FN Thomson Reuters Web of Science™ VR 1.0 PT J AU SUN, SQ SHI, SL LEAPMAN, R AF SUN, SQ SHI, SL LEAPMAN, R TI WATER DISTRIBUTIONS OF HYDRATED BIOLOGICAL SPECIMENS BY VALENCE ELECTRON-ENERGY-LOSS SPECTROSCOPY SO ULTRAMICROSCOPY LA English DT Article ID LOSS SPECTRUM; ICE; MICROSCOPY; MICROANALYSIS; MOLECULES; CELLS AB A technique has been developed for measuring the water distribution in thin frozen hydrated biological specimens by means of electron energy loss spectroscopy (EELS). The method depends on the quantification of subtle changes in the valence electron excitation spectrum as a function of composition. It involves determining the single-scattering intensities, calculating oscillator strengths and applying a multiple-least-squares fitting procedure to reference spectra for water and the organic constituents. The direct EELS approach has an important advantage over other indirect methods that are based on X-ray generation or elastic scattering measurements since these are applied to freeze-dried specimens where differential shrinkage between compartments may produce errors. Precision and accuracy of the EELS method have been tested on cryosectioned solutions of bovine serum albumin; data have also been obtained from cryosections of rapidly frozen erythrocytes. Results suggest that a precision of better than +/-5% (s.d.) is attainable from a single measurement and the accuracy may be as high as +/-2% if repeated measurements are made. The lateral spatial resolution of the water determinations is limited by radiation damage to approximately 100 nm which is of the same order as the specimen thickness. C1 NIH, NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13, RM 3W13, BETHESDA, MD 20892 USA. NR 41 TC 39 Z9 39 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3991 EI 1879-2723 J9 ULTRAMICROSCOPY JI Ultramicroscopy PD JUL PY 1993 VL 50 IS 2 BP 127 EP 139 DI 10.1016/0304-3991(93)90003-G PG 13 WC Microscopy SC Microscopy GA LQ573 UT WOS:A1993LQ57300003 PM 8367908 ER PT J AU RAZZAQUE, A WILLIAMS, O WANG, JH RHIM, JS AF RAZZAQUE, A WILLIAMS, O WANG, JH RHIM, JS TI NEOPLASTIC TRANSFORMATION OF IMMORTALIZED HUMAN EPIDERMAL-KERATINOCYTES BY 2 HHV-6 DNA CLONES SO VIROLOGY LA English DT Article ID VIRUS HUMAN HERPESVIRUS-6; TYPE-1 REPLICATION; IDENTIFICATION; INFECTION; HEPATITIS; SEQUENCES; LYMPHOMA; INVITRO; TROPISM; GENOME C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. RP RAZZAQUE, A (reprint author), US FDA,CBER,DNA VIRUS RES LAB,DIV VIRAL PROD,8800 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 36 TC 45 Z9 47 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD JUL PY 1993 VL 195 IS 1 BP 113 EP 120 DI 10.1006/viro.1993.1351 PG 8 WC Virology SC Virology GA LH710 UT WOS:A1993LH71000012 PM 8391179 ER PT J AU POPESCU, NC CHEN, MC SIMPSON, S SOLINAS, S DIPAOLO, JA AF POPESCU, NC CHEN, MC SIMPSON, S SOLINAS, S DIPAOLO, JA TI A BURKITT-LYMPHOMA CELL-LINE WITH INTEGRATED EPSTEIN-BARR-VIRUS AT A STABLE CHROMOSOME MODIFICATION SITE SO VIROLOGY LA English DT Note ID TRANSFORMED INVITRO; REL LOCUS; SEQUENCES; INSITU; DNA; EBV C1 SWISS FED INST TECHNOL,INST ANIM PROD,CH-8092 ZURICH,SWITZERLAND. RP POPESCU, NC (reprint author), NCI,DIV CANC ETIOL,BIOL LAB,BLDG 37,ROOM 2A19,BETHESDA,MD 20892, USA. NR 21 TC 20 Z9 21 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD JUL PY 1993 VL 195 IS 1 BP 248 EP 251 DI 10.1006/viro.1993.1367 PG 4 WC Virology SC Virology GA LH710 UT WOS:A1993LH71000028 PM 8391183 ER PT J AU COLLINS, PL MINK, MA HILL, MG CAMARGO, E GROSFELD, H STEC, DS AF COLLINS, PL MINK, MA HILL, MG CAMARGO, E GROSFELD, H STEC, DS TI RESCUE OF A 7502-NUCLEOTIDE (49.3-PERCENT OF FULL-LENGTH) SYNTHETIC ANALOG OF RESPIRATORY SYNCYTIAL VIRUS GENOMIC RNA SO VIROLOGY LA English DT Note ID NUCLEOTIDE-SEQUENCES; GENE RP COLLINS, PL (reprint author), NIAID,INFECT DIS LAB,BLDG 7,ROOM 100,BETHESDA,MD 20892, USA. NR 13 TC 25 Z9 25 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD JUL PY 1993 VL 195 IS 1 BP 252 EP 256 DI 10.1006/viro.1993.1368 PG 5 WC Virology SC Virology GA LH710 UT WOS:A1993LH71000029 PM 8317100 ER PT J AU ZHAO, TM ROBINSON, MA SAWASDIKOSOL, S SIMPSON, RM KINDT, TJ AF ZHAO, TM ROBINSON, MA SAWASDIKOSOL, S SIMPSON, RM KINDT, TJ TI VARIATION IN HTLV-I SEQUENCES FROM RABBIT-CELL LINES WITH DIVERSE INVIVO EFFECTS SO VIROLOGY LA English DT Note ID VIRUS TYPE-I; TROPICAL SPASTIC PARAPARESIS; COMPLETE NUCLEOTIDE-SEQUENCE; LEUKEMIA-LIKE DISEASE; VARIABILITY; VARIANTS; ISOLATE; ORIGIN C1 NIAID,IMMUNOGENET LAB,TWINBROOK II FACIL,12441 PARKLAWN DR,ROCKVILLE,MD 20852. NR 24 TC 34 Z9 35 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD JUL PY 1993 VL 195 IS 1 BP 271 EP 274 DI 10.1006/viro.1993.1373 PG 4 WC Virology SC Virology GA LH710 UT WOS:A1993LH71000034 PM 8317104 ER PT J AU DUFFY, CJ WURTZ, RH AF DUFFY, CJ WURTZ, RH TI AN ILLUSORY TRANSFORMATION OF OPTIC FLOW-FIELDS SO VISION RESEARCH LA English DT Article DE OPTIC FLOW; ILLUSION; PERCEPTION; VISION; MOTION ID MACAQUE MONKEY; RESPONSE SELECTIVITY; TEMPORAL AREA; EYE-MOVEMENTS; MST NEURONS; MOTION; DIRECTION; PURSUIT; MT; ORGANIZATION AB We compared a human observer's ability to locate the focus of expansion (FOE) of a radial optic flow field when this flow field was either combined with, or overlapped by, planar motion. With combined stimuli, in which the FOE was displaced in the direction opposite to the planar motion, subjects accurately located the displaced FOE. With overlapping (transparent) stimuli and the FOE remaining in the center of the display, we found an illusory transformation of the radial pattern: the focus of expansion appeared to be shifted in the direction of the planar motion. The speed of both the planar and radial patterns of motion influenced the illusion. Presence or absence of visual fixation had little effect. We suggest that this illusion might provide a clue as to the way the brain processes planar and radial motion which might in turn be relevant to the interaction of the planar and radial motion components of optic flow fields. RP DUFFY, CJ (reprint author), NEI,SENSORIMOTOR RES LAB,BLDG 10,ROOM 10C101,BETHESDA,MD 20892, USA. NR 36 TC 43 Z9 43 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0042-6989 J9 VISION RES JI Vision Res. PD JUL PY 1993 VL 33 IS 11 BP 1481 EP 1490 DI 10.1016/0042-6989(93)90141-I PG 10 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA LG796 UT WOS:A1993LG79600004 PM 8351820 ER PT J AU DOPPMAN, JL MILLER, DL CHANG, R GORDEN, P EASTMAN, RC NORTON, JA AF DOPPMAN, JL MILLER, DL CHANG, R GORDEN, P EASTMAN, RC NORTON, JA TI INTRAARTERIAL CALCIUM STIMULATION TEST FOR DETECTION OF INSULINOMAS SO WORLD JOURNAL OF SURGERY LA English DT Article ID ZOLLINGER-ELLISON SYNDROME; ISLET CELL TUMORS; INTRAOPERATIVE ULTRASONOGRAPHY; VEIN CATHETERIZATION; INJECTION TEST; LOCALIZATION; GASTRINOMAS; SECRETIN AB Occult insulinomas are adenomas not visualized by routine preoperative imaging studies, including ultrasonography (US), computed tomography (CT), magnetic resonance imaging (MRI), and arteriography. Reliance for detecting occult insulinomas has been placed on portal venous sampling (PVS), a sensitive (> 75%) but invasive procedure that requires considerable experience to enable sampling of small veins about the pancreatic head. For the past 2 years we have attempted to localize insulinomas by stimulating the release of insulin with a selective intraarterial injection of calcium gluconate and sampling for insulin gradients in the hepatic veins. This study replaces PVS by indicating the region of the pancreas within which the tumor lies, although, like PVS, it does not directly visualize the tumor. Our experience in 9 patients with surgically proved insulinomas is reviewed, comparing the results with PVS as well as with US, CT, MRI, and arteriography. C1 NIDDK,DIABETES BRANCH,BETHESDA,MD. NCI,SURG BRANCH,DIV CANC TREATMENT,BETHESDA,MD 20892. HENRY M JACKSON FDN,ROCKVILLE,MD. RP DOPPMAN, JL (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,900 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 17 TC 59 Z9 61 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2313 J9 WORLD J SURG JI World J.Surg. PD JUL-AUG PY 1993 VL 17 IS 4 BP 439 EP 443 PG 5 WC Surgery SC Surgery GA LP535 UT WOS:A1993LP53500004 PM 8362527 ER PT J AU ZEIGER, MA SHAWKER, TH NORTON, JA AF ZEIGER, MA SHAWKER, TH NORTON, JA TI USE OF INTRAOPERATIVE ULTRASONOGRAPHY TO LOCALIZE ISLET-CELL TUMORS SO WORLD JOURNAL OF SURGERY LA English DT Article ID ZOLLINGER-ELLISON SYNDROME; INSULINOMAS; GASTRINOMAS; PANCREAS; ULTRASOUND; RESECTION AB Because approximately 50% of insulinomas and a similar proportion of gastrinomas are not evident on preoperative imaging studies, precise intraoperative localization of these small tumors is imperative. Recently the use of high-resolution real-time B-mode ultrasonography has dramatically facilitated the operative detection of pancreatic islet cell tumors. The tumor appears sonolucent compared to the more echo-dense surrounding pancreas. This operative technique has been especially useful in patients with insulinoma because these tumors are generally located within the pancreas. In fact, it is so helpful during explorations for insulinoma some suggest that extensive preoperative localization studies are no longer indicated-that the patient can simply be explored with intraoperative ultrasonography (IOUS). It has not been as useful for gastrinomas because of their common extrapancreatic location. Accumulating evidence suggests that IOUS is an effective tool to aid in the operative localization and resection of pancreatic islet cell tumors. Not only can it precisely localize the tumor, it can accurately document the relation of the tumor to other vital pancreatic structures including ducts, veins, and arteries. C1 NCI,SURG BRANCH,SURG METAB SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2B07,BETHESDA,MD 20892. NIH,CTR CLIN,DEPT RADIOL,BETHESDA,MD 20892. NR 18 TC 38 Z9 42 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2313 J9 WORLD J SURG JI World J.Surg. PD JUL-AUG PY 1993 VL 17 IS 4 BP 448 EP 454 PG 7 WC Surgery SC Surgery GA LP535 UT WOS:A1993LP53500006 PM 8395749 ER PT J AU METZ, DC PISEGNA, JR FISHBEYN, VA BENYA, RV JENSEN, RT AF METZ, DC PISEGNA, JR FISHBEYN, VA BENYA, RV JENSEN, RT TI CONTROL OF GASTRIC-ACID HYPERSECRETION IN THE MANAGEMENT OF PATIENTS WITH ZOLLINGER-ELLISON SYNDROME SO WORLD JOURNAL OF SURGERY LA English DT Review ID LONG-TERM OMEPRAZOLE; NEOPLASIA TYPE-I; ENDOCRINE-CELLS; SYNDROME ZES; H2-RECEPTOR ANTAGONISTS; CARCINOID-TUMORS; OXYNTIC MUCOSA; DRUG-THERAPY; CIMETIDINE; SECRETION AB During the last 5 years important advances have occurred in the control of gastric acid hypersecretion in Zollinger-Ellison syndrome (ZES). The increased availability of potent gastric acid antisecretory agents such as histamine H-2-receptor antagonists and more recently the H+K+-ATPase inhibitors such as omeprazole and lansoprazole have made it possible to medically control acid secretion in all patients. Increased understanding of the variation in antisecretory drug dosage between individual patients has led to identification of criteria to ensure effective antisecretory control and to the recognition of subgroups of patients who require special monitoring. Effective regimens for parenteral antisecretory control during surgery have been established. The importance of parathyroidectomy in patients with multiple endocrine neoplasia type I with ZES and the possible usefulness of highly selective vagotomy have been investigated. We review here the new data that led to increased understanding in each of these areas from our studies and studies by others. C1 NIDDK,DIGEST DIS BRANCH,BETHESDA,MD. NR 99 TC 67 Z9 67 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2313 J9 WORLD J SURG JI World J.Surg. PD JUL-AUG PY 1993 VL 17 IS 4 BP 468 EP 480 PG 13 WC Surgery SC Surgery GA LP535 UT WOS:A1993LP53500009 PM 8362529 ER PT J AU LOPEZAPARICIO, P BELFRAGE, P MANGANIELLO, VC KONO, T DEGERMAN, E AF LOPEZAPARICIO, P BELFRAGE, P MANGANIELLO, VC KONO, T DEGERMAN, E TI STIMULATION BY INSULIN OF A SERINE KINASE IN HUMAN PLATELETS THAT PHOSPHORYLATES AND ACTIVATES THE CGMP-INHIBITED CAMP-PHOSPHODIESTERASE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID CYCLIC-AMP PHOSPHODIESTERASE; DEPENDENT PROTEIN-KINASE; RAT ADIPOCYTES; ADENYLATE-CYCLASE; S6 KINASE; FAT-CELLS; PURIFICATION; GMP; ATP C1 LUND UNIV,DEPT MED & PHYSIOL CHEM,POB 94,S-22100 LUND,SWEDEN. VANDERBILT UNIV,MED CTR,SCH MED,DEPT MOLEC PHYSIOL & BIOPHYS,NASHVILLE,TN 37232. NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 30 TC 29 Z9 29 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JUN 30 PY 1993 VL 193 IS 3 BP 1137 EP 1144 DI 10.1006/bbrc.1993.1744 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LJ912 UT WOS:A1993LJ91200048 PM 7686745 ER PT J AU SHEIKH, MS SHAO, ZM HUSSAIN, A CHEN, JC ROBERTS, CT LEROITH, D FONTANA, JA AF SHEIKH, MS SHAO, ZM HUSSAIN, A CHEN, JC ROBERTS, CT LEROITH, D FONTANA, JA TI RETINOIC ACID AND ESTROGEN MODULATION OF INSULIN-LIKE GROWTH-FACTOR BINDING PROTEIN-4 GENE-EXPRESSION AND THE ESTROGEN-RECEPTOR STATUS OF HUMAN BREAST-CARCINOMA CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID MOLECULAR-CLONING; IGF-II; CANCER; INHIBITION; PROLIFERATION; SEQUENCE; RAT; IDENTIFICATION; SERUM; LINES C1 UNIV MARYLAND,SCH MED,DEPT MED,DIV ONCOL,BALTIMORE,MD 21201. NIDDK,DIABET BRANCH,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,CTR CANC,BALTIMORE,MD 21201. VET ADM MED CTR,BALTIMORE,MD 21218. OI Fontana, Joseph/0000-0003-3829-3358; Roberts, Charles/0000-0003-1756-5772 NR 32 TC 25 Z9 25 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JUN 30 PY 1993 VL 193 IS 3 BP 1232 EP 1238 DI 10.1006/bbrc.1993.1757 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LJ912 UT WOS:A1993LJ91200061 PM 7686749 ER PT J AU KHOCHBIN, S WOLFFE, AP AF KHOCHBIN, S WOLFFE, AP TI DEVELOPMENTAL REGULATION AND BUTYRATE-INDUCIBLE TRANSCRIPTION OF THE XENOPUS HISTONE H1-CIRCLE PROMOTER SO GENE LA English DT Article DE RECOMBINANT DNA; NUCLEOTIDE SEQUENCE, EXPRESSION; TRANSCRIPTIONAL REGULATION; UPSTREAM CONTROL ELEMENT; CHROMATIN ID H-1 GENE; MESSENGER-RNA; S-PHASE; MUTAGENESIS; ELEMENTS; CELLS; DIFFERENTIATION; ACCUMULATION; EXPRESSION; ENHANCER AB We have isolated genomic clones of the Xenopus laevis histone H1-degrees promoter and identified regulatory elements mediating the transcriptional regulation of the H1-degrees gene. Expression of H1-degrees is associated with the terminal differentiation of many cell types. During X. laevis development, H1-degrees mRNA is present in the oocyte and egg, but remains at low levels during embryogenesis until hatching. After this time, mRNA levels accumulate dramatically correlating with the differentiation of many tissue types, e.g., liver and skin. Accumulation of H1-degrees mRNA can be induced at earlier developmental stages by treating embryos with butyrate. The enhanced transcription of H1-degrees in adult somatic cells, as well as the butyrate inducibility of the gene, have been investigated using transfection of adult X. laevis A6 somatic cells. We have defined specific protein-nucleic acid interactions with three cis-acting elements. Two previously defined gene regulatory elements: the H1 box, normally involved in the regulation of the H1 gene, and the H4TF2 site, normally involved in the regulation of the H4 gene, appear to have novel roles in determining differentiation-specific H1-degrees expression. These two elements act together with a new distal cis-acting element in order to sustain high levels of basal transcription and to potentiate transcription following butyrate treatment. C1 NICHHD,MOLEC EMBRYOL LAB,BLDG 6,RM BIA-13,BETHESDA,MD 20892. RI Khochbin, Saadi/M-8090-2013 NR 27 TC 56 Z9 56 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 PD JUN 30 PY 1993 VL 128 IS 2 BP 173 EP 180 DI 10.1016/0378-1119(93)90560-P PG 8 WC Genetics & Heredity SC Genetics & Heredity GA LK345 UT WOS:A1993LK34500004 PM 8514185 ER PT J AU LEEHUANG, S LIN, JJ KUNG, H HUANG, PL LEE, L HUANG, PL AF LEEHUANG, S LIN, JJ KUNG, H HUANG, PL LEE, L HUANG, PL TI THE HUMAN ERYTHROPOIETIN-ENCODING GENE CONTAINS A CAAT BOX, TATA BOXES AND OTHER TRANSCRIPTIONAL REGULATORY ELEMENTS IN ITS 5' FLANKING REGION SO GENE LA English DT Article DE GENE EXPRESSION; TRANSCRIPTION SIGNALS; GROWTH FACTORS; HORMONE; HEMATOPOIESIS ID TRANSGENIC MICE; STIMULATING FACTOR; NUCLEAR FACTORS; EXPRESSION; PROTEIN; INTERLEUKIN-6; SEQUENCES; PROMOTER; INVITRO; LIVER AB We have reported the cloning and expression of a human erythropoietin (hEp)-encoding cDNA [Lee-Huang, Proc. Natl. Acad. Sci. USA 81 (1984) 2708-2712]. Using this hEp cDNA as a probe, we isolated a 9.3-kb BamHI genomic Ep clone from a human leukocyte library soon thereafter. The size and restriction map of this clone is in agreement with restriction analysis of human genomic DNA probed with the hEp cDNA, demonstrating that this clone is representative of the single hEp gene. This clone is unique in that it extends beyond any reported hEp genomic clone by 3.9 kb on the 5' side and by 1.8 kb on the 3' side. The promoter function of the newly described 5' flanking region has been demonstrated by the expression of biologically active hEp in transfected cells. We find that, despite reports to the contrary, hEp does contain classic canonical TATA boxes and a CAAT box. The 5'-flanking region also contains cytokine-responsive consensus sequences, tissue-specific and metal-responsive elements, CRE and GRE sites, and binding sites for transcription factors, including AP1, NF-kappabeta and Spl. These regulatory elements have not been found in the hEp genomic clones thus far reported. The identification of these elements and their precise localization in hEp should be useful in studying the regulation of hEp expression, as well as in gene therapy and physiologic modulation of this hormone. C1 NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP LEEHUANG, S (reprint author), NYU,SCH MED,DEPT BIOCHEM,NEW YORK,NY 10016, USA. FU NHLBI NIH HHS [HL 30862, HL21683] NR 45 TC 29 Z9 29 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD JUN 30 PY 1993 VL 128 IS 2 BP 227 EP 236 DI 10.1016/0378-1119(93)90567-M PG 10 WC Genetics & Heredity SC Genetics & Heredity GA LK345 UT WOS:A1993LK34500011 PM 8514189 ER PT J AU ITOH, K YAMADA, F SHIBATA, N AF ITOH, K YAMADA, F SHIBATA, N TI THE FUNCTIONAL-ROLE OF MYOSIN PHOSPHORYLATION AND GLYCOPROTEIN-IIB/IIIA ACTIVATION IN PLATELETS STIMULATED BY THROMBIN SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. CTR ADULT DIS,DIV MOLEC CARDIOL,OSAKA 537,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 552 EP 552 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57700042 ER PT J AU HANSMANN, KE WILLIAMS, SB GRALNICK, HR AF HANSMANN, KE WILLIAMS, SB GRALNICK, HR TI RECOMBINANT FVIII INTERACTIONS WITH PLATELET VON-WILLEBRAND-FACTOR SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 NIH,HEMATOL SERV,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 559 EP 559 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57700062 ER PT J AU VAIL, M MCKEOWN, L HANSMANN, K GRALNICK, HR AF VAIL, M MCKEOWN, L HANSMANN, K GRALNICK, HR TI MODULATION OF ADHESIVE PROTEINS BOUND TO ACTIVATED PLATELETS SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 NIH,HEMATOL SERV,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 585 EP 585 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57700146 ER PT J AU MEHRINGER, JH KOZAK, CA VANDEERLIN, VMD TOLLEFSEN, DM AF MEHRINGER, JH KOZAK, CA VANDEERLIN, VMD TOLLEFSEN, DM TI STRUCTURE, CHROMOSOME LOCALIZATION, AND EXPRESSION OF THE GENE FOR MURINE HEPARIN COFACTOR-II SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 WASHINGTON UNIV,DEPT INTERNAL MED,DIV HEMATOL ONCOL,ST LOUIS,MO 63130. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 899 EP 899 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57701287 ER PT J AU RAULLI, R THURKAUF, A JACKSON, B GRECO, N TANDON, NN RICE, KC JAMIESON, GA AF RAULLI, R THURKAUF, A JACKSON, B GRECO, N TANDON, NN RICE, KC JAMIESON, GA TI A ROLE FOR SEROTONIN RECEPTORS IN EPINEPHRINE-INDUCED PLATELET ACTIVATION SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 AMER RED CROSS,DEPT CELL BIOL,ROCKVILLE,MD. NIDDKD,NEUROSCI LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 908 EP 908 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57701323 ER PT J AU WILLIAMS, SB MCKEOWN, LP KRUTZSCH, H HANSMANN, K GRALNICK, HR AF WILLIAMS, SB MCKEOWN, LP KRUTZSCH, H HANSMANN, K GRALNICK, HR TI PURIFICATION AND CHARACTERIZATION OF HUMAN PLATELET VON-WILLEBRAND-FACTOR SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 NIH,HEMATOL SERV,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 951 EP 951 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57701485 ER PT J AU VAIL, M MERRYMAN, P CHU, I WILSON, O GRALNICK, HR AF VAIL, M MERRYMAN, P CHU, I WILSON, O GRALNICK, HR TI PLATELETS FROM PATIENTS WITH PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA ARE ACTIVATED SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 NIH,HEMATOL SERV,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 967 EP 967 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57701530 ER PT J AU MCKEOWN, L VAIL, M HANSMANN, K WILLIAMS, S SHAFER, B GRALNICK, HR AF MCKEOWN, L VAIL, M HANSMANN, K WILLIAMS, S SHAFER, B GRALNICK, HR TI PLATELET-ADHESION TO COLLAGEN IN NAK(A) PERSONS SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 NIH,HEMATOL SERV,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 1000 EP 1000 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57701636 ER PT J AU RICK, ME MCKEOWN, LP HANSMANN, K MILLER, KD KRIZEK, DM AF RICK, ME MCKEOWN, LP HANSMANN, K MILLER, KD KRIZEK, DM TI VON-WILLEBRANDS DISEASE DUE TO DEFECTIVE BINDING OF FACTOR-VIII BY VON-WILLEBRAND-FACTOR SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 NIH,CTR CLIN,HEMATOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 1180 EP 1180 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57702282 ER PT J AU TANNENBAUM, SH CHAO, ES GRAINICK, HR AF TANNENBAUM, SH CHAO, ES GRAINICK, HR TI THE EFFECT OF HEPARIN ON ENDOTHELIAL-CELL VON-WILLEBRAND-FACTOR SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 NIH,HEMATOL SERV,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 1187 EP 1187 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57702303 ER PT J AU GHARAVI, AE SAMMARITANO, LR MORSE, JH ZARRABI, MH LOCKSHIN, MD AF GHARAVI, AE SAMMARITANO, LR MORSE, JH ZARRABI, MH LOCKSHIN, MD TI BINDING CHARACTERISTICS OF HIV AND CHLORPROMAZINE-INDUCED ANTIPHOSPHOLIPID ANTIBODIES SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 HOSP SPECIAL SURG,NEW YORK,NY 10021. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY 10032. VET ADM MED CTR,NORTHPORT,NY 11768. