTIONS FROM SCIENTISTS SUPPORTED BY THE NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN-DEVELOPMENT SO JOURNAL OF CHILD NEUROLOGY LA English DT Article RP LYON, GR (reprint author), NICHHD,CTR RES MOTHERS & CHILDREN,6100 BLDG,ROOM 4B05,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 13 TC 26 Z9 26 U1 1 U2 1 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON ST, PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD JAN PY 1995 VL 10 IS 1 SU S BP S120 EP S126 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA QB975 UT WOS:A1995QB97500026 PM 7751548 ER PT J AU LEE, JH MIRAGLIA, CC GROSH, WW MINTZ, PD AF LEE, JH MIRAGLIA, CC GROSH, WW MINTZ, PD TI PERIPHERAL-BLOOD STEM-CELL COLLECTION IN A PATIENT WITH CHRONIC MYELOGENOUS LEUKEMIA AND A HIGH CIRCULATING NUCLEATED RED-CELL FRACTION SO JOURNAL OF CLINICAL APHERESIS LA English DT Article DE CHRONIC MYELOGENOUS LEUKEMIA; NUCLEATED RED BLOOD CELLS; PERIPHERAL BLOOD STEM CELL COLLECTION ID BONE-MARROW AB A high level of circulating nucleated red blood cells (NRBC) in patients with chronic myeloproliferative syndromes could potentially complicate peripheral blood stem cell (PSC) collection. The mononuclear NRBC might comprise a significant fraction of the total mononuclear cells in the final product. We report a successful PSC collection in a patient with more NRBC than WBC in the peripheral blood. A 27-year-old man with chronic myelogenous leukemia underwent eight PSC collection procedures, seven using the Cobe Spectra (Spectra) and one using the Fenwal CS3000 Plus (CS). PSC product manipulations to remove NRBC were unnecessary. As assessed by post-collection NRBC:WBC ratio as a percent of the initial ratio, Spectra selectively harvested mononuclear leukocytes over NRBC. The collected products had a mean NRBC:WBC ratio that was 3.4% of the peripheral blood ratio. Adequate numbers of mononuclear leukocytes were collected with less than 6% NRBC contamination. The single CS procedure resulted in a comparable NRBC reduction efficiency as the Spectra. We conclude that PSC harvest using automated blood cell separators from patients with a high level of circulating NRBC may result in a product with an acceptable number of NRBC. (C) 1995 Wiley-Liss, Inc. C1 UNIV VIRGINIA,HLTH SCI CTR,DEPT PATHOL,CHARLOTTESVILLE,VA. UNIV VIRGINIA,HLTH SCI CTR,DEPT INTERNAL MED,CHARLOTTESVILLE,VA. RP LEE, JH (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BLDG 10,ROOM 1C-711,BETHESDA,MD 20892, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0733-2459 J9 J CLIN APHERESIS JI J. Clin. Apheresis PY 1995 VL 10 IS 2 BP 87 EP 89 DI 10.1002/jca.2920100207 PG 3 WC Hematology SC Hematology GA RQ569 UT WOS:A1995RQ56900006 PM 7592523 ER PT J AU Lee, JH Cullis, H Leitman, SF Klein, HG AF Lee, JH Cullis, H Leitman, SF Klein, HG TI Efficacy of pentastarch in granulocyte collection by centrifugal leukapheresis SO JOURNAL OF CLINICAL APHERESIS LA English DT Article DE erythrocyte sedimentation rate; granulocyte collection efficiency; hydroxyethyl starch ID HYDROXYETHYL STARCH; COAGULATION; BLOOD; HETASTARCH; DONORS; SYSTEM AB The efficacy of 6% hydroxyethyl starch (hetastarch, HS) in enhancing granulocyte harvest by centrifugal leukapheresis has been described by a simple equation which predicts the granulocyte collection efficiency (GCE) based on an intrinsic donor variable, the erythrocyte sedimentation rate (ESR): GCE (%) = 1.3 ESR (mm/hr) + 45. Ten percent low molecular weight hydroxyethyl starch (pentastarch, PS) has been reported to be as effective as HS with potentially fewer adverse donor reactions (ADR). The derivation of an analogous equation for PS under conditions previously reported for HS may quantify PS efficacy and allow comparison to HS. We prospectively measured the in vitro and the in vivo effects of PS on the donor ESR in 53 granulocyte collections from 44 donors using the model CS-3000 Plus blood cell separator (CS). We then correlated the findings with the GCE of each procedure and derived an equation which expresses GCE in terms of baseline donor ESR. The in vitro addition of PS increased the donor ESR 2.4-fold, but its administration to a donor during a collection procedure did not appreciably change the ESR. Higher baseline donor ESR was more likely to result in more efficient cell collections: GCE (%)= 0.8 ESR (mm/hr) + 20; (r = 0.37). For granulocyte harvests using the CS and PS as the sedimenting agent 1) baseline donor ESR affects granulocyte harvests, but the poor correlation does not allow an accurate prediction of GCE and cell yield from the baseline donor ESR; 2) in comparison with HS (results from a previous study), PS may be less effective in vitro and not effective in vivo in elevating ESR, and may be less effective in enhancing granulocyte harvest; and 3) the parameters (slope, y-intercept, correlation coefficient) which define the linear relationship between baseline donor ESR and GCE may serve collectively as a quantitative measure of the effectiveness of different hydroxyethyl starch agents in enhancing granulocyte harvests. These parameters may be helpful in rapidly assessing the clinical efficacy of new, potentially useful hydroxyethyl starch agents prior to initiating a randomized, controlled clinical trial. (C) 1995 Wiley-Liss, Inc. C1 BAXTER HLTHCARE CORP,BIOTECH DIV,DEERFIELD,IL. RP Lee, JH (reprint author), NIH,DEPT TRANSFUS MED,BLDG 10,ROOM 1C-711,BETHESDA,MD 20892, USA. NR 24 TC 7 Z9 7 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0733-2459 J9 J CLIN APHERESIS JI J. Clin. Apheresis PY 1995 VL 10 IS 4 BP 198 EP 202 DI 10.1002/jca.2920100408 PG 5 WC Hematology SC Hematology GA TN257 UT WOS:A1995TN25700007 PM 8770713 ER PT J AU OLSON, BR RUBINO, D GUMOWSKI, J OLDFIELD, EH AF OLSON, BR RUBINO, D GUMOWSKI, J OLDFIELD, EH TI ISOLATED HYPONATREMIA AFTER TRANSSPHENOIDAL PITUITARY SURGERY SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID PERMANENT BRAIN-DAMAGE; INAPPROPRIATE SECRETION; ANTIDIURETIC-HORMONE; VASOPRESSIN; WOMEN; WATER AB A retrospective analysis was performed to study the fluid and sodium status of patients undergoing transsphenoidal surgery (TS) for Cushing's disease. We evaluated the time of onset, duration, and relative incidence of isolated hyponatremia and identified possible factors associated with it. Of 58 patients that underwent TS over 1 yr, 52 without postoperative diabetes insipidus or Volume depletion were studied. Isolated hyponatremia after TS for Cushing's disease occurred in 21%, and symptomatic hyponatremia (plasma sodium, less than or equal to 125 mmol/L) with new onset headache, nausea, and emesis occurred in 7.0% of all operated. These later patients escaped monitoring and intervention for 24 h. The development of hyponatremia began early in the postoperative period and progressed slowly over 7 days. Maximum antidiuresis occurred on postoperative day 7. Vasopressin levels measured in two patients while hypoosmolar suggested that unregulated vasopressin release contributed to the hyponatremia. Cortisol levels, glucocorticoid replacement, and pituitary adenoma size were similar in normonatremic and hyponatremic patients. Patients combining a history of an estrogenic milieu and documented posterior pituitary trauma at surgery experienced lower nadir plasma sodium. All hyponatremic patients were fluid restricted, and none developed progressive neurological symptoms, morbidity, or mortality. We speculate that the mild degree and slow rate of development of hyponatremia and/or active monitoring and intervention contributed to the good outcome. C1 NINCDS, SURG NEUROL BRANCH, BETHESDA, MD 20892 USA. RP OLSON, BR (reprint author), NICHHD, WARREN G MAGNUSON CLIN CTR,DEPT NURSING, DEV ENDOCRINOL BRANCH,BLDG 10, ROOM 10N262, BETHESDA, MD 20892 USA. NR 24 TC 40 Z9 44 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1995 VL 80 IS 1 BP 85 EP 91 DI 10.1210/jc.80.1.85 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QC590 UT WOS:A1995QC59000015 PM 7829644 ER PT J AU HURST, BS ZILBERSTEIN, M CHOU, JY LITMAN, B STEPHENS, J LESLIE, KK AF HURST, BS ZILBERSTEIN, M CHOU, JY LITMAN, B STEPHENS, J LESLIE, KK TI ESTROGEN-RECEPTORS ARE PRESENT IN HUMAN GRANULOSA-CELLS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; PROGESTERONE RECEPTORS; LUTEAL CELLS; AROMATASE-ACTIVITY; MENSTRUAL-CYCLE; HUMAN-OVARY; ESTRADIOL; BINDING; INHIBITION; TISSUE AB Recent studies failed to detect estrogen receptors in primate follicles. This study was initiated to determine whether estrogen receptor (ER) messenger ribonucleic acid (mRNA) is present in human granulosa cells and, further, if functional ER proteins are present. To evaluate the presence of ER, RNA from human granulosa cells obtained at the time of oocyte retrieval for assisted reproduction was extracted, and complementary DNA synthesis was performed by the reverse transcriptase-polymerase chain reaction. Oligonucleotide primers were used to amplify basepairs 570-852 in the B- and C-domains of the ER mRNA. Southern blotting was performed and confirmed that the amplified DNA fragment identified in granulosa cells represented ER. By reverse transcriptase-polymerase chain reaction, mRNA for the ER is clearly identified in primary human granulosa cells obtained at the time of oocyte retrieval. To expand these studies and determine whether functional ER were present in human granulosa cells in culture, a simian virus-40-transformed human granulosa cell line was studied. Cells were transfected with a plasmid containing an estrogen response element up-stream from the bacterial reporter gene chloramphenicol acetyltransferase (CAT). In transfected cells, CAT activity is inducible by estradiol if endogenous functional ER are present. In these studies, the transfection analysis confirmed that functional, transcriptionally competent ER are present in a human granulosa cell line, with a 4- to 5-fold enhancement of CAT activity demonstrated after the addition of estradiol compared to that in nonhormone-treated cells. In conclusion, ER mRNA is present in human granulosa cells. Functional ER are also demonstrated in a transformed human granulosa cell line. We hypothesize that low, but biologically significant, amounts of ER protein are present in human granulosa cells, which are not routinely detectable by standard assays. C1 UNIV COLORADO, HLTH SCI CTR, DEPT PATHOL, DENVER, CO 80262 USA. NICHHD, HUMAN GENET BRANCH, BETHESDA, MD 20892 USA. FAULKNER CTR REPROD MED, BOSTON, MA 02130 USA. RP HURST, BS (reprint author), UNIV COLORADO, HLTH SCI CTR, DEPT OBSTET & GYNECOL, 4200 E 9TH AVE, BOX B198, DENVER, CO 80262 USA. FU NICHD NIH HHS [HD-31078-01] NR 27 TC 35 Z9 36 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 JAN PY 1995 VL 80 IS 1 BP 229 EP 232 DI 10.1210/jc.80.1.229 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QC590 UT WOS:A1995QC59000038 PM 7829617 ER PT J AU SCHNEIDER, AB GIERLOWSKI, TC SHOREFREEDMAN, E STOVALL, M RON, E LUBIN, J AF SCHNEIDER, AB GIERLOWSKI, TC SHOREFREEDMAN, E STOVALL, M RON, E LUBIN, J TI DOSE-RESPONSE RELATIONSHIPS FOR RADIATION-INDUCED HYPERPARATHYROIDISM SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID NECK IRRADIATION; CHILDHOOD AB It has been hard to establish with certainty that radiation exposure is a risk factor for developing hyperparathyroidism. In part this is because many cases of hyperparathyroidism remain asymptomatic and escape clinical detection. We present results from a study of 2555 subjects who received external beam radiotherapy to the head and neck area for benign conditions before their 16th birthday between 1939 and 1962. The average length of follow-up was 36.6 yr. There were 36 confused cases of hyperparathyroidism. Based on a relative risk model, the excess relative risk increased significantly by 0.11/ centigray; however, the confidence interval was wide (95% confidence interval, 0.0-17.2). The hyperparathyroidism rates and dose-response relationships were not affected by gender or age at first radiation treatment. The demonstration of a dose-response relationship within an irradiated cohort supports an association between radiation exposure and hyperparathyroidism and suggests that the calcium levels of individuals irradiated to the head and neck area should be monitored. C1 UNIV TEXAS, MD ANDERSON CANC CTR, DEPT RADIAT PHYS, HOUSTON, TX 77030 USA. NCI, RADIAT EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA. NCI, BIOSTAT BRANCH, BETHESDA, MD 20892 USA. RP SCHNEIDER, AB (reprint author), UNIV ILLINOIS, MICHAEL REESE HOSP & MED CTR, DIV ENDOCRINOL & METAB 216RC, 2929 S ELLIS AVE, CHICAGO, IL 60616 USA. OI Shore-Freedman, Eileen/0000-0001-6194-1814 FU NCI NIH HHS [CA-21518, N01-CP-05609, N01-CP-85604] NR 15 TC 62 Z9 63 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 EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1995 VL 80 IS 1 BP 254 EP 257 DI 10.1210/jc.80.1.254 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QC590 UT WOS:A1995QC59000043 PM 7829622 ER PT J AU ANASTI, JN FLACK, MR FROEHLICH, J NELSON, LM NISULA, BC AF ANASTI, JN FLACK, MR FROEHLICH, J NELSON, LM NISULA, BC TI A POTENTIAL NOVEL MECHANISM FOR PRECOCIOUS PUBERTY IN JUVENILE HYPOTHYROIDISM SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; CELLS; BINDING; THYROTROPIN; RECEPTOR; RADIOIMMUNOASSAY; EXPRESSION; TESTIS; RATS AB Some children with juvenile hypothyroidism exhibit unexplained precocious puberty. Interaction of TSH with the human FSH receptor (hFSH-R) is a possible pathophysiological mechanism for this syndrome that has not been explored due to the lack of hFSH-free TSH preparations and the scarcity of a suitable hFSH-R-based assay system. To devise an in vitro FSH bioassay suitable for exploring this mechanism, we expressed hFSH-R complementary DNA in COS-7 cells and stimulated them with recombinant hTSH (rec-hTSH). Rec-hTSH elicited a dose-dependent cAMP response in the in vitro hFSH-R bioassay; however, the concentration of rec-hTSH required for half-maximal stimulation was several logs greater than that of hFSH. Rec-hTSH acted as a competitive inhibitor of hFSH at the hFSH-R, indicating that hTSH and HFSH are acting through the same receptor, namely the hFSH-R. This provides a potential novel mechanism for the precocious puberty of juvenile hypothyroidism. RP ANASTI, JN (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10N262, BETHESDA, MD 20892 USA. NR 36 TC 112 Z9 118 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1995 VL 80 IS 1 BP 276 EP 279 DI 10.1210/jc.80.1.276 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QC590 UT WOS:A1995QC59000046 PM 7829625 ER PT J AU ROSE, SR LEONG, GM YANOVSKI, JA BLUM, D HEAVNER, G BARNES, KM CHIPMAN, JJ DICHEK, HL JACOBSEN, J KLEIN, KEO CUTLER, GB AF ROSE, SR LEONG, GM YANOVSKI, JA BLUM, D HEAVNER, G BARNES, KM CHIPMAN, JJ DICHEK, HL JACOBSEN, J KLEIN, KEO CUTLER, GB TI THYROID-FUNCTION IN NONGROWTH HORMONE-DEFICIENT SHORT CHILDREN DURING A PLACEBO-CONTROLLED DOUBLE-BLIND TRIAL OF RECOMBINANT GROWTH-HORMONE THERAPY SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Note ID NOCTURNAL THYROTROPIN SURGE; SHORT STATURE; THYROXINE; HYPOTHYROIDISM; TRIIODOTHYRONINE; HYPOPITUITARISM; CONVERSION; DWARFISM; HGH; T4 AB GH treatment in GH-deficient children has been reported to cause decreases in serum T-4 and TSH and an increase in serum T-3. We sought to determine whether GH treatment alters thyroid function in non-GH-deficient short children. Twenty children (18 boys) mere followed for 12 months while receiving either GH (Humatrope, Eli Lilly; 0.074 mg/kg, sc, 3 times/week; n = 9) or placebo (n = 11). Total T-4, free T-4, T-3, and TSH were measured every 6 months and in 12 children also at 1, 2, 3, and 9 months. A TRH test and measurement of nocturnal TSH surge were performed at baseline and after 6 months of treatment in 19 subjects. There were no significant differences at baseline in the clinical features between the placebo and GH groups. Total T-4, free T-4, T-3, and TSH levels did not significantly differ between the placebo and GH groups at baseline and at 1, 2, 3, 6, 9, and 12 months. There were no significant differences between the two groups in TSH response to TRH or nocturnal TSH surge. Although an early transient effect of GH treatment could not be excluded, we conclude that GH treatment for 12 months does not produce sustained alterations in thyroid function in non-GH-deficient children. C1 UNIV TENNESSEE, DEPT PEDIAT ENDOCRINOL, MEMPHIS, TN 38103 USA. ELI LILLY & CO, LILLY RES LABS, INDIANAPOLIS, IN 46285 USA. RP ROSE, SR (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10N262, BETHESDA, MD 20892 USA. NR 32 TC 18 Z9 18 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 EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1995 VL 80 IS 1 BP 320 EP 324 DI 10.1210/jc.80.1.320 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QC590 UT WOS:A1995QC59000053 PM 7829634 ER PT J AU KOH, GY KIM, SJ KLUG, MG PARK, K SOONPAA, MH FIELD, LJ AF KOH, GY KIM, SJ KLUG, MG PARK, K SOONPAA, MH FIELD, LJ TI TARGETED EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA-1 IN INTRACARDIAC GRAFTS PROMOTES VASCULAR ENDOTHELIAL-CELL DNA-SYNTHESIS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE C2C12 SKELETAL MYOBLASTS; INTRACARDIAC GRAFTS; CELL TRANSPLANTATION; GENE THERAPY; MYOCARDIAL REPAIR; ANGIOGENESIS ID LONG-TERM SURVIVAL; FACTOR-BETA; SYSTEMIC DELIVERY; GENE-TRANSFER; MOUSE MUSCLE; MYOBLASTS; PROTEINS; INVIVO; HEART; DIFFERENTIATION AB Intracardiac grafts comprised of genetically modified skeletal myoblasts were assessed for their ability to effect longterm delivery of recombinant transforming growth factor-beta (TGF-beta) to the heart. C2C12 myoblasts were stably transfected with a construct comprised of an inducible metallothionein promoter fused to a modified TGF-beta 1 cDNA. When cultured in medium supplemented with zinc sulfate, cells carrying this transgene constitutively secrete active TGF-beta 1. These genetically modified myoblasts were used to produce intracardiac grafts in syngeneic C3Heb/FeJ hosts. Viable grafts were observed as long as three months after implantation, and immunohistological analyses of mice maintained on water supplemented with zinc sulfate revealed the presence of grafted cells which stably expressed TGF-beta 1. Regions of apparent neovascularization, as evidenced by tritiated thymidine incorporation into vascular endothelial cells, were observed in the myocardium which bordered grafts expressing TGF-beta 1. The extent of vascular endothelial cell DNA synthesis could be modulated by altering dietary zinc. Similar effects on the vascular endothelial cells were not seen in mice with grafts comprised of nontransfected cells. This study indicates that genetically modified skeletal myoblast grafts can be used to effect the local, long-term delivery of recombinant molecules to the heart. C1 INDIANA UNIV,SCH MED,KRANNERT INST CARDIOL,INDIANAPOLIS,IN 46202. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. RI Koh, Gou Young /C-1615-2011 FU NHLBI NIH HHS [HL-45453] NR 43 TC 79 Z9 86 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1995 VL 95 IS 1 BP 114 EP 121 DI 10.1172/JCI117627 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QA882 UT WOS:A1995QA88200017 PM 7529257 ER PT J AU LEI, KJ SHELLY, LL LIN, BC SIDBURY, JB CHEN, YT NORDLIE, RC CHOU, JY AF LEI, KJ SHELLY, LL LIN, BC SIDBURY, JB CHEN, YT NORDLIE, RC CHOU, JY TI MUTATIONS IN THE GLUCOSE-6-PHOSPHATASE GENE ARE ASSOCIATED WITH GLYCOGEN-STORAGE-DISEASE TYPES 1A AND 1ASP BUT NOT 1B AND 1C SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE TYPE 1 GLYCOGEN STORAGE DISEASE; GLUCOSE-6-PHOSPHATASE; GENETIC MUTATION; MODELS OF G6PASE CATALYSIS ID MICROSOMAL GLUCOSE-6-PHOSPHATASE; SYSTEM; IB; NEUTROPHIL AB Glycogen storage disease (GSD) type 1, which is caused by the deficiency of glucose-6-phosphatase (G6Pase), is an autosomal recessive disease with heterogenous symptoms, Two models of G6Pase catalysis have been proposed to explain the observed heterogeneities. The translocase-catalytic unit model proposes that five GSD type 1 subgroups exist which correspond to defects in the G6Pase catalytic unit (1a), a stabilizing protein (1aSP), the glucose-6-P (1b), phosphate/pyrophosphate (1c), and glucose (1d) translocases. Conversely, the conformation-substrate-transport model suggests that G6Pase is a single multifunctional membrane channel protein possessing both catalytic and substrate (or product) transport activities, We have recently demonstrated that mutations in the G6Pase catalytic unit cause GSD type 1a. To elucidate whether mutations in the G6Pase gene are responsible for other GSD type 1 subgroups, we characterized the G6Pase gene of GSD type 1b, 1c, and 1aSP patients, Our results show that the G6Pase gene of GSD type 1b and 1c patients is normal, consistent with the translocase-catalytic unit model of G6Pase catalysis. However, a mutation in exon 2 that converts an Arg at codon 83 to a Cys (R83C) was identified in both G6Pase alleles of the type 1aSP patient. The R83C mutation was also demonstrated in one homozygous and five heterogenous GSD type la patients, indicating that type 1aSP is a misclassification of GSD type 1a. We have also analyzed the G6Pase gene of seven additional type 1a patients and uncovered two new mutations that cause GSD type 1a. C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT PEDIAT,DURHAM,NC 27710. UNIV N DAKOTA,SCH MED,DEPT BIOCHEM & MOLEC BIOL,GRAND FORKS,ND 58202. RI Lin, Baochuan/A-8390-2009 OI Lin, Baochuan/0000-0002-9484-0785 NR 22 TC 93 Z9 93 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1995 VL 95 IS 1 BP 234 EP 240 DI 10.1172/JCI117645 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QA882 UT WOS:A1995QA88200032 PM 7814621 ER PT J AU MAEDA, Y SMITH, BL AGRE, P KNEPPER, MA AF MAEDA, Y SMITH, BL AGRE, P KNEPPER, MA TI QUANTIFICATION OF AQUAPORIN-CHIP WATER CHANNEL PROTEIN IN MICRODISSECTED RENAL TUBULES BY FLUORESCENCE-BASED ELISA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Note DE PROXIMAL TUBULE; LOOP OF HENLE; COLLECTING DUCT; NEPHRON; WATER CHANNEL ID RAT-KIDNEY; SEGMENTS; NEPHRON; RECONSTITUTION; PERMEABILITY AB Several transporters have been localized along the nephron by physiological methods or immunocytochemistry. However, the actual abundance of these molecules has not been established. To accomplish this goal, we have developed a fluorescence-based ELISA method and have used it to quantitate Aquaporin-CHIP (AQP-CHIP) water channel protein in rat kidney tubules. Microdissected tubules (2 mm/sample, permeabilized with 0.5% Triton X-100) or purified AQP-CHIP standards (0-200 fmol) were utilized in a fluorescence ELISA protocol after covalent immobilization on epoxy-activated Sepharose beads. The lower limit of detection was 2.4 fmol of AQP-CHIP. Preabsorption with excess purified AQP-CHIP or use of nonimmune serum eliminated the signal. In proximal segments, the measured AQP-CHIP was linearly related to tubule length (1-10 mm). The measured AQP-CHIP was (mean+/-SE, fmol/mm): S-1 proximal, 10.8+/-2.1; S-2, 10.0+/-2.3; S-3, 21.3+/-3.1; type 1 thin descending limb (DTL), 12.9+/-4.6; type 2 DTL, 86.5+/-19.5; type 3 DTL, 43.0+/-11.2. In thin ascending limbs, thick ascending limbs, distal convoluted tubules, connecting tubules, and collecting ducts, the AQP-CHIP signal was indistinguishable from zero. Based on the unit water conductance of single CHIP molecules, our calculations show that the content of AQP-CHIP is sufficient