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 30 PY 1993 VL 69 IS 6 BP 1224 EP 1224 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LT577 UT WOS:A1993LT57702423 ER PT J AU BLUMBERG, B FAUCI, A MASSEY, W RAVEN, P WIESEL, T AF BLUMBERG, B FAUCI, A MASSEY, W RAVEN, P WIESEL, T TI LEADERS OF THE SCIENCE COMMUNITY ADDRESS NEW GRADUATES OF 1993 SO SCIENTIST LA English DT Editorial Material AB FROM THE HEART: in commencement speeches, eminent scientists and honorary degree recipients Baruch Blumberg, Anthony Fauci, Walter Massey, Peter Raven, and Torsten Wiesel shared their views on a broad range of topics-presented here in excerpts from their addresses. C1 ROCKEFELLER UNIV,NEW YORK,NY 10021. FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. NIAID,BETHESDA,MD 20892. MISSOURI BOT GARDEN,ST LOUIS,MO 63166. RP BLUMBERG, B (reprint author), UNIV CALIF BERKELEY,BERKELEY,CA 94720, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SCIENTIST INC PI PHILADELPHIA PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104 SN 0890-3670 J9 SCIENTIST JI Scientist PD JUN 28 PY 1993 VL 7 IS 13 BP 11 EP 11 PG 1 WC Information Science & Library Science; Multidisciplinary Sciences SC Information Science & Library Science; Science & Technology - Other Topics GA LJ263 UT WOS:A1993LJ26300008 ER PT J AU DEMICHELI, E LAMOUR, Y BASSANT, MH SONCRANT, TT AF DEMICHELI, E LAMOUR, Y BASSANT, MH SONCRANT, TT TI SUSTAINED CORTICAL METABOLIC RESPONSIVITY TO PHYSOSTIGMINE AFTER NUCLEUS BASALIS MAGNOCELLULARIS ABLATION IN RATS SO BRAIN RESEARCH LA English DT Article DE NUCLEUS BASALIS MAGNOCELLULARIS; [C-14]2-DEOXY-D-GLUCOSE; CHOLINERGIC SYSTEM; NICOTINE; ARECOLINE; PHYSOSTIGMINE; RAT ID CEREBRAL GLUCOSE-UTILIZATION; IBOTENIC ACID INJECTIONS; ALZHEIMERS-DISEASE; CHOLINE-ACETYLTRANSFERASE; ACETYLCHOLINE-RELEASE; BEHAVIORAL RECOVERY; UNILATERAL LESIONS; GLOBUS PALLIDUS; CORTEX; FOREBRAIN AB Unilateral nucleus basalis magnocellularis (NBM) ablation, which causes partial cholinergic denervation of the ipsilateral anterior neocortex, results in an acute but transient depression of regional cerebral metabolic rates for glucose (rCMRglc) in deafferented areas; rCMRglc normalizes within 2 weeks. To seek possible compensatory changes in cholinergic mechanisms following NBM ablation that could lead to rapid metabolic normalization, we studied rCMRglc responses to the receptor agonists nicotine and arecoline and the cholinesterase inhibitor physostigmine in rats at 2 weeks after unilateral NBM destruction. Physostigmine increased rCMRglc in 10 of 30 cortical areas contralateral to the NBM lesion. Compared to the unlesioned side, rCMRglc after physostigmine in the lesioned cortex was significantly lower in 2, significantly higher in 1 and not different (P < 0.05) in 27 areas. Neither arecoline nor nicotine treatment produced rCMRglc asymmetry in lesioned rats. These results demonstrate that responsivity to physostigmine is maintained in most regions of the rat neocortex after extrinsic cholinergic denervation by NBM ablation. This adaptive response appears not to result from cholinergic receptor upregulation and may reflect instead reorganization of cholinergic synapses. C1 NIA,NEUROSCI LAB,10-6C103,BETHESDA,MD 20892. NR 49 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 25 PY 1993 VL 615 IS 1 BP 80 EP 86 DI 10.1016/0006-8993(93)91116-A PG 7 WC Neurosciences SC Neurosciences & Neurology GA LK260 UT WOS:A1993LK26000009 PM 8364728 ER PT J AU MOODY, EJ HARRIS, BD SKOLNICK, P AF MOODY, EJ HARRIS, BD SKOLNICK, P TI STEREOSPECIFIC ACTIONS OF THE INHALATION ANESTHETIC ISOFLURANE AT THE GABA(A) RECEPTOR COMPLEX SO BRAIN RESEARCH LA English DT Article DE ANESTHESIA; BENZODIAZEPINE RECEPTOR; GABA(A) RECEPTOR; ISOFLURANE; STEREOSPECIFICITY; T-BUTYLBICYCLOPHOSPHOROTHIONATE (TBPS) ID RAT-BRAIN SYNAPTONEUROSOMES; CHLORIDE CHANNEL COMPLEX; BENZODIAZEPINE RECEPTORS; HALOTHANE; BINDING; CONVULSANT; CORTEX; DRUGS; SITES AB The inhalation anesthetic isoflurane stereoselectively modulates ligand binding to the GABA(A) receptor complex. The (+)-isomer of isoflurane was more potent and efficacious than the (-)-isomer in enhancing [H-3]flunitrazepam binding to benzodiazepine receptors. For example, concentration effect curves for Cl- enhancement of [H-3]flunitrazepam binding were significantly different (P < 0.001) in the presence of (+)-and (-)-isoflurane (0.44 and 0.88 mM). At the higher anesthetic concentration, the potency of Cl- to increase [H-3]flunitrazepam binding was increased 3.2- and 1.45-fold by (+)- and (-)-isoflurane, respectively (P < 0.05). Likewise, concentration-effect curves for (+) isoflurane-enhanced [H-3]flunitrazepam binding were significantly different (P < 0.05-P < 0.001) from the (-)-isomer in the presence of 0-200 mM Cl-. Stereoselectivity was not observed with respect to the potencies of these enantiomers as inhibitors of [S-35]t-butylbicyclophosphorothionate (TBPS) binding to sites within the Cl- ionophore. In this measure, the isomers had similar potencies (P > 0.05), although at higher concentrations ( > 0.1 mM) (+)-isoflurane produced significantly more inhibition than (-)-isoflurane. While the absolute potency differences between isomers were modest ( less-than-or-equal-to 2-fold) and measure dependent, these effects were manifested at clinically relevant concentrations of isoflurane and are consistent with in vivo studies demonstrating ( + )-isoflurane is a more effective anesthetic than the ( - )-isomer. This is the first demonstration of an inhalation anesthetic producing a stereoselective perturbation of the GABA(A) receptor complex. C1 JOHNS HOPKINS UNIV,DEPT ANESTHESIA & CRIT CARE MED,DIV CARDIAC ANESTHESIA,BALTIMORE,MD 21287. RP MOODY, EJ (reprint author), NIDDKD,NEUROSCI LAB,BLDG 8,RM 111,BETHESDA,MD 20892, USA. NR 30 TC 54 Z9 54 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 25 PY 1993 VL 615 IS 1 BP 101 EP 106 DI 10.1016/0006-8993(93)91119-D PG 6 WC Neurosciences SC Neurosciences & Neurology GA LK260 UT WOS:A1993LK26000012 PM 8395953 ER PT J AU JAKUS, J WOLFF, EC PARK, MH FOLK, JE AF JAKUS, J WOLFF, EC PARK, MH FOLK, JE TI FEATURES OF THE SPERMIDINE-BINDING SITE OF DEOXYHYPUSINE SYNTHASE AS DERIVED FROM INHIBITION STUDIES - EFFECTIVE INHIBITION BY BIS-GUANYLATED AND MONO-GUANYLATED DIAMINES AND POLYAMINES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INITIATION-FACTOR EIF-4D; PROTEIN-SYNTHESIS; HYPUSINE FORMATION; AMINO-ACID; FACTOR 4D; IDENTIFICATION; PRECURSOR; SUBSTRATE; CHEMISTRY; SECONDARY AB Several types of basic compounds structurally related to spermidine, one of the substrates for deoxyhypusine synthase, were tested as inhibitors of this enzyme. The results indicate that inhibitory compounds associate with the enzyme at the site of spermidine binding and must possess two charged primary amino or guanidino groups, or one of each. The efficiency of inhibition is related to the maximum possible distance between the primary amino groups and is adversely affected by substitutions on the secondary amino group or in the carbon chains of polyamines. The mono-guanyl derivatives are much more effective inhibitors than the parent amines or their bis-guanylated counterparts, N1-guanyl-1,7-diaminoheptane being the most effective compound with a K(i) value of about 10 nM. Based on these observations we have proposed a model for the spermidine-binding site of deoxyhypusine synthase. Studies with Chinese hamster ovary cells reveal a direct correlation between prevention of hypusine formation by several guanyldiamines and their in vitro inhibition of deoxyhypusine synthase. This evidence for disruption of the initial step in the post-translational maturation of eukaryotic initiation factor 5A provides a basis for the potential control of protein biosynthesis and cell proliferation. RP JAKUS, J (reprint author), NIDR,CELLULAR DEV & ONCOL LAB,BLDG 30,RM 211,BETHESDA,MD 20892, USA. NR 33 TC 132 Z9 135 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1993 VL 268 IS 18 BP 13151 EP 13159 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LH553 UT WOS:A1993LH55300023 PM 8514754 ER PT J AU ECKERT, KA KUNKEL, TA AF ECKERT, KA KUNKEL, TA TI EFFECT OF REACTION PH ON THE FIDELITY AND PROCESSIVITY OF EXONUCLEASE-DEFICIENT KLENOW POLYMERASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INVITRO DNA-SYNTHESIS; ESCHERICHIA-COLI; LARGE FRAGMENT; MUTATIONAL SPECIFICITY; REVERSE-TRANSCRIPTASE; KINETIC MECHANISM; THERMUS-AQUATICUS; BASE-PAIRS; ALPHA; REPLICATION AB We have examined as a function of pH the fidelity of DNA synthesis catalyzed by the 3'-->5' exonuclease-deficient form of the Klenow fragment of Escherichia coli DNA polymerase I. Increasing the pH of in vitro gap-filling reactions from pH 6.2 through 9.8 (37-degrees-C increased the frequency of base substitution and minus-one-base frameshift mutations 50- and 40-fold, respectively, as measured by reversion of a nonsense or frameshift mutation within the lacZalpha gene of bacteriophage M13mp2. To understand the mechanisms of high fidelity at low pH, we have examined the biochemical events associated with DNA synthesis at pH 6.2 that might be responsible for the observed accuracy in vitro. We show that while the steady-state frequency of T.dGTP misinsertion at the lacZalpha opal codon is 20-fold lower at pH 6.2 than at pH 7.6, pH-dependent changes in the frequencies of G.dATP and A.dCTP base misinsertions at the lacZalpha nonsense codon are insufficient to explain the fidelity changes observed in the gap-filling assay. However, the efficiency of steady-state extension synthesis from template-primers containing 3'-terminal T.G, G.A, and A.C (template-primer) mispairs was reduced up to 160-fold at pH 6.2 relative to pH 7.6. Analyses of the processivity of DNA polymerization versus pH demonstrated that at low pH the termination probability was decreased at specific template positions. Concomitantly, at sites where the termination probability was lower at pH 6.2, a decreased error rate was observed for base substitution mutations at three template positions and for minus-one-base frameshift mutations at two homopolymeric sequences relative to pH 7.6. We suggest that the observed increase in error discrimination by the exonuclease-deficient Klenow polymerase results from altered template binding properties of the enzyme at pH 6.2. C1 NIEHS, MOLEC GENET LAB, RES TRIANGLE PK, NC 27709 USA. NR 37 TC 47 Z9 47 U1 1 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1993 VL 268 IS 18 BP 13462 EP 13471 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LH553 UT WOS:A1993LH55300064 PM 8390464 ER PT J AU KUNO, K OKAMOTO, S HIROSE, K MURAKAMI, S MATSUSHIMA, K AF KUNO, K OKAMOTO, S HIROSE, K MURAKAMI, S MATSUSHIMA, K TI STRUCTURE AND FUNCTION OF THE INTRACELLULAR PORTION OF THE MOUSE INTERLEUKIN-1 RECEPTOR (TYPE-I) - DETERMINING THE ESSENTIAL REGION FOR TRANSDUCING SIGNALS TO ACTIVATE THE INTERLEUKIN-8 GENE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TUMOR-NECROSIS-FACTOR; IL-1 RECEPTOR; CYTOPLASMIC REGION; ENDOTHELIAL-CELLS; DOWN-REGULATION; LIGAND-BINDING; BETA-CHAIN; CYCLIC-AMP; PROTEIN; EXPRESSION AB The structural and functional relationships of the intracellular portion of mouse interleukin 1 receptor (muIL-1R) type I were examined with regard to activation of the human IL-8 gene in the Jurkat T cell line. C-terminal deletion mutations of muIL-1R revealed that the C-terminal boundary for receptor function is localized between 28 and 42 amino acids from the C-terminal end. The internal deletion mutants between amino acids 364 and 474 had a loss of activity, demonstrating the requirement for a large region of the mIL-1R cytoplasmic portion for receptor function. Amino acid substitution revealed that the putative nuclear localization elements (amino acids at 429-433, 523-527, and 507-519) and putative protein kinase C or A acceptor sites (Ser-431, Ser-509, Ser-528) do not participate in IL-1 signaling to induce IL-8 gene expression. A truncated mutation within the segment, which possesses homology with gp130, beta chain of IL-6R, or a point mutation of box 1- and box 2-like elements within the gp130 homologous segment, abolished the capacity to induce IL-8 gene expression, suggesting similar structural requirements in the cytoplasmic portion of several cytokine receptors. C1 KANAZAWA UNIV,CANC RES INST,DEPT PHARMACOL,13-1 TAKARA MACHI,KANAZAWA,ISHIKAWA 920,JAPAN. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. KANAZAWA UNIV,CANC RES INST,DEPT BIOPHYS,KANAZAWA,ISHIKAWA 920,JAPAN. NR 55 TC 43 Z9 43 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1993 VL 268 IS 18 BP 13510 EP 13518 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LH553 UT WOS:A1993LH55300071 PM 8514784 ER PT J AU NOGUCHI, M ADELSTEIN, S CAO, XQ LEONARD, WJ AF NOGUCHI, M ADELSTEIN, S CAO, XQ LEONARD, WJ TI CHARACTERIZATION OF THE HUMAN INTERLEUKIN-2 RECEPTOR GAMMA-CHAIN GENE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ALPHA-CHAIN; MOLECULAR-CLONING; EXPRESSION; PROMOTER; IDENTIFICATION; LOCALIZATION; ORGANIZATION; ACTIVATION; SEQUENCES; PROTEINS AB The interleukin-2 (IL-2) receptor gamma chain is an essential component of high and intermediate affinity IL-2 receptors (IL-2Rs), playing critical roles for ligand binding and internalization. We report here the isolation and characterization of the genomic locus for human IL-2Rgamma, which, like IL-2Rbeta, is a member of the cytokine receptor superfamily. The IL-2Rgamma gene is composed of eight exons and seven introns and spans approximately 4.2 kilobases. Analogous to the IL-2Rbeta gene, the two pairs of conserved cysteines typical of cytokine receptor superfamily proteins are located in adjacent exons, and the conserved WSXWS motif is located in the exon preceding the one that encodes the transmembrane domain and a Small part of the cytoplasmic domain. In each gene, the remainder of the cytoplasmic domain is encoded by the final two exons. Southern blot analysis suggests that IL-2Rgamma is encoded by a single copy gene. Cross-hybridizing sequences were detected in DNA derived from a number of other mammalian species but not from yeast. Primer extension analysis and ribonuclease protection assays revealed that there are three principal transcription initiation sites located 32-38 nucleotides 5' to the translation initiation AUG codon. These sites are upstream of the 5' end of the published IL-2Rgamma cDNA sequence. The region 5' to the transcription initiation sites exhibited promoter activity when cloned upstream of the luciferase reporter gene. With this study, the organization of the genes encoding all three chains (alpha, beta, and gamma) of the IL-2 receptor has been determined and promoters for each identified. C1 NHLBI,PULM & MOLEC IMMUNOL SECT,INTRAMURAL RES PROGRAM,OFF DIRECTOR,BETHESDA,MD 20892. RI Adelstein, Stephen/I-7936-2016 OI Adelstein, Stephen/0000-0001-7221-6298 NR 31 TC 69 Z9 72 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1993 VL 268 IS 18 BP 13601 EP 13608 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LH553 UT WOS:A1993LH55300083 PM 8514792 ER PT J AU PASH, JM ALFONSO, PJ BUSTIN, M AF PASH, JM ALFONSO, PJ BUSTIN, M TI ABERRANT EXPRESSION OF HIGH-MOBILITY GROUP CHROMOSOMAL PROTEIN-14 AFFECTS CELLULAR-DIFFERENTIATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN CDNA SEQUENCE; MULTIGENE FAMILY; TRANSCRIBED GENES; HMG-14; CHROMATIN; MYOD1; NUCLEOSOMES; INHIBITION; MYOGENESIS; MYOBLASTS AB High mobility group (HMG) 14 is a ubiquitous chromosomal protein that binds specifically to nucleosomal DNA and may be involved in a process that confers distinct properties to the chromatin structure of transcriptionally active genes. To explore the involvement of this protein in regulation of gene expression, we studied the effect of aberrant expression of HMG-14 protein on cellular differentiation. We produced stably transfected C2C12 mouse myoblasts expressing the human HMG-14 protein under the control of the mouse mammary tumor virus promoter. Transformed colonies retained their potential do differentiate into myotubes. Induction of human HMG-14 expression by dexamethasone inhibited the myogenic process. Revertant colonies, which lost the ability to express human HMG-14, regained the ability to differentiate into myotubes. Inhibition of myoblast differentiation by aberrantly expressed HMG-14 correlated with down-regulation of myogenic determination factors. The results suggest that proper cellular differentiation requires regulated expression of HMG-14 protein and are consistent with the possibility that this protein may be involved in gene regulation. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RI Bustin, Michael/G-6155-2015 NR 39 TC 23 Z9 23 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1993 VL 268 IS 18 BP 13632 EP 13638 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LH553 UT WOS:A1993LH55300087 PM 8514795 ER PT J AU CHIORINI, JA BOAL, TR MIYAMOTO, S SAFER, B AF CHIORINI, JA BOAL, TR MIYAMOTO, S SAFER, B TI A DIFFERENCE IN THE RATE OF RIBOSOMAL ELONGATION BALANCES THE SYNTHESIS OF EUKARYOTIC TRANSLATION INITIATION-FACTOR (EIF)-2 ALPHA AND EIF-2-BETA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-SYNTHESIS-INITIATION; MESSENGER-RNA; HEMOGLOBIN SYNTHESIS; FACTOR-II; PHOSPHORYLATION; SEQUENCE; SUBUNIT; PURIFICATION; RECOGNITION; MUTATIONS AB Eukaryotic translation initiation factor 2 (eIF-2) is a heterotrimer composed of three subunits designated alpha, beta, and gamma. These proteins exist in equimolar amounts in the cell and have not been detected as isolated subunits. Our research examines the basis of their balanced synthesis. Northern analysis of K562 cell mRNA revealed that eIF-2beta was five times more abundant than eIF-2alpha. However, immunoprecipitation of pulse-labeled K562 cells showed an equimolar rate of synthesis of eIF-2alpha and -beta despite the 5-fold difference in the size of their mRNA pools. Addition of equal amounts of synthetic capped mRNA for eIF-2alpha and eIF-2beta to an in vitro translation reaction produced five times more eIF-2alpha protein than eIF-2beta. Determination of the polysome profile for alpha and beta mRNA in K562 cells indicated eIF-2alpha was translated more efficiently than eIF-2beta. Substitution of either the initiation codon context or the leader of the beta mRNA for that of alpha had only a minor effect on the translational efficiency of beta. Comparison of the rate of ribosomal elongation for the two mRNAs indicated that ribosomes associated with the beta mRNA elongate at a rate 4-fold less than that of eIF-2alpha. Thus, the balanced translation of alpha and beta mRNA is primarily the result of a 4-fold difference in the rate of ribosomal elongation. C1 NHLBI,MOLEC HEMATOL BRANCH,RNA & PROT BIOSYNTH SECT,BETHESDA,MD 20892. NR 39 TC 11 Z9 12 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1993 VL 268 IS 18 BP 13748 EP 13755 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LH553 UT WOS:A1993LH55300102 PM 8514807 ER PT J AU WONG, G KOEHLER, KF SKOLNICK, P GU, ZQ ANANTHAN, S SCHONHOLZER, P HUNKELER, W ZHANG, WJ COOK, JM AF WONG, G KOEHLER, KF SKOLNICK, P GU, ZQ ANANTHAN, S SCHONHOLZER, P HUNKELER, W ZHANG, WJ COOK, JM TI SYNTHETIC AND COMPUTER-ASSISTED ANALYSIS OF THE STRUCTURAL REQUIREMENTS FOR SELECTIVE, HIGH-AFFINITY LIGAND-BINDING TO DIAZEPAM-INSENSITIVE BENZODIAZEPINE RECEPTORS SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID ANTAGONIST; SYSTEM AB Several 1,4-diazepines were recently reported to bind with high affinities to the ''diazepam-insensitive'' (DI) isoform of the benzodiazepine receptor (BzR) (Korpi, E. R.; Uusi-Oukari, M.; Wegelius, K. Eur. J. Pharm. 1992,213,323-329. Wong, G.; Skolnick, P. Eur. J. Pharmacol. Mol. Pharm. Sec. 1992, 225, 63-68). However, only the putative ethanol antagonist 1 (Ro 15-4513) displayed modest selectivity for the DI site compared to other ''diazepam-sensitive' (DS) BzR isoforms. In order to probe the requirements for selective, high-affinity binding to the DI site, the affinities of 47 benzodiazepines have been determined at both DI and DSBzR sites. In addition, single X-ray crystallographic analyses for three of these derivatives, 5 (Ro 17-1812), 6 (Ro 16-6028), and 42 (Ro 14-5974), are reported. The radioligand binding studies reveal that modifications to the 3-, 7-, and 8-positions of 6-oxoimidazo[1,5-a] [1,4] benzodiazepines have a marked influence on the K(i)(DI)/K(i)(DS) ratios. In order to more precisely determine the structural requirements for both high affinity and selectivity at DI BzR relative to DS, 3D-QSAR analyses were carried out on ligand affinities at both of these BzR isoforms. This analysis was based, in part, on the new X-ray crystallographic data. Satisfactory cross-validated regression equations were obtained individually for the logarithms of ligand affinities at DI and DS as well as for the differences of the logarithms of their affinities at these two isoforms (cross-validated R2 > 0.70 for all three regression equations). The steric and electrostatic 3D-QSAR DI and DS maps are in qualitative accord with the structure-activity relationship (SAR) data. Furthermore, the DI and DI/DS maps may be useful in the design of ligands with enhanced DI affinity and DI/DS selectivity, respectively. C1 SEARLE RES & DEV,DRUG DESIGN SECT,SKOKIE,IL 60077. F HOFFMANN LA ROCHE & CO LTD,DIV PHARMA,CH-4002 BASEL,SWITZERLAND. SO RES INST,ORGAN CHEM RES DEPT,BIRMINGHAM,AL 35255. UNIV WISCONSIN,DEPT CHEM,MILWAUKEE,WI 53201. RP WONG, G (reprint author), NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892, USA. NR 35 TC 67 Z9 67 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD JUN 25 PY 1993 VL 36 IS 13 BP 1820 EP 1830 DI 10.1021/jm00065a004 PG 11 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA LJ878 UT WOS:A1993LJ87800004 PM 8390574 ER PT J AU PRABHU, VV AF PRABHU, VV TI SYMMETRY OBSERVATIONS IN LONG NUCLEOTIDE-SEQUENCES SO NUCLEIC ACIDS RESEARCH LA English DT Article RP PRABHU, VV (reprint author), NIH,NATL CTR BIOTECHNOL INFORMAT,BLDG 38-A,8TH FLOOR,BETHESDA,MD 20892, USA. NR 6 TC 43 Z9 46 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD JUN 25 PY 1993 VL 21 IS 12 BP 2797 EP 2800 DI 10.1093/nar/21.12.2797 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LL721 UT WOS:A1993LL72100002 PM 8332488 ER PT J AU BHAT, KS MORRISON, SG AF BHAT, KS MORRISON, SG TI PRIMARY STRUCTURE OF HUMAN RIBOSOMAL-PROTEIN S21 SO NUCLEIC ACIDS RESEARCH LA English DT Article ID SACCHAROMYCES-CEREVISIAE; LIVER; YS25 RP BHAT, KS (reprint author), NIH,ROCKY MT LABS,HAMILTON,MT 59840, USA. NR 4 TC 7 Z9 9 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD JUN 25 PY 1993 VL 21 IS 12 BP 2939 EP 2939 DI 10.1093/nar/21.12.2939 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LL721 UT WOS:A1993LL72100022 PM 8332502 ER PT J AU BURKE, TR SMYTH, MS OTAKA, A ROLLER, PP AF BURKE, TR SMYTH, MS OTAKA, A ROLLER, PP TI SYNTHESIS OF 4-PHOSPHONO(DIFLUOROMETHYL)-D, L-PHENYLALANINE AND N-BOC AND N-FMOC DERIVATIVES SUITABLY PROTECTED FOR SOLID-PHASE SYNTHESIS OF NONHYDROLYZABLE PHOSPHOTYROSYL PEPTIDE ANALOGS SO TETRAHEDRON LETTERS LA English DT Article AB Synthesis of 4-phosphono(difluoromethyl)-D,L-phenylalanine as well as its diethyl phosphonate analogues bearing either Boc or Fmoc-amino protection are reported. The latter two derivatives were utilized for the solid-phase synthesis of SH2-related peptides containing nonhydrolyzable phosphotyrosyl mimetics. RP BURKE, TR (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BLDG 37,RM 5C06,BETHESDA,MD 20892, USA. RI Burke, Terrence/N-2601-2014 NR 7 TC 87 Z9 88 U1 0 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4039 J9 TETRAHEDRON LETT JI Tetrahedron Lett. PD JUN 25 PY 1993 VL 34 IS 26 BP 4125 EP 4128 DI 10.1016/S0040-4039(00)60508-7 PG 4 WC Chemistry, Organic SC Chemistry GA LJ936 UT WOS:A1993LJ93600002 ER PT J AU GERMAIN, RN RINKER, AG AF GERMAIN, RN RINKER, AG TI PEPTIDE BINDING INHIBITS PROTEIN AGGREGATION OF INVARIANT-CHAIN FREE CLASS-II DIMERS AND PROMOTES SURFACE EXPRESSION OF OCCUPIED MOLECULES SO NATURE LA English DT Article ID HLA-DR MOLECULES; HISTOCOMPATIBILITY ANTIGENS; INTRACELLULAR-TRANSPORT; MONOCLONAL-ANTIBODIES; CELL LINE; IA; ASSOCIATION; RECOGNITION; GENE; H-2 AB EFFICIENT egress of major histocompatibility complex (MHC) class I molecules from the endoplasmic reticulum (ER) depends on peptide binding1-7. For MHC class II molecules, invariant chain (Ii) promotes ER exit of newly assembled, peptide-free dimers8-14. This raises the question of whether a mechanism exists elsewhere in the cell that dictates selective expression of peptide-associated class II molecules. We report here that dissociation of MHC class II-Ii complexes at low pH and physiological temperature leads to inclusion of empty class II in protein aggregates, and that this aggregation is specifically prevented by peptide binding. Combined with data showing that antigen exposure increases cell surface class II expression on living cells by a post-translational mechanism12, these results provide evidence for peptide-dependent intracellular editing of class II dimers, which limits surface expression of empty molecules unsuitable for antigen-specific T-cell activation. RP GERMAIN, RN (reprint author), NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BETHESDA,MD 20892, USA. NR 37 TC 158 Z9 160 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JUN 24 PY 1993 VL 363 IS 6431 BP 725 EP 728 DI 10.1038/363725a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LJ339 UT WOS:A1993LJ33900057 PM 8515815 ER PT J AU STGEORGIEV, V AF STGEORGIEV, V TI IMMUNOMODULATING DRUGS - MAJOR ADVANCES IN RESEARCH-AND-DEVELOPMENT SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID GROWTH-FACTOR-BETA; ESTABLISHED PULMONARY METASTASES; ACTIVATED KILLER CELLS; T-CELL; INTERLEUKIN-2 RECEPTOR; MYCOPHENOLIC-ACID; INVITRO GROWTH; RECOMBINANT INTERLEUKIN-2; ADOPTIVE IMMUNOTHERAPY; TUMOR-CELLS RP STGEORGIEV, V (reprint author), NIAID,SOLAR BLDG,ROOM 4C-39,BETHESDA,MD 20892, USA. NR 79 TC 5 Z9 5 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 1 EP 10 PG 10 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700001 PM 8363213 ER PT J AU STGEORGIEV, V AF STGEORGIEV, V TI ENZYMES OF THE PURINE METABOLISM - INHIBITION AND THERAPEUTIC POTENTIAL SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID NUCLEOSIDE-PHOSPHORYLASE-DEFICIENCY; MOUSE T-LYMPHOMA; ADENOSINE-DEAMINASE DEFICIENCY; CYTOPLASMIC FREE CALCIUM; MYCOPHENOLIC-ACID; CYTO-TOXICITY; SELECTIVE TOXICITY; COMBINED IMMUNODEFICIENCY; NUCLEOTIDE DEPLETION; ARABINOSYL-GUANINE RP STGEORGIEV, V (reprint author), NIAID,SOLAR BLDG,ROOM 4C-39,BETHESDA,MD 20892, USA. NR 91 TC 10 Z9 10 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 207 EP 216 PG 10 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700025 PM 8103311 ER PT J AU JANIK, J KOPP, WC SMITH, JW LONGO, DL ALVORD, WG URBA, WJ AF JANIK, J KOPP, WC SMITH, JW LONGO, DL ALVORD, WG URBA, WJ TI LEVAMISOLE-INDUCED NEOPTERIN SYNTHESIS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID COLON-CARCINOMA; TETRAHYDROBIOPTERIN; BIOSYNTHESIS; INTERFERON; INVITRO C1 NCI,FREDERICK CANC RES & DEV CTR,CLIN SERV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,DATA MANAGEMENT SERV INC,FREDERICK,MD 21702. RP JANIK, J (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701, USA. NR 12 TC 3 Z9 3 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 252 EP 258 DI 10.1111/j.1749-6632.1993.tb35873.x PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700030 PM 8363229 ER PT J AU INMAN, JK AF INMAN, JK TI SYNTHESES OF MACROMOLECULAR IMMUNOMODULATORS AND CONJUGATES EMPLOYING HALOACETYL REAGENTS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article RP INMAN, JK (reprint author), NIAID,IMMUNOL LAB,BLDG 10,ROOM 11N311,BETHESDA,MD 20892, USA. NR 5 TC 1 Z9 1 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 347 EP 350 DI 10.1111/j.1749-6632.1993.tb35887.x PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700044 PM 8363239 ER PT J AU FAUCI, AS AF FAUCI, AS TI IMMUNOPATHOGENESIS OF HIV-INFECTION SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; CD4+ T-CELLS; TUMOR NECROSIS FACTOR; CD3/T-CELL RECEPTOR COMPLEX; FOLLICULAR DENDRITIC CELLS; GERMINAL-CENTERS; SAN-FRANCISCO; HTLV-III/LAV; EXPRESSION; ACTIVATION RP FAUCI, AS (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 63 TC 2 Z9 2 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 409 EP 419 DI 10.1111/j.1749-6632.1993.tb35899.x PG 11 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700054 ER PT J AU RUSCETTI, F VARESIO, L OCHOA, A ORTALDO, J AF RUSCETTI, F VARESIO, L OCHOA, A ORTALDO, J TI PLEIOTROPIC EFFECTS OF TRANSFORMING GROWTH-FACTOR-BETA ON CELLS OF THE IMMUNE-SYSTEM SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID COLONY-STIMULATING FACTOR; ACTIVATED KILLER ACTIVITY; TGF-BETA; LYMPHOCYTES-B; T-CELLS; CD8 EXPRESSION; HELPER-CELLS; FACTOR-BETA-1; INHIBITION; PROLIFERATION C1 PROGRAM RESOURCES INC DYNCORP,IMMUNOTHERAPY LAB,FREDERICK,MD. RP RUSCETTI, F (reprint author), NCI,FREDERICK CANC RES & DEV CTR,LEUKOCYTE BIOL MOLEC IMMUNOREGULAT & EXPTL IMMUNOL LABS,FREDERICK,MD 21702, USA. RI varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 56 TC 69 Z9 69 U1 0 U2 5 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 488 EP 500 DI 10.1111/j.1749-6632.1993.tb35911.x PG 13 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700064 PM 8363258 ER PT J AU PLAUT, M AF PLAUT, M TI CYTOKINES AND MODULATION OF DISEASES OF IMMEDIATE HYPERSENSITIVITY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID T-CELL CLONES; NECROSIS-FACTOR-ALPHA; HOUSE DUST MITE; FC-EPSILON-RI; MAST-CELLS; LATE-PHASE; PRODUCE INTERLEUKIN-4; FUNCTIONAL SUBSETS; IMMUNOGLOBULIN-E; BONE-MARROW RP PLAUT, M (reprint author), NIAID,DIV ALLERGY IMMUNOL & TRANSPLANTAT,ASTHMA & ALLERGY BRANCH,BETHESDA,MD 20892, USA. NR 55 TC 2 Z9 2 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 512 EP 520 DI 10.1111/j.1749-6632.1993.tb35913.x PG 9 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700066 PM 8363259 ER PT J AU STGEORGIEV, V ALBRIGHT, JF AF STGEORGIEV, V ALBRIGHT, JF TI CYTOKINES AND THEIR ROLE AS GROWTH-FACTORS AND IN REGULATION OF IMMUNE-RESPONSES SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Review ID LEUKEMIA INHIBITORY FACTOR; COLONY-STIMULATING FACTOR; ACTIVATED KILLER-CELLS; TUMOR-NECROSIS-FACTOR; HUMAN PERIPHERAL-BLOOD; INTERLEUKIN-1 RECEPTOR ANTAGONIST; HELPER T-CELLS; HUMAN B-CELLS; FACTOR-BETA; LYMPHOCYTES-T RP STGEORGIEV, V (reprint author), NIAID,SOLAR BLDG,ROOM 4C-39,BETHESDA,MD 20892, USA. NR 167 TC 9 Z9 10 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 584 EP 602 PG 19 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700075 PM 8363268 ER PT J AU WALDMANN, TA GOLDMAN, C TOP, L GRANT, A BURTON, J BAMFORD, R ROESSLER, E HORAK, I ZAKNOEN, S KASTENSPORTES, C WHITE, J ENGLAND, R HORAK, E MARTINUCCI, J TINUBU, SA MISHRA, B JUNGHANS, R DIPRE, M CARRASQUILLO, J REYNOLDS, J GANSOW, O NELSON, D AF WALDMANN, TA GOLDMAN, C TOP, L GRANT, A BURTON, J BAMFORD, R ROESSLER, E HORAK, I ZAKNOEN, S KASTENSPORTES, C WHITE, J ENGLAND, R HORAK, E MARTINUCCI, J TINUBU, SA MISHRA, B JUNGHANS, R DIPRE, M CARRASQUILLO, J REYNOLDS, J GANSOW, O NELSON, D TI THE INTERLEUKIN-2 RECEPTOR - A TARGET FOR IMMUNOTHERAPY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID T-CELL LEUKEMIA; ANTI-TAC-H; MONOCLONAL-ANTIBODY; HUMANIZED ANTIBODY; IL-2 RECEPTOR; GROWTH-FACTOR; ASSOCIATION; EXPRESSION; PEPTIDE; LYMPHOMA C1 NCI,WARREN GRANT MAGNUSON CLIN CTR,DEPT NUCL MED,BETHESDA,MD 20892. NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. RP WALDMANN, TA (reprint author), NCI,METAB BRANCH,BETHESDA,MD 20892, USA. RI Carrasquillo, Jorge/E-7120-2010; OI Carrasquillo, Jorge/0000-0002-8513-5734 NR 42 TC 6 Z9 6 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 603 EP 610 DI 10.1111/j.1749-6632.1993.tb35923.x PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700076 PM 8363269 ER PT J AU ALBRIGHT, JF AF ALBRIGHT, JF TI IMMUNE DYSFUNCTION RELATED TO DRUG-METABOLIZING-ENZYMES SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN TCDD; RECEPTOR; "2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN; THYMOCYTES; PROTEIN; DIOXIN; GENE RP ALBRIGHT, JF (reprint author), NIAID,DIV ALLERGY IMMUNOL & TRANSPLANTAT,SOLAR BLDG,ROOM 4A22,BETHESDA,MD 20892, USA. NR 15 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 620 EP 623 DI 10.1111/j.1749-6632.1993.tb35927.x PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700080 PM 8395782 ER PT J AU SNELLER, MC LANE, HC AF SNELLER, MC LANE, HC TI IMMUNOLOGICAL APPROACHES TO THE THERAPY OF HIV-1 INFECTION SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; IMMUNE-DEFICIENCY SYNDROME; PERIPHERAL-BLOOD LYMPHOCYTES; BONE-MARROW TRANSPLANTATION; CD4+ T-CELLS; INTERFERON-ALPHA; KAPOSI-SARCOMA; SYNDROME AIDS; RECOMBINANT INTERLEUKIN-2; MONONUCLEAR-CELLS C1 NIAID,IMMUNOREGULAT LAB,BLDG 10,RM 11B-13,BETHESDA,MD 20892. NR 50 TC 5 Z9 5 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 687 EP 696 DI 10.1111/j.1749-6632.1993.tb35932.x PG 10 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700085 PM 8363275 ER PT J AU ROHRBAUGH, ML MCGOWAN, JJ AF ROHRBAUGH, ML MCGOWAN, JJ TI GENE-TRANSFER FOR THERAPY AND PROPHYLAXIS OF HIV-1 INFECTION SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID IMMUNODEFICIENCY-VIRUS REPLICATION; HEMATOPOIETIC STEM-CELLS; RETROVIRAL VECTORS; INTRACELLULAR IMMUNIZATION; IMMUNE-RESPONSE; ANTISENSE RNA; BRAIN-TUMORS; SOLUBLE CD4; EXPRESSION; INHIBITION RP ROHRBAUGH, ML (reprint author), NIAID,DIV EXTRAMURAL ACTIVITIES,BETHESDA,MD 20892, USA. OI Rohrbaugh, Mark/0000-0002-6136-3337 NR 78 TC 2 Z9 2 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 697 EP 712 DI 10.1111/j.1749-6632.1993.tb35933.x PG 16 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700086 PM 8363276 ER PT J AU FITZGERALD, D PASTAN, I AF FITZGERALD, D PASTAN, I TI PSEUDOMONAS EXOTOXIN AND RECOMBINANT IMMUNOTOXINS DERIVED FROM IT SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID GROWTH-FACTOR-ALPHA; CD4-PSEUDOMONAS EXOTOXIN; TRANSFERRIN RECEPTOR; MONOCLONAL-ANTIBODY; ANTITUMOR-ACTIVITY; CELLULAR PROTEASE; DIPHTHERIA-TOXIN; CHIMERIC TOXINS; TUMOR-CELLS; MICE RP FITZGERALD, D (reprint author), NCI,DIV CANC BIOL DIAGN & CTR,MOLEC BIOL LAB,BLDG 36,1D-32,BETHESDA,MD 20892, USA. NR 43 TC 27 Z9 27 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 740 EP 745 DI 10.1111/j.1749-6632.1993.tb35935.x PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700088 PM 8363279 ER PT J AU SUHADOLNIK, RJ REICHENBACH, NL HITZGES, PM ABLASHI, DV STRAYER, DR CARTER, WA AF SUHADOLNIK, RJ REICHENBACH, NL HITZGES, PM ABLASHI, DV STRAYER, DR CARTER, WA TI RNA DRUG-THERAPY ACTING VIA THE 2-5A SYNTHETASE RNASE L PATHWAY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID VIRUS C1 NCI,BETHESDA,MD 20892. HAHNEMANN UNIV,DEPT NEOPLAST DIS,PHILADELPHIA,PA 19102. HEM PHARMACEUT CORP,PHILADELPHIA,PA 19103. RP SUHADOLNIK, RJ (reprint author), TEMPLE UNIV,HLTH SCI CTR,SCH MED,DEPT BIOCHEM,PHILADELPHIA,PA 19140, USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 756 EP 757 DI 10.1111/j.1749-6632.1993.tb35937.x PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700090 PM 8363281 ER PT J AU HOTH, DF AF HOTH, DF TI ISSUES IN THE DEVELOPMENT OF A PROPHYLACTIC HIV VACCINE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID INFECTION; VIRUS RP HOTH, DF (reprint author), NIAID,DIV AIDS,6003 EXECUT BLVD,ROOM 2A18,BETHESDA,MD 20892, USA. NR 10 TC 3 Z9 3 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 23 PY 1993 VL 685 BP 777 EP 783 DI 10.1111/j.1749-6632.1993.tb35943.x PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LL567 UT WOS:A1993LL56700096 PM 8363285 ER PT J AU HEALY, B AF HEALY, B TI NOTIFYING PHYSICIANS AND PRESS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP HEALY, B (reprint author), NIH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 23 PY 1993 VL 269 IS 24 BP 3096 EP 3096 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LH145 UT WOS:A1993LH14500008 ER PT J AU HEALY, B AF HEALY, B TI ENSURING JOURNAL PUBLICATION SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP HEALY, B (reprint author), NIH, BETHESDA, MD 20892 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 23 PY 1993 VL 269 IS 24 BP 3096 EP 3096 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LH145 UT WOS:A1993LH14500007 ER PT J AU HEALY, B AF HEALY, B TI ISSUING CLINICAL ALERTS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP HEALY, B (reprint author), NIH, BETHESDA, MD 20892 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 23 PY 1993 VL 269 IS 24 BP 3096 EP 3096 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LH145 UT WOS:A1993LH14500005 ER PT J AU HEALY, B AF HEALY, B TI WHEN TO DO A CLINICAL ALERT SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP HEALY, B (reprint author), NIH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 23 PY 1993 VL 269 IS 24 BP 3096 EP 3096 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LH145 UT WOS:A1993LH14500006 ER PT J AU LINDBERG, DAB SIEGEL, ER RAPP, BA WALLINGFORD, KT WILSON, SR AF LINDBERG, DAB SIEGEL, ER RAPP, BA WALLINGFORD, KT WILSON, SR TI USE OF MEDLINE BY PHYSICIANS FOR CLINICAL PROBLEM-SOLVING SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID INFORMATION AB Objective.-To understand the Ways in which computer-mediated searching of the biomedical literature affects patient care and other professional activities. Undertaken to determine the ways in which on-line access to the biomedical literature via the National Library of Medicine's MEDLINE database ''makes a difference'' in what physicians do when confronted with a medical problem requiring new or additional information. Design.-An adaptation of the Critical Incident Technique used to gather detailed reports of MEDLINE search results that were especially helpful (or not helpful) in carrying out the individual's professional activities. The individual physician was the source of the patient care incident reports. One thousand one hundred fifty-eight reports were systematically analyzed from three different perspectives: (1) why the information was sought; (2) the effect of having (or not having) the needed information on professional decisions and actions; and (3) the outcome of the search. Participants and Setting.-Telephone interviews were carried out with a purposive sample of 552 physicians, scientists, and other professionals working in a variety of clinical care and other settings. Of these, 65% were direct users of MEDLINE throughout the United States, and 35% had MEDLINE searches conducted for them either at a major health sciences center or in community hospitals. Results.-Three comprehensive and detailed inventories that describe the motivation for the searches, how search results affected the actions and decisions of the individual who initiated the search, and how they affected the outcome of the situation that motivated the search. Conclusions.-MEDLINE searches are being carried out by and for physicians to meet a wide diversity of clinical information needs. Physicians report that in situations involving individual patients, rapid access to the biomedical literature via MEDLINE is at times critical to sound patient care and favorably influences patient outcomes. C1 NATL LIB MED,8600 ROCKVILLE PIKE,BETHESDA,MD 20894. AMER INST RES,PALO ALTO,CA 94302. NR 17 TC 125 Z9 125 U1 0 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 23 PY 1993 VL 269 IS 24 BP 3124 EP 3129 DI 10.1001/jama.269.24.3124 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA LH145 UT WOS:A1993LH14500026 PM 8505815 ER PT J AU ROUAULT, TA AF ROUAULT, TA TI HEREDITARY HEMOCHROMATOSIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Discussion ID IRON DEPLETION; HYPOGONADISM RP ROUAULT, TA (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 22 TC 12 Z9 13 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 23 PY 1993 VL 269 IS 24 BP 3152 EP 3154 DI 10.1001/jama.269.24.3152 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA LH145 UT WOS:A1993LH14500031 PM 8505819 ER PT J AU PARKER, CE PERKINS, JR TOMER, KB SHIDA, Y OHARA, K AF PARKER, CE PERKINS, JR TOMER, KB SHIDA, Y OHARA, K TI NANOSCALE PACKED CAPILLARY LIQUID-CHROMATOGRAPHY ELECTROSPRAY-IONIZATION MASS-SPECTROMETRY - ANALYSIS OF PENICILLINS AND CEPHEMS SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS LA English DT Article ID FAST-ATOM-BOMBARDMENT; BETA-LACTAM ANTIBIOTICS; ZONE ELECTROPHORESIS; INNER DIAMETERS; BOVINE-MILK; DEGRADATION; INTERFACE; PHARMACOKINETICS; CEPHALOSPORINS; CONFIRMATION AB A series of seventeen penicillins and cephems (cephalosporins and cephamycins) was examined by electrospray ionization. Separations by nanoscale packed-capillary liquid chromatography, with sub-microliter flow-rates, were performed using methanol-water and acetonitrile-water both containing trifluoroacetic acid gradients. In the on-column analyses. the protonated species usually predominate, and the fragment ions are often present which can be used for confirmation of compound identity. With combined nanoscale packed-capillary liquid chromatography-electrospray ionization mass spectrometry, separations and full-scan mass spectra can be obtained on *q12-15 ng of analyte, allowing the analysis of therapeutic levels of these antibiotics from only a few microliters of serum. C1 TOKYO COLL PHARM,DEPT CHEM ANAL,TOKYO 19203,JAPAN. TOKYO COLL PHARM,DEPT MICROBIOL,TOKYO 19203,JAPAN. RP PARKER, CE (reprint author), NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709, USA. RI Tomer, Kenneth/E-8018-2013 NR 36 TC 24 Z9 24 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR-BIOMED JI J. Chromatogr.-Biomed. Appl. PD JUN 23 PY 1993 VL 616 IS 1 BP 45 EP 57 DI 10.1016/0378-4347(93)80470-O PG 13 WC Chemistry, Analytical SC Chemistry GA LL225 UT WOS:A1993LL22500006 PM 8376492 ER PT J AU SOLARY, E LETEURTRE, F PAULL, KD SCUDIERO, D HAMEL, E POMMIER, Y AF SOLARY, E LETEURTRE, F PAULL, KD SCUDIERO, D HAMEL, E POMMIER, Y TI DUAL INHIBITION OF TOPOISOMERASE-II AND TUBULIN POLYMERIZATION BY AZATOXIN, A NOVEL CYTOTOXIC AGENT SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID TUMOR-CELL-LINES; DNA STRAND BREAKS; PODOPHYLLOTOXIN; ADRIAMYCIN; TENIPOSIDE; CLEAVAGE; ANALOGS; DRUGS AB Azatoxin (NSC 640737) is a synthetic molecule that was rationally designed as a topoisomerase II inhibitor (Leteurtre et al., Cancer Res 52: 4478-4483, 1992). The present study was undertaken in order to investigate the molecular pharmacology and the cytotoxic activity of azatoxin in human tumor cells. Alkaline elution experiments performed in HL-60 cells demonstrated that: (1) azatoxin induces DNA-protein cross-links and protein-linked DNA single- and double-strand breaks characteristic of topoisomerase II inhibition in HL-60 cells; and (2) the potency of azatoxin is comparable to that of etoposide (VP-16). Testing of azatoxin in 45 human cell lines in the National Cancer Institute (NCI) in vitro Drug Screening Program indicated that azatoxin was potent (mean IC50 = 0.13 muM), but that its cell line sensitivity profile was correlated with that of tubule inhibitors rather than that of topoisomerase II inhibitors. These data led us to investigate the anti-tubulin activity of azatoxin. We found that azatoxin inhibited tubulin polymerization in vitro and was a mitotic inhibitor at 1 muM and above in the human colon cancer cell line KM20L2. In these cells topoisomerase II inhibition, as detected by the induction of protein-linked DNA strand breaks, required azatoxin concentrations of at least 10 muM. In summary, azatoxin is a potent cytotoxic agent that inhibited both tubulin and topoisomerase II. At lower azatoxin concentrations the former activity prevailed whereas at higher concentrations topoisomerase II inhibition became prominent. C1 NCI,BLDG 37,RM 5C25,BETHESDA,MD 20892. DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNACORP,FREDERICK,MD 21702. NR 27 TC 48 Z9 48 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD JUN 22 PY 1993 VL 45 IS 12 BP 2449 EP 2456 DI 10.1016/0006-2952(93)90226-M PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LK593 UT WOS:A1993LK59300012 PM 8392342 ER PT J AU JOHNSTON, PG DRAKE, JC STEINBERG, SM ALLEGRA, CJ AF JOHNSTON, PG DRAKE, JC STEINBERG, SM ALLEGRA, CJ TI QUANTITATION OF THYMIDYLATE SYNTHASE IN HUMAN TUMORS USING AN ULTRASENSITIVE ENZYME-LINKED IMMUNOASSAY SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID SYNTHETASE; 5-FLUOROURACIL; CHEMOTHERAPY; CARCINOMA; CANCER; CELLS; 2'-DEOXYURIDYLATE; INHIBITION; BINDING; TARGET AB Thymidylate synthase (TS; EC 2.1.1.45) is an important therapeutic target for fluoropyrimidine cytotoxic drugs that are widely used for the treatment of solid tumors. Using the monoclonal antibody TS 106, we have developed an ultrasensitive enzyme-linked immunoassay (ELISA) for the detection and quantitation of TS. Using a chemiluminescent ELISA technique, TS was detectable in serially diluted lysates from NCI H630 and HCT 116 human colon carcinoma cell lines. The ELISA assay was reliably able to detect activity down to a level of 30 attamol of TS protein above background (P2 = 0.016). The usable range of detection was from 0.03 to 500 fmol of enzyme. There was a close correlation between the optical density signal and the total TS enzyme between both cell lines (r2 = 0.96). The ELISA was used to measure TS in cytosolic extracts from human tumor samples, and it was able to quantitate TS levels using as little as 1-mg tumor biopsy samples. The mean total TS measured by ELISA in seven tumor samples from patients with breast cancer and sarcomas was 131 fmol/mg cytosolic protein (range 60-240) compared with a mean TS of 85 fmol/mg cytosolic protein (range 35-163) using the fluorodeoxyuridine monophosphate binding assay. While the TS levels were uniformly higher when measured by ELISA, there was close proportional agreement between both assays (r2 = 0.84). Thus, the chemiluminescent TS ELISA would appear to be an extremely sensitive and specific assay that may be used to quantitate TS in tumor tissue specimens. C1 NCI,DIV CANC TREATMENT,BIOSTAT & DATA MANAGEMENT SECT,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. RP JOHNSTON, PG (reprint author), NCI,NAVY MED ONCOL BRANCH,BLDG 8,ROOM 5101,8901 WISCONSIN AVE,BETHESDA,MD 20892, USA. NR 21 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 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD JUN 22 PY 1993 VL 45 IS 12 BP 2483 EP 2486 DI 10.1016/0006-2952(93)90230-T PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LK593 UT WOS:A1993LK59300016 PM 8328986 ER PT J AU POZSGAY, V GLAUDEMANS, CPJ ROBBINS, JB SCHNEERSON, R AF POZSGAY, V GLAUDEMANS, CPJ ROBBINS, JB SCHNEERSON, R TI SYNTHESIS OF A TETRASACCHARIDE DONOR CORRESPONDING TO THE O-SPECIFIC POLYSACCHARIDE OF SHIGELLA-DYSENTERIAE TYPE-1 SO CARBOHYDRATE RESEARCH LA English DT Article ID 2-(TRIMETHYLSILYL)ETHYL GLYCOSIDES; FACILE SYNTHESIS; TRI-SACCHARIDE; OLIGOSACCHARIDES; TRANSFORMATION; ANTIGEN; UNIT AB O-(2,4-Di-O-benzoyl-3-O-chloroacetyl-alpha-L-rhamnopyranosyl)-(1 --> 2)-O-(3,4,6-tri-O-benzoyl-alpha-D-galactopyranosyl)-(1 --> 3)-O-(2-acetamido-4,6-di-O-acetyl-2-deoxy-alpha-D-glucopyranosyl)-(1 --> 3)-2,4-di-O-benzoyl-alpha-L-rhamnopyranosyl trichloroacetimidate (1) was synthesized in a stepwise manner, using the following monosaccharide units: 2-(trimethylsilyl)ethyl 2,4-di-O-benzoyl-alpha-L-rhamnopyranoside, 2-azido-4,6-O-benzylidene-3-O-chloroacetyl-2-deoxy-beta-D-glucopyranosyl chloride, methyl 3,4,6-tri-O-benzoyl-2-O-(4-methoxybenzyl)-1-thio-beta-D-galactopyranoside, and 2,4-di-O-benzoyl-3-O-chloroacetyl-alpha-L-rhamnopyranosyl chloride. Compound 1 corresponds to a complete tetrasaccharide repeating unit of the O-specific polysaccharide of the lipopolysaccharide of Shigella dysenteriae type 1. C1 NIADDKD,MED CHEM LAB,BETHESDA,MD 20892. RP POZSGAY, V (reprint author), NICHHD,DEV & MOLEC IMMUN LAB,BETHESDA,MD 20892, USA. NR 23 TC 16 Z9 16 U1 1 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD JUN 21 PY 1993 VL 244 IS 2 BP 259 EP 273 PG 15 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA LH555 UT WOS:A1993LH55500006 PM 8348552 ER PT J AU REUVENY, S KIM, YJ KEMP, CW SHILOACH, J AF REUVENY, S KIM, YJ KEMP, CW SHILOACH, J TI PRODUCTION OF RECOMBINANT PROTEINS IN HIGH-DENSITY INSECT CELL-CULTURES SO BIOTECHNOLOGY AND BIOENGINEERING LA English DT Note DE INSECT CELLS; HIGH DENSITY CULTURE; RECOMBINANT PROTEIN PRODUCTION ID NUCLEAR POLYHEDROSIS-VIRUS; EXPRESSION SYSTEM; BACULOVIRUS AB The effect of the growth phase of Spodoptera frugiperda (Sf9) cells on the production of recombinant proteins (beta-galactosidase and glucocerebrosidase) was investigated. Cells infected with the recombinant Autographa californica nuclear polyhedrosis virus at the late exponential and stationary phases yielded low quantities of expressed protein. Highest enzyme yields were obtained using Sf9 cells from the early exponential phase (0.9 mg beta-galactosidase/10(6) cells and 1.7 mug glucocerebrosidase/10(6) cells). Infection of resuspension of cells collected from various phases of growth in fresh medium resulted in 75% restoration of maximal expression levels. This finding suggested either nutrient limitation or waste product accumulation as the cause of the decrease in productivity at the latter phases of growth. Further experiments revealed that the highest productivity levels could be obtained with cultures of Sf9 cells grown in a fermentor to a cell concentration of 4 x 10(6) mL-1. The medium needed to be replaced prior to infection with the recombinant virus and supplemented with a mixture of glucose, L-glutamine, and yeastolate ultrafiltrate. C1 NIDDK,LCDB,BIOTECHNOL UNIT,BETHESDA,MD 20892. NR 15 TC 51 Z9 51 U1 1 U2 3 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3592 J9 BIOTECHNOL BIOENG JI Biotechnol. Bioeng. PD JUN 20 PY 1993 VL 42 IS 2 BP 235 EP 239 DI 10.1002/bit.260420211 PG 5 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA LD110 UT WOS:A1993LD11000010 PM 18612984 ER PT J AU MERLO, GR BERNARDI, A DIELLA, F VENESIO, T CAPPA, APM CALLAHAN, R LISCIA, DS AF MERLO, GR BERNARDI, A DIELLA, F VENESIO, T CAPPA, APM CALLAHAN, R LISCIA, DS TI IN PRIMARY HUMAN BREAST CARCINOMAS MUTATIONS IN EXONS-5 AND 6 OF THE P53 GENE ARE ASSOCIATED WITH A HIGH S-PHASE INDEX SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID TUMOR SUPPRESSOR GENE; CELL-PROLIFERATION; TRANSFORMATION; CANCERS; MUTANT AB A series of 121 human breast tumors was screened for point mutations in exons 5 through 8 of the p53 gene, by SSCP analysis. On the same tumor samples, the S-phase index (SPI) was determined by the incorporation of BUdR in fresh tissue. p53 mutations were observed in 29% of the cases. The frequency of point mutations for the individual exons was: exon 5, 10.0%; exon 6, 9.9%; exon 7, 7. 