to explain water permeability measured in isolated proximal tubules and DTL segments. C1 NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21205. FU NHLBI NIH HHS [HL-33991, HL-48268] NR 23 TC 67 Z9 69 U1 0 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1995 VL 95 IS 1 BP 422 EP 428 DI 10.1172/JCI117672 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QA882 UT WOS:A1995QA88200055 PM 7529263 ER PT J AU TOLLERUD, DJ BROWN, LM BLATTNER, WA WEISS, ST MALONEY, EM KURMAN, CC NELSON, DL HOOVER, RN AF TOLLERUD, DJ BROWN, LM BLATTNER, WA WEISS, ST MALONEY, EM KURMAN, CC NELSON, DL HOOVER, RN TI RACIAL-DIFFERENCES IN SERUM IMMUNOGLOBULIN LEVELS - RELATIONSHIP TO CIGARETTE-SMOKING, T-CELL SUBSETS, AND SOLUBLE INTERLEUKIN-2 RECEPTORS SO JOURNAL OF CLINICAL LABORATORY ANALYSIS LA English DT Article DE BLACKS; WHITES; RACER IGG; IGA; IGM; SOLUBLE INTERLEUKIN-2 RECEPTORS ID BLACK; ANTIBODY; SMOKERS; RACE; NONSMOKERS; POPULATION; ANTIGENS; FARMERS; IMMUNE; VALUES AB To investigate the influence of race, cigarette smoking, and immunologic parameters on serum immunoglobulins, we analyzed serum IgG, IgA, and IgM levels in 455 healthy adults. The study population ranged in age from 20 to 69 years, including 282 whites and 173 blacks, 181 never-smokers, 93 ex-smokers, and 181 current smokers. Race and smoking were independently associated with alterations in serum IgG levels. Blacks had Significantly higher IgG levels than whites (1,587 vs. 1.209 mg/dl; P<0.001), and never smokers had significantly higher levels than current smokers (1,426 vs. 1,287 vs, mg/dl; P<0.001). IgA and IgM levels were unrelated to race or smoking. Serum IgG was also found to be directly related to the proportion of HLA-DR(+) cells and the level of soluble interleukin-2 receptors (slL-2R) and inversely related to the proportion of CD4(+) cells. Investigation of this racial heterogeneity may provide insights into the pathogenesis of immunologic diseases that exhibit unexplained racial variation. (C) 1995 Wiley-Liss. Inc. C1 BRIGHAM & WOMENS HOSP,DEPT MED,CHANNING LAB,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA. NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. NCI,METAB BRANCH,BETHESDA,MD 20892. RP TOLLERUD, DJ (reprint author), UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT ENVIRONM & OCCUPAT HLTH,GSPH A718,130 DESOTO ST,PITTSBURGH,PA 15261, USA. FU NCI NIH HHS [YO1-CP-30500] NR 28 TC 20 Z9 20 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-8013 J9 J CLIN LAB ANAL JI J. Clin. Lab. Anal. PY 1995 VL 9 IS 1 BP 37 EP 41 DI 10.1002/jcla.1860090107 PG 5 WC Medical Laboratory Technology SC Medical Laboratory Technology GA QF654 UT WOS:A1995QF65400006 PM 7722770 ER PT J AU BEI, R PARANAVITANA, C MILENIC, D KASHMIRI, SVS SCHLOM, J AF BEI, R PARANAVITANA, C MILENIC, D KASHMIRI, SVS SCHLOM, J TI GENERATION, PURIFICATION, AND CHARACTERIZATION OF A RECOMBINANT SOURCE OF HUMAN PROSTATE-SPECIFIC ANTIGEN SO JOURNAL OF CLINICAL LABORATORY ANALYSIS LA English DT Article DE PROSTATE CANCER; BACULOVIRUS; RECOMBINANT PROTEIN; GLYCOSYLATION; IMMUNOASSAY ID INFECTED INSECT CELLS; BACULOVIRUS VECTOR; TUMOR-MARKER; CANCER; ADENOCARCINOMA; PROTEIN; SERUM; VIRUS; GLYCOSYLATION; HEMAGGLUTININ AB Human prostate-specific antigen (PSA), a 33- to 34-kDa serine proteinase with extensive homology to glandular kallikrein, is a single-chain glycoprotein that contains 7% carbohydrate. The presence of PSA in the serum of patients with prostatic cancer is widely employed as a marker of disease status. PSA has also been thought of as a possible target for use in active specific immunotherapy protocols. To date, the source of PSA employed has been seminal fluid from different individuals; this has raised concerns about differences among PSA batches for standardization of assays. This report is the first description of the production and the purification of a recombinant source of PSA using a baculovirus expression system. A baculovirus recombinant of the cDNA encoding the full length PSA was expressed in insect cells yielding two major immunoreactive products of 31 and 29 kDa. The latter size conforms to the molecular weight of a core preprotein deduced from the sequence of the cDNA insert. The larger protein represents the N-linked glycosylated form of the preprotein. Western blot analysis showed that both the glycosylated and aglycosylated forms of PSA reacted with a polyclonal and two different monoclonal antibodies specific for PSA, bV-PSA, like commercially available PSA, showed also low-molecular-weight immunoreactive products when culture supernatants were concentrated or taken through steps of purification. bV-PSA was purified to a final product consisting of a major 29-kDa protein and a minor 31-kDa protein. This recombinant source of PSA will make it possible to further evaluate the biological, serological, and functional properties of the antigen and may serve as a more standardized source for serum assays to detect PSA, bV-PSA may also serve as a potential source for immunogen in active specific immunotherapy protocols. (C) 1995 Wiley-Liss, Inc.* C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NR 40 TC 11 Z9 12 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 0887-8013 J9 J CLIN LAB ANAL JI J. Clin. Lab. Anal. PY 1995 VL 9 IS 4 BP 261 EP 268 DI 10.1002/jcla.1860090408 PG 8 WC Medical Laboratory Technology SC Medical Laboratory Technology GA RJ015 UT WOS:A1995RJ01500007 PM 7562244 ER PT J AU LYMAN, CA DEVI, SJN NATHANSON, J FRASCH, CE PIZZO, PA WALSH, TJ AF LYMAN, CA DEVI, SJN NATHANSON, J FRASCH, CE PIZZO, PA WALSH, TJ TI DETECTION AND QUANTITATION OF THE GLUCURONOXYLOMANNAN-LIKE POLYSACCHARIDE ANTIGEN FROM CLINICAL AND NONCLINICAL ISOLATES OF TRICHOSPORON BEIGELII AND IMPLICATIONS FOR PATHOGENICITY SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID LATEX AGGLUTINATION-TEST; CRYPTOCOCCUS-NEOFORMANS; INFECTION; PATIENT; MODEL AB Sera from patients with systemic infections caused by the opportunistic fungus Trichosporon beigelii have been shown to cross-react with anticryptococcal antibodies. We quantitatively compared the amounts of antigen produced and examined the expression of O-acetyl epitopes from 35 strains of T. beigelii isolated from deep and superficial infections. By counterimmunoelectrophoresis, 10 of 10 isolates from deep infections were positive for polysaccharide, compared with 7 of 13 isolates from superficial infections (P = 0.02). All 23 strains tested were positive for polysaccharide when screened by immunodot, By enzyme immunoassay, the cross-reactive antigen produced by deep isolates (n = 9) had a mean titer of 1:5,500, In contrast, superficial isolates (n = 22) produced significantly less antigen than the deep isolates (P < 0.001), with a mean titer of 1:700, Isolates from environmental sources (n = 3) were similar to the superficial isolates, with a mean titer of 1:600, The mean concentrations +/- standard errors of cross-reactive polysaccharide released by deep isolates and superficial isolates were 3.09 +/- 0.44 and 1.74 +/- 0.30 mu g/ml, respectively, when measured by rocket immunoelectrophoresis (P = 0.02), O-Acetyl epitopes were detected on polysaccharide from 8 of 9 strains of T. beigelii isolated from deep sources, while only 2 of 12 superficial isolates expressed detectable O-acetyl epitopes (P = 0.01), Thus, while all isolates of T. beigelii tested were capable of producing glucuronoxylomannan-like cross-reactive antigen, pathogenic isolates produced significantly more antigen than superficial or environmental isolates, Furthermore, significantly more pathogenic isolates than superficial or environmental isolates expressed antigen that was O acetylated. C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,CTR BIOL EVALUAT & RES,BETHESDA,MD 20892. NR 31 TC 23 Z9 24 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1995 VL 33 IS 1 BP 126 EP 130 PG 5 WC Microbiology SC Microbiology GA PX472 UT WOS:A1995PX47200026 PM 7535310 ER PT J AU CARTWRIGHT, CP STOCK, F BEEKMANN, SE WILLIAMS, EC GILL, VJ AF CARTWRIGHT, CP STOCK, F BEEKMANN, SE WILLIAMS, EC GILL, VJ TI PCR AMPLIFICATION OF RIBOSOMAL-RNA INTERGENIC SPACER REGIONS AS A METHOD FOR EPIDEMIOLOGIC TYPING OF CLOSTRIDIUM-DIFFICILE SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; RIBOSOMAL-RNA GENES; ESCHERICHIA-COLI; SUSCEPTIBILITY; CLINDAMYCIN; OUTBREAK; STRAINS AB From January to March 1993, a suspected outbreak of antibiotic-associated diarrhea occurred on a pediatric oncology ward of the Clinical Center Hospital at the National Institutes of Health. Isolates of Clostridium difficile obtained from six patients implicated in this outbreak were typed by both PCR amplification of rRNA intergenic spacer regions (PCR ribotyping) and restriction endonuclease analysis of genomic DNA. Comparable results were obtained,vith both methods; five of the six patients were infected with the same strain of C. difficile. Subsequent analysis of 102 C. difficile isolates obtained from symptomatic patients throughout the Clinical Center revealed the existence of 41 distinct and reproducible PCR ribotypes, These data suggest that PCR ribotyping provides a discriminatory, reproducible, and simple alternative to conventional molecular approaches for typing strains of C. difficile. C1 NIH,WARREN G MAGNUSON CLIN CTR,HOSP EPIDEMIOL SERV,BETHESDA,MD 20892. RP CARTWRIGHT, CP (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,MICROBIOL SERV,BETHESDA,MD 20892, USA. NR 19 TC 65 Z9 67 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1995 VL 33 IS 1 BP 184 EP 187 PG 4 WC Microbiology SC Microbiology GA PX472 UT WOS:A1995PX47200037 PM 7699038 ER PT J AU HARLAN, L BRAWLEY, O POMMERENKE, F WALI, P KRAMER, B AF HARLAN, L BRAWLEY, O POMMERENKE, F WALI, P KRAMER, B TI GEOGRAPHIC, AGE, AND RACIAL VARIATION IN THE TREATMENT OF LOCAL/REGIONAL CARCINOMA OF THE PROSTATE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID COLLEGE-OF-SURGEONS; RADICAL PROSTATECTOMY; RADIATION-THERAPY; UNITED-STATES; CANCER; TRENDS; CARE; PATTERNS; RATES AB Purpose: Prostate cancer is one of the most common cancers in men. Incidence rates increase with age and are substantially higher in black men than white men. This study examines the variations in the use of radical prostatectomy and radiation by geographic area, age, and race. Materials and Methods: Data from the National Cancer Institute's Surveillance, Epidemiology, and End-Results Program (SEER) were used to examine treatment differences. Current treatments generally consist of prostatectomy, radiation, or careful observation for clinically localized or regional disease. Results: The age-adjusted proportion of men, age 50 and older, who received radical prostatectomy increased sharply between 1984 and 1991, from 11.0% to 32.3% among men with local/regional disease. The choice of treatment varied widely by geographic regions. In 1991, the proportion that received prostatectomy was highest in Utah (47.8%) end lowest in Connecticut (22.5%) among men with localized and regional disease. The increase in radical prostatectomy was not limited to younger men. Although the rates increased for blacks, black men had lower age-adjusted rates of prostatectomy than whites in all years of the study. Conclusion: The SEER data show a clear trend toward more aggressive treatment, especially prostatectomy. However, the proportion of black men who received prostatectomy was substantially lower than that of white men and this disparity does not appear to be changing. C1 INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD. RP HARLAN, L (reprint author), NCI,9000 ROCKVILLE PIKE EPN 313,BETHESDA,MD 20892, USA. NR 26 TC 150 Z9 151 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1995 VL 13 IS 1 BP 93 EP 100 PG 8 WC Oncology SC Oncology GA QA325 UT WOS:A1995QA32500015 PM 7799048 ER PT J AU JOHNSON, BE LINNOILA, RI WILLIAMS, JP VENZON, DJ OKUNIEFF, P ANDERSON, GB RICHARDSON, GE AF JOHNSON, BE LINNOILA, RI WILLIAMS, JP VENZON, DJ OKUNIEFF, P ANDERSON, GB RICHARDSON, GE TI RISK OF 2ND AERODIGESTIVE CANCERS INCREASES IN PATIENTS WHO SURVIVE FREE OF SMALL-CELL LUNG-CANCER FOR MORE THAN 2 YEARS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID LONG-TERM SURVIVAL; 2ND PRIMARY CANCERS; HODGKINS-DISEASE; COMBINATION CHEMOTHERAPY; BRONCHOGENIC-CARCINOMA; FOLLOW-UP; IRRADIATION; MALIGNANCIES; THERAPY; MORTALITY AB Purpose: patients who survived small-cell lung cancer (SCLC) for more than 2 years were evaluated to determine the frequency and anatomic pattern of redevelopment of smell-cell cancer and development of nonsmall-cell lung cancer (NSCLC) and aerodigestive cancers with the passage of time. Patients and Methods: From April 1973 through December 1991, 578 patients with previously untreated SCLC were entered onto prospective therapeutic trials at the National Cancer Institute (NCI), Bethesda, MD, Sixty-two (11%) were cancer-free 2 years after initiation of therapy and were assessable for redevelopment of SCLC and development of NSCLC, and aerodigestive cancers. Results: Twenty patients redeveloped SCLC 2.0 to 12.2 years after initiation of chemotherapy, of whom two patients were deemed to have a second primary small-cell cancer that involved the aerodigestive tract. Fifteen patients developed 16 cancers in the lung other than SCLC 3.4 to 14.9 years after initiation of therapy. Two developed other aerodigestive cancers that involved the larynx and lip. The risk of a NSCLC and aerodigestive cancer in these patients increased more than sixfold from 2% per patient per year during years 2 to 4 to 12.6% and 14.4%, respectively, after more than 10 years. The cumulative actuarial risk of a second primary NSCLC or aerodigestive cancer at 16 years is 69% and 72%, respectively. Conclusion: The increasing risk of second aerodigestive cancers with the passage of time is a mounting problem for patients cured of SCLC. Chemoprevention trials for these patients should be considered. C1 NCI, BIOMARKERS & PREVENT RES BRANCH, BETHESDA, MD 20892 USA. NCI, RADIAT ONCOL BRANCH, BETHESDA, MD 20892 USA. NCI, BIOSTAT & DATA MANAGEMENT SECT, BETHESDA, MD 20892 USA. NATL NAVAL MED CTR, DEPT PATHOL, BETHESDA, MD USA. NATL NAVAL MED CTR, DEPT MED, BETHESDA, MD USA. RP JOHNSON, BE (reprint author), NCI, NATL NAVAL MED CTR, NAVY MED ONCOL BRANCH, BLDG 8, ROOM 5105, BETHESDA, MD 20889 USA. RI Venzon, David/B-3078-2008 NR 43 TC 43 Z9 45 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 JAN PY 1995 VL 13 IS 1 BP 101 EP 111 PG 11 WC Oncology SC Oncology GA QA325 UT WOS:A1995QA32500016 PM 7799009 ER PT J AU FREIFELD, AG WALSH, T MARSHALL, D GRESS, J STEINBERG, SM HATHORN, J RUBIN, M JAROSINSKI, P GILL, V YOUNG, RC PIZZO, PA AF FREIFELD, AG WALSH, T MARSHALL, D GRESS, J STEINBERG, SM HATHORN, J RUBIN, M JAROSINSKI, P GILL, V YOUNG, RC PIZZO, PA TI MONOTHERAPY FOR FEVER AND NEUTROPENIA IN CANCER-PATIENTS - A RANDOMIZED COMPARISON OF CEFTAZIDIME VERSUS IMIPENEM SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ANTIBIOTIC-THERAPY; EMPIRIC THERAPY; CLINICAL-TRIAL; ACUTE-LEUKEMIA; FEBRILE; CILASTATIN; VANCOMYCIN; CHILDREN; AMIKACIN; GRANULOCYTOPENIA AB Purpose: To compare the efficacy of ceftazidime and imipenem monotherapy for fever and neutropenia, and to determine whether fewer antimicrobial modifications (additions or changes) are required by the broader-spectrum agent, imipenem. Patients and Methods: Adult and pediatric patients undergoing chemotherapy for solid tumors, leukemias, or lymphomas were randomized to receive open-label ceftazidime or imipenem on presentation with fever and neutropenia. Success with or without modifications of the initial antibiotic was defined os survival through neutropenia; failure was death due to infection. Comparisons were based on numbers of modifications made to each monotherapy during the course of neutropenia, in patients stratified as having unexplained fever or a documented infection. Results: Among 204 ceftazidime and 195 imipenem recipients, the overall success rate with or without modification was more than 98%, regardless of initial antibiotic regimen. Modifications occurred in half of all episodes, primarily in patients with documented infections on either monotherapy. Antianaerobic agents were more frequently added to ceftazidime (P < .001), but addition of other antibiotics, including vancomycin and aminoglycosides, was similar between the two monotherapy groups. Imipenem therapy was associated with significantly greater toxicity, manifested by Clostridium difficile-associated diarrhea and by nausea and vomiting, which required discontinuation of imipenem in 10% of recipients. Conclusion: Ceftazidime and imipenem are both effective in the management of fever and chemotherapy-related neutropenia, provided that modifications are mode in response to clinical and microbiologic data that emerge during the course of neutropenia. Imipenem, despite its broader antimicrobial spectrum, does not significantly decrease the overall need for antibiotic modifications and is more often complicated by gastrointestinal toxicity. RP FREIFELD, AG (reprint author), NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N-240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 31 TC 162 Z9 163 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1995 VL 13 IS 1 BP 165 EP 176 PG 12 WC Oncology SC Oncology GA QA325 UT WOS:A1995QA32500023 PM 7799016 ER PT J AU BLANEY, SM POPLACK, DG GODWIN, K MCCULLY, CL MURPHY, R BALIS, FM AF BLANEY, SM POPLACK, DG GODWIN, K MCCULLY, CL MURPHY, R BALIS, FM TI EFFECT OF BODY POSITION ON VENTRICULAR CSF METHOTREXATE CONCENTRATION FOLLOWING INTRALUMBAR ADMINISTRATION SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CEREBROSPINAL-FLUID; PHARMACOKINETICS; MODEL AB Purpose: Intralumbar methotrexate is one of the primary therapeutic modalities for the prevention and treatment of meningeal leukemia, However, methotrexate distribution to the ventricles is limited and highly variable following intralumbar dosing, and cytotoxic concentrations of methotrexate are not always achieved or sustained in the ventricular CSF. We used a nonhuman primate model to determine the effect of body position on the caudal distribution of an intralumbar dose of methotrexate. Methods: Methotrexate (1.0 mg) was administered by intralumbar injection to four animals, which were then immediately placed either in an upright sitting position or in a prone position for 1 hour, then upright. Each animal served as its own control and was studied in each position on at least one occasion. Results: The mean peak ventricular methotrexate concentration was 0.12 mu mol/L (range, 0.091 to 0.20) in animals that were immediately placed upright, compared with 2.81 mu mol/L (range, 0.21 to 8.9) in animals that remained prone for 1 hour. The mean area under the concentration-versus-time curves (AUG) was 0.51 mu mol/L.h (range, 0.26 to 1.1) in the upright animals and 12.0 mu mol/L.h (range, 0.9 to 35.4) in the prone animals, Conclusion: Maintaining a prone position for 1 hour after an intralumbar dose increased the peak methotrexate concentration and drug exposure in ventricular CSF. CSF drug distribution following intralumbar therapy can be influenced by body position after the injection. (C) 1995 by American Society of Clinical Oncology. C1 WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. TEXAS CHILDRENS HOSP,HOUSTON,TX 77030. RP BLANEY, SM (reprint author), NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 10 TC 28 Z9 29 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 JAN PY 1995 VL 13 IS 1 BP 177 EP 179 PG 3 WC Oncology SC Oncology GA QA325 UT WOS:A1995QA32500024 PM 7799017 ER PT J AU THOM, AK ALEXANDER, HR ANDRICH, MP BARKER, WC ROSENBERG, SA FRAKER, DL AF THOM, AK ALEXANDER, HR ANDRICH, MP BARKER, WC ROSENBERG, SA FRAKER, DL TI CYTOKINE LEVELS AND SYSTEMIC TOXICITY IN PATIENTS UNDERGOING ISOLATED LIMB PERFUSION WITH HIGH-DOSE TUMOR-NECROSIS-FACTOR, INTERFERON-GAMMA, AND MELPHALAN SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID INTERCELLULAR-ADHESION MOLECULE-1; ADVANCED MALIGNANT DISEASE; PHASE-I TRIAL; FACTOR-ALPHA; SERUM LEVELS; ANTITUMOR-ACTIVITY; SOLUBLE RECEPTORS; GENE-EXPRESSION; MELANOMA; ICAM-1 AB Purpose: Isolated limb perfusion (ILP) with tumor necrosis factor (TNF), interferon gamma, and melphalan (M) has been reported to result in high response rates for extremity melanoma and sarcoma. We have evaluated the relationship of systemic TNF exposure to induction of several secondary mediators and incidence of systemic toxicity. Patients and Methods: Nineteen patients with extremity melanoma (n = 16) or sarcoma (n = 3), underwent 90-minute ILP with TNF-alpha, interferon gamma (0.2 mg), and M (10 to 13 mg/L of limb volume) (TNF/IFN/M) (n = 12), or M alone (n = 7). Continuous intraoperative monitoring (CIM) for systemic leak from the perfusion circuit was performed using radioactive iodine-131 albumin. Cytokine levels in the perfusate and systemic circulation during and after ILP were measured by enzyme linked immunosorbent assay. Results: Systemic leaks greater than or equal to 1% from the perfusion circuit occurred in six patients who received TNF/IFN/M and in four who received M alone. Hypotension that required vasopressor support occurred in six of six patients with evidence of a leak(greater than or equal to 1%) and zero of six patients without a leak (< 1%). These six patients had significantly higher peak systemic TNF levels during and after perfusion than patients without a leak (2.8 and 8.2 ng/ mg v 0.7 and 2.0 ng/mL, respectively; P < .05). All patients who received TNF/IFN/M had significantly greater increases in systemic interleukin-6 (IL-6) levels than in patients with M alone (12,395 +/- 10,374 pg/mL v 79.4 +/- 7.2 pg/mL, respectively; P < .001), Intracellular adhesion molecule (ICAM), IL-8, and TNF-R levels were also increased after ILP with TNF/IFN/M. Conclusion: ILP with TNF/IFN/M can be safely performed, as I-131 albumin provides a sensitive measure of systemic leakage from the perfusion circuit. Patients with a measured leak of greater than or equal to 1% develop mild and transient postoperative hypotension with significantly higher systemic TNF levels and lower perfusate TNF levels than in patients without leaks, (C) 1995 by American Society of Clinical Oncology, C1 NCI,SURG BRANCH,BETHESDA,MD 20892. NR 54 TC 83 Z9 86 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1995 VL 13 IS 1 BP 264 EP 273 PG 10 WC Oncology SC Oncology GA QA325 UT WOS:A1995QA32500035 PM 7799030 ER PT J AU BIRKEDALHANSEN, H AF BIRKEDALHANSEN, H TI SYMPOSIUM - SCIENTIFIC HIGHLIGHTS OF THE NIDR INTRAMURAL RESEARCH-PROGRAM - AN ENVIRONMENT FOR CREATIVE RESEARCH AND TRAINING IN ORAL HEALTH SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 13 EP 13 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800014 ER PT J AU WHITE, BA AF WHITE, BA TI SYMPOSIUM - THE NEED FOR MEASURES OF OUTCOMES OF DENTAL TREATMENT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BEHAV SCI & HLTH SERV,RES GRP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 13 EP 13 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800011 ER PT J AU TESSLER, SJ MOORE, ML RESHKIN, SJ TURNER, RJ AF TESSLER, SJ MOORE, ML RESHKIN, SJ TURNER, RJ TI TISSUE DISTRIBUTION OF THE SECRETORY (SALIVARY) ISOFORM OF THE NA-K-2CL COTRANSPORTER SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 53 EP 53 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800331 ER PT J AU BASCH, C ZYBERT, P HOROWITZ, AM AF BASCH, C ZYBERT, P HOROWITZ, AM TI CARIES PREVENTION IN YOUNG-CHILDREN - LATINA MOTHERS BELIEFS, KNOWLEDGE AND PRACTICES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 COLUMBIA UNIV,NEW YORK,NY 10027. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 70 EP 70 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800463 ER PT J AU DSOUZA, RN LETTERIO, JJ DICKINSON, DP ROBERTS, AB LITZ, M AF DSOUZA, RN LETTERIO, JJ DICKINSON, DP ROBERTS, AB LITZ, M TI TRANSFORMING GROWTH-FACTOR-BETA GENES AND TOOTH DEVELOPMENT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. NCI,BETHESDA,MD 20892. RI Dickinson, Douglas/B-9111-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 72 EP 72 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800484 ER PT J AU CODE, JE BENNETT, PS ANTONUCCI, JM AF CODE, JE BENNETT, PS ANTONUCCI, JM TI EFFECTS OF ASCORBIC-ACID AND CAMPHORQUINONE ON DENTIN BONDING SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. ADAHF,GAITHERSBURG,MD. NIST,GAITHERSBURG,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 73 EP 73 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800493 ER PT J AU BEDI, GS SHARMA, A OCONNELL, BC TABAK, LA AF BEDI, GS SHARMA, A OCONNELL, BC TABAK, LA TI EXPRESSION OF A FUNCTIONAL-RAT SALIVARY CYSTATIN-S POLYPEPTIDE IN ESCHERICHIA-COLI SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 MED COLL PENN,PHILADELPHIA,PA 19129. SUNY BUFFALO,BUFFALO,NY 14260. UNIV ROCHESTER,ROCHESTER,NY 14627. NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 84 EP 84 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800579 ER PT J AU REDFORD, M GIFT, HC MONROECOOK, E BRONK, M AF REDFORD, M GIFT, HC MONROECOOK, E BRONK, M TI QUALITATIVE ASSESSMENT OF DECISIONS REGARDING RESTORATIVE TREATMENT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 86 EP 86 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800595 ER PT J AU SHKLAR, DP SHKLAR, G SCHWARTZ, JL AF SHKLAR, DP SHKLAR, G SCHWARTZ, JL TI GLUTATHIONE INHIBITS ORAL CARCINOGENESIS AND TUMOR ANGIOGENESIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TUFTS UNIV,SCH DENT,BOSTON,MA 02111. HARVARD UNIV,SCH DENT,BOSTON,MA 02115. NIDR,EODPP,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 88 EP 88 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800606 ER PT J AU SHKLAR, G SHKLAR, DP SCHWARTZ, JL AF SHKLAR, G SHKLAR, DP SCHWARTZ, JL TI VIT-E INHIBITS ORAL CARCINOGENESIS AND TUMOR ANGIOGENESIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH DENT,BOSTON,MA 02115. TUFTS UNIV,SCH DENT,BOSTON,MA 02111. NIDR,EODPP,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 88 EP 88 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800610 ER PT J AU KINGMAN, A BROWN, LJ ALBERTINI, TF AF KINGMAN, A BROWN, LJ ALBERTINI, TF TI EFFECTS OF ESTIMATING AMALGAM EXPOSURE INDIRECTLY BY THE CARIES FS SCORES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 98 EP 98 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800687 ER PT J AU FOX, PC BERMUDEZ, D SUN, D AF FOX, PC BERMUDEZ, D SUN, D TI IL-6 IN PRIMARY SJOGRENS-SYNDROME SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 100 EP 100 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800707 ER PT J AU SUN, D BERMUDEZ, D WU, AJ FOX, PC AF SUN, D BERMUDEZ, D WU, AJ FOX, PC TI IL-6 PRODUCTION IN A HUMAN SALIVARY CELL-LINE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 100 EP 100 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800703 ER PT J AU WU, AJ BAUM, BJ AF WU, AJ BAUM, BJ TI INTERFERON-GAMMA INDUCES PHOSPHORYLATION OF JAK2 AND STAT-1-ALPHA-IN A HUMAN SALIVARY-GLAND CELL-LINE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 100 EP 100 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800706 ER PT J AU CORRIGAN, JG AF CORRIGAN, JG TI CAREER OUTCOMES FOR DENTIST SCIENTISTS SUPPORTED BY THE NIDR SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 115 EP 115 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800827 ER PT J AU STRECKFUS, C BROWN, LJ BRUNELLE, JA AF STRECKFUS, C BROWN, LJ BRUNELLE, JA TI THE EFFECTS OF ESTROGEN ON SALIVARY FUNCTION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,EODPP,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 116 EP 116 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800831 ER PT J AU HAGHIGHAT, N SHENG, M FOX, PC ALHASHIMI, I AF HAGHIGHAT, N SHENG, M FOX, PC ALHASHIMI, I TI THE DIAGNOSTIC-VALUE OF IMMOBILIZED PH GRADIENT (IPG) ELECTROPHORESIS IN SJOGRENS-SYNDROME SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 BAYLOR COLL DENT,DEPT PERIODONT,DALLAS,TX 75246. NIDR,CIPCB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 121 EP 121 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800872 ER PT J AU SELWITZ, RH NOWJACKRAYMER, RE KINGMAN, A DRISCOLL, WS AF SELWITZ, RH NOWJACKRAYMER, RE KINGMAN, A DRISCOLL, WS TI PREVALENCE OF DENTAL-CARIES AND FLUOROSIS IN ILLINOIS AND NEBRASKA SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 147 EP 147 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801077 ER PT J AU SCHUMACHER, GE CODE, JE ANTONUCCI, JM BENNETT, PS AF SCHUMACHER, GE CODE, JE ANTONUCCI, JM BENNETT, PS TI N-PHENYLIMINODIACETIC ACID (PIDAA) AND SALTS THEREOF AS CONDITIONING PRIMERS FOR DENTIN BONDING SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NIST,GAITHERSBURG,MD. ADAHF,PRC,GAITHERSBURG,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 151 EP 151 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801109 ER PT J AU HART, TC TOLME, Z SCHENKEIN, HA DIEHL, SR AF HART, TC TOLME, Z SCHENKEIN, HA DIEHL, SR TI ASSOCIATION BETWEEN HLA CLASS-II ANTIGENS ANTIBODY-RESPONSE AND PERIODONTAL STATUS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC 27103. EASTMAN DENT CTR,ROCHESTER,NY 14620. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. NIDR,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 157 EP 157 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801160 ER PT J AU SCHWARTZ, J AF SCHWARTZ, J TI EGF AND RELATED PROTEINS DURING INHIBITION OF ORAL-CANCER CELL-DEVELOPMENT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,MEDPP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 167 EP 167 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801238 ER PT J AU GUCKES, AD MCCARTHY, GR BRAHIM, JS MCCULLAGH, LA AF GUCKES, AD MCCARTHY, GR BRAHIM, JS MCCULLAGH, LA TI USE OF TITANIUM SCREW IMPLANTS IN PREADOLESCENTS WITH ECTODERMAL DYSPLASIA SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV N CAROLINA,CHAPEL HILL,NC 27514. NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 169 EP 169 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801259 ER PT J AU KUZNETSOV, SA ROBEY, PG AF KUZNETSOV, SA ROBEY, PG TI HUMAN MARROW STROMAL FIBROBLASTS REQUIRE ONLY SERUM FOR MAXIMAL CLONING EFFICIENCY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 171 EP 171 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801271 ER PT J AU GORDON, SM DIONNE, RA BRAHIM, J DUBNER, R AF GORDON, SM DIONNE, RA BRAHIM, J DUBNER, R TI BLOCKADE OF PERIPHERAL NEURONAL BARRAGE REDUCES POSTOPERATIVE PAIN SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 178 EP 178 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801328 ER PT J AU SKRTIC, D EANES, ED TAKAGI, S ANTONUCCI, J AF SKRTIC, D EANES, ED TAKAGI, S ANTONUCCI, J TI IN-VITRO REMINERALIZATION OF ACP METHACRYLATE COATED ENAMEL LESIONS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. ADAFH,PRC,GAITHERSBURG,MD. NIST,GAITHERSBURG,MD. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 185 EP 185 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801385 ER PT J AU NOWJACKRAYMER, RE RAMS, TE WINN, DM KASTE, LM KIRKLAND, V BRUNELLE, JA AF NOWJACKRAYMER, RE RAMS, TE WINN, DM KASTE, LM KIRKLAND, V BRUNELLE, JA TI GINGIVAL TISSUE ALTERATIONS IN HIV - RELATION TO ORAL HYGIENE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 194 EP 194 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801452 ER PT J AU MARKOVIC, M FOWLERE, BO TUNG, MS AF MARKOVIC, M FOWLERE, BO TUNG, MS TI HIGH-PURITY MONOCLINIC AND HEXAGONAL CALCIUM HYDROXYAPATITES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 ADAHF,PRC,GAITHERSBURG,MD. NIDR,GAITHERSBURG,MD. NIST,GAITHERSBURG,MD. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 195 EP 195 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801464 ER PT J AU ADESANYA, MR OCONNELL, B WANG, S WALSH, CE BAUM, BJ AF ADESANYA, MR OCONNELL, B WANG, S WALSH, CE BAUM, BJ TI ADENOASSOCIATED VIRAL TRANSDUCTION OF A HUMAN SALIVARY-GLAND CELL-LINE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. NIH,CC HEMATOL SERV,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 197 EP 197 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801476 ER PT J AU KLIER, CM KOLENBRANDER, PE AF KLIER, CM KOLENBRANDER, PE TI CHARACTERIZATION OF A PUTATIVE COAGGREGATION-MEDIATING ADHESIN ON ACTINOMYCES SEROVAR WVA963 SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 198 EP 198 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801491 ER PT J AU WHITTAKER, CJ CLEMANS, DL KOLENBRANDER, PE AF WHITTAKER, CJ CLEMANS, DL KOLENBRANDER, PE TI GENETIC-ANALYSIS OF STREPTOCOCCAL COAGGREGATION-RELEVANT ADHESIONS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 198 EP 198 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801487 ER PT J AU TAKAHASHI, Y CISAR, JO RUHL, S SANDBERG, AL AF TAKAHASHI, Y CISAR, JO RUHL, S SANDBERG, AL TI A STREPTOCOCCUS-GORDONIL DL1 ANTIGEN ASSOCIATED WITH SIALIC-ACID LECTIN REACTIVITY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 201 EP 201 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801508 ER PT J AU PIHLSTROM, BL AF PIHLSTROM, BL TI SYMPOSIUM - CHALLENGES IN CLINICAL ORAL RESEARCH SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV MINNESOTA,NIDR,CORE CLIN RES CTR,MINNEAPOLIS,MN 55455. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 217 EP 217 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801640 ER PT J AU EIDELMAN, N GOLOMB, G BREUER, E FOWLER, BO AF EIDELMAN, N GOLOMB, G BREUER, E FOWLER, BO TI EFFECT OF PHOSPHONATES ON CALCIUM-PHOSPHATE FORMATION AND PHASE-TRANSFORMATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIST,ADAHF PRC,GAITHERSBURG,MD. NIDR,GAITHERSBURG,MD. HEBREW UNIV JERUSALEM,JERUSALEM,ISRAEL. RI Breuer, Eli/E-8382-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 222 EP 222 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801676 ER PT J AU SKRTIC, D GOLOMB, G BREUER, E VANGELDER, JM EANES, ED AF SKRTIC, D GOLOMB, G BREUER, E VANGELDER, JM EANES, ED TI PHOSPHONATE INHIBITION OF LIPOSOMAL CALCIUM-PHOSPHATE PRECIPITATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,JERUSALEM,ISRAEL. RI Breuer, Eli/E-8382-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 222 EP 222 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801679 ER PT J AU STANFORD, C JACOBSON, P EANES, ED MIDURA, R AF STANFORD, C JACOBSON, P EANES, ED MIDURA, R TI RAPIDLY FORMING APATITIC MINERAL IN AN OSTEOBLASTIC CELL-LINE (UMR 106-01 BSP) SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV IOWA,DOWS INST & ORTHOPAED SURG,IOWA CITY,IA 52242. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 222 EP 222 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801677 ER PT J AU REDFORD, M OLDAKOWSKI, R AF REDFORD, M OLDAKOWSKI, R TI TREND ANALYSES OF PROSTHODONTIC DATA FOR THE UNITED-STATES POPULATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 2 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 226 EP 226 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801714 ER PT J AU KOLENBRANDER, PE LONDON, J AF KOLENBRANDER, PE LONDON, J TI SYMPOSIUM - PLAQUE AS A BIOFILM IN HEALTH AND DISEASE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,MICROBIOL & IMMUNOL GRP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 229 EP 229 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801736 ER PT J AU SCHWARTZ, JL AF SCHWARTZ, JL TI SYMPOSIUM - MECHANISMS AND TREATMENTS FOR ORAL-DISEASES WITH ANTIOXIDANT MEDICATIONS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,MEODPP,PHARM & ORAL TOXICOL GRP,BETHESDA,MD 20892. NIDR,MEODPP,NUTR GRP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 229 EP 229 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801733 ER PT J AU BRUNELLE, JA BROWN, LJ STRECKFUS, C AF BRUNELLE, JA BROWN, LJ STRECKFUS, C TI THE ASSOCIATION OF ALVEOLAR BONE LOSS WITH PHYSIOLOGICAL-CHANGES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,EODPP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 233 EP 233 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801763 ER PT J AU RAMS, TE KINGMAN, A BROWN, LJ DAVIDSON, PL ANDERSEN, RM LISTGARTEN, MA AF RAMS, TE KINGMAN, A BROWN, LJ DAVIDSON, PL ANDERSEN, RM LISTGARTEN, MA TI INTRACLASS CORRELATION OF CPITN SEXTANT SCORES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UNIV PENN,PHILADELPHIA,PA 19104. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 233 EP 233 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801764 ER PT J AU BOUMA, C CAVEDON, K LONDON, J AF BOUMA, C CAVEDON, K LONDON, J TI CLONING AND EXPRESSION OF LACTOBACILLUS-CASEI CL16 RIBITOL-5-P DEHYDROGENASE AND THE RIBITOL PTS REPRESSOR SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 251 EP 251 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801907 ER PT J AU MATSUKI, Y NAKASHIMA, M AMIZUKA, N WARSHAWSKY, H GOLTZMAN, D YAMADA, KM YAMADA, Y AF MATSUKI, Y NAKASHIMA, M AMIZUKA, N WARSHAWSKY, H GOLTZMAN, D YAMADA, KM YAMADA, Y TI A COMPILATION OF PARTIAL SEQUENCES OF RANDOMLY SELECTED CDNA CLONES FROM THE RAT INCISOR SO JOURNAL OF DENTAL RESEARCH LA English DT Article DE GENE EXPRESSION; CDNA LIBRARY; SEQUENCE; RAT INCISOR ID EXPRESSION; COLLAGEN; GENES AB The formation of tooth organs is regulated by a series of developmental programs. We have initiated a genome project with the ultimate goal of identifying novel genes important for tooth development. As an initial approach, we constructed a unidirectional cDNA library from the non-calcified portion of incisors of 3- to 4-week-old rats, sequenced cDNA clones, and classified their sequences by homology search through the GenBank data base and the PIR protein data base. Here, we report partial DNA sequences obtained by automated DNA sequencing on 400 cDNA clones randomly selected from the library. Of the sequences determined, 51% represented sequences of new genes that were not related to any previously reported gene. Twenty-six percent of the clones strongly matched genes and proteins in the data bases, including amelogenin, alpha 1(I) and alpha 2(I) collagen chains, osteonectin, and decorin. Nine percent of clones revealed partial sequence homology to known genes such as transcription factors and cell surface receptors. A significant number of the previously identified genes were expressed redundantly and were found to encode extracellular matrix proteins. Identification and cataloging of cDNA clones in these tissues are the first step toward identification of markers expressed in a tissue- or stage-specific manner, as well as the genetic linkage study of tooth anomalies. Further characterization of the clones described in this paper should lead to the discovery of novel genes important for tooth development. C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. MCGILL UNIV,ROYAL VICTORIA HOSP,DEPT ANAT & CELL BIOL,MONTREAL,PQ H3A 1A1,CANADA. MCGILL UNIV,ROYAL VICTORIA HOSP,CALCIUM RES LAB,MONTREAL,PQ H3A 1A1,CANADA. MCGILL UNIV,DEPT MED,MONTREAL,PQ H3A 1A1,CANADA. OI Yamada, Kenneth/0000-0003-1512-6805 NR 13 TC 40 Z9 40 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD JAN PY 1995 VL 74 IS 1 BP 307 EP 312 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QK445 UT WOS:A1995QK44500003 PM 7876422 ER PT J AU MERGENHAGEN, SE AF MERGENHAGEN, SE TI PERSPECTIVES ON MOLECULAR MECHANISMS OF INFLAMMATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 401 EP 401 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100002 ER PT J AU KOLENBRANDER, PE PARRISH, K ANDERSEN, RN GREENBERG, EP AF KOLENBRANDER, PE PARRISH, K ANDERSEN, RN GREENBERG, EP TI COAGGREGATION OF ORAL TREPONEMA SPP WITH FUSOBACTERIUM SPP SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UNIV IOWA,IOWA CITY,IA 52242. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 407 EP 407 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100049 ER PT J AU DIONNE, RA GORDON, SM ROWAN, JS AF DIONNE, RA GORDON, SM ROWAN, JS TI PHARMACOKINETIC COMPARISON OF PERIPHERALLY VERSUS ORALLY-ADMINISTERED KETOPROFEN GEL SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 420 EP 420 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100157 ER PT J AU HOFFMAN, MP KIBBEY, MC NOMIZU, M KLEINMAN, HK AF HOFFMAN, MP KIBBEY, MC NOMIZU, M KLEINMAN, HK TI LAMININ PROMOTES ACINAR-LIKE DEVELOPMENT OF A HUMAN SUBMANDIBULAR-GLAND CELL-LINE (HSG) IN-VITRO SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 444 EP 444 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100347 ER PT J AU CHANG, DS PAIK, DI MOON, HS KIM, JB HOROWITZ, AM AF CHANG, DS PAIK, DI MOON, HS KIM, JB HOROWITZ, AM TI ORAL HEALTH KNOWLEDGE AND PRACTICES OF 4TH GRADE KOREAN STUDENTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 SEOUL NATL,SEOUL,SOUTH KOREA. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 458 EP 458 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100462 ER PT J AU KOBAYASHI, S SAKUMA, S YOSHIHARA, A HORII, K SAKAI, O HOROWITZ, AM AF KOBAYASHI, S SAKUMA, S YOSHIHARA, A HORII, K SAKAI, O HOROWITZ, AM TI A TARGETED SEALANT PROGRAM COMBINED WITH FLUORIDE MOUTHRINSING - 5-YEAR RESULTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIIGATA UNIV,SCH DENT,NIIGATA 95021,JAPAN. FUKUOKA DENT COLL,FUKUOKA 814,JAPAN. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 458 EP 458 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100459 ER PT J AU BIRKEDALHANSEN, B GRENETT, H PETERS, GE BIRKEDALHANSEN, H AF BIRKEDALHANSEN, B GRENETT, H PETERS, GE BIRKEDALHANSEN, H TI EXPRESSION OF STROMELYSIN-1 AND STROMELYSIN-2 IN ORAL SQUAMOUS-CELL CARCINOMAS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV ALABAMA,BIRMINGHAM,AL 35294. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 465 EP 465 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100513 ER PT J AU INOUE, K KOMATSU, F CHINO, T CREVELING, CR AF INOUE, K KOMATSU, F CHINO, T CREVELING, CR TI DOPA AND RELATED ENZYMES IN HUMAN DENTAL-PULP SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 485 EP 485 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100678 ER PT J AU PAIK, DI MOON, HS KIM, JB HOROWITZ, AM CHANG, DS AF PAIK, DI MOON, HS KIM, JB HOROWITZ, AM CHANG, DS TI KNOWLEDGE, OPINIONS AND PRACTICES ABOUT CARIES PREVENTION AMONG KOREAN DENTISTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 SEOUL NATL UNIV,SEOUL 151,SOUTH KOREA. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 533 EP 533 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08101060 ER PT J AU KORN, EL BAUMRIND, S BOYD, RL AF KORN, EL BAUMRIND, S BOYD, RL TI ROOT RESORPTION IN ADULT ORTHODONTIC TREATMENT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NCI,BIOMETR RES BRANCH,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DIV ORTHODONT,SAN FRANCISCO,CA 94143. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 537 EP 537 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08101090 ER PT J AU ALBANDAR, JM BROWN, LJ BRUNELLE, JA LOE, H AF ALBANDAR, JM BROWN, LJ BRUNELLE, JA LOE, H TI COMPARISON OF GINGIVAL STATE AND CALCULUS SCORES IN ADOLESCENTS WITH AND WITHOUT EARLY-ONSET PERIODONTITIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 542 EP 542 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08101131 ER PT J AU BROWN, LJ ALBANDAR, JM BRUUELLE, JA LOE, H AF BROWN, LJ ALBANDAR, JM BRUUELLE, JA LOE, H TI PATTERN OF TRANSITION OF CLINICAL-DISEASE STATUS IN CASES WITH EARLY-ONSET PERIODONTITIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 542 EP 542 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08101134 ER PT J AU GORDON, SM DIONNE, RA BRAHIM, J DUBNER, R AF GORDON, SM DIONNE, RA BRAHIM, J DUBNER, R TI BLOCKADE OF PERIPHERAL NEURONAL BARRAGE REDUCES POSTOPERATIVE PAIN SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 550 EP 550 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08101199 ER PT J AU CATERINA, NCM WINDSOR, LJ TAYLOR, KB BIRKEDALHANSEN, H ENGLER, JA AF CATERINA, NCM WINDSOR, LJ TAYLOR, KB BIRKEDALHANSEN, H ENGLER, JA TI FUNCTIONAL DOMAINS IN THE TISSUE INHIBITOR OF METALLOPROTEINASES-1 (TIMP-1) SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35233. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 590 EP 590 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08101520 ER PT J AU GALAZKA, G BIRKEDALHANSEN, H ENGLER, JE AF GALAZKA, G BIRKEDALHANSEN, H ENGLER, JE TI MUTATIONS IN THE HUMAN PROSL-1 PROPEPTIDE - EFFECT ON ORGANOMERCURIAL ACTIVATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35233. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 591 EP 591 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08101526 ER PT J AU Kozuch, P Cooney, TM AF Kozuch, P Cooney, TM TI Young adults' marital and family attitudes: The role of recent parental divorce, and family and parental conflict SO JOURNAL OF DIVORCE & REMARRIAGE LA English DT Article ID ADOLESCENTS; MARRIAGE; ADJUSTMENT; LIFE AB Only a few small studies have examined the effects of recent parental divorce on young adults, including how it influences attitudes toward marriage and divorce. Results from studies using parental marital status as a predictor of young adults' attitudes have been inconsistent. Other studies have suggested that parental and family conflict would be stronger predictors of young adults' marital and family attitudes. The main hypothesis of this study was that parental and family conflict would be stronger predictors of young adults' attitudes than would parental marital status. Randomly sampled, never-married, White young adults (ages 17-23) formed two groups: those with recently divorced parents (n = 231) and those with married parents (n = 213). All responded to structured telephone interviews. While level of family conflict did not predict any of the five attitudes measured, level of parental disagreement predicted four of the five attitudes. Parental marital status predicted two of the attitudes. C1 UNIV DELAWARE,NEWARK,DE 19716. NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. OI kozuch, patricia/0000-0002-7465-9671 NR 23 TC 8 Z9 8 U1 2 U2 14 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1050-2556 J9 J DIVORCE REMARRIAGE JI J. Divorce Remarriage PY 1995 VL 23 IS 3-4 BP 45 EP 62 DI 10.1300/J087v23n03_03 PG 18 WC Family Studies SC Family Studies GA TK913 UT WOS:A1995TK91300003 ER PT J AU AUGUSTYN, M SIMONSMORTON, BG AF AUGUSTYN, M SIMONSMORTON, BG TI ADOLESCENT DRINKING AND DRIVING - ETIOLOGY AND INTERPRETATION SO JOURNAL OF DRUG EDUCATION LA English DT Article ID ALCOHOL-RELATED EXPECTANCIES; DRUG-ABUSE PREVENTION; PSYCHOSOCIAL FACTORS; SITUATIONAL FACTORS; SMOKING PREVENTION; COLLEGE-STUDENTS; SOCIAL-CONTEXT; SCHOOL; RISK; BEHAVIOR AB In the adolescent population, drinking and driving is an important cause of injury, disability and premature death. A literature review of the demographics and etiology of drinking and drinking/driving reveals: 1) which subgroups of the adolescent population are more likely to drink and drink/ drive; 2) where and why adolescents drink and drink/drive; 3) peer and family issues associated with adolescent drinking and drinking/driving; and 4) adolescent expectancies and perceived efficacies associated with drinking and drinking/driving. A discussion of the role of theory and the use of etiologic data in intervention research precedes an overview of several types of school-based alcohol-prevention programs and recommendations for more theory based interventions. C1 NIH,BETHESDA,MD. RP AUGUSTYN, M (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MATERNAL & CHILD HLTH,HAMPTON HOUSE,RM 203,BALTIMORE,MD 21205, USA. OI Simons-Morton, Bruce/0000-0003-1099-6617 NR 87 TC 14 Z9 14 U1 2 U2 3 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0047-2379 J9 J DRUG EDUC JI J. Drug Educ. PY 1995 VL 25 IS 1 BP 41 EP 59 DI 10.2190/B041-Q1D9-YCXL-0BK0 PG 19 WC Substance Abuse; Education, Scientific Disciplines SC Substance Abuse; Education & Educational Research GA QV049 UT WOS:A1995QV04900005 PM 7776149 ER PT J AU WETLE, TT FULMER, TT AF WETLE, TT FULMER, TT TI A MEDICAL PERSPECTIVE SO JOURNAL OF ELDER ABUSE & NEGLECT LA English DT Article AB Elder mistreatment is explored from the perspective of the health care professional, beginning with a brief review of relevant values and ethical concepts. These include beneficence, nonmaleficence, autonomy, confidentiality, paternalism, filial piety, and justice. The chapter then raises several ethical dilemmas faced by health care professionals in evaluating, reporting, and caring for cases of elder mistreatment, These include the difficulty in balancing patient autonomy with the obligation to protect them from harm the problem of confidentiality and reporting requirements, the impact of reporting on relationships with patients and other professionals, and the problems in working with patients and their families. Approaches to developing appropriate institutional responses are suggested. The chapter concludes with a discussion of the three cases. C1 COLUMBIA UNIV,CTR GERIATR EDUC,NEW YORK,NY 10032. RP WETLE, TT (reprint author), NIA,BLDG 31,ROOM 5C35,31 CTR DR MSC 2292,BETHESDA,MD 20892, USA. NR 17 TC 0 Z9 0 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0894-6566 J9 J ELDER ABUSE NEGL JI J. Elder Abuse Negl. PY 1995 VL 7 IS 2-3 BP 31 EP 48 DI 10.1300/J084v07n02_03 PG 18 WC Gerontology SC Geriatrics & Gerontology GA TC741 UT WOS:A1995TC74100004 ER PT J AU VRHEL, MJ TRUSSELL, HJ BOSCH, J AF VRHEL, MJ TRUSSELL, HJ BOSCH, J TI DESIGN AND REALIZATION OF OPTIMAL COLOR FILTERS FOR MULTI-ILLUMINANT COLOR CORRECTION SO JOURNAL OF ELECTRONIC IMAGING LA English DT Article ID FUNDAMENTAL METAMERS; MIXTURE; IMAGES; SET AB A method of selecting optimal color filters to perform accurate multi-illuminant color correction is reviewed. The transmittances for a set of filters obtained by the method were provided to a color filter manufacturer. The manufacturer used a dichroic filter modeling program to produce transmittances that satisfied the physical constraints of the manufacturing process and approximated the optimal filter transmittances. The ideal and manufacturable filters are compared through computer simulation and their accuracy assessed during the CIE Delta E(L*a*b*) measure. The results show that the unconventional shapes of the optimal filters can be well approximated by actual filters with slight degradation in performance. C1 N CAROLINA STATE UNIV,DEPT ELECT & COMP ENGN,RALEIGH,NC 27695. BARR ASSOCIATES,DIV COLOR PROD,WESTFORD,MA 01886. RP VRHEL, MJ (reprint author), NIH,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13-3N13,13 SOUTH DR,MSC 5766,BETHESDA,MD 20892, USA. NR 25 TC 26 Z9 26 U1 0 U2 1 PU I S & T - SOC IMAGING SCIENCE TECHNOLOGY PI SPRINGFIELD PA 7003 KILWORTH LANE, SPRINGFIELD, VA 22151 SN 1017-9909 J9 J ELECTRON IMAGING JI J. Electron. Imaging PD JAN PY 1995 VL 4 IS 1 BP 6 EP 14 DI 10.1117/12.193812 PG 9 WC Engineering, Electrical & Electronic; Optics; Imaging Science & Photographic Technology SC Engineering; Optics; Imaging Science & Photographic Technology GA QV376 UT WOS:A1995QV37600002 ER PT J AU BARCHI, JJ COONEY, DA HAO, Z WEINBERG, M TAFT, C MARQUEZ, VE FORD, H AF BARCHI, JJ COONEY, DA HAO, Z WEINBERG, M TAFT, C MARQUEZ, VE FORD, H TI IMPROVED SYNTHESIS OF ZEBULARINE [1-(BETA-D-RIBOFURANOSYL)-DIHYDROPYRIMIDIN-2-ONE] NUCLEOTIDES AS INHIBITORS OF HUMAN DEOXYCYTIDYLATE DEAMINASE SO JOURNAL OF ENZYME INHIBITION LA English DT Article DE DCMP DEAMINASE; ZEBULARINE; MOLT-4; INHIBITION; DEOXYRIBONUCLEOTIDE POOLS; ANTICANCER THERAPEUTICS ID HUMAN LEUKEMIA-CELLS; DNA-SYNTHESIS; CYTIDINE DEAMINASE; ESCHERICHIA-COLI; TETRAHYDROURIDINE; MECHANISM; BINDING; TISSUES; LINES; HIV AB The 2'-deoxy (2a) and 2'-ara-fluoro (3a) derivatives of zebularine [1-(beta-D-ribofuranosyl)-dihydropyrimidin-2-one, 1a] were phosphorylated in high yield to the 5'-nucleotides 2b and 3b, respectively, and characterized by HPLC, enzyme degradation, H-1, C-13 and P-31 NMR, and high resolution mass spectral analysis. Their inhibitory activity against partially purified MOLT-4 deoxycytidylate deaminase (dCMPD) in the presence of the allosteric effector deoxycytidine triphosphate (dCTP) and Mg+2 ion was examined. Compounds 2b and 3b inhibited dCMPD with K-1 values of 2.1 x 10(-8) M and 1.2 x 10(-8) M, respectively. The parent nucleotide, zebularine monophosphate 1b was ineffective at concentrations > 100 mu mol. The effect of the nucleosides, 1a-3a, as well as tetrahydrouridine (THU) and 2'-deoxy THU (dTHU), on the cellular production of DNA precursors was examined in human MOLT-4 peripheral lymphoblasts. It was shown that 1a, 2a and 3a all elevated intracellular dCTP and TTP levels in whole cells with the most powerful effect elicited by la. The 2'-fluoro derivative 3a was chemically phosphorylated much more cleanly and higher yield than 2a, without the formation of diphosphorylated by-products. This compound was found to be infinitely less sensitive to acid-catalyzed degradation than 2a. Since the substitution of fluorine for hydrogen had a slight potentiating effect on the dCMPD inhibitory activity while stabilizing the compound toward acid-catalyzed and enzymatic depyrimidination, compound 3b emerges as a very attractive tool for the pharmacological modulation of pyrimidine deaminase activity. RP BARCHI, JJ (reprint author), NCI,DIV CANC TREATMENT,MED CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892, USA. RI Barchi Jr., Joseph/N-3784-2014 NR 35 TC 13 Z9 14 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 8755-5093 J9 J ENZYM INHIB JI J. Enzym. Inhib. PY 1995 VL 9 IS 2 BP 147 EP 162 DI 10.3109/14756369509042814 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QZ618 UT WOS:A1995QZ61800004 PM 8583252 ER PT J AU CLARK, CG MARTIN, DS DIAMOND, LS AF CLARK, CG MARTIN, DS DIAMOND, LS TI PHYLOGENETIC-RELATIONSHIPS AMONG ANURAN TRYPANOSOMES AS REVEALED BY RIBOPRINTING SO JOURNAL OF EUKARYOTIC MICROBIOLOGY LA English DT Article DE DISTANCE MATRIX; FROG; PARSIMONY; POLYMORPHISM; SMALL-SUBUNIT RIBOSOMAL RNA GENE; TOAD ID FALLISI; TOADS; KINETOPLASTIDA; INFECTIVITY; ONTARIO AB Twenty trypanosome isolates from Anura (frogs and toads) assigned to several species were characterized by riboprinting-restriction enzyme digestion of polymerase chain reaction amplified small subunit ribosomal RNA genes. Restriction site polymorphisms allowed distinction of all the recognized species and no intraspecific variation in riboprint patterns was detected. Phylogenetic reconstruction using parsimony and distance estimates based on restriction fragment comigration showed Trypanosoma chattoni to be only distantly related to the other species, while T. ranarum and T. fallisi appear to be sister taxa despite showing non-overlapping host specificities. C1 UNIV TORONTO,DEPT ZOOL,TORONTO,ON M5S 1A1,CANADA. RP CLARK, CG (reprint author), NIH,PARASIT DIS LAB,BETHESDA,MD 20892, USA. RI Clark, C Graham/H-3683-2011 OI Clark, C Graham/0000-0002-0521-0977 NR 13 TC 34 Z9 36 U1 0 U2 5 PU SOC PROTOZOOLOGISTS PI POTOMAC PA 12263 GREENLEAF AVE, POTOMAC, MD 20854 SN 1066-5234 J9 J EUKARYOT MICROBIOL JI J. Eukaryot. Microbiol. PD JAN-FEB PY 1995 VL 42 IS 1 BP 92 EP 96 DI 10.1111/j.1550-7408.1995.tb01546.x PG 5 WC Microbiology SC Microbiology GA QN884 UT WOS:A1995QN88400015 PM 7728144 ER PT J AU STANLEY, JR AF STANLEY, JR TI AUTOANTIBODIES AGAINST ADHESION MOLECULES AND STRUCTURES IN BLISTERING SKIN DISEASES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Editorial Material ID BULLOUS PEMPHIGOID ANTIGEN; PARANEOPLASTIC PEMPHIGUS; PASSIVE TRANSFER; TRANSMEMBRANE GLYCOPROTEIN; VULGARIS ANTIGEN; CELL-ADHESION; FOLIACEUS; PROTEIN; HEMIDESMOSOME; CADHERIN RP STANLEY, JR (reprint author), NIH,DERMATOL BRANCH,BETHESDA,MD 20892, USA. NR 35 TC 59 Z9 62 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 1 EP 4 DI 10.1084/jem.181.1.1 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200001 PM 7806996 ER PT J AU SEDER, RA LEGROS, GG AF SEDER, RA LEGROS, GG TI THE FUNCTIONAL-ROLE OF CD8(+) T-HELPER TYPE-2 CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Editorial Material ID HIV-INFECTION; SUBSETS; VIRUS; INTERLEUKIN-4; RESPONSES; PROFILES; SWITCH; CD4 C1 MALAGHAN INST MED RES,WELLINGTON,NEW ZEALAND. RP SEDER, RA (reprint author), NIAID,CLIN INVEST LAB,LYMPHOKINE REGULAT UNIT,BLDG 10,ROOM 11C215,BETHESDA,MD 20892, USA. RI Le Gros, Graham/C-6725-2011 NR 18 TC 118 Z9 122 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 5 EP 7 DI 10.1084/jem.181.1.5 PG 3 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200002 PM 7807025 ER PT J AU KEARSE, KP TAKAHAMA, Y PUNT, JA SHARROW, SO SINGER, A AF KEARSE, KP TAKAHAMA, Y PUNT, JA SHARROW, SO SINGER, A TI EARLY MOLECULAR EVENTS INDUCED BY T-CELL RECEPTOR (TCR) SIGNALING IN IMMATURE CD4(+)CD8(+) THYMOCYTES - INCREASED SYNTHESIS OF TCR-ALPHA PROTEIN IS AN EARLY RESPONSE TO TCR SIGNALING THAT COMPENSATES FOR TCR-ALPHA INSTABILITY, IMPROVES TCR ASSEMBLY, AND PARALLELS OTHER INDICATORS OF POSITIVE SELECTION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MONOCLONAL-ANTIBODY; CD4+CD8+ THYMOCYTES; CLONAL DELETION; NEGATIVE SELECTION; ANTIGEN RECEPTOR; CYCLOSPORINE-A; DEGRADATION; EXPRESSION; ACTIVATION; CHAINS AB Differentiation of immature CD4(+)CD8(+) thymocytes into mature CD4(+) or CD8(+) T cells occurs within the thymus and is dependent upon expression of antigen receptor complexes (T cell receptor [TCR]) containing clonotypic alpha/beta proteins. We have recently found that CD4(+) CD8(+) thymocytes express low levels of surface TCR because of limitations placed on TCR assembly by the instability of nascent TCR-alpha proteins within the endoplasmic reticulum (ER) of immature thymocytes. Because TCR-alpha/beta expression increases during development, a molecular mechanism must exist for increasing the number of assembled TCR complexes present in immature CD4(+)CD8(+) thymocytes that have been signaled to differentiate into mature T cells, although no such mechanism has yet been described. In the current report we have examined the molecular consequences of intracellular signals generated by engagement of surface TCR complexes on immature CD4(+)CD8(+) thymocytes. Isolated TCR engagement generated signals that increased TCR-alpha RNA levels and increased synthesis of TCR-a proteins, which, in turn, significantly increased assembly of complete TCR-alpha/beta complexes in CD4(+)CD8(+) thymocytes. Increased TCR-alpha protein levels in TCR-signaled CD4(+)CD8(+) thymocytes was the result of increased synthesis and not increased stability of TCR-alpha proteins, indicating that TCR engagement compensates for, but does not correct, the inherent instability of TCR-alpha proteins in the ER of immature thymocytes. Consistent with the delivery by TCR engagement of a positive selection signal, TCR engagement also increased CD5 expression, decreased RAG-1 expression, and decreased CD4/CD8 coreceptor expression in immature CD4(+)CD8(+) thymocytes. These data identify amplified TCR-alpha expression as an initial response of immature CD4(+)CD8(+) thymocytes to TCR-mediated positive selection signals and provide a molecular basis for increased surface TCR density on developing thymocytes undergoing selection events within the thymus. RP KEARSE, KP (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM 4B-17,BETHESDA,MD 20892, USA. RI Takahama, Yousuke/A-5863-2010 NR 29 TC 72 Z9 73 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 193 EP 202 DI 10.1084/jem.181.1.193 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200020 PM 7528767 ER PT J AU PAOLINI, R RENARD, V VIVIER, E OCHIAI, K JOUVIN, MH MALISSEN, B KINET, JP AF PAOLINI, R RENARD, V VIVIER, E OCHIAI, K JOUVIN, MH MALISSEN, B KINET, JP TI DIFFERENT ROLES FOR THE FC-EPSILON-RI GAMMA-CHAIN AS A FUNCTION OF THE RECEPTOR CONTEXT SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID CELL ANTIGEN RECEPTOR; PROTEIN-TYROSINE KINASE; AFFINITY IGE RECEPTOR; NATURAL-KILLER-CELLS; T-CELL; ZETA-CHAIN; SIGNAL TRANSDUCTION; CYTOPLASMIC TAIL; ACTIVATION; ASSOCIATION AB The high affinity immunoglobulin E receptor (Fc epsilon RI) and the B and T cell antigen receptors (TCR) are multimeric complexes containing subunits with cytoplasmic antigen recognition activation motifs (ARAMs). The presence of multiple motifs may be a way to amplify a single signal or provide independent activation modules. Here we have compared the signaling capacity of the same Fc epsilon RI gamma motif in the context of two different receptors, Fc epsilon RI and TCR/CD3, simultaneously reconstituted on the surface of the same zeta-deficient T cell line. Both reconstituted receptors mediate early (phosphorylation) and late (interleukin [IL]-2 release) signals. Mutation of the two tyrosine residues of ARAM gamma alters early signaling by both receptors, but the set of substrates phosphorylated via ARAM gamma is different for each receptor and is thus dependent on the receptor context. Furthermore, the mutations prevent Fc epsilon RI- but not TCR/CD3-mediated IL-2 release. These data demonstrate that ARAM gamma is necessary for allowing both receptors to phosphorylate the complete set of substrates, and that the CD3 complex, unlike the Fc epsilon RI beta chain, contains activation modules capable of compensating for the absence of a functional ARAM gamma in generating late signals such as IL-2 release. C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. CNRS,INSERM,CTR IMMUNOL,F-13288 MARSEILLE 9,FRANCE. NR 46 TC 37 Z9 37 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 247 EP 255 DI 10.1084/jem.181.1.247 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200025 PM 7528770 ER PT J AU KRAUSE, PR STANBERRY, LR BOURNE, N CONNELLY, B KURAWADWALA, JF PATEL, A STRAUS, SE AF KRAUSE, PR STANBERRY, LR BOURNE, N CONNELLY, B KURAWADWALA, JF PATEL, A STRAUS, SE TI EXPRESSION OF THE HERPES-SIMPLEX VIRUS TYPE-2 LATENCY-ASSOCIATED TRANSCRIPT ENHANCES SPONTANEOUS REACTIVATION OF GENITAL HERPES IN LATENTLY INFECTED GUINEA-PIGS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TRIGEMINAL GANGLIA; MESSENGER-RNA; LAT PROMOTER; SEQUENCE; NEURONS; REGION; MOUSE; GENE; ESTABLISHMENT; KINETICS AB The latency-associated transcript (LAT) is the only herpes simplex virus (HSV) gene product detectable in latently infected humans and animals. In this report, we show that a 624-bp deletion in the promoter of the HSV-2 LAT had no discernable effect on viral growth in tissue culture or in acute genital infection of guinea pigs, but impaired LAT accumulation and led to a marked decrease in spontaneous genital recurrences when compared with the behavior of wild-type and rescuant strains. Differences in the ability of the mutant to replicate, or in how readily it established or maintained latency did not account for this finding. Thus, HSV LAT expression facilitates the spontaneous reactivation of latent virus. C1 UNIV CINCINNATI,COLL MED,CHILDRENS HOSP RES FDN,DEPT PEDIAT,DIV INFECT DIS,CINCINNATI,OH 45229. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. RP KRAUSE, PR (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV VIRAL PROD,HFM-457,8800 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [AI-15101, AI-22667, AI-29687] NR 35 TC 67 Z9 68 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 297 EP 306 DI 10.1084/jem.181.1.297 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200029 PM 7807009 ER PT J AU ORTALDO, JR MASON, AT OSHEA, JJ AF ORTALDO, JR MASON, AT OSHEA, JJ TI RECEPTOR-INDUCED DEATH IN HUMAN NATURAL-KILLER-CELLS - INVOLVEMENT OF CD16 SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID DNA FRAGMENTATION; LYMPHOCYTES; APOPTOSIS; EXPRESSION; ANTIGEN; ENGAGEMENT; OCCURS; CYCLE; CHAIN AB Propriocidal regulation of T cells refers to apoptosis induced by inerleukin 2 (IL-2) activation with subsequent antigen receptor stimulation. We examined whether natural killer (NK) cells exhibited cytokine- and ligand-induced death similar to activated T cells. peripheral NK cells were examined for ligand-induced death using antibodies to surface moieties (CD2, CD3, CD8, CD16, CD56), with and without prior activation of IL-2. Only those NK cells stimulated first with IL-2 and then with CD16 exhibited ligand-induced death; none of the other antibody stimuli induced this phenomenon. Next we examined various cytokines (IL-2, IL-4, IL-6, IL-7, IL-12, IL-13, interferon a and gamma) that can activate NK cells and determined if CD16-induced killing occurred. Only IL-2 and IL-12 induced NK cell death after occupancy of this receptor by aggregated immunoglobulin or by cross-linking with antireceptor antibody. The CD16-induced death was inhibited by herbimycin A, indicating that cell death was dependent upon protein tyrosine kinases. Identical to T cells, the form of cell death for NK cells was demonstrated to be receptor-induced apoptosis. Overall these data indicate that highly activated NK cells mediate ligand-induced apoptosis via signaling molecules like CD16. Whereas the propriocidal regulation of T cells is antigen specific, this is not the case for NK cells due to the nature of the receptor The clinical implications of this finding are considered. RP ORTALDO, JR (reprint author), NCI,FREDERICK CANC RES FACIL,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702, USA. NR 25 TC 121 Z9 121 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 339 EP 344 DI 10.1084/jem.181.1.339 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200033 PM 7528771 ER PT J AU GRZEGORZEWSKI, KJ KOMSCHLIES, KL JACOBSEN, SEW RUSCETTI, FW KELLER, JR WILTROUT, RH AF GRZEGORZEWSKI, KJ KOMSCHLIES, KL JACOBSEN, SEW RUSCETTI, FW KELLER, JR WILTROUT, RH TI MOBILIZATION OF LONG-TERM RECONSTITUTING HEMATOPOIETIC STEM-CELLS IN MICE BY RECOMBINANT HUMAN INTERLEUKIN-7 SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID BONE-MARROW TRANSPLANTATION; MYELOID PROGENITOR CELLS; HUMAN PERIPHERAL-BLOOD; IL-7; INVITRO; GROWTH AB Administration of recombinant human interleukin 7 (rh)IL-7 to mice has been reported by our group to increase the exportation of myeloid progenitors (colony-forming unit [CFU]-c and CFU-granulocyte erythroid megakarocyte macrophage) from the bone marrow to peripheral organs (blood, spleen[s], and liver). We now report that IL-7 also stimulates a sixfold increase in the number of more primitive CFU-S day 8 (CFU-S-8) and day 12 (CFU-S-12) in the peripheral blood leukocytes (PBL) of mice treated with rhiL-7 for 7 d. Moreover, >90% of lethally irradiated recipient mice that received PBL from rhIL-7-treated donor mice have survived for >6 mo whereas none of the recipient mice that received an equal number of PBL. from diluent-treated donors survived. Flow cytometry analysis at 3 and 6 mo after transplantation revealed complete trilineage (T, B, and myelomonocytic cell) repopulation of bone marrow, thymus, and spleen by blood-borne stem/progenitor cells obtained from rhIL-7-treated donor mice. Thus, IL-7 may prove valuable for mobilizing pluripotent stem cells with long-term repopulating activity from the bone marrow to the peripheral blood for the purpose of gene modification and/or autologous or allogeneic stem cell transplantation. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESP MODIFIERS PROG,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESP MODIFIERS PROG,LEUKOCYTE BIOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NORWEGIAN RADIUM HOSP,DEPT IMMUNOL,N-0310 OSLO,NORWAY. NR 24 TC 23 Z9 23 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 369 EP 374 DI 10.1084/jem.181.1.369 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200038 PM 7807018 ER PT J AU ISAKOV, N WANGE, RL BURGESS, WH WATTS, JD AEBERSOLD, R SAMELSON, LE AF ISAKOV, N WANGE, RL BURGESS, WH WATTS, JD AEBERSOLD, R SAMELSON, LE TI ZAP-70 BINDING-SPECIFICITY TO T-CELL RECEPTOR TYROSINE-BASED ACTIVATION MOTIFS - THE TANDEM SH2 DOMAINS OF ZAP-70 BIND DISTINCT TYROSINE-BASED ACTIVATION MOTIFS WITH VARYING AFFINITY SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID ANTIGEN RECEPTOR; ZETA-CHAIN; KINASE; CD3-EPSILON; COMPONENTS; COMPLEX; TAIL AB Engagement of the T cell antigen receptor (TCR) results in activation of several tyrosine kinases leading to tyrosine phosphorylation of protein substrates and activation of multiple biochemical pathways. TCR-mediated activation of the src-family kinases, Lck and Fyn, results in tyrosine phosphorylation of the TCR zeta and CD3 chains. The site of phosphorylation in these chains is the tyrosine-based activation motif(TAM), a 15-16 amino acid module containing two tyrosine residues. Tyrosine-phosphorylated TAMs serve as targets for binding of the zeta-associated protein (ZAP-70) tyrosine kinase via its tandem SH2 domains. This binding correlates with activation of ZAP-70, a critical event in T cell activation. To further define the structural requirements for ZAP-70 interaction with the TCR, we developed a binding assay using immobilized glutathione S-transferase fusion proteins containing the NH2- and/or COOH-terminal SH2 domains of ZAP-70, and soluble synthetic peptides with the sequence of the cytoplasmic region of the TCR zeta chain (TCRS zeta(cyt) or individual TCR zeta and CD3 epsilon TAM motifs. Direct binding studies demonstrated that the tandem ZAP-70 SH2 domains bind phosphorylated, but not nonphosphorylated, TCR zeta(cyt). The NH2-terminal ZAP-70 SH2 domain also binds to TCR zeta(cyt) but with 100-fold lower affinity. No binding was observed with the COOH-terminal ZAP-70 SH2 domain. Similar studies demonstrated that the ZAP-70 tandem SH2 domain can bind a TCR zeta(3) TAM peptide in which both tyrosine residues are phosphorylated: Little or no binding was observed with peptides phosphorylated at only one tyrosine residue, or a nonphosphorylated peptide. Binding of the tandem SH2 domains to the other two TCR zeta TAM peptides and to a CD3 epsilon TAM peptide was also observed. AIL four doubly tyrosine phospholylated TAM peptides cross-compete with each other for binding to the tandem SH2 domains of ZAP-70. The affinity of these peptides for the tandem SH2 construct demonstrated a hierarchy of TAM zeta 1 greater than or equal to TAM zeta(2) > TAM epsilon greater than or equal to TAM zeta(3). The results provide further evidence that the ZAP-70 interaction with the TCR requires prior phosphorylation of both tyrosine residues within a TAM motif. Binding of ZAP-70 to phospho-TAMs is notable for the high level of cooperativity between the two SH2 domains, which individually demonstrate low affinity interaction with the ligand. The cooperativity ensures higher affinity for the doubly phosphorylated ligand. Affinity differences of as much as 30-fold indicates a significant specificity of interaction of ZAP-70 SH2 domains for different phospho-TAMs. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. BEN GURION UNIV NEGEV,DEPT MICROBIOL & IMMUNOL,IL-84105 BEER SHEVA,ISRAEL. BEN GURION UNIV NEGEV,CANC RES CTR,IL-84105 BEER SHEVA,ISRAEL. AMER RED CROSS,HOLLAND MED LAB,ROCKVILLE,MD 20850. UNIV BRITISH COLUMBIA,BIOMED RES CTR,VANCOUVER,BC V6T 1Z3,CANADA. RI ISAKOV, NOAH/F-1659-2012 FU NHLBI NIH HHS [HL 35762] NR 25 TC 155 Z9 160 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 375 EP 380 DI 10.1084/jem.181.1.375 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200039 PM 7528772 ER PT J AU BACON, CM MCVICAR, DW ORTALDO, JR REES, RC O'SHEA, JJ JOHNSTON, JA AF BACON, CM MCVICAR, DW ORTALDO, JR REES, RC O'SHEA, JJ JOHNSTON, JA TI INTERLEUKIN-12 (IL-12) INDUCES TYROSINE PHOSPHORYLATION OF JAK2 AND TYK2 - DIFFERENTIAL USE OF JANUS FAMILY TYROSINE KINASES BY IL-2 AND IL-12 SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID CELL STIMULATORY FACTOR; GAMMA SIGNAL-TRANSDUCTION; NATURAL-KILLER-CELLS; INTERFERON-GAMMA; CYTOKINE RECEPTORS; NK CELLS; PROLIFERATION; ALPHA/BETA; INDUCTION; PATHWAY AB Interleukin (IL-12) has many effects on the function of natural killer and T cells, and is important in the control of cell-mediated immunity. IL-2 and IL-12 display many similar activities, yet each also induces a distinct set of responses. A human IL-12 receptor subunit has recently been cloned and, like the IL-2R beta and IL-2R gamma, is a member of the hematopoietic receptor superfamily; however, the molecular mechanisms of IL-12 action are unknown. In this report we show that IL-12 and IL-2 induce tyrosine phosphorylation of distinct members of the Janus (JAK) family of protein tyrosine kinases in human T lymphocytes. IL-12, but not IL-2, stimulates the tyrosine phosphorylation of TYK2 and JAK2, whereas JAK1 and JAK3, which are phosphorylated in response to IL-2, are not phosphorylated after IL-12 treatment. The use of distinct but related JAK family tyrosine kinases by IL-12 and IL-2 may provide a biochemical basis for their different biological activities. C1 NCI, FREDERICK CANC RES & DEV CTR, BIOL RESPONSE MODIFIERS PROGRAM, EXPTL IMMUNOL LAB, FREDERICK, MD 21702 USA. UNIV SHEFFIELD, SCH MED, INST CANC STUDIES, SHEFFIELD S10 2RX, S YORKSHIRE, ENGLAND. RI McVicar, Daniel/G-1970-2015 NR 32 TC 262 Z9 265 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 399 EP 404 DI 10.1084/jem.181.1.399 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200043 PM 7528775 ER PT J AU THURMAN, RG GAO, WS CONNOR, HD ADACHI, Y STACHLEWITZ, RF ZHONG, Z KNECHT, KT BRADFORD, BU MASON, RP LEMASTERS, JJ AF THURMAN, RG GAO, WS CONNOR, HD ADACHI, Y STACHLEWITZ, RF ZHONG, Z KNECHT, KT BRADFORD, BU MASON, RP LEMASTERS, JJ TI ROLE OF KUPFFER CELLS IN FAILURE OF FATTY LIVERS FOLLOWING LIVER-TRANSPLANTATION AND ALCOHOLIC LIVER-INJURY SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY LA English DT Article; Proceedings Paper CT Satellite Symposium on Hepatic Sinusoidal Cells and Hepatic Disorders, of the 7th International Symposium on Cells of the Hepatic Sinusoid CY SEP 12, 1994 CL TOKYO, JAPAN DE ALCOHOLIC LIVER INJURY; ENDOTOXIN; ETHANOL; FATTY LIVER; FREE RADICALS; KUPFFER CELLS; ORTHOTOPIC LIVER TRANSPLANTATION; REPERFUSION INJURY ID TUMOR-NECROSIS-FACTOR; CALCIUM-CHANNEL BLOCKER; HEPATIC MACROPHAGES; PLASMA ENDOTOXIN; RAT-LIVER; ETHANOL; DISEASE; ENHANCEMENT; NISOLDIPINE; CIRRHOSIS AB Kupffer cells have been implicated in mechanisms of pathophysiology following liver transplantation. Recently, postoperative injury in ethanol-induced fatty liver has been evaluated because fatty livers often fail following transplantation. The low-flow, reflow liver perfusion model was used to study the role of Kupffer cells (KC) in reperfusion injury to fatty livers from rats fed a diet containing ethanol for 4-5 weeks. Treatment with GdCl3, which selectively destroys KC, decreased cell death significantly. Thus, destruction of KC minimized hepatic reperfusion injury, most likely by inhibiting free radical formation and improving microcirculation. Since it was demonstrated recently that destruction of KC prevented the hypermetabolic state observed with acute alcohol exposure, their involvement in events leading to alcohol-induced liver disease was investigated. In rats exposed to ethanol continuously via intragastric feeding for up to 4 weeks, GdCl3 treatment prevented elevation of aspartate aminotransferase (AST) and dramatically reduced the average hepatic pathological score. These results indicate that KC participate in the early phases of alcohol-induced liver injury. Endotoxaemia occurs in alcoholics and activates KC; therefore, we evaluated the effect of minimizing bacterial endotoxin by intestinal sterilization with the antibiotics polymyxin B and neomycin. Antibiotics diminished plasma endotoxin levels significantly and prevented ethanol-induced increases in AST values. These results indicate that endotoxin is involved in the mechanism of ethanol-induced liver injury. A six-line radical spectrum was detected with electron paramagnetic resonance spectroscopy in bile from alcohol-treated rats which was blocked by GdCl3. The free radical adducts had hyperfine coupling constants characteristic of lipid-derived free radical products. In conclusion, these studies demonstrate that KC are involved in reperfusion injury to ethanol-induced fatty livers and hepatic injury due to long-term treatment with ethanol. C1 UNIV N CAROLINA,CURRICULUM TOXICOL,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT ANAT & CELL BIOL,CHAPEL HILL,NC 27599. NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RP THURMAN, RG (reprint author), UNIV N CAROLINA,DEPT PHARMACOL,HEPATOBIOL & TOXICOL LAB,CB 7365,FLOB,CHAPEL HILL,NC 27599, USA. FU NIAAA NIH HHS [AA-03624, AA-09156]; NIDDK NIH HHS [DK-37034] NR 42 TC 16 Z9 17 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL AUSTR PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON 3053, AUSTRALIA SN 0815-9319 J9 J GASTROEN HEPATOL JI J. Gastroenterol. Hepatol. PY 1995 VL 10 SU 1 BP S24 EP S30 DI 10.1111/j.1440-1746.1995.tb01791.x PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA TD185 UT WOS:A1995TD18500006 PM 8589336 ER PT J AU AUERBACH, JD FIGERT, AE AF AUERBACH, JD FIGERT, AE TI WOMENS HEALTH RESEARCH - PUBLIC-POLICY AND SOCIOLOGY SO JOURNAL OF HEALTH AND SOCIAL BEHAVIOR LA English DT Review ID SEX-DIFFERENCES; GENDER DIFFERENCES; MARITAL-STATUS; MENTAL-HEALTH; MEDICALIZATION; MENOPAUSE; MORTALITY; IDENTITY; DISTRESS; ILLNESS AB In the space of just a few years, the amount and nature of scientific research on women's health has emerged as a major policy issue being addressed at the highest levels of the federal government and in the mainstream media. This debate has engaged members of Congress, the National Institutes of Health, and other federal agencies, and medical, scientific, health, and women's organizations. Sociologists have made significant contributions to both the process by which the women's health research issue has ascended to public awareness and the content of its agenda. Many of these contributions go unrecognized and other potential contributions by medical sociologists remain unrealized. In order to advance both science and practice in women's health-by ensuring the inclusion of the sociological perspective-we encourage sociologists to participate more directly in the policy debates. C1 LOYOLA UNIV, CHICAGO, IL 60611 USA. RP AUERBACH, JD (reprint author), NIH, OFF AIDS RES, BLDG 31, ROOM 4C06, BETHESDA, MD 20892 USA. NR 112 TC 4 Z9 5 U1 0 U2 0 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0022-1465 EI 2150-6000 J9 J HEALTH SOC BEHAV JI J. Health Soc. Behav. PY 1995 VL 35 SI SI BP 115 EP 131 DI 10.2307/2626960 PG 17 WC Public, Environmental & Occupational Health; Psychology, Social SC Public, Environmental & Occupational Health; Psychology GA RR555 UT WOS:A1995RR55500008 ER PT J AU DIBISCEGLIE, AM AF DIBISCEGLIE, AM TI LONG-TERM OUTCOME OF INTERFERON-ALPHA THERAPY FOR CHRONIC HEPATITIS-B SO JOURNAL OF HEPATOLOGY LA English DT Article; Proceedings Paper CT VI International Symposium on Viral Hepatitis CY FEB 03-05, 1994 CL MADRID, SPAIN DE HEPATITIS B; TREATMENT; PROGNOSIS ID CONTROLLED TRIAL AB Interferon-alpha therapy has a beneficial effect. in 30-40% of selected patients with chronic hepatitis B who respond by clearing hepatitis B e antigen (HBeAg) and hepatitis B viral (HBV) DNA from serum. This is usually associated with normalization of serum aminotransferase activities. On long-term follow-up of treated patients, it is apparent that many go on to clear hepatitis B surface antigen (HBsAg) from serum with considerable improvement in liver histopathology. Among patients with clinically apparent chronic HBV infection such as those with decompensated cirrhosis or the nephrotic syndrome, a serologic response is usually followed by slow but steady clinical and biochemical improvement. However, even among patients who have cleared HBsAg from serum, HBV-DNA remains detectable within the liver and may provide a source of reactivation in rare patients in association with immunosuppression. (C) Journal of Hepatology. C1 NIDDKD,DIGEST DIS BRANCH,LIVER DIS SECT,BETHESDA,MD 20892. NR 12 TC 15 Z9 15 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0169-5185 J9 J HEPATOL JI J. Hepatol. PY 1995 VL 22 SU 1 BP 65 EP 67 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QP392 UT WOS:A1995QP39200012 PM 7602080 ER PT J AU GIARDINA, SL ANDERSON, SK SAYERS, TJ CHAMBERS, WH PALUMBO, GA YOUNG, HA ORTALDO, JR AF GIARDINA, SL ANDERSON, SK SAYERS, TJ CHAMBERS, WH PALUMBO, GA YOUNG, HA ORTALDO, JR TI SELECTIVE LOSS OF NK CYTOTOXICITY IN ANTISENSE NK-TR1 RAT LGL CELL-LINES - ABROGATION OF ANTIBODY-INDEPENDENT TUMOR AND VIRUS-INFECTED TARGET-CELL KILLING SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NATURAL-KILLER-CELLS; MONOCLONAL-ANTIBODY; TYROSINE PHOSPHORYLATION; LYMPHOCYTES-T; MOLECULE; ANTIGEN; ACTIVATION; PURIFICATION; RECOGNITION; SPECIFICITY AB We have shown that NK-TR1, a protein containing a cyclophilin-like domain, is associated with a receptor/ triggering molecule on the surface of human large granular lymphocytes (1). In the present study, we have further defined the role of NK-TR1 in target cell recognition/killing by generating antisense NK-TR1 transfectants in the rat LGL cell line, RNK-16. Stable transfectants were identified by analyzing permeabilized cells with the anti-NK-TR1 mAb, 4F9. Transfectants with low levels of 4F9 staining showed drastically reduced levels of killing against three NK-susceptible target cell lines. Lytic activity against vaccinia virus-infected cell lines also was dramatically reduced. In contrast, transfected cells showing normal levels of NK-TR1 expression demonstrated normal killing of all target cells. The ability of all transfectants to form conjugates was identical to that observed with the wild-type RNK cell line. Lectin-dependent cytotoxicity, reverse ADCC via NKR-PI, and ADCC-mediated killing were comparable in both high or low NK-TR1 expressing clones, demonstrating that the lytic machinery was still intact. BLT-esterase activity, PF levels, and surface marker phenotype were not significantly affected. These results provide strong evidence that NK-TR1 is an essential element in a signaling pathway leading to MHC unrestricted killing of tumor and virus-infected cells. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. UNIV PITTSBURGH,PITTSBURGH CANC INST,PITTSBURGH,PA 15213. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. RP GIARDINA, SL (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702, USA. RI Anderson, Stephen/B-1727-2012; Sayers, Thomas/G-4859-2015 OI Anderson, Stephen/0000-0002-7856-4266; NR 32 TC 18 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 JAN 1 PY 1995 VL 154 IS 1 BP 80 EP 87 PG 8 WC Immunology SC Immunology GA PY218 UT WOS:A1995PY21800009 PM 7995961 ER PT J AU SELVEY, LA MORSE, HC JUNE, CH HODES, RJ AF SELVEY, LA MORSE, HC JUNE, CH HODES, RJ TI ANALYSIS OF ANTIGEN RECEPTOR SIGNALING IN B-CELLS FROM MICE WITH A RETROVIRUS-INDUCED ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PROTEIN-TYROSINE KINASES; LYMPHOCYTE-B; MEMBRANE IMMUNOGLOBULIN; CROSS-LINKING; MOLECULAR-COMPONENTS; C57BL/6 MICE; SRC-FAMILY; T-CELLS; PHOSPHORYLATION; ACTIVATION AB MAIDS is a retrovirus-induced immunodeficiency syndrome in mice that has similarities to human AIDS. Because the functional defects in B cells from retroviral immunodeficiency syndromes have not been characterized in detail, we examined early and late parameters of B cell responses to IgM cross-linking in B cells from MAIDS and normal mice. Splenic B cells from mice with MAIDS have defective in vitro proliferative responses to LPS and anti-IgM-mediated stimuli, as well as to PMA plus calcium ionophore, indicating a generalized defect in proliferative response potential independent of specific receptor-mediated signaling. When early signaling parameters were analyzed in response to IgM cross-linking, it was found that calcium flux in B cells from MAIDS mice was significantly reduced; this reduction was not accounted for by quantitative differences in cell-surface IgM expression and therefore indicates a defect in early signal transduction through the IgM receptor. The tyrosine phosphorylation response to IgM cross-linking was also markedly deficient; tyrosine phosphorylation of Ig-alpha, Ig-beta, and an undefined protein of 80 kDa was detected in MAIDS B cells after anti-IgM stimulation, at levels substantially less than those observed in normal B cells. Multiple other tyrosine phosphorylation events observed in normal B cells, including phosphorylation of GTPase-activating protein, PI3-kinase, and syk kinase, were not detected in MAIDS B cells in response to IgM cross-linking. The defect in tyrosine phosphorylation seemed to correlate with reduced surface IgM levels on a subpopulation of MAIDS B cells. B cells from mice expressing the MAIDS retrovirus-induced immunodeficiency thus reflect defects in early signaling through the Ag-specific IgM receptor as well as a generalized defect in proliferative responsiveness. C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20889. NIA,BETHESDA,MD 20892. RI Selvey, Linda/B-8473-2017; OI Selvey, Linda/0000-0001-8493-0974; Morse, Herbert/0000-0002-9331-3705 NR 37 TC 10 Z9 10 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1995 VL 154 IS 1 BP 171 EP 179 PG 9 WC Immunology SC Immunology GA PY218 UT WOS:A1995PY21800018 PM 7995937 ER PT J AU SIDNEY, J DELGUERCIO, MF SOUTHWOOD, S ENGELHARD, VH APPELLA, E RAMMENSEE, HG FALK, K ROTZSCHKE, O TAKIGUCHI, M KUBO, RT GREY, HM SETTE, A AF SIDNEY, J DELGUERCIO, MF SOUTHWOOD, S ENGELHARD, VH APPELLA, E RAMMENSEE, HG FALK, K ROTZSCHKE, O TAKIGUCHI, M KUBO, RT GREY, HM SETTE, A TI SEVERAL HLA ALLELES SHARE OVERLAPPING PEPTIDE SPECIFICITIES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-I MOLECULES; TOXIC LYMPHOCYTES-T; IMMUNODEFICIENCY-VIRUS TYPE-1; SELF-PEPTIDES; MONOCLONAL-ANTIBODY; CELL RECOGNITION; VIRAL PEPTIDES; MHC MOLECULES; C MOLECULES AB Herein we describe the establishment of assays to measure peptide binding to purified HLA-B*0701, -B*0801, -B*2705, -B*3501-03, -B*5401, -Cw*0401,-Cw*0602, and -Cw*0702 molecules. The binding of known peptide epitopes or naturally processed peptides correlates well with HLA restriction or origin, underscoring the immunologic relevance of these assays. Analysis of the sequences of various HLA class I alleles suggested that alleles with peptide motifs characterized by proline in position 2 and aromatic or hydrophobic residues at their C-terminus shared key consensus residues at positions 9, 63, 66, 67, and 70 (B pocket) and residue 116 (F pocket). Prediction of the peptide-binding specificity of HLA-B*5401, on the basis of this consensus B and F pocket structure, verified this hypothesis and suggested that a relatively large family of HLA-B alleles (which we have defined as the HLA-B7-like supertype) may significantly overlap in peptide binding specificity. Availability of quantitative binding assays allowed verification that, indeed, many (25%) of the peptide ligands carrying proline in position 2 and hydrophobic/aromatic residues at the C-terminus (the B7-like supermotif) were capable of binding at least three of five HLA-B7-like supertype alleles. Identification of epitopes carrying the B7-like super motif and binding to a family of alleles represented in over 40% of individuals from all major ethnic groups may be of considerable use in the design of peptide vaccines. C1 CYTEL CORP,SAN DIEGO,CA 92121. UNIV VIRGINIA,CHARLOTTESVILLE,VA 22908. NCI,BETHESDA,MD 20892. GERMAN CANC RES CTR,W-6900 HEIDELBERG,GERMANY. HARVARD UNIV,CAMBRIDGE,MA 02138. UNIV TOKYO,TOKYO,JAPAN. RI Takiguchi, Masafumi/E-7468-2013 FU NIAID NIH HHS [AI18634, R37AI20963] NR 91 TC 159 Z9 161 U1 1 U2 7 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1995 VL 154 IS 1 BP 247 EP 259 PG 13 WC Immunology SC Immunology GA PY218 UT WOS:A1995PY21800026 PM 7527812 ER PT J AU GUSELLA, GL MUSSO, T ROTTSCHAFER, SE PULKKI, K VARESIO, L AF GUSELLA, GL MUSSO, T ROTTSCHAFER, SE PULKKI, K VARESIO, L TI POTENTIAL REQUIREMENT OF A FUNCTIONAL DOUBLE-STRANDED RNA-DEPENDENT PROTEIN-KINASE (PKR) FOR THE TUMORICIDAL ACTIVATION OF MACROPHAGES BY LIPOPOLYSACCHARIDE OR IFN-ALPHA-BETA, BUT NOT IFN-GAMMA SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INITIATION FACTOR-II; MESSENGER-RNA; TRANSLATIONAL CONTROL; MURINE MACROPHAGES; TRANSFECTED CELLS; MAMMALIAN-CELLS; SELECTIVE-INHIBITION; EIF-2-ALPHA KINASE; INTERFERON-BETA; P68 KINASE AB We analyzed the expression of the dsRNA-dependent protein kinase (PKR) during the activation of murine macrophages to the tumoricidal state by LPS and/or IFNs. LPS induced PKR expression in a dose-dependent manner at levels that were comparable with those observed in response to IFNs. By using the PKR inhibitor 2-aminopurine (2-AP), we have shown that the pathways of macrophage tumoricidal activation elicited by LPS and IFN-alpha beta, but not by IFN-gamma, included a 2-AP-sensitive step. In fact, LPS- and IFN-alpha beta-induced activation was inhibited by 2-AP, whereas the activation by IFN-gamma was not affected by the presence of the inhibitor. 2-AP did not affect the activation of protein kinase C or protein kinase A in intact cells. In the presence of 2-AP the up-regulation of IFN-beta mRNA by LPS was specifically inhibited, whereas the expression of glyceraldehyde-3-phosphate dehydrogenase mRNA or the induction of PKR remained unchanged, thereby demonstrating that 2-AP inhibited selective macrophage genes. The differential sensitivity to 2-AP suggested that the expression of a functional PKR may be required for the macrophage tumoricidal response triggered by LPS and IFN-alpha beta but not IFN-gamma. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. RP GUSELLA, GL (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,BLDG 560,FREDERICK,MD 21702, USA. RI varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 58 TC 47 Z9 47 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1995 VL 154 IS 1 BP 345 EP 354 PG 10 WC Immunology SC Immunology GA PY218 UT WOS:A1995PY21800036 PM 7995954 ER PT J AU DHAWAN, S WEEKS, BS SODERLAND, C SCHNAPER, HW TORO, LA ASTHANA, SP HEWLETT, IK STETLERSTEVENSON, WG YAMADA, SS YAMADA, KM MELTZER, MS AF DHAWAN, S WEEKS, BS SODERLAND, C SCHNAPER, HW TORO, LA ASTHANA, SP HEWLETT, IK STETLERSTEVENSON, WG YAMADA, SS YAMADA, KM MELTZER, MS TI HIV-1 INFECTION ALTERS MONOCYTE INTERACTIONS WITH HUMAN MICROVASCULAR ENDOTHELIAL-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS DEMENTIA COMPLEX; TISSUE INHIBITOR; IV COLLAGENASE; MONONUCLEAR PHAGOCYTES; EXTRACELLULAR-MATRIX; ADHESION MOLECULE-1; RHEUMATOID SYNOVIUM; TNF-ALPHA; MACROPHAGES AB HIV infection of monocytes resulted in a twofold elevation of adhesion molecule LFA-1 (both alpha(L)/CD11a and beta(2)/CD18 subunits) and LFA-3 (CD58), with no apparent increase in LFA-2 (CD2) or various beta(1)-integrins. Homotypic aggregation of monocytes was evident 2 h after exposure to virus and was inhibited by mAbs to both the alpha(L)- and beta(2)-subunits of LFA-1. HIV-infected monocytes also showed a marked increase in adherence to human capillary endothelial cell monolayers derived from brain, lung, and skin. This adherence was inhibited by mAb to either LFA-1 subunit and by mAb to the counter-receptor intercellular adhesion molecule-1. Cocultivation of HIV-infected monocytes with endothelial cells increased permeability of endothelial cell monolayers to I-125 albumin in transwell assay systems. The increased endothelial permeability induced by HIV-infected monocytes was associated with a substantial disruption of the endothelial cell monolayer. Morphologic disruption was not a direct toxic effect on endothelial cells, but appeared to be secondary to changes in endothelial cell-cell or cell-matrix interactions. Northern blot analysis showed increased expression of gelatinase B (92-kDa gelatinase), tissue inhibitor of metalloproteinase TIMP-1, and TIMP-2 in the HIV-infected monocytes. Consistent with these Northern analyses, secretion of gelatinase activity in culture fluids of HIV-infected monocytes was also increased and was dependent on the stage of virus replication. Incubation of HIV-infected monocytes with the proteinase inhibitors TIMP-1 and TIMP-2 inhibited the increased permeability of endothelial cell monolayers to I-125 albumin. These results suggest possible mechanisms for extravasation of HIV-infected monocytes through vascular endothelium into tissue in early stages of HIV disease. C1 APPL CELL BIOL RES INST,KIRKLAND,WA 98034,AUSTRALIA. HAMILTON COLL,DEPT BIOL,CLINTON,NY 13323. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. WALTER REED ARMY INST RES,DEPT CELLULAR IMMUNOL,WASHINGTON,DC 20307. RP DHAWAN, S (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV TRANSFUS TRANSMITTED DIS HFM310,1401 ROCKVILLE PIKE,ROCKVILLE,MD 20852, USA. RI Stetler-Stevenson, William/H-6956-2012; OI Stetler-Stevenson, William/0000-0002-5500-5808; Yamada, Kenneth/0000-0003-1512-6805 NR 49 TC 100 Z9 100 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1995 VL 154 IS 1 BP 422 EP 432 PG 11 WC Immunology SC Immunology GA PY218 UT WOS:A1995PY21800043 PM 7527819 ER PT J AU ALEXANDER, RB FITZGERALD, EB MIXON, A CARTER, CS JAKOBSEN, M COHEN, PA ROSENBERG, SA AF ALEXANDER, RB FITZGERALD, EB MIXON, A CARTER, CS JAKOBSEN, M COHEN, PA ROSENBERG, SA TI HELPER T-CELLS INFILTRATING HUMAN RENAL-CELL CARCINOMAS HAVE THE PHENOTYPE OF ACTIVATED MEMORY-LIKE T-LYMPHOCYTES SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE RENAL CARCINOMA CELLS; CD4(+) T CELLS; SURFACE MARKERS; PHENOTYPE; T-LYMPHOCYTES ID SIGNAL TRANSDUCTION; PERIPHERAL-BLOOD; HUMAN MELANOMAS; TUMOR; INTERLEUKIN-2; EXPRESSION; PROFILES; CD4+; MOLECULES; LYSIS AB Human renal cell carcinomas are characterized by an inflammatory infiltrate containing many T lymphocytes. Attempts to grow T cells from such tumors by culture in interleukin (IL)-2 have yielded heterogeneous populations of cells with functional characteristics typical of lymphokine-activated killer cells obtained by similar culture of cells from peripheral blood mononuclear cells. We examined a panel of surface markers expressed on T lymphocytes to determine if the CD4(+) T cells infiltrating human renal cell carcinomas are different from those in peripheral blood mononuclear cells. By flow cytometry analysis the CD4(+) T cells in a panel of freshly digested human renal cell carcinoma primary and metastatic tumors expressed the activation markers CD69 and HLA-DR and manifested an increase in CD45RO and a reciprocal decrease in CD45RA expression as compared with peripheral blood CD4(+) T cells. This suggests that CD4(+) T cells infiltrating renal cell carcinomas are activated and have encountered antigen. However, the expression of the IL-2R a chain (CD25) was not different in tumor-infiltrating CD4(+) T cells and peripheral blood CD4(+) T cells, suggesting that T cells infiltrating human renal cell carcinomas may have a block in proliferative capacity. The general failure of cultured tumor-infiltrating lymphocyte (TIL) from renal cell carcinoma to demonstrate tumor-specific reactivity may be due to the failure of such cells to grow in IL-2. C1 NCI,SURG BRANCH,BETHESDA,MD 20892. NIH,CTR CLIN,DEPT TRANSFUS MED,BETHESDA,MD 20892. NR 30 TC 17 Z9 17 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1995 VL 17 IS 1 BP 39 EP 46 DI 10.1097/00002371-199501000-00005 PG 8 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA QG223 UT WOS:A1995QG22300005 PM 7728304 ER PT J AU ANDERSON, LJ HEILMAN, CA AF ANDERSON, LJ HEILMAN, CA TI PROTECTIVE AND DISEASE-ENHANCING IMMUNE-RESPONSES TO RESPIRATORY SYNCYTIAL VIRUS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID ANTIGENIC SUBGROUP-A; PULMONARY PATHOLOGY; COTTON RATS; MATERNAL ANTIBODY; YOUNG-CHILDREN; RSV CHALLENGE; BALB/C MICE; N-PROTEINS; T-CELLS; INFECTION AB The National Institutes of Health, Centers for Disease Control and Prevention, and World Health Organization jointly sponsored a workshop on protective and disease-enhancing immune responses to respiratory syncytial virus (RSV). The primary purpose of the meeting was to discuss protective and disease-enhancing immune responses to RSV in the context of opportunities and barriers to the development of RSV vaccines. Although both live attenuated and subunit vaccines have been developed, it is not yet clear if any of these vaccines will be safe and effective. The fact that neither the disease-enhancing nor the protective immune response to RSV is well understood or well characterized is an important barrier to development of these vaccines. Studies in animal model systems and newly developed immunologic tools, however, provide hope that these barriers can be overcome and a safe and effective RSV vaccine can be developed. C1 NIAID,DIV MICROBIOL & INFECT DIS,BETHESDA,MD. RP ANDERSON, LJ (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV VIRAL & RICKETTSIAL DIS,ROOM 144,MAILSTOP G17,ATLANTA,GA 30333, USA. NR 51 TC 66 Z9 69 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1995 VL 171 IS 1 BP 1 EP 7 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA PZ873 UT WOS:A1995PZ87300001 PM 7798649 ER PT J AU LANG, DR GUERRANT, RL AF LANG, DR GUERRANT, RL TI SUMMARY OF THE 29TH UNITED-STATES-JAPAN JOINT CONFERENCE ON CHOLERA AND RELATED DIARRHEAL DISEASES SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID TOXIN-COREGULATED PILI; VIBRIO-CHOLERAE; ESCHERICHIA-COLI; ENTEROTOXIN; MUTANTS; INVITRO; INVIVO C1 UNIV VIRGINIA,DIV GEOG MED,CHARLOTTESVILLE,VA. RP LANG, DR (reprint author), NIAID,DIV MICROBIOL & INFECT DIS,ENTER DIS BRANCH,SOLAR BLDG,ROOM 3A21,6003 EXEC BLVD,BETHESDA,MD 20892, USA. NR 16 TC 5 Z9 5 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1995 VL 171 IS 1 BP 8 EP 12 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA PZ873 UT WOS:A1995PZ87300002 PM 7798685 ER PT J AU KUHNS, DB ALVORD, WG GALLIN, JI AF KUHNS, DB ALVORD, WG GALLIN, JI TI INCREASED CIRCULATING CYTOKINES, CYTOKINE ANTAGONISTS, AND E-SELECTIN AFTER INTRAVENOUS ADMINISTRATION OF ENDOTOXIN IN HUMANS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID TUMOR-NECROSIS-FACTOR; NEUTROPHIL-SPECIFIC GRANULES; INFLAMMATORY RESPONSE; SOLUBLE RECEPTORS; BINDING-PROTEIN; INTERLEUKIN-1; RELEASE; PLASMA; SERUM; LACTOFERRIN AB Intravenous administration of endotoxin into humans causes transient fever, alteration in the number of circulating neutrophils, and transient release into plasma of cytokines, cytokine antagonists, and other cellular products. The release can be temporally differentiated, and the extent of release is dose-dependent. By 1 h after endotoxin challenge, levels of tumor necrosis factor (TNF)-alpha and soluble TNF receptor increase; interleukin (IL)-6 and IL-8 increase by 1.5 h, and IL-1 receptor antagonist, granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor, and lactoferrin increase by 2 h. Increased G-CSF is temporally associated with neutrophilia and the appearance of band neutrophils. Increased plasma lactoferrin and altered neutrophil surface antigen expression suggest that intravascular activation of neutrophils has occurred. The level of soluble E-selectin (sE-sel), an adhesion molecule released from endothelial cells, is elevated at 4 h and remains elevated at 24 h. sE-sel levels increase with higher doses of endotoxin at 4, 6, and 24 h. C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. PRI DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD. DATA MANAGEMENT SERV,FREDERICK,MD. NR 35 TC 125 Z9 125 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1995 VL 171 IS 1 BP 145 EP 152 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA PZ873 UT WOS:A1995PZ87300021 PM 7528250 ER PT J AU BOPPANA, SB POLIS, MA KRAMER, AA BRITT, WJ KOENIG, S AF BOPPANA, SB POLIS, MA KRAMER, AA BRITT, WJ KOENIG, S TI VIRUS-SPECIFIC ANTIBODY-RESPONSES TO HUMAN CYTOMEGALOVIRUS (HCMV) IN HUMAN-IMMUNODEFICIENCY-VIRUS TYPE 1-INFECTED PERSONS WITH HCMV RETINITIS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID MONOCLONAL-ANTIBODIES; NEWBORN-INFANTS; AIDS; DISEASE; INFECTIONS AB Human cytomegalovirus (HCMV) causes retinitis and is the leading cause of blindness in patients infected with the human immunodeficiency virus (HIV). While most patients with HIV are HCMV seropositive, not all will develop clinical complications from it. The immune responses that can prevent the development of HCMV retinitis are unknown. The levels of anti-HCMV antibodies, including responses to the two major envelope proteins, gpUL55 (gB) and gpUL75 (gH), which are the targets of neutralizing antibody (NA), were examined in HIV-infected patients with and without retinitis. No specific deficiency in the antibody response of retinitis patients was observed. However, higher levels of NA were associated with a more favorable clinical course. These results indicate that antibodies may modulate progression of disease, and they suggest a possible role for the exogenous administration of NA in patients who develop HCMV retinitis. C1 MEDIMMUNE INC,GAITHERSBURG,MD 20878. UNIV ALABAMA,DEPT PEDIAT,DIV INFECT DIS,BIRMINGHAM,AL. NIAID,IMMUNOREGULAT LAB,GAITHERSBURG,MD. OI Polis, Michael/0000-0002-9151-2268 FU NIAID NIH HHS [AI-30105]; NIDCD NIH HHS [DC-00079] NR 15 TC 40 Z9 40 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1995 VL 171 IS 1 BP 182 EP 185 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA PZ873 UT WOS:A1995PZ87300026 PM 7798660 ER PT J AU SCHNEIDER, JA CLARK, KF GREENE, AA REISCH, JS MARKELLO, TC GAHL, WA THOENE, JG NOONAN, PK BERRY, KA AF SCHNEIDER, JA CLARK, KF GREENE, AA REISCH, JS MARKELLO, TC GAHL, WA THOENE, JG NOONAN, PK BERRY, KA TI RECENT ADVANCES IN THE TREATMENT OF CYSTINOSIS SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article; Proceedings Paper CT 32nd Annual Symposium of the SSIEM CY SEP 06-09, 1994 CL EDINBURGH, SCOTLAND SP SSIEM ID NEPHROPATHIC CYSTINOSIS; RENAL-FUNCTION; CYSTEAMINE; CHILDREN; PHOSPHOCYSTEAMINE; DEPLETION; THERAPY AB Cysteamine bitartrate capsules (Cystagon) have been approved by the US Food and Drug Administration for use in patients with nephropathic cystinosis. Plasma cysteamine concentrations were virtually identical at various times following ingestion of either cysteamine hydrochloride or Cystagon capsules in 24 normal control subjects. A transfer study was done with eight cystinosis patients who had been receiving either cysteamine hydrochloride or phosphocysteamine for many years. The plasma cysteamine concentration was significantly higher 2h after Cystagon and the leukocyte cystine content was significantly lower at all times after Cystagon compared to older forms of the drug. These differences are probably the result of greater patient compliance in taking the capsules compared to the older, liquid forms of the drug. A new method for following the course of renal, glomerular deterioration in diseases such as cystinosis has been published recently. This method was used to re-analyse data on the efficacy of cysteamine treatment and to re-analyse new data on treating cystinosis patients with either of two doses of cysteamine (1.30g/m(2) per day and 1.95 g/m(2) per day). This new method agrees well with other methods and shows that both doses of drug are equally effective in maintaining glomerular function. C1 UNIV TEXAS,SW MED CTR,DALLAS,TX 75235. NICHHD,BETHESDA,MD. UNIV MICHIGAN,ANN ARBOR,MI 48109. MYLAN PHARMACEUT INC,MORGANTOWN,WV. RP SCHNEIDER, JA (reprint author), UNIV CALIF SAN DIEGO,DEPT PEDIAT,DIV PEDIAT METAB,9500 GILMAN DR DEPT 0609 F,LA JOLLA,CA 92093, USA. FU NCRR NIH HHS [M01-RR-00042, M01-RR-00827]; NICHD NIH HHS [HD-6-2927] NR 19 TC 36 Z9 36 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1995 VL 18 IS 4 BP 387 EP 397 DI 10.1007/BF00710051 PG 11 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA RR958 UT WOS:A1995RR95800004 PM 7494398 ER PT J AU ESPINOZADELGADO, I BOSCO, MC MUSSO, T GUSELLA, GL LONGO, DL VARESIO, L AF ESPINOZADELGADO, I BOSCO, MC MUSSO, T GUSELLA, GL LONGO, DL VARESIO, L TI INTERLEUKIN-2 AND HUMAN MONOCYTE ACTIVATION SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Review ID TUMOR-NECROSIS-FACTOR; PERIPHERAL-BLOOD MONOCYTES; COLONY-STIMULATING FACTOR; GROWTH FACTOR-BETA; RECEPTOR GAMMA-CHAIN; NEUTROPHIL CHEMOTACTIC FACTOR; FACTOR-ALPHA PRODUCTION; PROTO-ONCOGENE PRODUCT; NATURAL-KILLER-CELLS; HUMAN LYMPHOCYTES-T C1 DIV CANC TREATMENT,CLIN ONCOL PROGRAM,MED BRANCH,BETHESDA,MD. PROGRAM RESOURCES INC DYNCORP,FCRDC,BIOL CARCINOGENESIS DEV PROGRAM,FREDERICK,MD. NCI,DIV CANC TREATMENT,BRMP,FREDERICK,MD 21701. RP ESPINOZADELGADO, I (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,EXPTL IMMUNOL LAB,FREDERICK,MD 21702, USA. RI Bosco, Maria Carla/J-7928-2016; varesio, luigi/J-8261-2016 OI Bosco, Maria Carla/0000-0003-1857-7193; varesio, luigi/0000-0001-5659-2218 NR 128 TC 68 Z9 70 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD JAN PY 1995 VL 57 IS 1 BP 13 EP 19 PG 7 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA QC581 UT WOS:A1995QC58100003 PM 7829965 ER PT J AU SHEFFLER, LA WINK, DA MELILLO, G COX, GW AF SHEFFLER, LA WINK, DA MELILLO, G COX, GW TI CHARACTERIZATION OF NITRIC OXIDE-STIMULATED ADP-RIBOSYLATION OF VARIOUS PROTEINS FROM THE MOUSE MACROPHAGE CELL-LINE ANA-1 USING SODIUM-NITROPRUSSIDE AND THE NOVEL NITRIC-OXIDE DONATING COMPOUND DIETHYLAMINE DINITRIC OXIDE SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE INTERFERON-GAMMA; LIPOPOLYSACCHARIDE; PERTUSSIS TOXIN; CHOLERA TOXIN; NITRIC OXIDE SYNTHASE; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE ID GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; L-ARGININE; VASCULAR ENDOTHELIUM; NEOPLASTIC-CELLS; INHIBITION; SYNTHASE; RELEASE; RIBOSYLTRANSFERASE; CEREBELLUM; EXPRESSION AB We examined the ability of nitric oxide (NO) to stimulate the ADP-ribosylation of proteins from the mouse macrophage cell line ANA-1. To demonstrate a specific effect of NO, we used a novel compound named diethylamine dinitric oxide (DEA/NO; 1,1-diethyl-2-hydroxy-2-nitrosohydrazine, sodium salt; [Et(2)NN(O)NO]Na), which releases NO in aqueous solution at neutral pH. DEA/NO stimulated the ADP-ribosylation of at least three cytosolic proteins (M(r) = 28,000, 33,000, and 39,000) from ANA-1 macrophages. The effect of DEA/NO on the ADP-ribosylation of the predominant target p39 was dose dependent(EC(50) = 80 mu M). Moreover, the effect of DEA/NO was attributed specifically to released NO rather than diethylamine or nitrite. Sodium nitroprusside (SNP) also stimulated the ADP-ribosylation of cytosolic proteins from ANA-1 mouse macrophages. However, SNP exhibited different time- and dose-dependent effects on the modification of p39. NO synthesized via the act activity of interferon-gamma plus lipopolysaccharide-induced NO synthase also enhanced the ADP-ribosylation of p39, confirming that the effects of DEA/NO and SNP could be attributed to NO or reactive nitrogen oxide species. Neither pertussis toxin nor cholera toxin stimulated the ADP-ribosylation of p39; however, cholera toxin stimulated the ADP-ribosylation of proteins with approximate molecular weights of 28,000 and 33,000. These data suggest that the induced expression of NO synthase in tumoricidal macrophages may be associated with autocrine and paracrine effects of NO that include the ADP-ribosylation of various proteins. Moreover, these results indicate that DEA/NO and related compounds may be useful as pharmacologic tools for investigating the-effects of NO and reactive nitrogen oxide species on macrophages. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC ETIOL,COMPARAT CARCINOGENESIS LAB,CHEM SECT,FREDERICK,MD 21702. NR 47 TC 13 Z9 13 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD JAN PY 1995 VL 57 IS 1 BP 152 EP 159 PG 8 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA QC581 UT WOS:A1995QC58100021 PM 7530278 ER PT J AU DU, QH ZHANG, TY ITO, Y AF DU, QH ZHANG, TY ITO, Y TI PURIFICATION OF 25-HYDROXY-CHOLECALCIFEROL FROM IRRADIATION OF CHOLESTA-5,7-DIOL BY HIGH-SPEED COUNTERCURRENT CHROMATOGRAPHY SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article AB High-speed countercurrent chromatography (HSCCC) was used for the separation of 25-hydroxycholecalciferol (25-HCC) from a post-irradiation mixture of cholesta-5,7-diene-3 beta,25-diol. With a two-phase solvent system composed of hexane/ethyl acetate/methanol/water (5:1:5:1, v/v/v/v), 500 mg of reaction mixture containing 245 mg of 25-HCC was separated with 207 mg of the product obtained at a purity of 97.7%. The separation was completed within 2 hours. C1 BEIJING INST NEW TECHNOL APPLICAT,BEIJING 100035,PEOPLES R CHINA. NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. RP DU, QH (reprint author), CHINESE ACAD AGR SCI,TEA RES INST,HANGZHOU 310008,PEOPLES R CHINA. NR 6 TC 2 Z9 2 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1995 VL 18 IS 1 BP 181 EP 188 DI 10.1080/10826079508009230 PG 8 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QD412 UT WOS:A1995QD41200014 ER PT J AU ISSAQ, HJ AF ISSAQ, HJ TI THE INTERNATIONAL-CONGRESS ON NATURAL-PRODUCTS RESEARCH - HALIFAX, NOVA-SCOTIA, CANADA, JULY 31 AUGUST 4, 1994 SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Editorial Material RP ISSAQ, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1995 VL 18 IS 1 BP 207 EP 208 PG 2 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QD412 UT WOS:A1995QD41200016 ER PT J AU ROTH, JS KELLEY, JA AF ROTH, JS KELLEY, JA TI DETERMINATION OF THE ANTI-HIV DRUG 2'-BETA-FLUORO-2',3'-DIDEOXYADENOSINE IN BIOLOGICAL-FLUIDS BY REVERSED-PHASE HPLC SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; IMMUNODEFICIENCY-VIRUS INFECTION; ANTIRETROVIRAL AGENT; HUMAN PLASMA; HTLV-III; 2',3'-DIDEOXYINOSINE; 2',3'-DIDEOXYADENOSINE; BRAIN; PHARMACOKINETICS; DIDANOSINE AB 2'-beta-Fluoro-2',3'-dideoxyadenosine (F-ddA) is a synthetic dideoxynucleoside analogue that has been designed to overcome the acid stability problems of the anti-AIDS drug didanosine. F-ddA is also a clinical candidate and will be tested in AIDS patients upon completion of its preclinical evaluation. We have developed a straightforward reversed-phase HPLC method to measure both F-ddA and its deaminated metabolite, 2'-beta-fluoro-2',3'-dideoxyinosine, in plasma and urine. This method employs an adenosine deaminase inhibitor to prevent sample degradation, an internal standard far quantitation, and C-18 solid-phase extraction to isolate and concentrate the fluorinated dideoxynucleosides. Gradient HPLC analysis on a reversed-phase phenyl column with UV detection at 260 nm gives a limit of quantitation of 50 ng/ml (0.2 mu M) for both analytes. This assay has been applied to preclinical studies in rats and monkeys to determine drug stability, disposition, metabolism and plasma kinetics. RP ROTH, JS (reprint author), NCI,MED CHEM LAB,DEV THERAPEUT PROGRAM,BLDG 37,ROOM 5C-02,BETHESDA,MD 20892, USA. NR 30 TC 5 Z9 5 U1 2 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1995 VL 18 IS 3 BP 441 EP 462 DI 10.1080/10826079508009249 PG 22 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QE327 UT WOS:A1995QE32700002 ER PT J AU ISSAQ, HJ AF ISSAQ, HJ TI 16TH INTERNATIONAL-SYMPOSIUM ON CAPILLARY CHROMATOGRAPHY SEPTEMBER 27-30, 1994 RIVA-DEL-GARDA, ITALY SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Editorial Material RP ISSAQ, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1995 VL 18 IS 5 BP 1035 EP 1036 PG 2 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QN492 UT WOS:A1995QN49200016 ER PT J AU ISSAQ, HJ CHAN, KC MUSCHIK, GM JANINI, GM AF ISSAQ, HJ CHAN, KC MUSCHIK, GM JANINI, GM TI APPLICATIONS OF CAPILLARY ZONE ELECTROPHORESIS AND MICELLAR ELECTROKINETIC CHROMATOGRAPHY IN CANCER-RESEARCH SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; TAXUS-BREVIFOLIA; PHASE-II; TAXOL; SEPARATION; VARIABILITY; CAFFEINE; ACIDS; URINE; DRUG AB The purpose of this communication is to illustrate the utility and advantages of capillary zone electrophoresis and micellar electrokinetic chromatography in cancer research. In our laboratory, both techniques have been used to explore many aspects of cancer research from the search for biological markers in urine, serum and tissue, to epidemiological studies, to the exploration of anti-cancer drugs in plant materials and marine organisms. Both CE and MEKC have proven to be useful in solving problems which faced us. We present a series of examples which illustrates the application of these techniques to problems faced by our laboratory. RP ISSAQ, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,POB B,FREDERICK,MD 21702, USA. NR 33 TC 13 Z9 13 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1995 VL 18 IS 7 BP 1273 EP 1288 DI 10.1080/10826079508010413 PG 16 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QU841 UT WOS:A1995QU84100003 ER PT J AU DU, QZ XIONG, XP ITO, Y AF DU, QZ XIONG, XP ITO, Y TI SEPARATION OF BIOACTIVE QUADRI-TERPENIC ACIDS FROM THE FRUIT OF LIGUSTRUM-LUCIDUM AIT BY HIGH-SPEED COUNTERCURRENT CHROMATOGRAPHY SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article AB High-speed countercurrent chromatography (HSCCC) was used for the separation of quadri-terpenic acids from the fruit of Ligustrum lucidum Ait using a two-phase solvent system composed of hexane/ethyl acetate/methanol/water (3:6:2:1, v/v). From 250mg of the crude extract, the method yielded 87 mg of oleanolic acid at 91.5% purity and 58 mg of ursolic acid at 93.2% purity in about 2.5 h. C1 NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. RP DU, QZ (reprint author), CHINESE ACAD AGR SCI,TEA RES INST,HANGZHOU 310008,PEOPLES R CHINA. NR 8 TC 8 Z9 9 U1 1 U2 3 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1995 VL 18 IS 10 BP 1997 EP 2004 DI 10.1080/10826079508013955 PG 8 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA RD540 UT WOS:A1995RD54000007 ER PT J AU JANINI, GM FISHER, RJ HENDERSON, LE ISSAQ, HJ AF JANINI, GM FISHER, RJ HENDERSON, LE ISSAQ, HJ TI APPLICATION OF CAPILLARY ZONE ELECTROPHORESIS FOR THE ANALYSIS OF PROTEINS, PROTEIN-SMALL MOLECULES, AND PROTEIN-DNA INTERACTIONS SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; AMYLOID-P COMPONENT; SILICA CAPILLARIES; BINDING; SEPARATION; PEPTIDES; BUFFERS; PRECONCENTRATION AB Capillary electrophoresis with a polyacrylamide-coated capillary was used for the separation of proteins, and the study of protein-small molecule and protein-DNA interactions. The coating (10% T polyacrylamide) is of sufficient thickness and hydrophilicity to reduce protein adsorption and eliminate electroosmotic flow. Data on the effect of sample solvent constituents on the peak shape and position of protein solutes was investigated. The results show that CE is a relevant and fast technique for the study of protein-DNA and protein-drug interaction. Also, the addition of TRIS-buffer to the sample solution resulted in the CE focusing of some basic proteins, while others were not affected. RP JANINI, GM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,POB B,FREDERICK,MD 21702, USA. RI Fisher, Robert/B-1431-2009 NR 22 TC 17 Z9 17 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1995 VL 18 IS 18-19 BP 3617 EP 3628 DI 10.1080/10826079508014614 PG 12 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA TJ400 UT WOS:A1995TJ40000006 ER PT J AU ISSAQ, HJ AF ISSAQ, HJ TI DEDICATED TO PROFESSOR HJERTEN,STELLAN SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Item About an Individual RP ISSAQ, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1995 VL 18 IS 18-19 BP R11 EP R14 PG 4 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA TJ400 UT WOS:A1995TJ40000001 ER PT J AU KUSZEWSKI, J QIN, J GRONENBORN, AM CLORE, GM AF KUSZEWSKI, J QIN, J GRONENBORN, AM CLORE, GM TI THE IMPACT OF DIRECT REFINEMENT AGAINST C-13(ALPHA) AND C-13(BETA) CHEMICAL-SHIFTS ON PROTEIN-STRUCTURE DETERMINATION BY NMR SO JOURNAL OF MAGNETIC RESONANCE SERIES B LA English DT Note ID SECONDARY; DYNAMICS C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 12 TC 187 Z9 189 U1 0 U2 7 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 1064-1866 J9 J MAGN RESON SER B JI J. Magn. Reson. Ser. B PD JAN PY 1995 VL 106 IS 1 BP 92 EP 96 DI 10.1006/jmrb.1995.1017 PG 5 WC Physics, Atomic, Molecular & Chemical SC Physics GA QE359 UT WOS:A1995QE35900017 PM 7850178 ER PT J AU BAER, SM RINZEL, J CARRILLO, H AF BAER, SM RINZEL, J CARRILLO, H TI ANALYSIS OF AN AUTONOMOUS PHASE MODEL FOR NEURONAL PARABOLIC BURSTING SO JOURNAL OF MATHEMATICAL BIOLOGY LA English DT Article DE EXCITABLE MEMBRANE; BURSTING OSCILLATIONS; NEURONAL MODELING ID SINGULAR HOPF-BIFURCATION; RELAXATION OSCILLATIONS; DYNAMICS AB An understanding of the nonlinear dynamics of bursting is fundamental in unraveling structure-function relations in nerve and secretory tissue. Bursting is characterized by alternations between phases of rapid spiking and slowly varying potential. A simple phase model is developed to study endogenous parabolic bursting, a class of burst activity observed experimentally in excitable membrane. The phase model is motivated by Rinzel and Lee's dissection of a model for neuronal parabolic bursting (J. Math. Biol. 25, 653-675 (1987)). Rapid spiking is represented canonically by a one-variable phase equation that is coupled bi-directionally to a two-variable slow system, The model is analyzed in the slow-variable phase plane? using quasi steady-state assumptions and formal averaging, We derive a reduced system to explore where the full model exhibits bursting, steady-states, continuous and modulated spiking. The relative speed of activation and inactivation of the slow variables strongly influences the burst pattern as well as other dynamics. We find conditions of the bistability of solutions between