1% and exon 8, 5.5%. Two mutations detected by SSCP were confirmed by sequencing the p53 cDNA. The presence of a p53 mutation, irrespective of its location, correlates (p = 0.003) with a high SPI. This association appears to primarily reflect mutations in exon 5 (p = 0.0002) and exon 6 (p = 0.05), since mutations in exons 7 and 8 failed to show any association. These results indicate that mutations in the pS3 gene identify highly proliferating tumors, and that the position of the p53 mutation may have different effects upon the proliferative activity of tumor cells in vivo. (C) 1993 Wiley-Liss, Inc. C1 NCI,TUMOR IMMUNOL & BIOL LAB,ONCOGENE SECT,BETHESDA,MD 20892. S GIOVANNI HOSP USL 1,ANAT PATHOL SECT,I-10123 TURIN,ITALY. NR 24 TC 33 Z9 33 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD JUN 19 PY 1993 VL 54 IS 4 BP 531 EP 535 DI 10.1002/ijc.2910540402 PG 5 WC Oncology SC Oncology GA LJ491 UT WOS:A1993LJ49100001 PM 8514444 ER PT J AU KNIGHT, RD PARSHAD, R PRICE, FM TARONE, RE SANFORD, KK AF KNIGHT, RD PARSHAD, R PRICE, FM TARONE, RE SANFORD, KK TI X-RAY-INDUCED CHROMATID DAMAGE IN RELATION TO DNA-REPAIR AND CANCER INCIDENCE IN FAMILY MEMBERS SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID CELL-CYCLE PERIOD; ATAXIA-TELANGIECTASIA; CHROMOSOMAL RADIOSENSITIVITY; G2; IRRADIATION; ABERRATIONS; LYMPHOCYTES; SENSITIVITY AB The cytogenetic response to G2-phase X-irradiation was examined in phytohemagglutinin-stimulated peripheral-blood lymphocytes from 69 individuals, a few of whom were cancer patients. The cancer patients had not received radiation or chemotherapy. The responses of cells arrested by Colcemid 30 to 90 min after X-irradiation (58R) could be divided into 2 distinct categories: 51 individuals had aberration frequencies typical of normal individuals in previous studies, while 18 others had a 2- to 3-fold higher frequency of chromatid breaks and gaps. Because chromatid breaks and gaps result from unrepaired DNA strand breaks, the first category may represent an efficient DNA repair phenotype, while the second may represent a deficient repair phenotype. The individuals with the deficient G2 response reported having first- and second-degree relatives with a 3.6- and 2.2-fold higher mean frequency of cancer, respectively. The present results, together with those from earlier studies of families with a genetic disorder predisposing to cancer, suggest that this deficient cytogenetic response to G2 phase X-irradiation is associated with a high risk of cancer. (C) 1993 Wiley-Liss, Inc. C1 NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,RM 2015,BETHESDA,MD 20892. NCI,BIOSTAT BRANCH,BETHESDA,MD 20892. WALTER REED ARMY INST RES,DIV HEMATOL,WASHINGTON,DC 20307. HOWARD UNIV,COLL MED,DEPT PATHOL,WASHINGTON,DC 20059. NR 23 TC 62 Z9 63 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD JUN 19 PY 1993 VL 54 IS 4 BP 589 EP 593 DI 10.1002/ijc.2910540412 PG 5 WC Oncology SC Oncology GA LJ491 UT WOS:A1993LJ49100011 PM 8514450 ER PT J AU THOMAS, DL MAHLEY, RW BADUR, S PALAOGLU, KE QUINN, TC AF THOMAS, DL MAHLEY, RW BADUR, S PALAOGLU, KE QUINN, TC TI EPIDEMIOLOGY OF HEPATITIS-E VIRUS-INFECTION IN TURKEY SO LANCET LA English DT Note ID NON-B HEPATITIS; TRANSMITTED NON-A; TRANSMISSION AB The seroprevalence and risk factors for infection with hepatitis E virus (HEV) were analysed in five regions of Turkey, where one-third of acute hepatitis cases are non-A, non-B. Antibodies to HEV (anti-HEV) were found in 80 (5.9%) of 1350 subjects. Independent predictors of anti-HEV were age over 25 years, less than elementary education, antibodies to hepatitis C virus, and residence in the warmest region (Adana). Whereas none of 105 subjects in the second decade of life were HEV seropositive, 17 (3.7%) of 464 and 28 (9.1%) of 308 of those in the third and fourth decades of life, respectively, had anti-HEV (p < 0.001). These data demonstrate that in Turkey HEV is more prevalent in warmer regions and in adults, beginning in the third decade of life. C1 ISTANBUL FAC MED,DEPT MICROBIOL,ISTANBUL,TURKEY. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. AMER BRISTOL HOSP,GLADSTONE RES INST,ISTANBUL,TURKEY. RP THOMAS, DL (reprint author), JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,1155 ROSS BLDG,720 RUTLAND AVE,BALTIMORE,MD 21205, USA. NR 10 TC 70 Z9 72 U1 0 U2 2 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD JUN 19 PY 1993 VL 341 IS 8860 BP 1561 EP 1562 DI 10.1016/0140-6736(93)90698-G PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA LH550 UT WOS:A1993LH55000005 PM 8099641 ER PT J AU COTTLERFOX, M SPITZER, TR AF COTTLERFOX, M SPITZER, TR TI IMMUNOGLOBULIN PREPARATIONS, ACUTE GRAFT-VERSUS-HOST DISEASE, AND INFECTION AFTER MARROW TRANSPLANT SO LANCET LA English DT Letter C1 MASSACHUSETTS GEN HOSP,BONE MARROW TRANSPLANT UNIT,BOSTON,MA 02114. RP COTTLERFOX, M (reprint author), NIH,DEPT TRANSFUS MED,BETHESDA,MD 20892, USA. NR 4 TC 2 Z9 3 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD JUN 19 PY 1993 VL 341 IS 8860 BP 1592 EP 1592 DI 10.1016/0140-6736(93)90726-W PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LH550 UT WOS:A1993LH55000026 PM 8099659 ER PT J AU MARGOLIS, RL CHUANG, DM DICK, D WEISS, SRB POST, RM AF MARGOLIS, RL CHUANG, DM DICK, D WEISS, SRB POST, RM TI EFFECT OF COCAINE, LIDOCAINE KINDLING AND CARBAMAZEPINE ON BATRACHOTOXIN-INDUCED PHOSPHOINOSITIDE HYDROLYSIS IN RAT-BRAIN SLICES SO BRAIN RESEARCH LA English DT Article DE PHOSPHOINOSITIDE; KINDLING; COCAINE, LIDOCAINE; ANESTHETIC; NA; BATRACHOTOXIN; IBOTENATE ID SENSITIVE SODIUM-CHANNELS; LOCAL-ANESTHETICS; SYNAPTONEUROSOMES; INHIBITION; CELLS; STIMULATION; BREAKDOWN; CORTEX; AGENTS; INFLUX AB Repeated administration of a subconvulsant dose of a local anesthetic will eventually induce seizures, a phenomenon similar to electrical kindling. We have investigated the effect of repeated lidocaine and cocaine administration on the phosphoinositide (PI) hydrolysis induced by batrachotoxin (BTX), a specific Na channel activator. Rats were injected with cocaine or saline daily for 6 days and PI hydrolysis was assayed in sliced frontal cortex. Cocaine treatment had no effect on BTX-induced PI hydrolysis while in vitro cocaine blocked the BTX effect. In a second experiment, rats received daily injections of lidocaine or saline. After a rat developed at least two seizures, it was sacrificed together with a rat receiving lidocaine injections which had never seized and a rat receiving saline injections. Basal, BTX and ibotenic acid (IBO; a glutamate receptor agonist)-stimulated PI hydrolysis did not differ among the three groups in slices of either hippocampus (HC) or piriform cortex (PC) though IBO-stimulated PI hydrolysis was much greater in the HC than in the PC. Neither in vitro nor in vivo carbamazepine altered the effect of cocaine on BTX-induced PI hydrolysis. These results demonstrate that local anesthetic kindling does not alter PI hydrolysis coupled to Na channel or IBO activation. C1 NIMH,BIOL PSYCHIAT BRANCH,BLDG 10,ROOM 3N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 31 TC 4 Z9 4 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 18 PY 1993 VL 614 IS 1-2 BP 185 EP 190 DI 10.1016/0006-8993(93)91033-O PG 6 WC Neurosciences SC Neurosciences & Neurology GA LJ044 UT WOS:A1993LJ04400024 PM 8394185 ER PT J AU SCHAAD, NC PARFITT, A RUSSELL, JT SCHAFFNER, AE KORF, HW KLEIN, DC AF SCHAAD, NC PARFITT, A RUSSELL, JT SCHAFFNER, AE KORF, HW KLEIN, DC TI SINGLE-CELL [CA2+]I ANALYSIS AND BIOCHEMICAL-CHARACTERIZATION OF PINEALOCYTES IMMOBILIZED WITH NOVEL ATTACHMENT PEPTIDE PREPARATION SO BRAIN RESEARCH LA English DT Article DE PINEALOCYTE; CALCIUM; NOREPINEPHRINE; MELATONIN; CYCLIC NUCLEOTIDE; N-ACETYLTRANSFERASE; IMAGE ANALYSIS ID RAT PINEALOCYTES; GLAND; CULTURE; CALCIUM; ADENOSINE-3',5'-MONOPHOSPHATE; BINDING; NEURONS AB Single-cell image analysis of rat pinealocytes has been difficult because they do not attach readily to coated or uncoated surfaces and typically adhere in clusters to fibroblast-like cells. In the present report, a new method for the rapid attachment of rat pinealocytes is described. Cells were prepared using papain digestion and density centrifugation and then were placed on coverslips or slides coated with PepTite-2000TM, a preparation containing the attachment peptide sequence Arg-Gly-Asp. Cells immobilized with this preparation responded to norepinephrine treatment with an increase in cyclic AMP and melatonin production. Single-cell analysis of Fura-2-loaded cells revealed that norepinephrine increased [Ca2+]i. This development makes it possible to conduct routine single-cell image analysis and other studies of freshly isolated rat pinealocytes. C1 NICHHD,NEUROENDOCRINOL SECT,BETHESDA,MD 20892. NINCDS,NEUROPHYSIOL LAB,BETHESDA,MD 20892. NICHHD,DEV NEUROBIOL LAB,NEURONAL SECRETORY SYST SECT,BETHESDA,MD 20892. UNIV FRANKFURT,CTR MORFOL,NEUROBIOL SECT,W-6000 FRANKFURT,GERMANY. NR 27 TC 35 Z9 35 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 18 PY 1993 VL 614 IS 1-2 BP 251 EP 256 DI 10.1016/0006-8993(93)91042-Q PG 6 WC Neurosciences SC Neurosciences & Neurology GA LJ044 UT WOS:A1993LJ04400033 PM 8394187 ER PT J AU MURPHY, E HIENY, S SHER, A OGARRA, A AF MURPHY, E HIENY, S SHER, A OGARRA, A TI DETECTION OF IN-VIVO EXPRESSION OF INTERLEUKIN-10 USING A SEMIQUANTITATIVE POLYMERASE CHAIN-REACTION METHOD IN SCHISTOSOMA-MANSONI-INFECTED MICE SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE SCHISTOSOMA-MANSONI; T-HELPER; INTERLEUKIN; REVERSE TRANSCRIPTION; POLYMERASE CHAIN REACTION, SEMIQUANTITATIVE ID MESSENGER-RNA; CYTOKINE PRODUCTION; CELLS AB A modified polymerase chain reaction (PCR) assay for analysis of cytokine gene expression from reverse-transcribed (R/T) RNA obtained from small numbers of cells is described in detail. This method employs a previously described dot-blot format and utilizes a target specific radioactive oligonucleotide probe which hybridizes to the PCR amplified product, thus increasing both specificity and sensitivity. This obviates the need for repeated electrophoresis gels and easily accommodates large experiments (e.g., numerous samples or kinetic studies), using small amounts of RNA from low cell numbers. Manipulation of many samples is further enhanced with the use of a PCR thermocycler, which like the dot-blot apparatus is designed in a 96-well format. We describe the use of the house-keeping enzyme hypoxanthine phosphoribosyltransferase (HPRT) as an internal standard, which is especially suitable since its range of detectability of expression is similar to that of the cytokines under test. This enables one to obtain an accurate measure of losses or degradation of RNA, as well as controlling for efficiency of the R/T and PCR reactions. These reactions are further controlled by inclusion of a standard curve consisting of a titration of a known amount of RNA from a cell line expressing the cytokine under test. As well as controlling for the R/T-PCR, this standard curve also enables one to obtain a semi-quantitative measure of cytokine expression by different cell populations during an immune response. We show that this method can be used successfuly for studying differential expression of IL-10 in different microenvironments during infection of mice with Schistosoma mansoni. C1 DNAX RES INST MOLEC & CELLULAR BIOL INC,DEPT IMMUNOL,901 CALIF AVE,PALO ALTO,CA 94304. NIAID,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,BETHESDA,MD 20892. OI O'Garra, Anne/0000-0001-9845-6134 NR 18 TC 105 Z9 105 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD JUN 18 PY 1993 VL 162 IS 2 BP 211 EP 223 DI 10.1016/0022-1759(93)90386-L PG 13 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA LK095 UT WOS:A1993LK09500008 PM 7686199 ER PT J AU TAKIZAWA, F KINET, JP ADAMCZEWSKI, M AF TAKIZAWA, F KINET, JP ADAMCZEWSKI, M TI BINDING OF PHYCOERYTHRIN AND ITS CONJUGATES TO MURINE LOW-AFFINITY RECEPTORS FOR IMMUNOGLOBULIN-G SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Note DE PHYCOERYTHRIN; FLOW CYTOMETRY; FC RECEPTOR; (MOUSE) ID FC-RECEPTORS; MACROPHAGE AB Conjugates of R-phycoerythrin are widely used for immunohistochemistry, especially for two-color flow cytometry. Their use is however limited by their apparent tendency to bind non-specifically. Using cells transfected with cDNAs for the murine low affinity receptors for immunoglobulin G (FcgammaRII and -III) and cells naturally expressing these receptors, we demonstrate that R-phycoerythrin and its conjugates bind specifically and inhibitably to FcgammaRII and -III. Immunofluorescence stainings of cells bearing these receptors, such as macrophages, monocytes, neutrophils, mast cells, subsets of T cells, and natural killer cells, may therefore not reflect the binding of antibody to antigen, but rather the binding of R-phycoerythrin to the receptors. C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,TWINBROOK II,RM 108,12441 PARKLAWN DR,ROCKVILLE,MD 20852. NR 8 TC 13 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD JUN 18 PY 1993 VL 162 IS 2 BP 269 EP 272 DI 10.1016/0022-1759(93)90392-K PG 4 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA LK095 UT WOS:A1993LK09500014 PM 8315294 ER PT J AU LANDSMAN, D AF LANDSMAN, D TI NO HMG-1 BOX SIGNATURE SO NATURE LA English DT Letter RP LANDSMAN, D (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BLDG 38A,ROOM 8N-807,BETHESDA,MD 20894, USA. RI Landsman, David/C-5923-2009; OI Landsman, David/0000-0002-9819-6675 NR 11 TC 5 Z9 5 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JUN 17 PY 1993 VL 363 IS 6430 BP 590 EP 590 DI 10.1038/363590b0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LH139 UT WOS:A1993LH13900038 PM 8510750 ER PT J AU DUFFNER, PK HOROWITZ, ME KRISCHER, JP FRIEDMAN, HS BURGER, PC COHEN, ME SANFORD, RA MULHERN, RK JAMES, HE FREEMAN, CR SEIDEL, FG KUN, LE AF DUFFNER, PK HOROWITZ, ME KRISCHER, JP FRIEDMAN, HS BURGER, PC COHEN, ME SANFORD, RA MULHERN, RK JAMES, HE FREEMAN, CR SEIDEL, FG KUN, LE TI POSTOPERATIVE CHEMOTHERAPY AND DELAYED RADIATION IN CHILDREN LESS-THAN 3 YEARS OF AGE WITH MALIGNANT BRAIN-TUMORS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID RANDOMIZED TRIAL; PHASE-II; IRRADIATION; SURVIVAL; VINCRISTINE; THERAPY; GROWTH AB Background. Among patients with malignant brain tumors, infants and very young children have the worst prognosis and the most severe treatment-related neurotoxic effects. Therefore, in 1986, the Pediatric Oncology Group began a study in which postoperative chemotherapy was given in order to permit a delay in the delivery of radiation to the developing brain. Methods. Children under 36 months of age with biopsy-proved malignant brain tumors were treated postoperatively with two 28-day cycles of cyclophosphamide plus vincristine, followed by one 28-day cycle of cisplatin plus etoposide. This sequence was repeated until the disease progressed or for two years in 132 children under 24 months of age at diagnosis and for one year in 66 children 24 to 36 months of age at diagnosis. After this, the patients received radiation therapy. The response to the first two cycles of chemotherapy was measured in 102 patients with residual postoperative disease. Results. The first two cycles of cyclophosphamide and vincristine produced complete or partial responses in 39 percent of the 102 patients who could be evaluated. The response rates were highest among patients with medulloblastomas, malignant gliomas, or ependymomas. Patients with brain-stem gliomas or embryonal tumors (primitive neuroectodermal tumors) had little or no response. The progression-free survival rate was 41 percent at one year for children who were 24 to 36 months old at diagnosis and 39 percent at two years for those under 24 months of age at diagnosis. Multivariate analysis identified embryonal tumors as a significant adverse prognostic feature (relative risk, 2.2; 95 percent confidence interval, 1.4 to 3.4) and complete resection as a favorable feature (relative risk, 0.33; 95 percent confidence interval, 0.20 to 0.54). Complete responses to chemotherapy were associated with a progression-free survival rate approaching that achieved with gross total resection. A comparison of cognitive evaluations obtained at base line and after one year of chemotherapy revealed no evidence of deterioration in cognitive function. Conclusions. Chemotherapy appears to be an effective primary postoperative treatment for many malignant brain tumors in young children. Disease control for one or two years in a large minority of patients permitted a delay in the delivery of radiation and, on the basis of preliminary results, a reduction in neurotoxicity. For patients who had undergone total surgical resection or who had a complete response to chemotherapy, the results are sufficiently encouraging to suggest that radiation therapy may not be needed in this subgroup of children after at least one year of chemotherapy. C1 SUNY Buffalo, SCH MED & BIOMED SCI, BUFFALO, NY 14260 USA. ROSWELL PK CANC INST, BUFFALO, NY USA. UNIV FLORIDA, PEDIAT ONCOL GRP STAT OFF, GAINESVILLE, FL 32611 USA. DUKE UNIV, MED CTR, DURHAM, NC 27710 USA. NCI, PEDIAT BRANCH, BETHESDA, MD 20892 USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA. CHILDRENS MERCY HOSP, KANSAS CITY, MO 64108 USA. UNIV CALIF SAN DIEGO, MED CTR, SAN DIEGO, CA 92103 USA. MONTREAL GEN HOSP, MONTREAL H3G 1A4, QUEBEC, CANADA. NR 34 TC 486 Z9 490 U1 1 U2 7 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUN 17 PY 1993 VL 328 IS 24 BP 1725 EP 1731 DI 10.1056/NEJM199306173282401 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA LG038 UT WOS:A1993LG03800001 PM 8388548 ER PT J AU KRICKA, LJ SCHMERFELDPRUSS, D KALADAS, P COLCHER, D SCASSELLATI, GA SECCAMANI, E COURTENAYLUCK, NS KOSMAS, C BEATTY, BG BEATTY, JD CHATENOUD, L ZIMMER, AM AUERBACH, B HEAL, AV AF KRICKA, LJ SCHMERFELDPRUSS, D KALADAS, P COLCHER, D SCASSELLATI, GA SECCAMANI, E COURTENAYLUCK, NS KOSMAS, C BEATTY, BG BEATTY, JD CHATENOUD, L ZIMMER, AM AUERBACH, B HEAL, AV TI SURVEY OF METHODS FOR MEASURING HUMAN ANTI-MOUSE ANTIBODIES SO CLINICA CHIMICA ACTA LA English DT Article DE HUMAN ANTI-MOUSE ANTIBODIES (HAMA); INTER-LABORATORY SURVEY ID MONOCLONAL-ANTIBODY; CARCINOEMBRYONIC ANTIGEN; 2-SITE IMMUNOASSAYS; THERAPY; INTERFERENCE; DIAGNOSIS AB Human anti-mouse antibodies (HAMA) methods were surveyed using a panel of 17 serum and two plasma specimens which were circulated to ten laboratories for analysis. The panel included HAMA-negative and HAMA-positive specimens (from patients given a variety of mouse monoclonal antibodies) and a specimen with a high rheumatoid factor titer. The participating laboratories used a diverse range of methods to determine HAMA and all three of the commercially available quantitative methods for HAMA were represented. The survey revealed significant differences in HAMA results among the different laboratories. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. SORIN BIOMED SPA,I-13040 SALUGGIA,ITALY. HAMMERSMITH HOSP,ROYAL POSTGRAD MED SCH,DEPT CLIN ONCOL,LONDON W12 0HS,ENGLAND. CITY HOPE NATL MED CTR,DIV SURG,DUARTE,CA 91010. NW MEM HOSP,DEPT CANC,CHICAGO,IL 60611. CYTOGEN CORP,PRINCETON,NJ 08540. HOP NECKER ENFANTS MALAD,CNRS,U25,INSERM,F-75730 PARIS,FRANCE. TAMPA VA,DEPT NUCL MED,TAMPA,FL 33612. BEHRINGWERKE AG,RES LABS,W-3550 MARBURG,GERMANY. RP KRICKA, LJ (reprint author), HOSP UNIV PENN,DEPT PATHOL & LAB MED,3400 SPRUCE ST,PHILADELPHIA,PA 19104, USA. NR 25 TC 15 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0009-8981 J9 CLIN CHIM ACTA JI Clin. Chim. Acta PD JUN 16 PY 1993 VL 215 IS 2 BP 153 EP 163 PG 11 WC Medical Laboratory Technology SC Medical Laboratory Technology GA LN371 UT WOS:A1993LN37100003 ER PT J AU SALIVE, ME HAVLIK, RJ AF SALIVE, ME HAVLIK, RJ TI BLOOD-PRESSURE AND SERUM CREATININE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP SALIVE, ME (reprint author), NIA,BETHESDA,MD 20892, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 16 PY 1993 VL 269 IS 23 BP 2983 EP 2984 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA LF941 UT WOS:A1993LF94100013 PM 8501833 ER PT J AU JOHNSON, CL RIFKIND, BM SEMPOS, CT CARROLL, MD BACHORIK, PS BRIEFEL, RR GORDON, DJ BURT, VL BROWN, CD LIPPEL, K CLEEMAN, JI AF JOHNSON, CL RIFKIND, BM SEMPOS, CT CARROLL, MD BACHORIK, PS BRIEFEL, RR GORDON, DJ BURT, VL BROWN, CD LIPPEL, K CLEEMAN, JI TI DECLINING SERUM TOTAL CHOLESTEROL LEVELS AMONG UNITED-STATES ADULTS - THE NATIONAL-HEALTH AND NUTRITION EXAMINATION SURVEYS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID DENSITY-LIPOPROTEIN CHOLESTEROL; LIPID RESEARCH CLINICS; MINNESOTA-HEART-SURVEY; EDUCATION-PROGRAM; DISEASE; TRENDS; MORTALITY; PLASMA; RISK AB Objective.-To examine the secular trend in serum total cholesterol levels of the US adult population. Design.-Nationally representative cross-sectional surveys with both an in-person interview and a medical examination that included the measurement of blood lipid levels. Setting/Participants.-Between 6000 and 13 000 adults aged 20 through 74 years examined in each of four separate national surveys during 1960 through 1962, 1971 through 1974, 1976 through 1980, and 1988 through 1991. Results.-Mean serum total cholesterol levels in US adults aged 20 through 74 years have consistently declined over the time period 1960 through 1991. More than half of the decline occurred during the time period 1976 through 1991. This decline occurred across the entire distribution of serum cholesterol levels and in all age-sex groups. High-density lipoprotein cholesterol and very low-density lipoprotein cholesterol levels have not changed, suggesting that the decline in total cholesterol levels is due to a decline in low-density lipoprotein cholesterol levels. Conclusions.-These results document a continuing and substantial decline in serum cholesterol levels among US adults. They suggest that public health programs, designed to reduce cholesterol levels, are proving successful. The observed downward trend in serum cholesterol levels has coincided with a continuing decline in coronary heart disease mortality. These observations suggest that the Healthy People 2000 goal of reducing the mean serum cholesterol level of US adults to no more than 200 mg/dL (5.17 mmol/L) is attainable. C1 NHLBI,NATL CHOLESTEROL EDUC PROGRAM,BLDG 31,ROOM 4A-05,BETHESDA,MD 20892. CTR DIS CONTROL & PREVENT,NATL CTR HLTH STAT,DIV HLTH EXAMINAT STAT,HYATTSVILLE,MD. NR 52 TC 388 Z9 399 U1 0 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 16 PY 1993 VL 269 IS 23 BP 3002 EP 3008 DI 10.1001/jama.269.23.3002 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA LF941 UT WOS:A1993LF94100029 PM 8501842 ER PT J AU SEMPOS, CT CLEEMAN, JI CARROLL, MD JOHNSON, CL BACHORIK, PS GORDON, DJ BURT, VL BRIEFEL, RR BROWN, CD LIPPEL, K RIFKIND, BM AF SEMPOS, CT CLEEMAN, JI CARROLL, MD JOHNSON, CL BACHORIK, PS GORDON, DJ BURT, VL BRIEFEL, RR BROWN, CD LIPPEL, K RIFKIND, BM TI PREVALENCE OF HIGH BLOOD CHOLESTEROL AMONG UNITED-STATES ADULTS - AN UPDATE BASED ON GUIDELINES FROM THE 2ND REPORT OF THE NATIONAL-CHOLESTEROL-EDUCATION-PROGRAM ADULT TREATMENT PANEL SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article AB Objective.-To estimate the current levels and trends in the proportion of US adults with high blood cholesterol based on guidelines from the second report of the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP II). Design.-Nationally representative cross-sectional surveys. Setting/Participants.-Data for 7775 participants 20 years of age and older from phase 1 of the third National Health and Nutrition Examination Survey (NHANES III) (data collected from 1988 through 1991) and for 9797 participants 20 through 74 years of age from NHANES II (data collected from 1976 through 1980) were used. Results.-From the data collection period in NHANES II (1976 through 1980) to the period in NHANES III (1988 through 1991), the proportion of adults with high blood cholesterol levels (greater-than-or-equal-to 240 mg/dL [6.21 mmol/L]) fell from 26% to 20%, while the proportion with desirable levels (<200 mg/dL [5.17 mmol/L]) rose f rom 44% to 49%. Currently, using the ATP II guidelines and NHANES III data, 40% of all adults 20 years of age and older would require fasting lipoprotein analysis; and 29% of all adults would be candidates for dietary therapy (as compared with 36%, using NHANES II data). Based on 1990 population data, it is estimated that approximately 52 million Americans 20 years of age and older would be candidates for dietary therapy. Assuming that dietary intervention would reduce low-density lipoprotein (LDL) cholesterol levels by 10%, as many as 7% of all adult Americans (approximately 12.7 million) might be candidates for cholesterol-lowering drugs. This estimate reflects approximately 4 million adults with established coronary heart disease, of whom half are aged 65 years and older, and up to 8.7 million adults without established coronary heart disease, of whom up to 3.1 million are aged 65 years and older. Conclusions.-Substantial progress has been made in reducing the prevalence of high blood cholesterol; yet a large proportion of all adults, approximately 29%, require dietary intervention for high blood cholesterol. C1 NHLBI,NATL CHOLESTEROL EDUC PROGRAM,BLDG 31,ROOM 4A-05,BETHESDA,MD 20892. CTR DIS CONTROL & PREVENT,NATL CTR HLTH STAT,DIV HLTH EXAMINAT STAT,HYATTSVILLE,MD. JOHNS HOPKINS UNIV,CTR CHILDRENS MED & SURG,BALTIMORE,MD 21218. NR 18 TC 298 Z9 304 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 16 PY 1993 VL 269 IS 23 BP 3009 EP 3014 DI 10.1001/jama.269.23.3009 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA LF941 UT WOS:A1993LF94100030 PM 8501843 ER PT J AU GRUNDY, SM BILHEIMER, D CHAIT, A CLARK, LT DENKE, M HAVEL, RJ HAZZARD, WR HULLEY, SB HUNNINGHAKE, DB KREISBERG, RA KRISETHERTON, P MCKENNEY, JM NEWMAN, MA SCHAEFER, EJ SOBEL, BE SOMELOFSKI, C WEINSTEIN, MC BREWER, HB CLEEMAN, JI DONATO, KA ERNST, N HOEG, JM RIFKIND, BM ROSSOUW, J SEMPOS, CT GALLIVAN, JM HARRIS, MN QUINTADLER, L AF GRUNDY, SM BILHEIMER, D CHAIT, A CLARK, LT DENKE, M HAVEL, RJ HAZZARD, WR HULLEY, SB HUNNINGHAKE, DB KREISBERG, RA KRISETHERTON, P MCKENNEY, JM NEWMAN, MA SCHAEFER, EJ SOBEL, BE SOMELOFSKI, C WEINSTEIN, MC BREWER, HB CLEEMAN, JI DONATO, KA ERNST, N HOEG, JM RIFKIND, BM ROSSOUW, J SEMPOS, CT GALLIVAN, JM HARRIS, MN QUINTADLER, L TI SUMMARY OF THE 2ND REPORT OF THE NATIONAL-CHOLESTEROL-EDUCATION-PROGRAM (NCEP) EXPERT PANEL ON DETECTION, EVALUATION, AND TREATMENT OF HIGH BLOOD CHOLESTEROL IN ADULTS (ADULT-TREATMENT-PANEL-II) SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article C1 NHLBI,NATL CHOLESTEROL EDUC PROGRAM,BLDG 31,ROOM 4A-05,BETHESDA,MD 20892. NR 0 TC 1826 Z9 1855 U1 1 U2 44 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 16 PY 1993 VL 269 IS 23 BP 3015 EP 3023 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA LF941 UT WOS:A1993LF94100031 ER PT J AU VERMUND, SH AF VERMUND, SH TI RISING HIV-RELATED MORTALITY IN YOUNG AMERICANS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID UNITED-STATES; AIDS; INFECTION; TRENDS; PREVALENCE; ZIDOVUDINE; EPIDEMIC; WOMEN RP VERMUND, SH (reprint author), NIAID,DIV AIDS,VACCINE TRIALS & EPIDEMIOL BRANCH,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. OI Vermund, Sten/0000-0001-7289-8698 NR 41 TC 8 Z9 8 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 16 PY 1993 VL 269 IS 23 BP 3034 EP 3035 DI 10.1001/jama.269.23.3034 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA LF941 UT WOS:A1993LF94100034 PM 8501847 ER PT J AU VUISTER, GW WANG, AC BAX, A AF VUISTER, GW WANG, AC BAX, A TI MEASUREMENT OF 3-BOND NITROGEN CARBON-J COUPLINGS IN PROTEINS UNIFORMLY ENRICHED IN N-15 AND C-13 SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Note ID 3-DIMENSIONAL NMR; CONSTANTS; MACROMOLECULES C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NR 19 TC 143 Z9 143 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD JUN 16 PY 1993 VL 115 IS 12 BP 5334 EP 5335 DI 10.1021/ja00065a071 PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA LH977 UT WOS:A1993LH97700071 ER PT J AU SCHIFFMAN, MH BAUER, HM HOOVER, RN GLASS, AG CADELL, DM RUSH, BB SCOTT, DR SHERMAN, ME KURMAN, RJ WACHOLDER, S STANTON, CK MANOS, MM AF SCHIFFMAN, MH BAUER, HM HOOVER, RN GLASS, AG CADELL, DM RUSH, BB SCOTT, DR SHERMAN, ME KURMAN, RJ WACHOLDER, S STANTON, CK MANOS, MM TI EPIDEMIOLOGIC EVIDENCE SHOWING THAT HUMAN PAPILLOMAVIRUS INFECTION CAUSES MOST CERVICAL INTRAEPITHELIAL NEOPLASIA SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID CANCER; WOMEN; RISK AB Background: Experimental studies have provided strong evidence that human papillomavirus (HPV) is the long-sought venereal cause of cervical neoplasia, but the epidemiologic evidence has been inconsistent. Purpose: Given improvements in HPV testing that have revealed a strong link between sexual activity history and cervical HPV infection, we conducted a large case-control study of HPV and cervical intraepithelial neoplasia (CIN) to evaluate whether sexual behavior and the other established risk factors for CIN influence risk primarily via HPV infection. Methods: We studied 500 women with CIN and 500 control subjects receiving cytologic screening at Kaiser Permanente, a large prepaid health plan, in Portland, Ore. The established epidemiologic risk factors for CIN were assessed by telephone interview. We performed HPV testing of cervicovaginal lavage specimens by gene amplification using polymerase chain reaction with a consensus primer to target the L1 gene region of HPV. Unconditional logistic regression analysis was used to estimate relative risk of CIN and to adjust the epidemiologic associations for HPV test results to demonstrate whether the associations were mediated by HPV. Results: The case subjects demonstrated the typical epidemiologic profile of CIN: They had more sex partners, more cigarette smoking, earlier ages at first sexual intercourse, and lower socioeconomic status. Statistical adjustment for HPV infection substantially reduced the size of each of these case-control differences. Seventy-six percent of cases could be attributed to HPV infection; the results of cytologic review suggested that the true percentage was even higher. Once HPV infection was taken into account, an association of parity with risk of CIN was observed in both HPV-negative and HPV-positive women. Conclusion: The data show that the great majority of all grades of CIN can be attributed to HPV infection, particularly with the cancer-associated types of HPV. Implications: In light of this conclusion, the investigation of the natural history of HPV has preventive as well as etiologic importance. C1 KAISER PERMANENTE,PORTLAND,OR. CETUS CORP,EMERYVILLE,CA 94608. JOHNS HOPKINS MED INST,DEPT PATHOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH PUBL HLTH,BALTIMORE,MD 21218. RP SCHIFFMAN, MH (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,EXECUT PLAZA N,RM 443,BETHESDA,MD 20892, USA. NR 29 TC 890 Z9 925 U1 0 U2 23 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JUN 16 PY 1993 VL 85 IS 12 BP 958 EP 964 DI 10.1093/jnci/85.12.958 PG 7 WC Oncology SC Oncology GA LF842 UT WOS:A1993LF84200011 PM 8388478 ER PT J AU ADAMSON, PC PITOT, HC BALIS, FM RUBIN, J MURPHY, RF POPLACK, DG AF ADAMSON, PC PITOT, HC BALIS, FM RUBIN, J MURPHY, RF POPLACK, DG TI VARIABILITY IN THE ORAL BIOAVAILABILITY OF ALL-TRANS-RETINOIC ACID SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ACUTE PROMYELOCYTIC LEUKEMIA; THERAPEUTIC ANTICANCER AGENTS; DIFFERENTIATION THERAPY AB Background: Orally administered all-trans-retinoic acid (all-trans-RA) can induce complete remission in a high proportion of patients with acute promyelocytic leukemia. A previous pharmacokinetic study in patients with acute promyelocytic leukemia raised the possibility that the absorption of orally administered all-trans-RA is a saturable process that would have significant clinical impact on dosing strategies. Purpose: This study was specifically designed to examine the saturability of all-trans-RA absorption by measuring the effect of doubling the oral dose of all-trans-RA on plasma drug concentration in patients receiving long-term oral therapy. Methods: Six patients with solid tumors received oral doses of 10-mg gelatin capsules of all-trans-RA. Patients were studied on 2 consecutive days after they receive d 28 days of all-trans-RA administered as two daily 78-mg/m2 doses. The study assigned the patients to two groups. Three patients took a 156-mg/m2 dose on day 28 and a 78-mg/m2 dose on day 29; the other three patients took the lower dose on day 28 and the double dose on day 29. Blood samples for the determination of all-trans-RA plasma concentration were obtained at 30-minute intervals starting just prior to drug administration and continuing for a total of 7 hours. The plasma concentration of all-trans-RA was measured by high-performance liquid chromatography. Results: Plasma concentrations following an oral dose of all-trans-RA were highly variable, with peak concentrations ranging from 0.07 to 1.2 muM for the 78-mg/m2 dose level. Doubling the dose from 78 to 156 mg/m2 increased plasma concentration in all six patients, but the increase was unpredictable and not related to dose, ranging from less than a 1.2-fold to more than a 10-fold increase. Conclusion: The current study does not support the hypothesis that the gastrointestinal absorption of all-trans-RA involves a saturable process but instead suggests that absorption is highly variable among patients. This wide interpatient variability suggests that pharmacokinetic drug monitoring may have an important role in the management of patients receiving all-trans-RA. C1 MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. RP ADAMSON, PC (reprint author), NCI,DEPT CANC TREATMENT,PEDIAT BRANCH,BLDG 10,RM 13N240,BETHESDA,MD 20892, USA. NR 19 TC 45 Z9 45 U1 1 U2 3 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JUN 16 PY 1993 VL 85 IS 12 BP 993 EP 996 DI 10.1093/jnci/85.12.993 PG 4 WC Oncology SC Oncology GA LF842 UT WOS:A1993LF84200016 PM 8388479 ER PT J AU SINGH, P PEDERSEN, LG AF SINGH, P PEDERSEN, LG TI ORTHORHOMBIC FORM OF THIOPURINOL - 1,5-DIHYDRO-4H-PYRAZOLO[3,4-D]PYRIMIDINE-4-THIONE SO ACTA CRYSTALLOGRAPHICA SECTION C-CRYSTAL STRUCTURE COMMUNICATIONS LA English DT Article ID LEISHMANIA-DONOVANI; CRYSTAL-STRUCTURE AB Thiopurinol crystallizes ill two forms. The crystal structure of the monoclinic form has been reported [Gadret, Goursolle & Leger (1974). Acta Cryst. B30, 1598-1602]. The orthorhombic form reported here has a hydrogen-bonded layered structure similar to the monoclinic form but differs from it in the stacking pattern of the purine bases. The interlayer separation (3.292 angstrom) is slightly smaller than that in the monoclinic form (3.426 angstrom). The H atom on the diazole ring is bonded to N(9). The relative magnitudes of the two exocyclic bond angles at N(9) subtended by H(9) are similar to those in the monoclinic form and in allopurinol, but differ from those in hypoxanthine, the related normal nucleobase. This trend for N(8)-purines is corroborated by ab initio molecular-orbital calculations and a literature search for related structures via the Cambridge Structural Database [Allen, Kennard & Taylor (1983). Acc. Chem. Res. 16, 146-153]. C1 NIEHS,DIV BIOMETRY & RISK ASSESSMENT,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,DEPT CHEM,CHAPEL HILL,NC 27599. RP SINGH, P (reprint author), N CAROLINA STATE UNIV,DEPT CHEM,RALEIGH,NC 27695, USA. RI Pedersen, Lee/E-3405-2013 OI Pedersen, Lee/0000-0003-1262-9861 NR 22 TC 2 Z9 2 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0108-2701 J9 ACTA CRYSTALLOGR C JI Acta Crystallogr. Sect. C-Cryst. Struct. Commun. PD JUN 15 PY 1993 VL 49 BP 1211 EP 1215 DI 10.1107/S0108270192013453 PN 6 PG 5 WC Chemistry, Multidisciplinary; Crystallography SC Chemistry; Crystallography GA LP186 UT WOS:A1993LP18600068 ER PT J AU HARRIS, TB BALLARDBARBASCH, R MADANS, J MAKUC, DM FELDMAN, JJ AF HARRIS, TB BALLARDBARBASCH, R MADANS, J MAKUC, DM FELDMAN, JJ TI OVERWEIGHT, WEIGHT-LOSS, AND RISK OF CORONARY HEART-DISEASE IN OLDER WOMEN - THE NHANES-I EPIDEMIOLOGIC FOLLOW-UP-STUDY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE AGING; BODY WEIGHT; CORONARY DISEASE; GERIATRICS; WEIGHT LOSS; WOMEN ID BODY-FAT DISTRIBUTION; BLOOD-PRESSURE; MORTALITY; OBESITY; POPULATION; GAIN; PROGNOSIS; LONGEVITY; PROJECT; PROGRAM AB Little is known about the relation of Overweight to risk of coronary heart disease in older women. In this paper, the authors used measured weight for 1,259 white women aged 65-74 years from the Epidemiologic Follow-up StudY of the First National Health and Nutrition Examination Survey to examine the effect of overweight on coronary heart disease incidence (mean length of follow-up, 14 years). They also used reported lifetime maximum weight to examine the effect of weight loss on this association. women with a Quetelet index (weight (kg)/height (m)2) of 29 or more showed an increased risk of coronary heart disease (relative risk (RR) = 1.5, 95% confidence interval (CI) 1.1-2.1) after adjustment for age and smoking in comparison with those with a Quetelet index of less than 21, while women with a Quetelet index of 23-24 had a lower risk of coronary heart disease (RR = 0.6,95% CI 0.4-0.9). However, the pattern of risk associated with measured weight was modified by weight loss. Among heavier women whose weight was relatively stable, those with a Quetelet index of 29 Or more had an increased risk of heart disease (RR = 2.7, 95% CI 1.7-4.4). Among those with greater weight loss, the relation between Quetelet index and risk of coronarY heart disease was J-shaped. overweight is an independent risk factor for coronary heart disease in older women, a finding strengthened after previous weight loss is accounted for. Reasons for the unexpected increase in risk of coronary heart disease in thinner women who lost weight are unclear, and further investigation is warranted. C1 NCI,BETHESDA,MD 20892. NATL CTR HLTH STAT,OFF ANALYSIS & EPIDEMIOL,HYATTSVILLE,MD 20782. RP HARRIS, TB (reprint author), NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,GATEWAY BLDG,ROOM 3C-309,BETHESDA,MD 20892, USA. NR 41 TC 74 Z9 77 U1 1 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 15 PY 1993 VL 137 IS 12 BP 1318 EP 1327 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LP660 UT WOS:A1993LP66000003 PM 8333413 ER PT J AU BURCHFIEL, CM REED, DM MARCUS, EB STRONG, JP HAYASHI, T AF BURCHFIEL, CM REED, DM MARCUS, EB STRONG, JP HAYASHI, T TI ASSOCIATION OF DIABETES-MELLITUS WITH CORONARY ATHEROSCLEROSIS AND MYOCARDIAL LESIONS - AN AUTOPSY STUDY FROM THE HONOLULU HEART PROGRAM SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ATHEROSCLEROSIS; AUTOPSY; DIABETES-MELLITUS; PROSPECTIVE STUDIES; RISK FACTORS ID ARTERY DISEASE; LIFESTYLE CHARACTERISTICS; INSULIN RESISTANCE; RISK-FACTORS; FRAMINGHAM; PREDICTORS; PATHOGENESIS; SEVERITY; ONSET; MEN AB While the excess risk of clinical cardiovascular disease among persons with diabetes mellitus is well established, most autopsy Studies have not been able to elucidate reasons for the excess, to assess potential selection bias, or to adjust for other cardiovascular risk factors. The purpose of this study was to examine the predictive relation between diabetes and autopsy evidence of coronary atherosclerosis and myocardial lesions. Among 8,006 Japanese-American men examined at baseline in 1965-1968 as part of the Honolulu Heart Program, 7,591 were free of cardiovascular disease, and 1,515 of these men died over a 17-year follow-up period. Protocol autopsies were performed for 83 diabetic men and 159 nondiabetic men. Diabetes status was defined using self-reported history and treatment at several examinations, as well as physician diagnoses during hospitalization between 1965 and 1984. An excess of coronary artery atherosclerosis, assessed by mean panel score (3.4 vs. 3.0, p = 0.017) and percentage of intimal surface with raised lesions (56.6% vs. 47.4%, p = 0.024), was present among diabetic men but diminished to nonsignificant levels (3.3 vs. 3.0, p = 0. 1 02, and 53.9% vs. 48.8%, p = 0.183, respectively) after adjustment for other cardiovascular risk factors. Myocardial lesions (acute, healing, or fibrotic) occurred significantly more frequently among diabetics than among nondiabetics (77.7% vs. 63.4%, p = 0.035), even after adjustment for other risk factors. Potential autopsy selection bias assessed in several ways appeared minimal. Among men with mild atherosclerosis, diabetics had more small and large myocardial lesions than did nondiabetics, although differences were not statistically significant (p < 0.10). It appears that the more adverse risk factor profile among diabetics accounts for some of the observed excess of coronary atherosclerosis. However, diabetes was independently associated with myocardial lesions, and these findings suggest a role for nonatherosclerotic mechanisms, such as clotting abnormalities or microvascular disease, in accounting for the excess clinical heart disease found in persons with diabetes. C1 LOUISIANA STATE UNIV,MED CTR,DEPT PATHOL,NEW ORLEANS,LA 70112. KUAKINI MED CTR,HONOLULU HEART PROGRAM,HONOLULU,HI. KUAKINI MED CTR,DEPT PATHOL,HONOLULU,HI. RP BURCHFIEL, CM (reprint author), NHLBI,HONOLULU HEART PROGRAM,347 N KUAKINI ST,HONOLULU,HI 96817, USA. FU NHLBI NIH HHS [N01-HC-02901] NR 69 TC 65 Z9 66 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 15 PY 1993 VL 137 IS 12 BP 1328 EP 1340 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LP660 UT WOS:A1993LP66000004 PM 8333414 ER PT J AU TAYLOR, JA WILCOX, AJ BOWES, WA LI, Y LIU, ET YOU, M AF TAYLOR, JA WILCOX, AJ BOWES, WA LI, Y LIU, ET YOU, M TI RISK OF MISCARRIAGE AND A COMMON VARIANT OF THE ESTROGEN-RECEPTOR GENE SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Note DE ABORTION; CASE-CONTROL STUDIES; DISEASE SUSCEPTIBILITY; GENES; POLYMERASE CHAIN REACTION; POLYMORPHISM (GENETIC); RECEPTORS, ESTROGEN ID SPONTANEOUS-ABORTION; BREAST-CANCER; POLYMORPHISM AB An inherited variant of the estrogen receptor gene was previously suggested to be a major determinant of a woman's risk of miscarriage. The authors tested this hypothesis in a case-control study of 29 women who had two or more miscarriages and 29 women with no miscarriages. All of the women had given birth in North Carolina between 1987 and 1990. Estrogen receptor genotype was determined by direct sequencing of DNA. The gene variant that supposedly produced the risk was found to contain only a silent substitution at codon 87. Furthermore, instead of an odds ratio of 25 (predicted by the previous study), the odds ratio found was 1.8 (95% confidence interval 0.3-11). For a hypothesis which now lacks biologic plausibility, this weak association provides little reason for further investigation. C1 UNIV N CAROLINA,SCH MED,DEPT OBSTET & GYNECOL,CHAPEL HILL,NC 27514. UNIV N CAROLINA,SCH MED,DEPT MED,CHAPEL HILL,NC 27514. MED COLL OHIO,DEPT PATHOL,TOLEDO,OH 43699. RP TAYLOR, JA (reprint author), NIEHS,EPIDEMIOL BRANCH,MD A3-05,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Liu, Edison/C-4141-2008; OI Wilcox, Allen/0000-0002-3376-1311; taylor, jack/0000-0001-5303-6398 NR 13 TC 25 Z9 27 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 15 PY 1993 VL 137 IS 12 BP 1361 EP 1364 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LP660 UT WOS:A1993LP66000007 PM 8333417 ER PT J AU KIPNIS, V FREEDMAN, LS BROWN, CC HARTMAN, A SCHATZKIN, A WACHOLDER, S AF KIPNIS, V FREEDMAN, LS BROWN, CC HARTMAN, A SCHATZKIN, A WACHOLDER, S TI INTERPRETATION OF ENERGY ADJUSTMENT MODELS FOR NUTRITIONAL EPIDEMIOLOGY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE EPIDEMIOLOGIC METHODS; MODELS, STATISTICAL; NUTRITION AB The authors discuss the interpretation of three alternative energy adjustment models for nutritional epidemiology. It is shown that four different effects are addressed by these models: 1) adding nutrient N, 2) substituting nutrient N for ''other'' nutrients, 3) adding ''other'' nutrients, and 4) adding both N and ''Other'' nutrients in a specific ratio. Each of these effects may be estimated from any of the three models. The relative standard errors for the four estimated effects are also provided. C1 NCI,DIV CANC PREVENT & CONTROL,APPL RES BRANCH,BETHESDA,MD 20892. NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. NCI,DIV CANC ETIOL,BIOSTAT BRANCH,BETHESDA,MD 20892. RP KIPNIS, V (reprint author), NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,EXECUT PLAZA N,BETHESDA,MD 20892, USA. NR 4 TC 79 Z9 79 U1 0 U2 3 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 15 PY 1993 VL 137 IS 12 BP 1376 EP 1380 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LP660 UT WOS:A1993LP66000009 PM 8333419 ER PT J AU ZIERDT, CH NAGY, B AF ZIERDT, CH NAGY, B TI ANTIBODY-RESPONSE TO BLASTOCYSTIS-HOMINIS INFECTIONS SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP ZIERDT, CH (reprint author), NIH,BETHESDA,MD 20892, USA. RI Nagy, Balint/F-6943-2012 NR 5 TC 11 Z9 11 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JUN 15 PY 1993 VL 118 IS 