continuous spiking and bursting. Although the phase model is simple, we demonstrate that it captures many dynamical features of more complex biophysical models. C1 NIDDK,MATH RES BRANCH,BETHESDA,MD 20892. NATL AUTONOMOUS UNIV MEXICO,FAC CIENCIAS,DINAM NO LINEAL LAB,MEXICO CITY 04510,DF,MEXICO. RP BAER, SM (reprint author), ARIZONA STATE UNIV,DEPT MATH,TEMPE,AZ 85287, USA. RI Carrillo Calvet, Humberto/E-2265-2012 OI Carrillo Calvet, Humberto/0000-0003-3659-6769 NR 33 TC 25 Z9 25 U1 1 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0303-6812 J9 J MATH BIOL JI J. Mathemat. Biol. PD JAN PY 1995 VL 33 IS 3 BP 309 EP 333 PG 25 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA QE418 UT WOS:A1995QE41800006 PM 7897331 ER PT J AU SHARP, TW HYAMS, KC WATTS, D TROFA, AF MARTIN, GJ KAPIKIAN, AZ GREEN, KY JIANG, X ESTES, MK WAACK, M SAVARINO, SJ AF SHARP, TW HYAMS, KC WATTS, D TROFA, AF MARTIN, GJ KAPIKIAN, AZ GREEN, KY JIANG, X ESTES, MK WAACK, M SAVARINO, SJ TI EPIDEMIOLOGY OF NORWALK VIRUS DURING AN OUTBREAK OF ACUTE GASTROENTERITIS ABOARD A US-AIRCRAFT-CARRIER SO JOURNAL OF MEDICAL VIROLOGY LA English DT Article DE TRANSMISSION; CROWDING; ENTERIC INFECTION ID INFECTIOUS NONBACTERIAL GASTROENTERITIS; VOLUNTEERS; CHALLENGE; ANTIBODY; DISEASE AB A large outbreak of acute gastroenteritis occurred over a 5-week period aboard an aircraft carrier. The estimated cumulative attack rate was 13% among the 4,500-man crew. Eight percent of the crew sought medical attention, nearly all of whom missed 1 day or more of work. The risk of developing illness was 2 to 3 times greater for individuals living in more crowded sleeping quarters (>50 persons per compartment). Occurrence of gastroenteritis was associated with a fourfold or more rise in Norwalk virus antibody levels, as measured by an enzyme-linked immunoassay utilizing a baculovirus expressed recombinant antigen. In addition, 27 nm Norwalk virus-like particles were visualized in two of six stools examined by immune electron microscopy. The presence of a low (<1:50) or a high (greater than or equal to 1:6,400) pre-illness antibody level was associated with a lower incidence of illness. This investigation indicates that Norwalk virus can adversely impact operations of a military vessel and that crowding is a major risk factor in transmission. (C) 1995 Wiley-Liss, Inc. C1 USN, ENVIRONM & PREVENT MED UNIT 7, NAPLES, 20889, ITALY. USN, INST MED RES, BETHESDA, MD USA. NATL NAVAL MED CTR, BETHESDA, MD 20307 USA. NIH, INFECT DIS LAB, BETHESDA, MD 77030 USA. WALTER REED ARMY MED CTR, WALTER REED ARMY INST RES, WASHINGTON, DC USA. BAYLOR COLL MED, DIV MOLEC VIROL, HOUSTON, TX USA. USN, INST AEROSP & OPERAT MED, PENSACOLA, FL USA. FU NIAID NIH HHS [AI 30448] NR 22 TC 46 Z9 50 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 0146-6615 J9 J MED VIROL JI J. Med. Virol. PD JAN PY 1995 VL 45 IS 1 BP 61 EP 67 DI 10.1002/jmv.1890450112 PG 7 WC Virology SC Virology GA QJ606 UT WOS:A1995QJ60600011 PM 7714493 ER PT J AU ROJAS, E STOKES, CL MEARS, D ATWATER, I AF ROJAS, E STOKES, CL MEARS, D ATWATER, I TI SINGLE-MICROELECTRODE VOLTAGE-CLAMP MEASUREMENTS OF PANCREATIC BETA-CELL MEMBRANE IONIC CURRENTS IN-SITU SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE ISLET OF LANGERHANS; K+ CURRENTS; CA2+ CURRENTS; L-TYPE CA2+ CHANNEL; GLUCOSE; BICARBONATE ID BURSTING ELECTRICAL-ACTIVITY; ACTIVATED K+ CHANNELS; B-CELLS; POTASSIUM CHANNEL; CALCIUM-CHANNEL; MOUSE ISLETS; EXTERNAL TETRAETHYLAMMONIUM; INSULIN RELEASE; GLUCOSE; LANGERHANS AB A conventional patch clamp amplifier was used to test the feasibility of measuring whole-cell ionic currents under voltage clamp conditions from beta-cells in intact mouse islets of Langerhans perifused with bicarbonate Krebs buffer at 37 degrees C. Cells impaled with a high resistance microelectrode (ca. 0.150 G Ohm) were identified as beta-cells by the characteristic burst pattern of electrical activity induced by 11 mM glucose. Voltage-dependent outward K+ currents were enhanced by glucose both in the presence and absence of physiological bicarbonate buffer and also by bicarbonate regardless of the presence or absence of glucose. For comparison with the usual patch clamp protocol, similar measurements were made from single rat beta-cells at room temperature; glucose did not enhance the outward currents in these cells. Voltage-dependent inward currents were recorded in the presence of tetraethylammonium (TEA), an effective blocker of the K+ channels known to be present in the beta-cell membrane. Inward currents exhibited a fast component with activation-inactivation kinetics and a delayed component with a rather slow inactivation; inward currents were dependent on Ca2+ in the extracellular solution. These results suggest the presence of either two types of voltage-gated Ca2+ channels or a single type with fast and slow inactivation. We conclude that it is feasible to use a single intracellular microelectrode to measure voltage-gated membrane currents in the beta-cell within the intact islet at 37 degrees C, under conditions that support normal glucose-induced insulin secretion and that glucose enhances an as yet unidentified voltage-dependent outward K+ current. C1 NIDDK,MATH RES BRANCH,BETHESDA,MD 20893. RP ROJAS, E (reprint author), NIDDK,CELL BIOL & GENET LAB,BETHESDA,MD 20893, USA. NR 53 TC 9 Z9 9 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 JAN PY 1995 VL 143 IS 1 BP 65 EP 77 PG 13 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA QB174 UT WOS:A1995QB17400006 PM 7714889 ER PT J AU SHERMAN, A XU, L STOKES, CL AF SHERMAN, A XU, L STOKES, CL TI ESTIMATING AND ELIMINATING JUNCTIONAL CURRENT IN COUPLED CELL-POPULATIONS BY LEAK SUBTRACTION - A COMPUTATIONAL STUDY SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE PANCREATIC BETA-CELL; ISLET OF LANGERHANS; VOLTAGE CLAMP; GAP JUNCTIONS; ELECTROTONIC COUPLING ID PANCREATIC BETA-CELLS; B-CELLS; MOUSE; CALCIUM; INACTIVATION; CHANNELS; ISLETS AB The quantitative characterization of ion channel properties in pancreatic beta-cells under typical patch clamp conditions can be questioned because of the unreconciled differences in experimental conditions and observed behavior between microelectrode recordings of membrane potential in intact islets of Langerhans and patch recordings of single cells. Complex bursting is reliably observed in islets but not in isolated cells under patch clamp conditions. E. Rojas et al. (J. Membrane Biol. 143:65-77, 1995) have attempted to circumvent these incompatibilities by measuring currents in beta-cells in intact islets by voltage-clamping with intracellular microelectrodes (150-250 M Omega tip resistance). The major potential pitfall is that beta-cells within the islet are electrically coupled, and contaminating coupling currents must be subtracted from current measurements, just as linear leak currents are typically subtracted. To characterize the conditions under which such coupling current subtraction is valid, we have conducted a computational study of a model islet. Assuming that the impaled cell is well clamped, we calculate the native and coupling components of the observed current. Our simulations illustrate that coupling can be reliably subtracted when neighbor cells' potentials are constant or vary only slowly (e.g., during their silent phases) but not when they vary rapidly (e.g., during their active phases). We also show how to estimate coupling conductances in the intact islet from measurements of coupling currents. C1 UNIV HOUSTON,DEPT CHEM ENGN,HOUSTON,TX 77204. NIH,BETHESDA,MD 20892. NR 19 TC 14 Z9 14 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 JAN PY 1995 VL 143 IS 1 BP 79 EP 87 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA QB174 UT WOS:A1995QB17400007 PM 7714890 ER PT J AU BLANDINO, JKW VIGLIONE, MP BRADLEY, WA OIE, HK KIM, YI AF BLANDINO, JKW VIGLIONE, MP BRADLEY, WA OIE, HK KIM, YI TI VOLTAGE-DEPENDENT SODIUM-CHANNELS IN HUMAN SMALL-CELL LUNG-CANCER CELLS - ROLE IN ACTION-POTENTIALS AND INHIBITION BY LAMBERT-EATON SYNDROME IGG SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE SMALL-CELL LUNG CANCER CELLS; VOLTAGE-GATED SODIUM CHANNELS; ACTION POTENTIALS; LAMBERT-EATON SYNDROME; PARANEOPLASTIC NEUROLOGICAL DISORDERS ID PATCH-CLAMP TECHNIQUE; CALCIUM CHANNELS; MYASTHENIC SYNDROME; CHROMAFFIN CELLS; ION CHANNELS; NA+ CHANNELS; LINE; CARCINOMA; CURRENTS; MUSCLE AB Sodium channels of human small-cell lung cancer (SCLC) cells were examined with whole-cell and single-channel patch clamp methods. In the tumor cells from SCLC cell line NCI-H146, the majority of the voltage-gated Na+ channels are only weakly tetrodotoxin (TTX)-sensitive (K-d = 215 nm). With the membrane potential maintained at -60 to -80 mV, these cells produced all-or-nothing action potentials in response to depolarizing current injection (>20 pA). Similar all-or-nothing spikes were also observed with anodal break excitation. Removal of external Ca2+ did not affect the action potential production, whereas 5 mu M TTX or substitution of Na+ with choline abolished it. Action potentials elicited in the Ca2+-free condition were reversibly blocked by 4 mM MnCl2 due to the Mn2+-induced inhibition of voltage-dependent sodium currents (I-Na). Therefore, Na+ channels, not Ca2+ channels, underlie the excitability of SCLC cells. Whole-cell I-Na was maximal with step-depolarizing stimulations to 0 mV, and reversed at +45.2 mV, in accord with the predicted Nernst equilibrium potential for a Na+-selective channel. I-Na evoked by depolarizing test potentials (-60 to +40 mV) exhibited a transient time course and activation/ inactivation kinetics typical of neuronal excitable membranes; the plot of the Hodgkin-Huxley parameters, m(infinity) and h(infinity), also revealed biophysical similarity between SCLC and neuronal Na+ channels. The single channel current amplitude, as measured with the inside-out patch configuration, was 1.0 pA at -20 mV with a slope conductance of 12.1 pS. The autoantibodies implicated in the Lambert-Eaton myasthenic syndrome (LES), which are known to inhibit I-Ca and I-Na in bovine adrenal chromaffin cells, also significantly inhibited I-Na in SCLC cells. These results indicate that (i) action potentials in human SCLC cells result from the regenerative increase in voltage-gated Na+ channel conductance; (ii) fundamental characteristics of SCLC Na+ channels are the same as the classical sodium channels found in a variety of excitable cells; and (iii) in some LES patients, SCLC Na+ channels are an additional target of the pathological IgG present in the patients' sera. C1 UNIV VIRGINIA,SCH MED,DEPT BIOMED ENGN,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,SCH MED,DEPT NEUROSCI,CHARLOTTESVILLE,VA 22908. NCI,NAVAL HOSP,NAVY MED ONCOL BRANCH,BETHESDA,MD 20892. UNIV VIRGINIA,SCH MED,DEPT NEUROL,CHARLOTTESVILLE,VA 22908. FU NINDS NIH HHS [NS18607] NR 38 TC 35 Z9 35 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD JAN PY 1995 VL 143 IS 2 BP 153 EP 163 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA QD009 UT WOS:A1995QD00900007 PM 7731034 ER PT J AU SUN, SQ SHI, SL HUNT, JA LEAPMAN, RD AF SUN, SQ SHI, SL HUNT, JA LEAPMAN, RD TI QUANTITATIVE WATER MAPPING OF CRYOSECTIONED CELLS BY ELECTRON-ENERGY-LOSS SPECTROSCOPY SO JOURNAL OF MICROSCOPY-OXFORD LA English DT Article DE WATER CONTENT; VITREOUS ICE; VALENCE ELECTRON EXCITATIONS; ELECTRON ENERGY-LOSS SPECTROSCOPY; PARALLEL EELS; SCANNING TRANSMISSION ELECTRON MICROSCOPY; HEPATOCYTES ID MICROSCOPY; SPECIMENS; SPECTROMETER; SECTIONS; LIVER AB A direct technique based on electron energy-loss spectroscopy (EELS) in the scanning transmission electron microscope (STEM) has been developed to map subcellular distributions of water in frozen-hydrated biological cryosections. Previously, methods for water determination have been indirect in that they have required the cryosections to be dehydrated first. The new approach makes use of spectrum-imaging, where EELS data are collected in parallel at each pixel. Several operations are required to process the spectra including: subtraction of the detector dark current, deconvolution by the detector point-spread function, removal of plural inelastic scattering and correction for the support film, The resulting single scattering distributions are fitted to standard reference spectra at each pixel, and water content can be determined from the fitting coefficients. Although the darkfield or brightfield image from a hydrated cryosection shows minimal structure, the processed EELS image reveals strong contrast due to variations in water content. Reference spectra have been recorded from the major biomolecules (protein, lipid, carbohydrate, nucleic acid) as well as from vitrified water and crystalline ice. It has been found that quantitative results can be obtained for the majority of subcellular compartments by fitting only water and protein reference spectra, and the accuracy of the method for these compartments has been estimated as +/- 3.5%. With the present instrumentation the maximum allowed dose of 2 x 10(3) e/nm(2) limits the useful spatial resolution to around 80 nm for +/- 5% precision at a single pixel. By averaging pixel intensities a value of 56.8% with a precision of +/- 2 0% has been determined for the water content of liver mitochondria. The water mapping technique may prove useful for applications to cell physiology and pathophysiology. C1 NIH,NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. GATAN RES & DEV INC,PLEASANTON,CA 94588. NR 48 TC 34 Z9 34 U1 0 U2 11 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0022-2720 J9 J MICROSC-OXFORD JI J. Microsc.-Oxf. PD JAN PY 1995 VL 177 BP 18 EP 30 PN 1 PG 13 WC Microscopy SC Microscopy GA QH316 UT WOS:A1995QH31600003 PM 7897645 ER PT J AU YAMAMOTO, A WENTHOLD, RJ ZHANG, J HERMAN, EH FERRANS, VJ AF YAMAMOTO, A WENTHOLD, RJ ZHANG, J HERMAN, EH FERRANS, VJ TI IMMUNOFLUORESCENCE TECHNIQUES FOR THE IDENTIFICATION OF IMMUNE EFFECTOR-CELLS IN RAT-HEART - APPLICATIONS TO THE STUDY OF THE MYOCARDITIS INDUCED BY INTERLEUKIN-2 SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE INTERLEUKIN-2; MYOCARDITIS; IMMUNOFLUORESCENCE; DENDRITIC CELLS; LYMPHOCYTES; LAK CELLS; MACROPHAGES ID INTERSTITIAL DENDRITIC CELLS; TNF-ALPHA; CLASS-II; LYMPHOCYTES; EXPRESSION; ANTIGENS; MACROPHAGES; ANTIBODIES; ACTIVATION; INFARCTION AB A detailed description is presented of immunohistochemical methods for identification of various types of immune effector cells in rat heart, involving the use of antibodies conjugated with different fluorochromes for the simultaneous demonstration of 2 or 3 different antigens by means of fluorescence microscopy. The initial results of the application of these techniques to the study of the myocarditis induced by interleukin-2 (IL-2) are also presented. Antibodies used included: OX6 antibody (for MHC class II molecules, mainly expressed by dendritic cells); W3/25 and OX8 antibody, for the demonstration of the rat equivalents of CD5 and CD8, respectively; asialo-GM(1), ganglioside antibody for the identification of natural killer (NK) cells and lymphokine activated killer (LAK) cells, and ED2 antibody for labeling of macrophages. Fluorochromes used were: fluorescein isothiocyanate (green), tetramethylrhodamine isothiocyanate (red), Texas red sulfonyl chloride (red), and 7-amino-4-methylcoumarin-3-acetic acid (blue), IL-2-induced myocarditis was characterized histologically by infiltration of the myocardium by mononuclear inflammatory cells, microvascular alteration, interstitial edema, and myocyte damage and necrosis, In the initial stages, Ng/LAK cells were the predominant type of infiltrating lymphocytes; however, the numbers of these cells decreased sharply in subsequent stages, Macrophages also were initially abundant, and continued to be prevalent throughout the late stages. CD8(+) lymphocytes were more numerous than CD4(+) lymphocytes. Dendritic cells showed a diffuse increase in number and also accumulated around foci of myocyte necrosis. Three phenotypes of dendritic cells were recognized, and the possible implications of these findings are dicussed. It is hoped that these techniques will prove useful for the immunohistochemical evaluation of various inflammatory diseases of the heart. C1 NHLBI, PATHOL BRANCH, ULTRASTRUCT SECT, BETHESDA, MD 20892 USA. US FDA, CTR DRUG EVALUAT & RES, DIV RES & TESTING, LAUREL, MD USA. NR 28 TC 5 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD JAN PY 1995 VL 27 IS 1 BP 307 EP 319 DI 10.1016/S0022-2828(08)80029-6 PG 13 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA QK489 UT WOS:A1995QK48900028 PM 7539083 ER PT J AU MCCUNE, SK HILL, JM AF MCCUNE, SK HILL, JM TI ONTOGENIC EXPRESSION OF 2 ALPHA-1-ADRENERGIC RECEPTOR SUBTYPES IN THE RAT-BRAIN SO JOURNAL OF MOLECULAR NEUROSCIENCE LA English DT Article DE IN SITU HYBRIDIZATION; CNS DEVELOPMENT; G-PROTEIN COUPLED RECEPTORS; CATECHOLAMINE RECEPTORS ID ALPHA-2-ADRENERGIC RECEPTOR; MOLECULAR-CLONING; ALPHA-1-ADRENERGIC RECEPTOR; MESSENGER-RNAS; CDNA; GENE; NORADRENALINE AB alpha-1A/D and alpha-1B adrenergic receptor subtype mRNA expression was studied during pre- and postnatal rat brain development. Oligonucleotide probes were generated to distinguish these two homologous subtypes by in situ histochemical analysis in E14, E16, E19, P0, P8, P14, P21, and adult animals. alpha-1B adrenergic receptor mRNA expression was noted as early as the E14 animal and demonstrated specific regional and temporal expression. alpha-1A/D adrenergic receptor mRNA expression was limited in the E19 and P0 animal but increased in intensity with aging. Specific regional and temporal expression differed between the two subtypes. The regional localization for both subtypes appeared to be stable after P21 but the intensity of expression for both subtypes decreased between P21 and adulthood, which is a finding that correlates with previous ligand-binding data. Different subtypes of homologous receptors have very different ontogenic patterns of distribution and may account for previous discrepancies in ligand-binding data and differential tissue responses to various ligands during development. C1 NICHHD,DEV NEUROBIOL LAB,DEV & MOLEC PHARMACOL SECT,BETHESDA,MD 20892. RP MCCUNE, SK (reprint author), JOHNS HOPKINS UNIV HOSP,DEPT PEDIAT,DIV NEONATOL,BALTIMORE,MD 21205, USA. NR 36 TC 5 Z9 6 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07012 SN 0895-8696 J9 J MOL NEUROSCI JI J. Mol. Neurosci. PY 1995 VL 6 IS 1 BP 51 EP 62 DI 10.1007/BF02736759 PG 12 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA TA741 UT WOS:A1995TA74100006 PM 8562320 ER PT J AU Schafer, MKH Weihe, E Erickson, JD Eiden, LE AF Schafer, MKH Weihe, E Erickson, JD Eiden, LE TI Human and monkey cholinergic neurons visualized in paraffin-embedded tissues by immunoreactivity for VAChT, the vesicular acetylcholine transporter SO JOURNAL OF MOLECULAR NEUROSCIENCE LA English DT Article DE basal forebrain; rhesus monkey; ventral horn; vesicular acetylcholine transporter; cholinergic neurons; cerebral cortex; human ID SENILE DEMENTIA; ACETYLTRANSFERASE; INNERVATION; HISTOCHEMISTRY; ORGANIZATION; BRAIN AB The predicted C-terminal dodecapeptide of the human vesicular acetylcholine transporter (VAChT), deduced from the unique open reading frame of the recently cloned human VAChT cDNA, was conjugated through an N-terminal cysteine to keyhole limpet hemocyanin and used as an immunogen to generate polyclonal antihuman VAChT antibodies in rabbits. The distribution of the VAChT antigen in representative regions of the cholinergic nervous system was examined and compared to that of the acetylcholine biosynthetic enzyme choline acetyltransferase (ChAT), a specific marker for cholinergic neurons. VAChT immunoreactivity was localized in cell bodies of neurons in the basal forebrain and ventral horn of the spinal cord, regions in which major cholinergic projection systems to the cerebral cortex and to skeletal muscle, respectively, originate. The primate caudate nucleus contained numerous VAChT-positive interneurons. VAChT immunoreactivity was visualized in both cell bodies and extensive terminals in striatal interneurons, in contrast to formalin-fixed, deparaffinized sections stained for ChAT, in which cell bodies and fibers were stained but nerve terminals were less well visualized than with the VAChT antiserum. VAChT-positive nerve fibers were visualized in routinely immersion-fixed, paraffin-embedded human cerebral cortex, comparable to the density of fibers observed in perfusion-fixed Bouin's-postfixed monkey cerebral cortex. Extensive investment of virtually all principal ganglion cells of thoracic sympathetic ganglia of monkey and human with VAChT-positive nerve terminals was observed. VAChT-positive cell bodies, presumably corresponding to cholinergic sympathetic sudomotor neurons, were a significant fraction of the total principal cell population in monkey and human thoracic sympathetic ganglia. VAChT is a specific marker for cholinergic neurons in human and rhesus monkey, visualizing especially nerve terminals more extensively than antibodies against the cholinergic biosynthetic enzyme ChAT, in routinely fixed tissue. VAChT immunoreactivity in cholinergic nerve terminals of the central and peripheral nervous systems ought to prove useful for visualizing cholinergic synapses and neuroeffector junctions, and their functional status during development and in neurodegenerative and autonomic disease. C1 NIMH,MOLEC NEUROSCI SECT,CELL BIOL LAB,NIH,BETHESDA,MD 20892. UNIV MARBURG,DEPT ANAT & CELL BIOL,W-3550 MARBURG,GERMANY. OI Eiden, Lee/0000-0001-7524-944X NR 34 TC 65 Z9 66 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0895-8696 J9 J MOL NEUROSCI JI J. Mol. Neurosci. PY 1995 VL 6 IS 4 BP 225 EP 235 DI 10.1007/BF02736782 PG 11 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA UJ947 UT WOS:A1995UJ94700001 PM 8860234 ER PT J AU Erickson, JD Eiden, LE Schafer, MKH Weihe, E AF Erickson, JD Eiden, LE Schafer, MKH Weihe, E TI Reserpine- and tetrabenazine-sensitive transport of H-3-histamine by the neuronal isoform of the vesicular monoamine transporter SO JOURNAL OF MOLECULAR NEUROSCIENCE LA English DT Article DE vesicular monoamine transporter isoforms; VMAT1; VMAT2; histamine; reserpine; tetrabenazine; posterior hypothalamus; tuberomammillary nucleus; mast cells ID RAT-BRAIN; HISTAMINE SYNTHESIS; MOUSE-BRAIN; ALPHA-FLUOROMETHYLHISTIDINE; IN-VIVO; RELEASE; CELLS; HYPOTHALAMUS; SLICES; 5-HYDROXYTRYPTAMINE AB The transport of H-3-histamine by the endocrine-specific (VMAT1) and neuronal (VMAT2) isoforms of the vesicular monoamine transporter has been evaluated in digitonin-permeabilized fibroblasts transfected with either VMAT1 or VMAT2. Transport of H-3-histamine by both VMAT1 and VMAT2 was reserpine-sensitive but only transport by VMAT2 was inhibited by tetrabenazine. Maximal equilibrated levels of H-3-histamine accumulation by VMAT2 (K-m similar to 300 mu M) were approximately three times greater than that mediated by VMAT1 when using a subsaturating concentration of exogenous H-3-histamine (50 mu M). The expression of VMAT2 in histaminergic neurons in the rat brain was examined with polyclonal antipeptide antibodies specific for VMAT1 or VMAT2. VMAT2-positive and tyrosine hydroxylase-negative immunoreactive cell bodies were localized to the ventral part of the posterior hypothalamus in the region of the mamillary nuclei. The transport properties of VMAT2 and the distribution of VMAT2 in cell bodies in the tuberomammillary nucleus of the posterior hypothalamus reported here and the apparent absence of VMAT1 and VMAT2 in tissue mast cells support previous findings of reserpine-sensitive and reserpine-resistant pools of histamine in brain and peripheral tissues. C1 UNIV MARBURG,DEPT ANAT & CELL BIOL,W-3550 MARBURG,GERMANY. RP Erickson, JD (reprint author), NIMH,MOLEC NEUROSCI SECT,CELL BIOL LAB,NIH,BETHESDA,MD 20892, USA. NR 46 TC 26 Z9 26 U1 4 U2 4 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0895-8696 J9 J MOL NEUROSCI JI J. Mol. Neurosci. PY 1995 VL 6 IS 4 BP 277 EP 287 DI 10.1007/BF02736786 PG 11 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA UJ947 UT WOS:A1995UJ94700005 PM 8860238 ER PT J AU JAIN, P GARRAFFO, HM SPANDE, TF YEH, HJC DALY, JW AF JAIN, P GARRAFFO, HM SPANDE, TF YEH, HJC DALY, JW TI A NEW SUBCLASS OF ALKALOIDS FROM A DENDROBATID POISON FROG - A STRUCTURE FOR DEOXYPUMILIOTOXIN 251H SO JOURNAL OF NATURAL PRODUCTS-LLOYDIA LA English DT Article ID SKIN ALKALOIDS; PUMILIOTOXINS; MYOBATRACHIDAE; QUINOLIZIDINES; PYRROLIZIDINES; INDOLIZIDINES AB Deoxypumiliotoxin 251H [4], representing a new subclass of the pumiliotoxin-A class of alkaloids, has been isolated from a dendrobatid frog, Epipedobates tricolor. The structure, elucidated by nmr, gc-Ftir, and mass spectral analyses, is proposed to be an 8-methyl-6-(5-hydroxy-2-methylhexylidene)-1-azabicyclo[4.3.0]nonane. The absolute stereochemistry and the relative configuration of the hydroxyl group are unknown. C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NIDDKD,ANALYT CHEM LAB,BETHESDA,MD 20892. NR 11 TC 35 Z9 35 U1 1 U2 3 PU AMER SOC PHARMACOGNOSY PI CINCINNATI PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202 SN 0163-3864 J9 J NAT PRODUCTS JI J. Nat. Prod. PD JAN PY 1995 VL 58 IS 1 BP 100 EP 104 DI 10.1021/np50115a012 PG 5 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA QM442 UT WOS:A1995QM44200012 PM 7760066 ER PT J AU MONTOYA, ID HAERTZEN, C HESS, JM COVI, L FUDALA, PJ JOHNSON, RE GORELICK, DA AF MONTOYA, ID HAERTZEN, C HESS, JM COVI, L FUDALA, PJ JOHNSON, RE GORELICK, DA TI COMPARISON OF PSYCHOLOGICAL SYMPTOMS BETWEEN DRUG-ABUSERS SEEKING AND NOT SEEKING TREATMENT SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Note ID COCAINE ABUSERS; PSYCHOPATHOLOGY; ADDICTS C1 UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. RP MONTOYA, ID (reprint author), NIDA,INTRAMURAL RES PROGRAM,POB 5180,BALTIMORE,MD 21224, USA. FU Intramural NIH HHS [Z99 DA999999] NR 16 TC 5 Z9 6 U1 0 U2 2 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 JAN PY 1995 VL 183 IS 1 BP 50 EP 53 DI 10.1097/00005053-199501000-00011 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QB802 UT WOS:A1995QB80200010 PM 7807072 ER PT J AU MAURICE, T SU, TP PARISH, DW PRIVAT, A AF MAURICE, T SU, TP PARISH, DW PRIVAT, A TI PREVENTION OF NIMODIPINE-INDUCED IMPAIRMENT OF LEARNING BY THE SELECTIVE SIGMA-LIGAND PRE-084 SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Article DE SIGMA SITES; PRE-084; NIMODIPINE; CALCIUM CHANNELS; PASSIVE AVOIDANCE; ALTERNATION BEHAVIOR; WATER-MAZE; AMNESIA ID EXTRACELLULAR ACETYLCHOLINE LEVEL; INDUCED NEURONAL ACTIVATION; LONG-TERM POTENTIATION; RAT FRONTAL-CORTEX; CA-2+ CHANNELS; ANTIPSYCHOTIC-DRUGS; NEUROPEPTIDE-Y; BINDING-SITES; ION-TRANSPORT; RECEPTORS AB The high selectivity of the phencyclidine derivative PRE-084 for sigma (sigma) sites is demonstrated. We previously reported that this compound is able to markedly attenuate the impairment of learning induced in mice by the non-competitive NMDA antagonist MK-801, and the cholinergic nicotinic antagonist mecamylamine. In this study, we examined the effect of PRE-084 on the impairment of learning induced by acute administration of the calcium channel antagonist nimodipine. Nimodipine (0.3 mg/kg i.p.) impaired the spontaneous alternation behaviour in a Y-maze, decreased the step-down latency (SDL) in a passive avoidance task, and altered place learning and retention in a water-maze paradigm, with no marked effect on the motility observed using an open-field test. Preadministration of PRE-084 resulted in an attenuation of the impairment of alternation, in the 0.3-1 mg/kg s.c. range, in a marked increase in SDL, at 1-3 mg/kg, and improved place learning and retention in the water-maze, at 1 mg/kg. The effects on alternation behaviour and passive avoidance were completely prevented by co-administration of the purported sigma antagonist BMY-14802 (10 mg/kg i.p.), implicating the sigma sites. These results confirm the beneficial effect of the sigma ligand PRE-084 on pharmacological models of learning impairments, and indicate that sigma sites may modulate Ca2+ fluxes through VDCC, which may in turn bear some as yet unknown relationship to the previously described interaction with neurotransmitter systems. C1 NIDA,INTRAMURAL RES PROGRAM,BALTIMORE,MD. MOLEC SIMULAT INC,SUNNYVALE,CA. RP MAURICE, T (reprint author), ECOLE NATL SUPER CHIM MONTPELLIER,INSERM,U336,8 RUE ECOLE NORMALE,F-34053 MONTPELLIER 1,FRANCE. NR 39 TC 23 Z9 25 U1 2 U2 4 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1995 VL 102 IS 1 BP 1 EP 18 DI 10.1007/BF01276561 PG 18 WC Neurosciences SC Neurosciences & Neurology GA RZ789 UT WOS:A1995RZ78900001 PM 8785020 ER PT J AU WOLF, SS HYDE, TM SAUNDERS, RC HERMAN, MM WEINBERGER, DR KLEINMAN, JE AF WOLF, SS HYDE, TM SAUNDERS, RC HERMAN, MM WEINBERGER, DR KLEINMAN, JE TI AUTORADIOGRAPHIC CHARACTERIZATION OF NEUROTENSIN RECEPTORS IN THE ENTORHINAL CORTEX OF SCHIZOPHRENIC-PATIENTS AND CONTROL SUBJECTS SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Article DE AUTORADIOGRAPHY; NEUROTENSIN; SCHIZOPHRENIA ID HUMAN-BRAIN; BINDING-SITES; HIPPOCAMPAL-FORMATION; BASAL GANGLIA; RAT-BRAIN; ALZHEIMERS-DISEASE; SUBSTANTIA NIGRA; RHESUS-MONKEY; ACETYLCHOLINESTERASE; EXPRESSION AB Neurotensin, an endogenous peptide and putative neurotransmitter, exhibits a wide range of interactions with dopaminergic neurons and displays some actions akin to neuroleptics. Moreover, neurotensin receptors are abundant in specific layers of the entorhinal cortex where cytoarchitectural abnormalites have been reported in schizophrenia. We therefore examined the entorhinal cortex from postmortem specimens of five control patients and six schizophrenic patients for alterations in neurotensin receptor quantitation and distribution using receptor autoradiography. Specific I-125-neurotensin binding was concentrated in layer II cell clusters, with a 40% reduction in binding in the schizophrenic group (p < 0.05). Moderate binding was observed in both cohorts in deep layers V/VI, with negligible binding in the hippocampus. There was no statistical difference in quantitative neurotensin binding in other lamina of the entorhinal cortex of schizophrenics compared with controls. The characteristic laminar pattern of binding did not differ between cohorts. The reduction in neurotensin binding in schizophrenics is consistent with an increasing number of reports of structural abnormalities in the medial temporal lobe of schizophrenics in general and the entorhinal cortex in particular. Further studies are required to examine the evidence for neuroanatomic and neurochemical pathology in the entorhinal cortex. RP WOLF, SS (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,DIV INTRAMURAL RES PROGRAMS,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. NR 45 TC 33 Z9 33 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1995 VL 102 IS 1 BP 55 EP 65 DI 10.1007/BF01276565 PG 11 WC Neurosciences SC Neurosciences & Neurology GA RZ789 UT WOS:A1995RZ78900005 PM 8785024 ER PT J AU WU, RM MURPHY, DL CHIUEH, CC AF WU, RM MURPHY, DL CHIUEH, CC TI NEURONAL PROTECTIVE AND RESCUE EFFECTS OF DEPRENYL AGAINST MPP(+) DOPAMINERGIC TOXICITY SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Article DE DEPRENYL (SELEGILINE); MPTP; MPP(+); PARKINSONS DISEASE; DOPAMINE; SUBSTANTIA NIGRA; NIGROSTRIATAL NEURON ID HYDROXYL RADICAL GENERATION; PARKINSONS-DISEASE; SUBSTANTIA-NIGRA; PRIMATE MODEL; MPTP; STRESS; BRAIN; MPP+; MECHANISMS; SELEGILINE AB Intranigral infusion of 1-Methyl-4-phenylpyridinium ion (MPP(+), 2.1-16.8 nmol) dose-dependently injured nigral neurons as reflected by reduced dopamine levels in the ipsilateral striatum four days after the infusion of this toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Coadministration of deprenyl (4.2 nmol) with MPP(+) into the substantia nigra protected against MPP(+)-induced moderate (20-50%) but not severe (over 70%) nigral injury as reflected in striatal dopamine reductions. However, supplementary treatment with deprenyl (0.25 mg/kg, s.c., twice daily for 4 days) after intranigral infusion of MPP(+) significantly rescued nigral neurons from more severe damage caused by a higher MPP(+) does (8.4 nmol) manifested by a lesser striatal dopamine decrease (-31%) compared to the non-deprenyl treated group (-70%). Thus, in addition to the blockade of bioactivation of MPTP, deprenyl can protect and/or rescue nigral neurons from MPP(+)-induced dopaminergic neurotoxicity. These in vivo data add further evidence to suggest that deprenyl, a putative and clinically unproven neuroprotective agent, may be of value in slowing the progressive nigral degeneration in ''early'' Parkinson's disease, but may prove to be less so in its terminal stages. C1 NIMH,NIH CLIN CTR 103D41,CLIN SCI LAB,NEUROTOXICOL & NEUROPROT UNIT,BETHESDA,MD 20892. NIMH,NIH CLIN CTR 103D41,CLIN SCI LAB,CLIN NEUROPHARMACOL SECT,BETHESDA,MD 20892. NATL TAIWAN UNIV HOSP,DEPT NEUROL,TAIPEI,TAIWAN. OI Wu, Ruey-Meei/0000-0002-4947-5467 NR 45 TC 32 Z9 32 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1995 VL 100 IS 1 BP 53 EP 61 DI 10.1007/BF01276865 PG 9 WC Neurosciences SC Neurosciences & Neurology GA QV938 UT WOS:A1995QV93800005 PM 8748663 ER PT J AU Jellinger, K Linert, L Kienzl, E Herlinger, E Youdim, MBH AF Jellinger, K Linert, L Kienzl, E Herlinger, E Youdim, MBH TI Chemical evidence for 6-hydroxydopamine to be an endogenous toxic factor in the pathogenesis of Parkinson's disease SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Article ID IRON-MELANIN COMPLEX; SUBSTANTIA-NIGRA; OXIDATIVE STRESS; FREE-RADICALS; NEURONS; FERRITIN; BRAIN; HYPOTHESIS; ALUMINUM AB The presence of 5-Hydroxydopamine (5-OHDA) and 6-Hydroxydopamine (6-OHDA) in the urine of parkinsonian patients on levodopa medication was reported by Andrew et al. (1993). To answer the question about the putative relevance of 6-OHDA endogenously formed in the brain for the pathogenesis of Parkinson's disease (PD), the chemical mechanisms leading to dopamine-coordinative complexes were investigated in vitro. Kinetic studies of the reaction of dopamine (DA) with dioxygen over the pH range 7.0-9.0, where it reacts spontaneously without the necessity of metal-ion analysis, show that stoichiometric amounts of H2O2 are produced. Pink dopaminochrome, another oxidation product, is not stable and further reacts - without the consumption of dioxygen - to form the insoluble polymeric material known as melanin. Based on these results, the in vitro chemistry of the reactions of DA, 5-OHDA, and 6-OHDA in the presence of Fe3+ and dioxygen are studied. A mechanism for the initiation of a chain reaction is suggested by which excess Fe3+ could arise, and its relevance for the degeneration of dopaminergic neurons in PD is discussed. Detailed studies on the release of ferritin bound iron (0.2-1.4 mu M Fe3+) by synthetic DA (200 mu M) may provide further insight into the pathogenesis of PD,but further studies are warranted to elucidate the molecular basis of this neurodegenerative disorder of the extrapyramidal system. C1 TECH UNIV VIENNA, INST INORGAN CHEM, A-1060 VIENNA, AUSTRIA. FAC MED, DEPT PHARMACOL, HAIFA, ISRAEL. NIH, DEPT HLTH & HUMAN SERV, BETHESDA, MD 20892 USA. RP Jellinger, K (reprint author), LAINZ HOSP, LUDWIG BOLTZMANN INST CLIN NEUROBIOL, WOLKERSBERGENSTR 1, A-1130 VIENNA, AUSTRIA. NR 56 TC 74 Z9 74 U1 2 U2 4 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0303-6995 J9 J NEURAL TRANSM-SUPP JI J. Neural Transm.-Suppl. PY 1995 IS 46 BP 297 EP 314 PG 18 WC Neurosciences SC Neurosciences & Neurology GA TQ521 UT WOS:A1995TQ52100031 ER PT J AU HIESIGER, EM GREEN, SB SHAPIRO, WR BURGER, PC SELKER, RG MAHALEY, MS RANSOHOFF, J VANGILDER, JC MEALEY, J ROBERTSON, JT HOCHBERG, FH YOUNG, RF AF HIESIGER, EM GREEN, SB SHAPIRO, WR BURGER, PC SELKER, RG MAHALEY, MS RANSOHOFF, J VANGILDER, JC MEALEY, J ROBERTSON, JT HOCHBERG, FH YOUNG, RF TI RESULTS OF A RANDOMIZED TRIAL COMPARING INTRAARTERIAL CISPLATIN AND INTRAVENOUS PCNU FOR THE TREATMENT OF PRIMARY BRAIN-TUMORS IN ADULTS - BRAIN-TUMOR COOPERATIVE GROUP TRIAL 8420A SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE GLIOMA; INTRAARTERIAL CISPLATIN; PCNU; RANDOMIZED TRIAL ID MALIGNANT GLIOMA; POSTOPERATIVE TREATMENT; ANAPLASTIC GLIOMAS; RADIOTHERAPY; INTRAARTERIAL; CHEMOTHERAPY; BCNU; CIS-DIAMMINEDICHLOROPLATINUM(II); INFUSION; SURGERY AB Purpose: To test the efficacy of intra-arterial (IA) cisplatin versus intravenous (IV) PCNU for treating primary brain tumors, in a randomized trial (Brain Tumor Cooperative Group [BTCG] Trial 8420A). Methods: 311 adult patients (ages 19-79 years; median 45) with supratentorial tumors (confirmed histologically) were randomized by nine participating institutions. Patients were required to have completed radiotherapy (4500-6020 cGy to the tumor bed) before randomization. Patients were stratified as either nonprogressive (clinically and radiologically stable) or progressive. Results were analyzed for the 311 patients in the randomized population (RP), and for the 281 patients in the Valid Study Group (VSG) meeting protocol eligibility requirements. 56% of patients in the VSG had glioblastoma multiforme, 33% had other malignant glioma, and 11% had low-grade glioma. 64% were stratified as progressive. 12% had received prior chemotherapy. Results: The group randomized to PCNU had the longer survival (p = 0.06 for the RP, p = 0.07 for the VSG). In the VSG, median survival was 10 months for the cisplatin group, 13 months for the PCNU group. The difference between treatment groups was significant (p less than or equal to 0.02) when adjusted for important prognostic factors. PCNU lead to greater hematotoxicity; cisplatin lead to greater renal toxicity and some ototoxicity. Some cisplatin patients experienced complications associated with IA administration, including six cases of encephalopathy. Conclusion: The trial showed a survival advantage to the group randomized to PCNU, although the difference was modest. Coupled with previous BTCG results, these trials suggest that PCNU is an active drug for brain tumors. C1 NCI,BETHESDA,MD 20892. NYU,MED CTR,NEW YORK,NY 10016. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. DUKE UNIV,MED CTR,DURHAM,NC 27706. UNIV PITTSBURGH,MONTEFIORE HOSP,PITTSBURGH,PA 15213. UNIV N CAROLINA,CHAPEL HILL,NC 27599. UNIV IOWA,IOWA CITY,IA 52242. INDIANA UNIV,BLOOMINGTON,IN 47405. UNIV TENNESSEE,KNOXVILLE,TN 37996. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV CALIF IRVINE,IRVINE,CA 92717. FU NCI NIH HHS [CA 36005, CA 36047, CA 36014] NR 33 TC 22 Z9 23 U1 1 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1995 VL 25 IS 2 BP 143 EP 154 DI 10.1007/BF01057758 PG 12 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA RU192 UT WOS:A1995RU19200007 PM 8543970 ER PT J AU BASILE, AS KUSTOVA, Y HA, JH PAUL, I SKOLNICK, P SEI, Y AF BASILE, AS KUSTOVA, Y HA, JH PAUL, I SKOLNICK, P SEI, Y TI THE CONTRIBUTION OF GLIAL PATHOLOGIES TO THE NEUROCHEMICAL AND COGNITIVE DEFICITS IN LP-BM5 INFECTED MICE - A MURINE MODEL OF AIDS DEMENTIA SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD 20892. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. NR 0 TC 0 Z9 0 U1 2 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S119 EP S119 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100470 ER PT J AU BRENNEMAN, DE GOZES, I AF BRENNEMAN, DE GOZES, I TI A FEMTOMOLAR ACTING NEUROPROTECTIVE PEPTIDE SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. TEL AVIV UNIV,SACKLER SCH MED,TEL AVIV,ISRAEL. 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S203 EP S203 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100801 ER PT J AU BRENNER, M ZHANG, Q MESSING, A AF BRENNER, M ZHANG, Q MESSING, A TI GFAP TRANSCRIPTION AND TRANSGENES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV WISCONSIN,MADISON,WI 53706. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S73 EP S73 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100285 ER PT J AU CADET, JL AF CADET, JL TI SUPEROXIDE RADICALS, CUZN-SUPERXOIDE DISMUTASE TRANSGENIC MICE, AND DOPAMINERGIC TOXICITY SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIDA,INTRAMURAL RES PROGRAM,MOLEC NEUROPSYCHIAT SECT,LEXINGTON,KY 40583. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S208 EP S208 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100821 ER PT J AU DOHURA, K PERRYMAN, S RACE, R CHESEBRO, B AF DOHURA, K PERRYMAN, S RACE, R CHESEBRO, B TI DIFFERENTIALLY EXPRESSED GENES IN SCRAPIE-INFECTED NEUROBLASTOMA-CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 MIE UNIV,SCH MED,DEPT BIOCHEM,TSU,MIE 514,JAPAN. NIAID,RML,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S43 EP S43 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100167 ER PT J AU FUKUYAMA, R FU, J HATANPAA, K JONES, C BRADY, DR CHANDRASEKARAN, K RAPOPORT, SI AF FUKUYAMA, R FU, J HATANPAA, K JONES, C BRADY, DR CHANDRASEKARAN, K RAPOPORT, SI TI REDUCTION OF GENE-EXPRESSION OF ND4, A SUBUNIT OF NADH DEHYDROGENASE, IN VULNERABLE NEURONS IN ALZHEIMERS-DISEASE BRAIN SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S76 EP S76 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100297 ER PT J AU GOZES, I LILLING, G BARDEA, A RESHEF, A WOLLMAN, Y RUBINRAUT, S FRIDKIN, M BRENNEMAN, DE AF GOZES, I LILLING, G BARDEA, A RESHEF, A WOLLMAN, Y RUBINRAUT, S FRIDKIN, M BRENNEMAN, DE TI LIPOPHILIC AND HYBRID PEPTIDES - NOVEL DRUGS FOR NONINVASIVE TREATMENT OF NEURODEGENERATIVE DISEASES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 WEIZMANN INST SCI,IL-76100 REHOVOT,ISRAEL. TEL AVIV UNIV,MED CTR,IL-69978 TEL AVIV,ISRAEL. NICHHD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S203 EP S203 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100803 ER PT J AU KIM, SJ ROBERTS, AB SPORN, MB AF KIM, SJ ROBERTS, AB SPORN, MB TI MOLECULAR AND CELLULAR BIOLOGY OF THE TRANSFORMING GROWTH FACTOR-BETA-S AND THEIR RECEPTORS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S63 EP S63 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100245 ER PT J AU KRIZBAI, I SZABO, G DELI, M MADERSPACH, K OLAH, Z LEHEL, C JOO, E AF KRIZBAI, I SZABO, G DELI, M MADERSPACH, K OLAH, Z LEHEL, C JOO, E TI EXPRESSION OF PKC ISOFORMS IN CEREBRAL ENDOTHELIAL-CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 BIOL RES CTR,INST BIOPHYS,H-6701 SZEGED,HUNGARY. BIOL RES CTR,INST BIOCHEM,H-6701 SZEGED,HUNGARY. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S96 EP S96 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100377 ER PT J AU LESTER, DS LYON, R LEWIS, EN LEVIN, IW HANIG, JP AF LESTER, DS LYON, R LEWIS, EN LEVIN, IW HANIG, JP TI SPECTROSCOPIC ANALYSIS OF BRAIN-SLICES AS A SYSTEM FOR STUDYING NEUROTOXICITY SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 US FDA,CDER,DIV RES & TESTING,LAUREL,MD. NIDDKD,CHEM PHYS LAB,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S171 EP S171 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100673 ER PT J AU MOHANAKUMAR, KP CHIUEH, CC AF MOHANAKUMAR, KP CHIUEH, CC TI FREE-RADICALS (NITRIC-OXIDE AND HYDROXYL RADICALS) AND FERROUS CITRATE INDUCED NIGRAL INJURY SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 INDIAN INST CHEM BIOL,CALCUTTA 700032,W BENGAL,INDIA. NIMH,LCS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S52 EP S52 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100202 ER PT J AU PENDE, M GALLO, V AF PENDE, M GALLO, V TI GENE-TRANSCRIPTION IN GLIAL-CELLS FOLLOWING NON-NMDA RECEPTOR STIMULATION REQUIRES PROTEIN-KINASE-C ACTIVATION SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,CELL MOLEC NEUROPHYSIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S98 EP S98 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100387 ER PT J AU SEKI, K CHEN, HC HUANG, KP AF SEKI, K CHEN, HC HUANG, KP TI DEPHOSPHORYLATION OF PROTEIN-KINASE-C SUBSTRATES, NEUROGRANIN, NEUROMODULIN, AND MARCKS BY CALCINEURIN AND PROTEIN PHOSPHATASE-1 AND PHOSPHATASE-2A SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S19 EP S19 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100075 ER PT J AU VITKOVIC, L DACUNHA, A AF VITKOVIC, L DACUNHA, A TI ROLE FOR ASTROCYTOSIS IN AIDS DEMENTIA COMPLEX SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S129 EP S129 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100507 ER PT J AU VOLONTE, C STEPHENS, R KAPLAN, DR GREENE, LA AF VOLONTE, C STEPHENS, R KAPLAN, DR GREENE, LA TI DISSECTING THE MECHANISMS OF ACTIVATION OF PKN BY NGF SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 CNR,INST NEUROBIOL,I-00156 ROME,ITALY. NCI,FREDERK CANC RES & DEV CTR,FREDERICK,MD 21702. COLUMBIA UNIV,DEPT PATHOL,NEW YORK,NY 10032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S83 EP S83 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100325 ER PT J AU KAUFMAN, MJ HARTIG, PR HOFFMAN, BJ AF KAUFMAN, MJ HARTIG, PR HOFFMAN, BJ TI SEROTONIN 5-HT2C RECEPTOR STIMULATES CYCLIC-GMP FORMATION IN CHOROID-PLEXUS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE SEROTONIN 5-HT2C RECEPTOR; SEROTONIN 5-HT1C RECEPTOR; CYCLIC GMP; CHOROID PLEXUS; PHOSPHOINOSITIDE TURNOVER; CALCIUM; CEREBROSPINAL FLUID FORMATION ID DEPENDENT PROTEIN-KINASE; VASCULAR SMOOTH-MUSCLE; CEREBROSPINAL-FLUID; EPITHELIAL-CELLS; PHOSPHOINOSITIDE HYDROLYSIS; GUANYLATE-CYCLASE; CALCIUM ELEVATION; MESSENGER-RNA; RAT-BRAIN; ACTIVATION AB The serotonin 5-HT2C receptor (formerly designated the 5-HT1C receptor) of the choroid plexus triggers phosphoinositide turnover. In the present study, we demonstrate that receptor activation also triggers the formation of cyclic GMP (cGMP). Application of 1 mu M 5-HT to porcine choroid plexus tissue slices resulted in stimulation of cGMP formation to a maximum of five-fold basal level, with an EC(50) of 11 nM. This response was not inhibited by muscarinic or beta-adrenergic receptor antagonists. Serotonin receptor antagonists inhibited cGMP formation with apparent K-i values of 1.3 (mianserin), 200 (ketanserin), and 5,500 (spiperone) nM, respectively. Neither serotonin-stimulated cGMP formation nor PI turnover was inhibited by pertussis toxin pretreatment. Preliminary biochemical studies suggested that serotonin-stimulated cGMP formation was calcium, phospholipase A(2), and lipoxygenase dependent, as incubation in low calcium buffers or inclusion of the phospholipase A(2) or lipoxygenase inhibitors p-bromophenacyl bromide or BW 755c resulted in significant reduction of cGMP formation. The present results suggest that in addition to triggering phosphoinositide turnover, choroid plexus serotonin 5-HT2C receptors trigger cGMP formation in a calcium-sensitive manner. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,DEPT ENVIRONM HLTH SCI,BALTIMORE,MD 21205. FU NIEHS NIH HHS [5T32ES07141] NR 64 TC 55 Z9 57 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1995 VL 64 IS 1 BP 199 EP 205 PG 7 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA PX199 UT WOS:A1995PX19900022 PM 7798914 ER EF