12 BP 985 EP 985 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LF937 UT WOS:A1993LF93700018 PM 8489119 ER PT J AU HUH, TL RYU, JH HUH, JW SUNG, HC OH, IU SONG, BJ VEECH, RL AF HUH, TL RYU, JH HUH, JW SUNG, HC OH, IU SONG, BJ VEECH, RL TI CLONING OF A CDNA-ENCODING BOVINE MITOCHONDRIAL NADP+-SPECIFIC ISOCITRATE DEHYDROGENASE AND STRUCTURAL COMPARISON WITH ITS ISOENZYMES FROM DIFFERENT SPECIES SO BIOCHEMICAL JOURNAL LA English DT Article ID TRICARBOXYLIC-ACID CYCLE; ESCHERICHIA-COLI; PIG-HEART; SACCHAROMYCES-CEREVISIAE; NUCLEOTIDE-SEQUENCE; PHOSPHORYLATION; PURIFICATION; BINDING; INACTIVATION; ORGANIZATION AB Mitochondrial NADP+-specific isocitrate dehydrogenase (IDP) was co-purified with the pyruvate dehydrogenase complex from bovine kidney mitochondria. The determination of its N-terminal 16-amino-acid sequence revealed that it is highly similar to the IDP from yeast. A cDNA clone (1.8 kb long) encoding this protein was isolated from a bovine kidney lambdagt11 cDNA library using a synthetic oligodeoxynucleotide. The deduced protein sequence of this cDNA clone rendered a precursor protein of 452 amino-acid residues (50830 Da) and a mature protein of 413 amino-acid residues (46 519 Da). It is 100 % identical to the internal tryptic peptide sequences of the autologous form from pig heart and 62 % similar to that from yeast. However, it shares little similarity with the mitochondrial NAD+-specific isoenzyme from yeast. Structural analyses of the deduced proteins of IDP isoenzymes from different species indicated that similarity exists in certain regions, which may represent the common domains for the active sites or coenzyme-binding sites. In Northern-blot analysis, one species of mRNA (about 2.2 kb for both bovine and human) was hybridized with a P-32-labelled cDNA probe. Southern-blot analysis of genomic DNAs verified simple patterns of hybridization with this cDNA. These results strongly indicate that the mitochondrial IDP may be derived from a single gene family which does not appear to be closely related to that of the NAD+-specific isoenzyme. C1 NIAAA,METAB & MOLEC BIOL LAB,12501 WASHINGTON AVE,ROCKVILLE,MD 20852. KYUNGPOOK NATL UNIV,COLL NAT SCI,DEPT GENET ENGN,TAEGU,SOUTH KOREA. KOREA UNIV,COLL AGR SCI,DEPT GENET ENGN,SEOUL,SOUTH KOREA. NR 36 TC 39 Z9 41 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD JUN 15 PY 1993 VL 292 BP 705 EP 710 PN 3 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LJ401 UT WOS:A1993LJ40100015 PM 8318002 ER PT J AU HARTLEY, RW AF HARTLEY, RW TI DIRECTED MUTAGENESIS AND BARNASE-BARSTAR RECOGNITION SO BIOCHEMISTRY LA English DT Article ID BACILLUS-AMYLOLIQUEFACIENS BARNASE; EXTRACELLULAR RIBONUCLEASE; DODECYL-SULFATE; EXPRESSION; PROTEINS; MUTATION AB Directed mutagenesis has been applied to the cloned genes of barnase and barstar, the extracellular ribonuclease of Bacillus amyloliquefaciens and its intracellular inhibitor, to locate residues involved in the mutual recognition of these two proteins. Arg59 and His102 of barnase and Asp35 and Asp39 of barstar have been so identified. With both Cys40 and Cys82 mutated to alanines, barstar is still produced in high yield and is functional both in vitro and in vivo. Methods devised for determining relative and absolute dissociation coefficients for various combinations of mutant and wild-type proteins have allowed us to determine a dissociation coefficient for the complex of wild-type barnase and barstar of about 10(-13) M, with off and on rate constants of 10(-5) s-1 and 10(8) M-1 s-1, respectively. RP HARTLEY, RW (reprint author), NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892, USA. NR 21 TC 98 Z9 99 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JUN 15 PY 1993 VL 32 IS 23 BP 5978 EP 5984 DI 10.1021/bi00074a008 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LG870 UT WOS:A1993LG87000008 PM 8507637 ER PT J AU MURTAGH, JJ LEE, FJS DEAK, P HALL, LM MONACO, L LEE, CM STEVENS, LA MOSS, J VAUGHAN, M AF MURTAGH, JJ LEE, FJS DEAK, P HALL, LM MONACO, L LEE, CM STEVENS, LA MOSS, J VAUGHAN, M TI MOLECULAR CHARACTERIZATION OF A CONSERVED, GUANINE NUCLEOTIDE-DEPENDENT ADP-RIBOSYLATION FACTOR IN DROSOPHILA-MELANOGASTER SO BIOCHEMISTRY LA English DT Article ID GTP-BINDING PROTEINS; GLUTATHIONE-S-TRANSFERASE; POLYMERASE CHAIN-REACTION; CHOLERA-TOXIN; ADENYLATE-CYCLASE; ESCHERICHIA-COLI; ALPHA-SUBUNIT; GENE; YEAST; DNA AB ADP-Ribosylation factors (ARFs) are ubiquitous approximately 20-kDa guanine nucleotide-binding proteins that stimulate cholera toxin-catalyzed ADP-ribosylation in vitro. Because the functional role(s) of ARF in mammalian systems is (are) elusive, we looked for ARF in Drosophila melanogaster, and report the partial purification and molecular cloning of an ARF from Drosophila. We cloned the Drosophila ARF 1 gene without library screening by a combination of 5 polymerase chain reactions (PCRs), yielding a 546-base open reading frame encoding 182 amino acids, which are >93% identical to those of mammalian class I ARFs. This ARF gene maps to 79F3-6 in the proximal region of the left arm of Drosophila chromosome 3. The Drosophila ARF 1 gene structure, including placement of introns, is highly conserved relative to mammalian class 1 ARF genes. A single ARF mRNA species of 1.8 kb was abundant in all Drosophila body segments. Recombinant Drosphila ARF 1 synthesized in Escherichia coli had biochemical and immunochemical activities similar to those of mammalian ARF. The similarities of sequence and biochemical properties between Drosophila and mammalian ARFs contrast with their differences from Drosophila arl (ARF-like protein), which does not stimulate cholera toxin-catalyzed ADP-ribosylation, and is only approximately 52-56% identical in amino acid sequence to mammalian ARFs. C1 SUNY Buffalo, DEPT BIOCHEM PHARMACOL, BUFFALO, NY 14260 USA. RP MURTAGH, JJ (reprint author), NHLBI, CELLULAR METAB LAB, ROOM SN-307, BLDG 10, BETHESDA, MD 20892 USA. RI Monaco, Lucia/A-4031-2010; Deak, Peter/F-7751-2012; OI LEE, FANG-JEN/0000-0002-2167-2426; LEE, CHII-MING/0000-0002-1075-5787 FU NINDS NIH HHS [NS16204] NR 44 TC 27 Z9 28 U1 1 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JUN 15 PY 1993 VL 32 IS 23 BP 6011 EP 6018 DI 10.1021/bi00074a012 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LG870 UT WOS:A1993LG87000012 PM 8507638 ER PT J AU DELACADENA, RA SUFFREDINI, AF PAGE, JD PIXLEY, RA KAUFMAN, N PARRILLO, JE COLMAN, RW AF DELACADENA, RA SUFFREDINI, AF PAGE, JD PIXLEY, RA KAUFMAN, N PARRILLO, JE COLMAN, RW TI ACTIVATION OF THE KALLIKREIN-KININ SYSTEM AFTER ENDOTOXIN ADMINISTRATION TO NORMAL HUMAN VOLUNTEERS SO BLOOD LA English DT Article ID TUMOR-NECROSIS-FACTOR; MOLECULAR-WEIGHT KININOGEN; HUMAN-PLASMA KALLIKREIN; FACTOR-XII; INTRAVENOUS ENDOTOXIN; HAGEMAN-FACTOR; PREKALLIKREIN; PLASMINOGEN; COAGULATION; INTERLEUKIN-1 C1 TEMPLE UNIV,HLTH SCI CTR,SCH MED,DEPT MED,SOL SHERRY THROMBOSIS RES CTR,PHILADELPHIA,PA 19140. NIH,CTR CLIN,DEPT CRIT CARE MED,BETHESDA,MD 20892. RUSH PRESBYTERIAN ST LUKES MED CTR,SCH MED,CHICAGO,IL 60612. RP DELACADENA, RA (reprint author), TEMPLE UNIV,HLTH SCI CTR,SCH MED,DEPT PATHOL,ROOM 403 OMS,3400 N BROAD ST,PHILADELPHIA,PA 19140, USA. FU NHLBI NIH HHS [HL45486, HL02681-01] NR 41 TC 77 Z9 77 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD JUN 15 PY 1993 VL 81 IS 12 BP 3313 EP 3317 PG 5 WC Hematology SC Hematology GA LG659 UT WOS:A1993LG65900020 PM 7685203 ER PT J AU DEVESA, SS CHOW, WH AF DEVESA, SS CHOW, WH TI VARIATION IN COLORECTAL-CANCER INCIDENCE IN THE UNITED-STATES BY SUBSITE OF ORIGIN SO CANCER LA English DT Article DE COLON CANCER; RECTUM CANCER; SUBSITE; INCIDENCE ID LARGE-BOWEL-CANCER; ALCOHOLIC BEVERAGE CONSUMPTION; COLON CANCER; REPRODUCTIVE FACTORS; MORTALITY TRENDS; CASE-REFERENT; RISK; SEX; AGE; CHOLECYSTECTOMY AB Background. Colorectal cancer incidence rates vary widely internationally, by race and gender, and have changed over time. Investigation of the patterns by subsite within the colorectum may suggest clue's of possible etiologic significance for further study. Methods. Using population-based data on more than 120,000 cases diagnosed 1976-1987 in the United States Surveillance, Epidemiology, and End Results program, colorectal cancer incidence was evaluated by subsite of origin. Results. Little racial variation was evident for cecum and ascending colon cancers; rates were higher among blacks than whites for transverse and descending colon cancers but lower for sigmoid, rectosigmoid, and rectal cancers. Rates generally increased over time for most colon sites, especially sigmoid colon among white men, but declined slightly for rectal cancer among whites. The sex ratio increased among whites monotonically from 1.12 for cecum to 1.71 for rectal cancers. The distal colon cancer excess among men was most notable at older ages, contrasting with slightly higher rates among women at younger ages. Geographic differences were particularly notable for transverse and rectosigmoid colon cancers. Conclusions. It may be fruitful for future studies to evaluate factors affecting colorectal carcinogenesis by subsite of origin. RP DEVESA, SS (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTATIST PROGRAM,BIOSTAT BRANCH,BETHESDA,MD 20892, USA. NR 54 TC 108 Z9 113 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JUN 15 PY 1993 VL 71 IS 12 BP 3819 EP 3826 DI 10.1002/1097-0142(19930615)71:12<3819::AID-CNCR2820711206>3.0.CO;2-L PG 8 WC Oncology SC Oncology GA LH256 UT WOS:A1993LH25600005 PM 8508350 ER PT J AU DAVIDSON, M BRAZIEL, RM LAIRMORE, MD JACOBSON, S SPROTT, JM TUCKER, SB LEVINE, PH KAPLAN, JE AF DAVIDSON, M BRAZIEL, RM LAIRMORE, MD JACOBSON, S SPROTT, JM TUCKER, SB LEVINE, PH KAPLAN, JE TI ATYPICAL HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I-ASSOCIATED T-CELL LYMPHOMA IN A LOW-PREVALENCE ALASKA NATIVE POPULATION - IMPLICATIONS FOR DISEASE SURVEILLANCE SO CANCER LA English DT Article DE LYMPHOMA; ADULT T-CELL LYMPHOMA LEUKEMIA; HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I (HTLV-I); ALASKA NATIVE; ESKIMO ID POLYMERASE CHAIN-REACTION; HTLV-I; LEUKEMIA-LYMPHOMA; HODGKINS-DISEASE; UNITED-STATES; CLASSIFICATION; RETROVIRUS; MYELOPATHY; FEATURES; REGION AB An atypical case of adult T-cell leukemia/lymphoma (ATL) associated with human T-cell lymphotropic virus type I (HTLV-I) occurred in a 46-year-old Inupiat Eskimo man with no behavioral risk factors for HTLV-I infection. The case was characterized by lack of atypical circulating lymphocytes, hypercalcemia, and opportunistic infections; and by complete remission of the initial renal parenchymal lymphoma. The lymphoma cells had a helper T-cell (CD4) immunophenotype. Serum antibodies to HTLV I/II, detected by Western immunoblot, were identified in specimens collected 31 months before the onset of illness, at the time of diagnosis, and up to 37 months later, shortly before the patient's death. Polymerase chain reaction was used to identify HTLV-I DNA in peripheral blood mononuclear cells and in lymphoma in involved skin. Clinicians should be alert to sporadic cases of both atypical and classic ATL, even in populations in which the prevalence of HTLV-I infection is low. C1 CTR DIS CONTROL,DIV VIRAL & RICKETTSIAL DIS,RETROVIRUS DIS BRANCH,ATLANTA,GA 30333. ALASKA NATIVE MED CTR,ANCHORAGE,AK. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. OREGON HLTH SCI UNIV,DEPT PATHOL,PORTLAND,OR 97201. NIMH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. RP DAVIDSON, M (reprint author), CTR DIS CONTROL & PREVENT,ARCTIC INVEST PROGRAM,225 EAGLE ST,ANCHORAGE,AK 99501, USA. NR 34 TC 1 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JUN 15 PY 1993 VL 71 IS 12 BP 4072 EP 4076 DI 10.1002/1097-0142(19930615)71:12<4072::AID-CNCR2820711244>3.0.CO;2-O PG 5 WC Oncology SC Oncology GA LH256 UT WOS:A1993LH25600043 PM 8099530 ER PT J AU MAKOS, M NELKIN, BD REITER, RE GNARRA, JR BROOKS, J ISAACS, W LINEHAN, M BAYLIN, SB AF MAKOS, M NELKIN, BD REITER, RE GNARRA, JR BROOKS, J ISAACS, W LINEHAN, M BAYLIN, SB TI REGIONAL DNA HYPERMETHYLATION AT D17S5 PRECEDES 17P STRUCTURAL-CHANGES IN THE PROGRESSION OF RENAL TUMORS SO CANCER RESEARCH LA English DT Note ID HUMAN NEOPLASIA; CELL CARCINOMA; SHORT ARM; METHYLATION; MUTATIONS; GENE AB In a preceding paper for brain tumors, we demonstrate a tight association between regional hypermethylation at locus D17S5 of chromosome 17p and allelic loss of this chromosome. Because 17p allelic losses occur at the earliest stages of brain tumors, the exact temporal relationship between this event and the hypermethylation could not be elucidated. In renal cancers, two linked structural changes on chromosome 17p, allelic loss and p53 gene mutations, generally occur late in progression. We now show that D17S5 hypermethylation is tightly coupled to both of these genetic changes in late stage renal tumors. However, the methylation change is the only one of the 17p abnormalities which occurs at a high incidence in early-stage renal cancers (hypermethylation. 50%; 17p allelic loss, 13%; p53 mutations, 0%). Our results firmly suggest that D17S5 regional hypermethylation precedes the appearance of the consistent 17p genetic changes in renal cancers, suggesting that this event either marks, or may even cause, chromatin changes which predispose to genetic instability. C1 JOHNS HOPKINS MED INST,CTR ONCOL,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,HUMAN GENET PROGRAM,BALTIMORE,MD 21205. NCI,SURG BRANCH,UROL ONCOL SECT,BETHESDA,MD 20892. FU NCI NIH HHS [R01-CA43318] NR 20 TC 113 Z9 114 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 15 PY 1993 VL 53 IS 12 BP 2719 EP 2722 PG 4 WC Oncology SC Oncology GA LG354 UT WOS:A1993LG35400007 PM 8504410 ER PT J AU HURSTING, SD SWITZER, BR FRENCH, JE KARI, FW AF HURSTING, SD SWITZER, BR FRENCH, JE KARI, FW TI THE GROWTH-HORMONE - INSULIN-LIKE GROWTH FACTOR-I AXIS IS A MEDIATOR OF DIET RESTRICTION-INDUCED INHIBITION OF MONONUCLEAR CELL LEUKEMIA IN FISCHER RATS SO CANCER RESEARCH LA English DT Article ID FACTOR-I; SOMATOMEDIN-C; LUNG-CANCER; 344 RATS; IGF-I; MICE; INVITRO; HYPOPHYSECTOMY; TRANSFORMATION; PROTEIN AB A leukemia cell transplant model and both in situ and in vitro bioassays were used to assess the roles of endogenous factors in mediating diet restriction (DR)-induced inhibition of mononuclear cell leukemia (MNCL) in Fischer 344 rats. DR-treated male rats (n = 35), which were fed 75% of ad libitum (AL) intake of NIH-07 open formula diet, had lower transplanted MNCL incidence (54 versus 77 %; P = 0.039) with longer latency (P = 0.015) and decreased severity (P = 0.01) than AL-treated rats 12 weeks after inoculation with MNCL cells. Five-day proliferation rates of cultured MNCL (CR.NK-16) cells in diffusion chambers implanted in DR-treated rats were 22% less than in AL-treated rats (P = 0.03), indicating that DR-dependent diffusible factor(s) modulate in situ MNCL cell growth. Serum from DR-treated rats supported lower in vitro CRNK-16 cell proliferation rates relative to serum from AL-treated rats. Serum levels of both growth hormone (GH) and insulin-like growth factor 1 (IGF-1) were over 50% lower in DR-versus AL-treated rats. An evaluation of the in vitro cell proliferative activity of a panel of purified factors showed that GH and IGF-1, but not 15 other growth factors, stimulated thymidine incorporation in CRNK-16 cells. Infusion of either GH or IGF-1 via osmotic minipumps restored in situ and in vitro CRNK-16 cell proliferation in DR-treated rats up to rates measured in AL-treated rats. Splenocytes from DR-treated rats, relative to AL-treated rats, were more sensitive to mitogen stimulation, displayed increased cell surface expression of receptors for class 1 and 2 major histocompatibility complex molecules, and were more cytotoxic to target tumor cells. Infusion of either GH or IGF-1 in DR-treated rats further enhanced mitogen responsiveness and natural cytotoxicity but reversed the DR-induced increase in major histocompatibility complex receptors. We conclude that DR modulates MNCL progression in Fischer 344 rats through both its influence on MNCL cell proliferation via suppression of the GH:IGF-1 axis and its enhancement of host defenses against tumor cells. C1 UNIV N CAROLINA,DEPT NUTR,CHAPEL HILL,NC 27599. NIEHS,RES TRIANGLE PK,NC 27709. NR 48 TC 81 Z9 83 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 15 PY 1993 VL 53 IS 12 BP 2750 EP 2757 PG 8 WC Oncology SC Oncology GA LG354 UT WOS:A1993LG35400014 PM 8389243 ER PT J AU CAMERA, L KINUYA, S PAI, LH GARMESTANI, K BRECHBIEL, MW GANSOW, OA PAIK, CH PASTAN, I CARRASQUILLO, JA AF CAMERA, L KINUYA, S PAI, LH GARMESTANI, K BRECHBIEL, MW GANSOW, OA PAIK, CH PASTAN, I CARRASQUILLO, JA TI PRECLINICAL EVALUATION OF IN-111 LABELED B3 MONOCLONAL-ANTIBODY - BIODISTRIBUTION AND IMAGING STUDIES IN NUDE-MICE BEARING HUMAN EPIDERMOID CARCINOMA XENOGRAFTS SO CANCER RESEARCH LA English DT Article ID NONMALIGNANT COLONIC TISSUES; IMPROVED TUMOR-LOCALIZATION; ANTIGENIC HETEROGENEITY; COLORECTAL-CARCINOMA; IN-111; DTPA; ADENOCARCINOMAS; EXPRESSION; FRAGMENTS; F(AB')2 AB Biodistribution and imaging characteristics of monoclonal antibody B3 were evaluated in nude mice bearing A431 human epidermoid carcinoma xenografts. B3 is a murine IgG1k, recently isolated, reacting with a carbohydrate epitope abundantly and uniformly expressed by most carcinomas. B3 was conjugated to a new backbone-substituted derivative of diethylenetriaminepentaacetic acid, 2-(p-isothiocyanato benzyl)-cyclohexyl-diethylenetriaminepentaacetic acid, and labeled with In-111. Tumor-bearing mice were given i.v. injections of approximately 5 muCi of either In-111-B3 or In-111-MOPC-21, an isotype-matched control, and sacrificed in groups of five at 6 h and daily up to 168 h. Imaging was performed at 24, 72, and 144 h. Significant differences were observed in tumor uptake at all time points with peak values at 48 h (25 +/- 5.2% versus 6.3 +/- 0.4% of the injected dose/g tissue) (mean +/- SD) for In-111-B3 and In-111-MOPC-21, respectively (P < 0.001). All tumor to organ ratios increased with time for In-111-B3. In particular, tumor:liver ratios rose from 3.2 +/- 0.6 at 24 h to 6.3 +/- 1.2 at 168 h. Imaging results showed selective and progressive accumulation of In-111-B3 at the tumor site, whereas In-111-MOPC-21 did not show specific localization. In summary, In-111-labeled B3 demonstrated good and specific tumor targeting, which warrants its future clinical evaluation. C1 NCI,WARREN G MAGNUSON CLIN CTR,DEPT NUCL MED,BLDG 10,ROOM 1C-401,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. RI Carrasquillo, Jorge/E-7120-2010 NR 47 TC 32 Z9 32 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 15 PY 1993 VL 53 IS 12 BP 2834 EP 2839 PG 6 WC Oncology SC Oncology GA LG354 UT WOS:A1993LG35400028 PM 8504427 ER PT J AU MARCHETTI, A BUTTITTA, F MERLO, G DIELLA, F PELLEGRINI, S PEPE, S MACCHIARINI, P CHELLA, A ANGELETTI, CA CALLAHAN, R BISTOCCHI, M SQUARTINI, F AF MARCHETTI, A BUTTITTA, F MERLO, G DIELLA, F PELLEGRINI, S PEPE, S MACCHIARINI, P CHELLA, A ANGELETTI, CA CALLAHAN, R BISTOCCHI, M SQUARTINI, F TI P53 ALTERATIONS IN NONSMALL CELL LUNG CANCERS CORRELATE WITH METASTATIC INVOLVEMENT OF HILAR AND MEDIASTINAL LYMPH-NODES SO CANCER RESEARCH LA English DT Article ID TUMOR-ANTIGEN; PROGNOSTIC FACTORS; POINT MUTATIONS; CHAIN-REACTION; GENE; EXPRESSION; TRANSFORMATION; RETINOBLASTOMA; PROTOONCOGENES; ABNORMALITIES AB Alterations of p53 are one of the most common molecular changes found in all types of lung tumors, suggesting a crucial role for p53 in bronchial carcinogenesis. However, the prognostic significance of p53 abnormalities in lung cancer patients is still unclear. By using genetic and immunohistochemical methods we have found p53 alterations in 40 of 53 (75%) primary, resected non-small cell lung cancer. A strong association (P = 0.0015) was found between deletions on chromosome region 17p13.3 and p53 mutations suggesting that loss of the wild-type p53 allele might be necessary for tumorigenesis. Correlations to clinicopathological parameters showed that p53 alterations (structural aberration of the gene and/or nuclear accumulation of the protein) are significantly linked with metastatic involvement of hilar and mediastinal lymph nodes (P < 0.01). Since the latter are well established prognostic factors for non-small cell lung cancer, p53 aberrations may also be a predictor of tumor aggressiveness. C1 UNIV PISA,SERV THORAC SURG,I-56100 PISA,ITALY. FRIEDRICH MIESCHER INST,CH-4002 BASEL,SWITZERLAND. UNIV NAPLES,DEPT MED ONCOL,I-80138 NAPLES,ITALY. NIH,LTIB,BETHESDA,MD 20892. RP MARCHETTI, A (reprint author), UNIV PISA,INST PATHOL ANAT & HISTOL,VIA ROMA 57,I-56100 PISA,ITALY. RI Pellegrini, Silvia/C-3770-2011; Macchiarini, Paolo/E-6878-2013 NR 55 TC 136 Z9 140 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 15 PY 1993 VL 53 IS 12 BP 2846 EP 2851 PG 6 WC Oncology SC Oncology GA LG354 UT WOS:A1993LG35400030 PM 8389245 ER PT J AU IZENWASSER, S KATZ, JL AF IZENWASSER, S KATZ, JL TI DIFFERENTIAL EFFICACIES OF DOPAMINE D1 RECEPTOR AGONISTS FOR STIMULATING ADENYLYL-CYCLASE IN SQUIRREL-MONKEY AND RAT SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION LA English DT Article DE DOPAMINE D1 RECEPTOR; ADENYLYL CYCLASE ID DISCRIMINATIVE STIMULUS PROPERTIES; ASSAY METHOD; COCAINE; SUBTYPES; STRIATUM; AFFINITY AB Adenylyl cyclase activity was stimulated by dopamine to approximately 200% over basal activity in both squirrel monkey caudate and rat caudate-putamen. The selective dopamine D1 receptor agonists SKF 82958, A68930, dihydrexidine, CY 208-243, and SKF 75670 each produced similar maximal stimulation across the two species. SKF 38393, SKF 81297, and 6-Br-APB, however, each had higher efficacy in rat than in monkey. These results suggest differences in dopamine D1 receptors in the two species. RP IZENWASSER, S (reprint author), NIDA,ADDICT RES CTR,PSYCHOBIOL SECT,POB 5180,BALTIMORE,MD 21224, USA. RI Izenwasser, Sari/G-9193-2012; OI Katz, Jonathan/0000-0002-1068-1159 NR 22 TC 71 Z9 71 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0922-4106 J9 EUR J PHARM-MOLEC PH JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect. PD JUN 15 PY 1993 VL 246 IS 1 BP 39 EP 44 DI 10.1016/0922-4106(93)90007-V PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LJ284 UT WOS:A1993LJ28400006 PM 8102607 ER PT J AU HOESS, R BRINKMANN, U HANDEL, T PASTAN, I AF HOESS, R BRINKMANN, U HANDEL, T PASTAN, I TI IDENTIFICATION OF A PEPTIDE WHICH BINDS TO THE CARBOHYDRATE-SPECIFIC MONOCLONAL ANTIBODY-B3 SO GENE LA English DT Article; Proceedings Paper CT MEETING ON SURFACE DISPLAY AND PEPTIDE LIBRARIES CY APR 04-07, 1992 CL COLD SPRING HARBOR LAB, BANBURY CTR, COLD SPRING HARBOR, NY HO COLD SPRING HARBOR LAB, BANBURY CTR DE PHAGE LIBRARIES; ADENOCARCINOMA CELLS; LEWISY ANTIGEN; SELECTINS; MONOCLONAL ANTIBODY BIOPANNING; EPITOPE; PEPTIDE MINIC; ALA SCAN MUTAGENESIS IMMUNOTOXIN; DISPLAY VECTORS ID ALPHA-AMYLASE INHIBITOR; STREPTOMYCES-TENDAE 4158; LIBRARY; LIGANDS; PHAGE; SITE; B3 AB The monoclonal antibody (mAb) B3 recognizes an antigen found on the surface of many adenocarcinoma cells. While the structure of the cellular antigen is unknown, epitope mapping using neoglycoproteins with known carbohydrate moieties indicates that the mAb B3 reacts with the Lewis(Y) (Le(Y)) antigen [Pastan et al., Cancer Res. 51 (1991) 3781-3787]. We have used mAb B3 to select for peptides that mimic the carbohydrate structure using libraries of filamentous phage displaying random peptides on their surface. Phage that were selected coded for the sequence APWLYGPA. The corresponding peptide was synthesized and tested for its ability to bind to mAb B3. The peptide was found to inhibit specifically the binding of In-111-labeled mAb B3 to A431 adenocarcinoma cells, as well as to inhibit killing of these cells by a B3 immunotoxin. In addition, the Le(Y) carbohydrate, lactodifucotetraose, was able to compete with the phage displaying this peptide for binding to mAb B3. Alanine-scanning mutagenesis of the sequence coding for this peptide indicates that four residues, PWLY, were critical for binding to the mAb. The sequence is similar to other sequences known to mimic carbohydrate structures. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892. RP HOESS, R (reprint author), DUPONT MERCK PHARMACEUT CO,EXPTL STN,BOX 8032,WILMINGTON,DE 19980, USA. NR 21 TC 150 Z9 152 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD JUN 15 PY 1993 VL 128 IS 1 BP 43 EP 49 DI 10.1016/0378-1119(93)90151-R PG 7 WC Genetics & Heredity SC Genetics & Heredity GA LH133 UT WOS:A1993LH13300007 PM 7685300 ER PT J AU OLMSTED, EA OBRIEN, L HENSHAW, EC PANNIERS, R AF OLMSTED, EA OBRIEN, L HENSHAW, EC PANNIERS, R TI PURIFICATION AND CHARACTERIZATION OF EUKARYOTIC INITIATION-FACTOR (EIF)-2-ALPHA KINASES FROM EHRLICH ASCITES TUMOR-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID POLYPEPTIDE-CHAIN INITIATION; NUCLEOTIDE-EXCHANGE FACTOR; DOUBLE-STRANDED-RNA; PROTEIN-SYNTHESIS INITIATION; FACTOR-II; TRANSLATIONAL INHIBITOR; RABBIT RETICULOCYTE; PHYSIOLOGICAL STRESSES; ALPHA-SUBUNIT; PHOSPHORYLATION AB A major mechanism of regulation of mammalian protein synthesis initiation is accomplished by the phosphorylation of the alpha subunit of eukaryotic initiation factor (eIF) 2 . This modification inhibits the activity of another initiation factor, guanine nucleotide exchange factor, preventing conversion of eIF-2.GDP to eIF-2.GTP and hence binding of initiator tRNA and formation of ternary complex (eIF-2.GTP.Met-tRNA(f)). Inhibition of protein synthesis and phosphorylation of eIF-2 occurs in Ehrlich cells when they are amino acid- or serum-deprived or heat-shocked as well as in other nucleated cells under similar conditions. This paper describes the purification of two eIF-2alpha kinases from Ehrlich cells. Unlike the two well characterized eIF-2alpha kinases, HRI (heme-regulated inhibitor from reticulocytes) and P68 (double-stranded RNA-dependent kinase found in interferon-treated cells), the Ehrlich cell kinases do not appear to auto-phosphorylate. The two kinases chromatograph differently on DEAE-cellulose and Mono Q. Furthermore, their Michaelis constants (K(m) values) for ATP are different. Both kinases can inhibit purified guanine nucleotide exchange factor (GEF) from stimulating ternary complex formation. However, only one kinase inhibits reticulocyte lysate cell free protein synthesis. The other kinase co-purifies with a factor that suppresses inhibition of protein synthesis in reticulocyte lysates by eIF-2alpha kinases. This suppressing activity is probably guanine nucleotide exchange factor. C1 NIH,DIV RES GRANTS,RM 2A17,WESTWOOD BLDG,5333 WESTBARD AVE,BETHESDA,MD 20892. UNIV ROCHESTER,DEPT BIOCHEM,ROCHESTER,NY 14642. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14642. FU NCI NIH HHS [R01 CA21663] NR 38 TC 18 Z9 18 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 15 PY 1993 VL 268 IS 17 BP 12552 EP 12559 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LG658 UT WOS:A1993LG65800050 PM 8099583 ER PT J AU HU, RQ GAN, YX LIU, JL MILLER, D ZOON, KC AF HU, RQ GAN, YX LIU, JL MILLER, D ZOON, KC TI EVIDENCE FOR MULTIPLE BINDING-SITES FOR SEVERAL COMPONENTS OF HUMAN LYMPHOBLASTOID INTERFERON-ALPHA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID I-125-LABELED MOUSE INTERFERON; CELL-SURFACE RECEPTOR; HIGH-AFFINITY BINDING; COMMON RECEPTORS; GAMMA; EXPRESSION; BETA AB The antiproliferative and competitive binding activities of 20 purified components of human lymphoblastoid interferon (IFN)-alpha were compared with that of recombinant human IFN-alpha2b on Daudi and AU937 cells. We observed broad ranges of antiproliferative activities of the IFN-alpha components on these cell lines. Daudi cells were more sensitive to the IFN-alpha components than AU937 cells; the concentrations of the components that resulted in 50% inhibition of cell growth ranged from 0.003 ng/ml to >10 ng/ml on Daudi cells and 0.05 ng/ml to >200 ng/ml on AU937 cells. Component o was the most active human IFN-alpha on both cell lines. Scatchard analysis demonstrated that the number of IFN-alpha2b binding sites is greater on Daudi cells (12,700 binding sites/cell) than AU937 cells (3,300 binding sites/cell); however, their receptor affinities were similar. Component o, which exhibited high antiproliferative activity on both cell lines, had low affinity for the IFN-alpha2b binding site on AU937 and Daudi cells. Several human IFN-alphas (components b', b'', and e) appeared to have high affinity binding sites but low antiproliferative activity on both Daudi and AU937 cells. These data suggest that there may be more than one binding site or receptor for human IFN-alpha, and/or there may be a multicomponent receptor involved in the biological actions of these molecules. C1 US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,BLDG 29,RM 130,8800 ROCKVILLE PIKE,BETHESDA,MD 20892. NICHHD,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT PATHOL,BETHESDA,MD 20814. NR 33 TC 47 Z9 47 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 15 PY 1993 VL 268 IS 17 BP 12591 EP 12595 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LG658 UT WOS:A1993LG65800055 PM 8509399 ER PT J AU KIM, IG GORMAN, JJ PARK, SC CHUNG, SI STEINERT, PM AF KIM, IG GORMAN, JJ PARK, SC CHUNG, SI STEINERT, PM TI THE DEDUCED SEQUENCE OF THE NOVEL PROTRANSGLUTAMINASE-E (TGASE3) OF HUMAN AND MOUSE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMINO-ACID-SEQUENCE; HUMAN EPIDERMAL TRANSGLUTAMINASE; CROSS-LINKED ENVELOPE; FACTOR-XIII; GUINEA-PIG; KERATINOCYTE TRANSGLUTAMINASE; TERMINAL DIFFERENTIATION; ERYTHROCYTE-MEMBRANE; I TRANSGLUTAMINASE; MOLECULAR-CLONING AB At least three transglutaminases are involved in terminal differentiation events in the epidermis and its derivatives, such as the hair follicle, presumably in cross-linking structural proteins and in the formation of the cornified cell envelope. Of these, only the transglutaminase 3 is a proenzyme, requiring activation by proteolytic cleavage, and is the least understood. Using oligonucleotides designed from the amino acid sequences of peptides of the guinea pig enzyme, we amplified mRNA and deduced the complete amino acid sequences of the mouse and human protransglutaminase 3 enzymes. Both proteins contain 692 amino acids of molecular mass about 77 kDa. Following expression in yeast, the proenzymes encoded by the full-length cDNA clones are active enzymes and can be further activated 15-fold on treatment with dispase. Although these proteins share 38-53% identity to other members of the transglutaminase family, surprisingly, the mouse, human, and guinea pig enzymes have not been highly conserved and show only 50-75% identity to each other. Much of the sequence variation occurs in the vicinity of the proteolytic activation site which lies at the most flexible and hydrophilic region of the molecule and is flanked by a sequence of 12 residues that are absent from other transglutaminases. We suggest that cleavage of this exposed flexible hinge region promotes a conformational change in the protein to a more compact form, resulting in activation of the enzyme. Expression of mouse and human protransglutaminase 3 mRNAs is regulated by calcium, as for other late differentiation products of the epidermis, suggesting that this enzyme is responsible for the later stages of cell envelope formation in the epidermis and hair follicle. C1 NIH,BLDG 6,RM 425,BETHESDA,MD 20892. BIOMOLEC RES INST,PARKVILLE,VIC 3052,AUSTRALIA. SEOUL NATL UNIV,SCH MED,DEPT BIOCHEM,SEOUL 110460,SOUTH KOREA. NIDA,CELLULAR DEV & ONCOL LAB,BETHESDA,MD. NIAMSD,SKIN BIOL BRANCH,BETHESDA,MD. NR 56 TC 109 Z9 112 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 15 PY 1993 VL 268 IS 17 BP 12682 EP 12690 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LG658 UT WOS:A1993LG65800068 PM 8099584 ER PT J AU CARROLL, K ELROYSTEIN, O MOSS, B JAGUS, R AF CARROLL, K ELROYSTEIN, O MOSS, B JAGUS, R TI RECOMBINANT VACCINIA VIRUS K3L GENE-PRODUCT PREVENTS ACTIVATION OF DOUBLE-STRANDED RNA-DEPENDENT, INITIATION FACTOR-2-ALPHA-SPECIFIC PROTEIN-KINASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INTERFERON; TRANSLATION; EIF-2-ALPHA; INHIBITION; BINDING; CELLS; DNA; AUTOPHOSPHORYLATION; PHOSPHORYLATION; PURIFICATION AB Deletion of the vaccinia virus K3L gene, a homologue of the alpha subunit of protein synthesis initiation factor 2, has been reported to reduce the ability of the virus to grow in interferon-treated cells (Beattie, E., Tattaglia, J., and Paoletti, E. (1991) Virology 183, 419-422). Purified recombinant K3L gene product, pK3r, has potent effects on activation of double-stranded (ds) RNA-dependent, initiation factor-2alpha (eIF-2alpha)-specific protein kinase (PKR) in in vitro reactions. Recombinant pK3 prevents the inhibition of protein synthesis by dsRNA in a cell-free translation system from rabbit reticulocytes at levels equal to, or lower than, the level of endogenous eIF-2alpha. In the cell-free translation system, pK3r exerts its effects at all dsRNA concentrations tested, by preventing phosphorylation of eIF-2alpha. In addition, pK3r reduces the autophosphorylation of immunopurified PKR, as well as its ability to phosphorylate the alpha subunit of purified eIF-2. At 400 mM NaCl, in vitro translated [S-35]methionine-radiolabeled pK3 can be co-immunoprecipitated with human PKR, using a monoclonal antibody to PKR. This tight binding is consistent with a role for pK3 as a pseudosubstrate for the kinase, and identifies the amino-terminal 30% of eIF-2alpha as the domain recognized by the eIF-2alpha-specific protein kinases. In addition, the tight binding opens up the possibility of using binding assays to identify functional domains within the kinase and pK3. Recombinant pK3 also prevents activation of the heme-sensitive eIF-2alpha-specific protein kinase, eIF-2alpha-PK(h), in both cell-free translation systems as well as in partially purified preparations. This suggests some similarity between the eIF-2alpha binding domains of the two eIF-2alpha specific protein kinases. C1 CTR MARINE BIOTECHNOL,600 E LOMBARD ST,BALTIMORE,MD 21202. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. OI Elroy-Stein, Orna/0000-0002-3716-1540 NR 52 TC 129 Z9 131 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 15 PY 1993 VL 268 IS 17 BP 12837 EP 12842 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LG658 UT WOS:A1993LG65800089 PM 8099586 ER PT J AU KELLEY, CA TAKAHASHI, M YU, JH ADELSTEIN, RS AF KELLEY, CA TAKAHASHI, M YU, JH ADELSTEIN, RS TI AN INSERT OF 7 AMINO-ACIDS CONFERS FUNCTIONAL DIFFERENCES BETWEEN SMOOTH-MUSCLE MYOSINS FROM THE INTESTINES AND VASCULATURE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHAIN MESSENGER-RNAS; LIGHT CHAIN; HEAVY-CHAIN; CYTOPLASMIC MYOSINS; DNA-SEQUENCE; SINGLE GENE; NONMUSCLE; ISOFORMS; CHICKEN; KINASE AB The molecular mechanisms underlying the heterogeneity in contractile properties observed among smooth muscle tissues are unknown. We examined whether part of this diversity might be intrinsic to myosin by comparing structural and enzymatic properties of myosins from two physiologically diverse tissues. Using the reverse transcriptase polymerase chain reaction, we compared avian intestinal smooth muscle and vascular smooth muscle myosin heavy chain (MHC) mRNA. We found that intestinal, but not vascular, MHC mRNA contains an insert of 21 nucleotides, encoding 7 amino acids, in a region near the ATP binding site in the myosin head. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of purified myosin revealed that the relative mobilities of the previously described intestinal MHC isoforms SM1 (204 kDa) and SM2 (200 kDa) were slower than the corresponding vascular SM1 and SM2 isoforms. Furthermore, antibodies raised against a synthetic peptide corresponding to the deduced amino acid sequence of the intestinal insert strongly recognized intestinal SM1 and SM2 but only weakly recognized the vascular isoforms. The presence of the insert in intestinal myosin correlated with a higher velocity of movement of actin filaments in vitro and a higher actin-activated Mg2+-ATPase activity, compared with vascular myosin. Other than the MHC insert, one other structural difference distinguished intestinal and vascular myosins: two isoforms of the 17-kDa myosin light chain were found in vascular myosin, whereas a single isoform was found in intestinal myosin. Exchange of the intestinal myosin light chains onto the vascular MHC did not alter its activity in the in vitro motility assay, suggesting that the 7-amino acid MHC insert is responsible for the different enzymatic activities of vascular and intestinal myosins. RP KELLEY, CA (reprint author), NHLBI,MOLEC CARDIOL LAB,BLDG 10,RM 8N202,BETHESDA,MD 20892, USA. RI Takahashi, Masayuki/D-8079-2012 NR 46 TC 219 Z9 219 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 15 PY 1993 VL 268 IS 17 BP 12848 EP 12854 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LG658 UT WOS:A1993LG65800091 PM 8509418 ER PT J AU DARDEN, T YORK, D PEDERSEN, L AF DARDEN, T YORK, D PEDERSEN, L TI PARTICLE MESH EWALD - AN N.LOG(N) METHOD FOR EWALD SUMS IN LARGE SYSTEMS SO JOURNAL OF CHEMICAL PHYSICS LA English DT Note ID CRYSTAL-STRUCTURE; LATTICE SUMS; CONFORMATION; SIMULATIONS AB An N. log(N) method for evaluating electrostatic energies and forces of large periodic systems is presented. The method is based on interpolation of the reciprocal space Ewald sums and evaluation of the resulting convolutions using fast Fourier transforms. Timings and accuracies are presented for three large crystalline ionic systems. RP DARDEN, T (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. RI Pedersen, Lee/E-3405-2013 OI Pedersen, Lee/0000-0003-1262-9861 NR 23 TC 10261 Z9 10350 U1 68 U2 576 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0021-9606 J9 J CHEM PHYS JI J. Chem. Phys. PD JUN 15 PY 1993 VL 98 IS 12 BP 10089 EP 10092 DI 10.1063/1.464397 PG 4 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA LG101 UT WOS:A1993LG10100091 ER PT J AU LASZLO, G HATHCOCK, KS DICKLER, HB HODES, RJ AF LASZLO, G HATHCOCK, KS DICKLER, HB HODES, RJ TI CHARACTERIZATION OF A NOVEL CELL-SURFACE MOLECULE EXPRESSED ON SUBPOPULATIONS OF ACTIVATED T-CELL AND B-CELL SO JOURNAL OF IMMUNOLOGY LA English DT Article ID FC IGG RECEPTORS; MEMBRANE MOLECULES; LYMPHOCYTES-T; ANTIGEN; HYALURONATE; ANTIBODIES AB A mAb, GL7, is described that reacts with a 35-kDa protein on subsets of activated mouse B cells as well as activated CD4+ and CD8+ peripheral T cells. In normal mice analyzed by flow cytometry, GL7 bound at low surface density to 0 to 9% of splenic B cells and 0 to 1% of splenic T cells. In contrast, GL7 bound at high density to a subpopulation comprising approximately 20% of TCR-bright thymocytes, and to B220+ cells in the bone marrow. The activation of B cells by various stimuli resulted in high levels of expression of the surface molecule identified by GL7 on up to 70% of B cells after 48 h; the remaining B cells expressed low or undetectable levels of this molecule, despite evidence of other activation-specific changes in cell-surface phenotype. The GL7-positive population of B cells induced by IL-5 stimulation exhibited high levels of both proliferative and IgM secretory activity, whereas the GL7-negative population showed little of either activity. Activation of splenic T cells with Con A for 48 h resulted in the expression of this determinant at high density on both CD4+ and CD8+ cells. GL7 thus appears to identify a previously uncharacterized cell-surface molecule expressed selectively on subpopulations of activated B and T cells as well as on discrete subpopulations of T and B lineage cells in vivo. C1 NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM 4B17,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 28 TC 57 Z9 57 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 15 PY 1993 VL 150 IS 12 BP 5252 EP 5262 PG 11 WC Immunology SC Immunology GA LH978 UT WOS:A1993LH97800005 PM 8515058 ER PT J AU HORGAN, C BROWN, K PINCUS, SH AF HORGAN, C BROWN, K PINCUS, SH TI STUDIES ON ANTIGEN-BINDING BY INTACT AND HINGE-DELETED CHIMERIC ANTIBODIES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MONOCLONAL-ANTIBODIES; COMPLEMENT ACTIVATION; SEGMENTAL FLEXIBILITY; SYNTHETIC POLYPEPTIDES; HUMAN-IMMUNOGLOBULINS; AFFINITY DIFFERENCES; EFFECTOR FUNCTIONS; VARIABLE REGIONS; SUBCLASS; IGG1 AB A matched set of chimeric IgG1 and IgG4 antibodies were used to investigate the role of the IgG hinge in binding to Ag with differing space between the epitopes. Antibodies bearing identical V regions and either IgG1 or IgG4 C regions were engineered with and without hinges. We measured the binding of these antibodies to the peptide CYYYEEEEY and to CYYYEEEEY-BSA conjugates with decreasing numbers of peptides per BSA molecule. We earlier showed that V region differences in antibodies could affect Ag binding patterns in solid-phase but not solution-phase assays; however, both types of assay yielded similar results for the hinge-deleted antibodies. Binding of CYYYEEEEY-BSA by hinge-deleted and intact IgG1 was similar, but intact IgG1 bound free peptide better than did hinge-deleted IgG1. Intact IgG4 antibody bound less well to CYYYEEEEY and CYYYEEEEY-BSA than did IgG1 but, surprisingly, hinge-deleted IgG4 showed better binding than did intact IgG4 and was more like the IgG1 antibodies in binding affinity. Thus, the IgG4 hinge may impart a structural constraint that prevents high affinity binding to Ag. The hinge-deleted IgG4 antibody did not activate C, although it bound Ag similarly to IgG1. This study is the first to address the effect of the IgG hinge on Ag binding by using well defined Ag with different epitope densities. Our results may provide an explanation for the apparent low affinity of IgG4 antibodies. C1 NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,HAMILTON,MT 59840. NR 27 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 JUN 15 PY 1993 VL 150 IS 12 BP 5400 EP 5407 PG 8 WC Immunology SC Immunology GA LH978 UT WOS:A1993LH97800020 PM 7685795 ER PT J AU JAIN, VK JUDDE, JG MAX, EE MAGRATH, IT AF JAIN, VK JUDDE, JG MAX, EE MAGRATH, IT TI VARIABLE IGH CHAIN ENHANCER ACTIVITY IN BURKITTS LYMPHOMAS SUGGESTS AN ADDITIONAL, DIRECT MECHANISM OF C-MYC DEREGULATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID GENE-TRANSCRIPTION; LOCUS; FORMS; CELLS AB The deregulation of the c-myc gene in small non-cleaved cell lymphomas (SNCL) with 8;14 translocations is thought to be due to the juxtaposition of this gene with the IgH chain locus, but exactly how the Ig locus contributes to the deregulation is unclear. One widely considered hypothesis is that Ig gene enhancers, when moved near c-myc, might stimulate inappropriate transcription of this gene. To evaluate this hypothesis, we have tested the ability of the two known H chain enhancers, the J(H)-Cmu intronic enhancer and the 3'alpha enhancer, to support transcription from c-myc promoters, by using transient transfection assays in a panel of 32 SNCL cell lines with 8;14 translocations. The activity of the J(H)-Cmu, intronic enhancer varied widely among the cell lines tested and correlated with the presence of nuclear factors binding to the E4/octamer regions of the enhancer. The 3'alpha enhancer was much less active than the intronic enhancer in all of our cell lines and seems unlikely to account for the c-myc deregulation (although the enhancer we tested was from the rat, because the human homologue is unidentified at present). A marked difference was also seen in the ability of individual cell lines to support transcription from the unenhanced c-myc constructs. Cell lines supporting the lowest enhancer activity tended to support the highest level of transcription from unenhanced c-myc promoters. The differences in transcription from c-myc promoters were confirmed by stably transfecting constructs containing c-myc promoters in SNCL cell lines. Our data strongly suggest that the importance of Ig enhancers for c-myc deregulation varies markedly in different cell lines and that, for many, trans-acting regulators of the c-myc promoters are as important or more important, than Ig enhancers in the deregulation of the c-myc gene. C1 NCI,PEDIAT BRANCH,LYMPHOMA BIOL SECT,BLDG 10,ROOM 13N240,BETHESDA,MD 20892. NR 22 TC 12 Z9 12 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 JUN 15 PY 1993 VL 150 IS 12 BP 5418 EP 5428 PG 11 WC Immunology SC Immunology GA LH978 UT WOS:A1993LH97800022 PM 8515068 ER PT J AU MCKENZIE, ANJ LI, X LARGAESPADA, DA SATO, A KANEDA, A ZURAWSKI, SM DOYLE, EL MILATOVICH, A FRANCKE, U COPELAND, NG JENKINS, NA ZURAWSKI, G AF MCKENZIE, ANJ LI, X LARGAESPADA, DA SATO, A KANEDA, A ZURAWSKI, SM DOYLE, EL MILATOVICH, A FRANCKE, U COPELAND, NG JENKINS, NA ZURAWSKI, G TI STRUCTURAL COMPARISON AND CHROMOSOMAL LOCALIZATION OF THE HUMAN AND MOUSE IL-13 GENES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN-LYMPHOCYTES; GROWTH-FACTORS; INTERLEUKIN-4; ACTIVATION; MAP; RECEPTORS; MONOCYTES AB The genomic structure of the recently described cytokine IL-13 has been determined for both human and mouse genes. The nucleotide sequence of a 4.6-kb DNA segment of the human gene is described. The human IL-13 gene (IL13) occurs as a single copy in the haploid genome and maps to human chromosome 5. A 4.3-kb DNA fragment of the mouse IL-13 gene (Il13) has been sequenced and found to occur as a single copy, mapping to mouse chromosome 11. Intrachromosomal mapping studies revealed that both genes contain four exons and three introns and show a high degree of sequence identity throughout their length. Potential recognition sequences for transcription factors that are present in the 5'-flanking region and are conserved between both genes include IFN-responsive elements, binding sites for AP-1, AP-2 and AP-3, an NF-IL 6 site, and a TATA-like sequence. Both genes map to chromosomal locations adjacent to genes encoding other cytokines, including IL-3, GM-CSF, IL-5, and IL-4, suggesting that IL-13 is another member of this cytokine gene family that may have arisen by gene duplication. C1 STANFORD UNIV,MED CTR,SCH MED,DEPT GENET,STANFORD,CA 94305. STANFORD UNIV,MED CTR,SCH MED,HOWARD HUGHES MED INST,STANFORD,CA 94305. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP MCKENZIE, ANJ (reprint author), DNAX RES INST CELLULAR & MOLEC BIOL,DEPT MOLEC BIOL,901 CALIF AVE,PALO ALTO,CA 94304, USA. RI Largaespada, David/C-9832-2014 FU NCI NIH HHS [N01-CO-74101] NR 26 TC 150 Z9 159 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 15 PY 1993 VL 150 IS 12 BP 5436 EP 5444 PG 9 WC Immunology SC Immunology GA LH978 UT WOS:A1993LH97800024 PM 8099936 ER PT J AU EPSTEIN, SL MISPLON, JA LAWSON, CM SUBBARAO, EK CONNORS, M MURPHY, BR AF EPSTEIN, SL MISPLON, JA LAWSON, CM SUBBARAO, EK CONNORS, M MURPHY, BR TI BETA-2-MICROGLOBULIN-DEFICIENT MICE CAN BE PROTECTED AGAINST INFLUENZA-A INFECTION BY VACCINATION WITH VACCINIA-INFLUENZA RECOMBINANTS EXPRESSING HEMAGGLUTININ AND NEURAMINIDASE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CD8+ T-CELLS; VIRUS-INFECTION; LYMPHOCYTIC CHORIOMENINGITIS; NUCLEOPROTEIN; IMMUNITY; PROTEINS; RECOVERY; ANTIGENS; INVIVO; IMMUNIZATION AB Immunity to viral infections includes both antibody and T cell components. The contributions of humoral and cell-mediated immune responses vary depending on virus and host factors. We have used an in vivo challenge system to examine protective immunity to influenza A(H1N1) virus infection in immunocompetent B6 (H-2b) mice, and in H-2b mice homozygous for disruption of the gene for beta2-microglobulin, termed beta2mu(-/-) mice. The latter mice do not express conventional MHC class I complexes on cell surfaces and lack CD8+ class I-restricted T cells. Ten vaccinia virus recombinants, each expressing 1 of the 10 proteins of influenza virus, were used to immunize the mice. Normal mice were protected against challenge with influenza virus by vaccination with HA-VAC and NA-VAC, but not by any of the vaccinia vectors expressing one of the eight other influenza virus proteins nor by a mixture of all eight of the latter vectors. Similar results were observed in mice of H-2d or H-2k MHC haplotypes. The beta2mu(-/-) mice were also protected by immunization with HA-VAC and NA-VAC, demonstrating that classical CD8+ CTL responses were not required for protection. Depletion of CD4+ T cells in either normal or beta2mu(-/-) mice at the time of challenge had little or no effect on protection induced by HA-VAC or NA-VAC, suggesting that preformed antibody is the dominant mediator of protective immunity induced by these recombinants. Antibody responses to vaccinia virus Ag and expressed influenza virus Ag were lower in titer in beta2mu(-/-) mice than in normal B6 mice, suggesting an influence of MHC class I complexes, CD8+ T cells, or their products on antibody production. C1 NIAID,INFECT DIS LAB,BETHESDA,MD 20892. RP EPSTEIN, SL (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV BIOCHEM & BIOPHYS,MOLEC IMMUNOL LAB,BLDG 29,RM 522,BETHESDA,MD 20892, USA. NR 49 TC 70 Z9 72 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 JUN 15 PY 1993 VL 150 IS 12 BP 5484 EP 5493 PG 10 WC Immunology SC Immunology GA LH978 UT WOS:A1993LH97800029 PM 8390536 ER PT J AU STEEL, C NUTMAN, TB AF STEEL, C NUTMAN, TB TI REGULATION OF IL-5 IN ONCHOCERCIASIS - A CRITICAL ROLE FOR IL-2 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; TRICHINELLA-SPIRALIS INFECTION; HUMAN T-CELLS; SCHISTOSOMA-MANSONI; CYTOKINE PRODUCTION; INTERLEUKIN-5 PRODUCTION; PROTECTIVE IMMUNITY; CHROMOSOMAL GENE; RESPONSES; HELPER AB The cytokine profiles of PBMC obtained from individuals ''immune'' to onchocerca volvulus infection were compared to those from infected individuals. The immune individuals had significantly higher levels of both IL-2 and IL-5 in response to parasite Ag than did those individuals with active infection (mean IL-2 = 1.3 and 0.138 U/ml, respectively; mean IL-5 = 973 and 147.4 pg/ml, respectively), and there was a direct correlation between the production of IL-2 and IL-5. To examine the mechanism underlying the possible association between these two cytokines in patients infected with onchocerciasis, reverse transcription followed by polymerase chain reaction was used to measure IL-5 mRNA. In response to rIL-2, IL-5 mRNA appeared as early as 3 h after stimulation of patient PBMC, reaching a peak at 24 h; further, this response was inhibited with neutralizing antibodies to IL-2. IL-2 was unable to induce mRNA expression for IL-4, IFN-gamma, IL-10, or granulocyte-macrophage-CSF. To assess whether IL-2 was specifically responsible for the up-regulation of Ag-induced IL-5 production in patients with onchocerciasis, IL-5 mRNA expression was measured in PBMC stimulated with parasite Ag. Up-regulation of IL-5 mRNA was seen in all patients (peaking at 72 h) in response to Ag stimulation and was found to be independent of proliferation to Ag; in addition, this up-regulation was specifically inhibited by neutralizing anti-IL-2 antibodies. Further, the primary source of IL-5 mRNA was determined to be CD4+ T cells. These findings suggest that IL-2 production is required to induce IL-5 and further implicates IL-5 as a possible mediator of protection in onchocerciasis. RP STEEL, C (reprint author), NIAID,PARASIT DIS LAB,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA. NR 47 TC 74 Z9 74 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 JUN 15 PY 1993 VL 150 IS 12 BP 5511 EP 5518 PG 8 WC Immunology SC Immunology GA LH978 UT WOS:A1993LH97800032 PM 8099937 ER PT J AU AHLERS, JD PENDLETON, CD DUNLOP, N MINASSIAN, A NARA, PL BERZOFSKY, JA AF AHLERS, JD PENDLETON, CD DUNLOP, N MINASSIAN, A NARA, PL BERZOFSKY, JA TI CONSTRUCTION OF AN HIV-1 PEPTIDE VACCINE CONTAINING A MULTIDETERMINANT HELPER PEPTIDE LINKED TO A V3 LOOP PEPTIDE-18 INDUCING STRONG NEUTRALIZING ANTIBODY-RESPONSES IN MICE OF MULTIPLE MHC HAPLOTYPES AFTER 2 IMMUNIZATIONS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; B-CELL EPITOPES; T-CELL; SYNTHETIC PEPTIDES; MONOCLONAL-ANTIBODIES; ENVELOPE PROTEIN; LYMPHOCYTES-T; SEROPOSITIVE INDIVIDUALS; INFECTED INDIVIDUALS; ANTIGEN RECOGNITION AB Peptide constructs comprised of multideterminant Th peptides from the envelope glycoprotein of HIV previously identified to induce proliferative responses in four different haplotypes of mice and IL-2 responses in 52 to 73% of HIV positive, Ag-responsive patients, were colinearly synthesized with the peptide 18 of the V3 loop of HIV-1 gp 160, corresponding to the principal neutralizing determinant of HIV-IIIB. The segments containing clusters of overlapping Th epitopes were called cluster peptides. Cognate help for peptide 18 antibody was elicited after a single immunization in all strains of mice that had previously responded to a T cell epitope encompassed by the cluster peptides. Animals boosted with cluster peptide-peptide 18 constructs 36 to 52 wk later displayed secondary antibody responses. Cluster peptide 3-peptide 18 induced antibody that neutralized homologous virus in one strain of mice although strong peptide 18 antibody responses were detected in all four strains of mice. The most promising construct, cluster peptide 6-peptide 18, induced neutralizing antibody in all strains of mice tested, and in two strains the level of neutralizing antibody achieved was comparable to levels adequate for protection from homologous viral challenge in chimpanzees. After a single boost, antibody titers for 90% neutralization in the range of 1/1000 to 1/16,000 were achieved. These neutralizing titers against the homologous viral strain, after just two immunizations, are at least four- to eight fold higher than the highest titered other polyclonal V3-specific immune sera we have ever observed in our laboratories. We also asked why some sera neutralized and others with similar ELISA titers did not. No correlation was found between neutralization and isotype or affinity for peptide or gp120. We could not account for neutralization by antibodies to the helper sites. Substitutions made in the central loop region of peptide 18, amino acid residues PGRAF, dramatically reduced binding of both neutralizing and nonneutralizing sera although some fine specificity differences between neutralizing and nonneutralizing sera were noted. These results have implications for the design of synthetic peptide vaccines for HIV. C1 NCI,METAB SECT,MOLEC IMMUNOGENET & VACCINE RES SECT,BLDG 10,6B-12,BETHESDA,MD 20892. NCI,FREDERICK CANC RES FACIL,FREDERICK,MD 21701. PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 80 TC 78 Z9 78 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 15 PY 1993 VL 150 IS 12 BP 5647 EP 5665 PG 19 WC Immunology SC Immunology GA LH978 UT WOS:A1993LH97800046 PM 8515081 ER PT J AU REN, K KIBBEY, MC KLEINMAN, HK RUDA, MA AF REN, K KIBBEY, MC KLEINMAN, HK RUDA, MA TI 110/140 LAMININ-BINDING PROTEIN IMMUNOREACTIVITY IN SPINAL DORSAL-ROOT GANGLIA - A CAPSAICIN-INSENSITIVE REDUCTION INDUCED BY CONSTRICTION INJURY OF THE SCIATIC-NERVE IN RATS SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE LAMININ-BINDING PROTEIN; PRIMARY SENSORY NEURONS; NERVE INJURY; IMMUNOCYTOCHEMISTRY; CAPSAICIN ID CONDUCTION-VELOCITY; CELLS; NEURONS; EXPRESSION; ADULT; PAIN; RECEPTORS; PEPTIDE; SYSTEM; AXONS AB The distribution of 110/140 laminin-binding protein (110/140 LBP) in the spinal dorsal root ganglia (DRG) and its regulation by partial constriction of the sciatic nerve was studied in adult rats. The cross-sectional area of neurons with 110/140 LBP-immunoreactivity (-I) showed an approximately normal frequency distribution. The 110/140 LBP-I was observed in neuronal cell bodies exclusive of the nucleus. Following sciatic nerve constriction, the 110/140 LBP-I was downregulated in the ipsilateral L4-5 DRG. DRG neurons with a cross-sectional area less-than-or-equal-to 1600 mum2 were preferentially affected. Neonatal capsaicin-treatment, a procedure that selectively destroys a subpopulation of DRG neurons with fine unmyelinated axons, had no effect on the reduction of 110/140 LBP in the DRG induced by sciatic nerve constriction. Western immunoblot analysis confirmed a reduction of 110/140 LBP on the side ipsilateral to the constriction. These results demonstrate a LBP within primary sensory neurons and its suppression by peripheral nerve injury. The data support a role for LBP in the adult nervous system. C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. RP REN, K (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 30,BETHESDA,MD 20892, USA. NR 35 TC 3 Z9 3 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD JUN 15 PY 1993 VL 35 IS 3 BP 227 EP 236 DI 10.1002/jnr.490350302 PG 10 WC Neurosciences SC Neurosciences & Neurology GA LF785 UT WOS:A1993LF78500001 PM 8350386 ER PT J AU BROWNSTEIN, MJ AF BROWNSTEIN, MJ TI A BRIEF-HISTORY OF OPIATES, OPIOID-PEPTIDES, AND OPIOID RECEPTORS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Review ID STEREOSPECIFIC BINDING; NARCOTIC ANALGESICS; SEQUENCE-ANALYSIS; NG108-15 CELLS; HIGH-AFFINITY; HUMAN BRAIN; RAT-BRAIN; MORPHINE; CDNA; LIPOTROPIN RP BROWNSTEIN, MJ (reprint author), NIMH,CELL BIOL LAB,BETHESDA,MD 20892, USA. RI Brownstein, Michael/B-8609-2009 NR 40 TC 158 Z9 166 U1 5 U2 32 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 15 PY 1993 VL 90 IS 12 BP 5391 EP 5393 DI 10.1073/pnas.90.12.5391 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LH129 UT WOS:A1993LH12900004 PM 8390660 ER PT J AU NASH, TE MOWATT, MR AF NASH, TE MOWATT, MR TI VARIANT-SPECIFIC SURFACE-PROTEINS OF GIARDIA-LAMBLIA ARE ZINC-BINDING PROTEINS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE METAL BINDING; PROTOZOA; ANTIGENIC VARIATION ID EXCRETORY-SECRETORY PRODUCTS; ANTIGENIC VARIATION; TRANSCRIPTION FACTOR; GENE; MOTIF; HOMEODOMAIN AB Giardia lamblia undergoes surface antigenic variation. The variant-specific surface proteins (VSPs) are a distinct family of cysteine-rich proteins. Characteristically, cysteine residues occur mostly as CXXC tetrapeptides. Four of the reported five VSPs contain a putative metal-binding domain that resembles other metal-binding motifs; the fifth is closely related but lacks an essential histidine. Three different native VSPs bound Zn2+. Co2+, Cu2+, and Cd2+ inhibited Zn2+ binding. Analysis of recombinant VSP fusion proteins showed that the putative binding motif bound Zn2+. Surprisingly, peptide fragments from other regions of the VSP contain numerous CXXCX(n)CXXC motifs that also bound Zn2+. Analysis of deduced amino acid sequences showed well-conserved CXXC spacing in three out of rive VSPs, suggesting conservation of structure despite amino acid sequence divergence. The function of VSPs is unknown, but by binding Zn2+ or other metals in the intestine, VSPs may contribute to Zn2+ malnutrition or inhibition of metal-dependent intestinal enzymes, which would lead to malabsorption, a well-known consequence of giardiasis. RP NASH, TE (reprint author), NIAID,PARASIT DIS LAB,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA. NR 46 TC 32 Z9 32 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 15 PY 1993 VL 90 IS 12 BP 5489 EP 5493 DI 10.1073/pnas.90.12.5489 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LH129 UT WOS:A1993LH12900025 PM 8516291 ER PT J AU JOHNSON, MR LOOK, AT DECLUE, JE VALENTINE, MB LOWY, DR AF JOHNSON, MR LOOK, AT DECLUE, JE VALENTINE, MB LOWY, DR TI INACTIVATION OF THE NF1 GENE IN HUMAN-MELANOMA AND NEUROBLASTOMA CELL-LINES WITHOUT IMPAIRED REGULATION OF GTP.RAS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID TUMOR SUPPRESSOR GENES; VONRECKLINGHAUSEN NEUROFIBROMATOSIS; SACCHAROMYCES-CEREVISIAE; NEURO-BLASTOMA; RAS ONCOGENES; PROTEIN; GAP; MUTATIONS; SARCOMA; DIFFERENTIATION AB The NF1 gene, which is altered in patients with type 1 neurofibromatosis, encodes neurofibromin, a protein whose GTPase-activating function can negatively regulate GTP.Ras by accelerating its conversion to inactive GDP.Ras. In schwannoma cell lines from patients with neurofibromatosis, loss of neurofibromin was previously shown to be associated with impaired regulation of GTP-Ras. Our analysis of other neural crest-derived tumor cell lines has shown that some melanoma and neuroblastoma cell lines established from tumors occurring in patients without neurofibromatosis contain reduced or undetectable levels of neurofibromin, with concomitant genetic abnormalities of the NF1 locus. In contrast to the schwannoma cell lines, GTP.Ras was appropriately regulated in the melanoma and neuroblastoma lines that were deficient in neurofibromin, even when c-H-ras was overexpressed in the lines. These results demonstrate that some neural crest tumors not associated with neurofibromatosis have acquired somatically inactivated NF1 genes and suggest a tumor-suppressor function for neurofibromin that is independent of Ras GTPase activation. C1 NCI, CELLULAR ONCOL LAB, BETHESDA, MD 20892 USA. ST JUDE CHILDRENS RES HOSP, DEPT EXPTL ONCOL, MEMPHIS, TN 38105 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT PEDIAT, MEMPHIS, TN 38163 USA. FU NCI NIH HHS [CA-23099, CA-21675] NR 50 TC 127 Z9 127 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 15 PY 1993 VL 90 IS 12 BP 5539 EP 5543 DI 10.1073/pnas.90.12.5539 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LH129 UT WOS:A1993LH12900035 PM 8516298 ER PT J AU TURNER, BC TONKS, NK RAPP, UR REED, JC AF TURNER, BC TONKS, NK RAPP, UR REED, JC TI INTERLEUKIN-2 REGULATES RAF-1 KINASE-ACTIVITY THROUGH A TYROSINE PHOSPHORYLATION-DEPENDENT MECHANISM IN A T-CELL LINE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE T-LYMPHOCYTE; SIGNAL TRANSDUCTION; PHOSPHATASE ID COLONY-STIMULATING FACTOR; PROTEIN-KINASE; RAPID PHOSPHORYLATION; SIGNAL TRANSDUCTION; RECEPTOR-BETA; GROWTH-FACTOR; KILLER-CELLS; C-RAF; ACTIVATION; INCREASE AB Previously we found that interleukin 2 (IL-2) induces tyrosine phosphorylation and activation of the serine/threonine-specific kinase encoded by the raf-1 protooncogene in a T-cell line, CTLL-2. Here we extended these findings by exploring the effects of selective removal of phosphate from tyrosines in p72-74-Raf-1 kinase that had been immunoprecipitated from IL-2-stimulated CTLL-2 cells. Treatment in vitro of IL-2-activated Raf-1 with the tyrosine-specific phosphatases CD45 and TCPTP (formerly called T-cell protein tyrosine phosphatase) reduced Raf kinase activity to nearly baseline levels. This effect was completely inhibited by the phosphatase inhibitor sodium orthovanadate. In contrast, treatment of Raf-1 with a serine/threonine-specific phosphatase, protein phosphatase 1 (PP-1), resulted in a more modest decrease in Raf in vitro kinase activity, and this effect was prevented by okadaic acid. Two-dimensional phosphoamino acid analysis confirmed the selective removal of phosphate from tyrosine by CD45 and from serine and threonine by PP-1. The immunoreactivity of p72-74-Raf-1 with anti-phosphotyrosine antibodies was also completely abolished by treatment with CD45 in the absence but not in the presence of sodium orthovanadate. These findings provide evidence that the IL-2-stimulated phosphorylation of Raf-1 on tyrosines plays an important role in upregulating the activity of this serine/threonine-specific kinase in CTLL-2 cells and, as such, provides a model system for studying the transfer of growth factor-initiated signals from protein tyrosine kinases to serine/threonine-specific kinases. C1 UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. COLD SPRING HARBOR LAB,COLD SPRING HARBOR,NY 11724. FU NCI NIH HHS [CA-54957, CA-53840] NR 31 TC 41 Z9 41 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 15 PY 1993 VL 90 IS 12 BP 5544 EP 5548 DI 10.1073/pnas.90.12.5544 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LH129 UT WOS:A1993LH12900036 PM 7685905 ER PT J AU DAVEY, RT DEWAR, RL REED, GF VASUDEVACHARI, MB POLIS, MA KOVACS, JA FALLOON, J WALKER, RE MASUR, H HANEIWICH, SE ONEILL, DG DECKER, MR METCALF, JA DELORIA, MA LASKIN, OL SALZMAN, N LANE, HC AF DAVEY, RT DEWAR, RL REED, GF VASUDEVACHARI, MB POLIS, MA KOVACS, JA FALLOON, J WALKER, RE MASUR, H HANEIWICH, SE ONEILL, DG DECKER, MR METCALF, JA DELORIA, MA LASKIN, OL SALZMAN, N LANE, HC TI PLASMA VIREMIA AS A SENSITIVE INDICATOR OF THE ANTIRETROVIRAL ACTIVITY OF L-697,661 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; REVERSE-TRANSCRIPTASE INHIBITORS; HIV-1 REPLICATION; TYPE-1; DERIVATIVES; ZIDOVUDINE AB L-697,661 is a non-nucleoside analogue with potent, selective inhibitory activity against the reverse transcriptase of human immunodeficiency virus type 1 (HIV-1). The present study evaluated the potential role of this compound in the treatment of HIV-1-infected patients in a double-blinded, placebo- and zidovudine-controlled trial using plasma viremia as a marker of antiviral activity and real-time phenotypic evaluation of viral isolates for the emergence of resistance. Participants received 12 weeks of either placebo, 25 mg twice a day, 100 mg three times a day, or 500 mg twice a day of L-697,661, or zidovudine, 100 mg rive times a day. Mean logarithmic reciprocal titers of plasma virus in patients taking either L-697,661 or zidovudine decreased by week 4 of therapy; for L-697,661 recipients these changes were dose-dependent and, at the highest dose tested, were comparable in magnitude to those seen with zidovudine. Viral suppression induced by L-697,661 persisted through 8 weeks of treatment but decreased by week 12. This rebound paralleled emergence of viral isolates showing resistance to L-697,661. We conclude that although L-697,661 has potent antiretroviral activity in vivo, its utility may be compromised by rapid emergence of L-697,661-resistant virus. Plasma viremia is a highly sensitive technique affording considerable utility in the early testing of such agents. C1 GEORGETOWN UNIV,MED CTR,DIV MOLEC VIROL & IMMUNOL,WASHINGTON,DC 20007. NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. MERCK SHARP & DOHME LTD,CLIN PHARMACOL,RAHWAY,NJ 07065. RP DAVEY, RT (reprint author), NIAID,BLDG 10,ROOM 11B13,BETHESDA,MD 20892, USA. OI Polis, Michael/0000-0002-9151-2268 NR 12 TC 53 Z9 53 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 15 PY 1993 VL 90 IS 12 BP 5608 EP 5612 DI 10.1073/pnas.90.12.5608 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LH129 UT WOS:A1993LH12900049 PM 8516307 ER PT J AU BENNETT, CB LEWIS, AL BALDWIN, KK RESNICK, MA AF BENNETT, CB LEWIS, AL BALDWIN, KK RESNICK, MA TI LETHALITY INDUCED BY A SINGLE SITE-SPECIFIC DOUBLE-STRAND BREAK IN A DISPENSABLE YEAST PLASMID SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DNA REPAIR; RECOMBINATION; CELL CYCLE ID PROGRAMMED CELL-DEATH; SACCHAROMYCES-CEREVISIAE; DNA DAMAGE; ESCHERICHIA-COLI; CYCLE ARREST; RAD9 GENE; MAT LOCUS; RECOMBINATION; REPAIR; TRANSFORMATION AB Cells of the yeast Saccharomyces cerevisiae are delayed in the G2 phase of the cell cycle following chromosomal DNA damage. This arrest is RAD9-dependent and suggests a signaling mechanism(s) between chromosomal lesions and cell cycling. We examined the global nature of growth inhibition caused by an HO endonuclease-induced double-strand break (DSB) at a 45-bp YZ sequence (from MAT YZ) in a non-yeast region of a dispensable single-copy plasmid. The presence of an unrepaired DSB results in cellular death even though the plasmid is dispensable. Loss of cell viability is partially dependent on the RAD9 gene product. Following induction of the DSB, 40% of RAD+ and 49% of rad9DELTA cells [including both unbudded (G1) and budded (S plus G2) cells] did not progress further in the cell cycle. The remaining RAD+ cells progressed to form microcolonies (<30 cells) containing aberrantly shaped inviable cells. For the rad9DELTA mutant, the majority of the remaining cells produced viable colonies accounting for the greater survival of the rad9DELTA strain. Based on the profound effects of a single nonchromosomal DNA lesion, this system provides a convenient means for studying the signaling effects of a DNA lesion, as well as for designing strategies for modulating cell proliferation. RP BENNETT, CB (reprint author), NIEHS,MOLEC GENET LAB,BOX 12233,RES TRIANGLE PK,NC 27709, USA. NR 33 TC 162 Z9 165 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 15 PY 1993 VL 90 IS 12 BP 5613 EP 5617 DI 10.1073/pnas.90.12.5613 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LH129 UT WOS:A1993LH12900050 PM 8516308 ER PT J AU WERNER, H RE, GG DRUMMOND, IA SUKHATME, VP RAUSCHER, FJ SENS, DA GARVIN, AJ LEROITH, D ROBERTS, CT AF WERNER, H RE, GG DRUMMOND, IA SUKHATME, VP RAUSCHER, FJ SENS, DA GARVIN, AJ LEROITH, D ROBERTS, CT TI INCREASED EXPRESSION OF THE INSULIN-LIKE GROWTH FACTOR-I RECEPTOR GENE, IGF1R, IN WILMS-TUMOR IS CORRELATED WITH MODULATION OF IGF1R PROMOTER ACTIVITY BY THE WT1 WILMS-TUMOR GENE-PRODUCT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MESSENGER-RNA; MESANGIAL CELLS; REGION; PROGRESSION; BINDING; PROTEIN; CULTURE; LOCUS AB Wilms tumor is a pediatric neoplasm that arises from the metanephric blastema. The expression of the gene encoding insulin-like growth factor II (IGF-II) is often elevated in these tumors. Since many of the actions of IGF-II are mediated through activation of the IGF-I receptor (IGF-IR), we have measured the levels of IGF-IR mRNA in normal kidney and in Wilms tumor samples using solution hybridization/RNase protection assays. IGF-IR mRNA levels in the tumors were 5.8-fold higher than in adjacent normal kidney tissue. Among the tumors themselves, the levels of IGF-IR mRNA in those containing heterologous stromal elements were 2-fold higher (P < 0.01) than in tumors without these elements. IGF-IR gene (designated IGF1R) expression in the tumors was inversely correlated with the expression of the Wilms tumor suppressor gene WT1, whose inactivation appears to be a key step in the etiology of Wilms tumor. Cotransfection of Chinese hamster ovary cells with rat and human IGF-IR gene promoter constructs driving luciferase reporter genes and with WT1 expression vectors showed that the active WT1 gene product represses IGF-IR promoter activity in a dose-dependent manner. These results suggest that underexpression, deletion, or mutation of WT1 may result in increased expression of the IGF-IR, whose activation by IGF-II may be an important aspect of the biology of Wilms tumor. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. UNIV CHICAGO,HOWARD HUGHES MED INST,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MOLEC GENET,CHICAGO,IL 60637. UNIV CHICAGO,DEPT CELL BIOL & MED,CHICAGO,IL 60637. WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. RP WERNER, H (reprint author), NIDDKD,DIABET BRANCH,MOLEC & CELLULAR PHYSIOL SECT,BLDG 10,ROOM 8S-239,BETHESDA,MD 20892, USA. OI Roberts, Charles/0000-0003-1756-5772 FU NCI NIH HHS [CA 10817, CA 47983, CA 52009] NR 33 TC 238 Z9 244 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 15 PY 1993 VL 90 IS 12 BP 5828 EP 5832 DI 10.1073/pnas.90.12.5828 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LH129 UT WOS:A1993LH12900095 PM 8390684 ER PT J AU KARLIN, S ALTSCHUL, SF AF KARLIN, S ALTSCHUL, SF TI APPLICATIONS AND STATISTICS FOR MULTIPLE HIGH-SCORING SEGMENTS IN MOLECULAR SEQUENCES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SEQUENCE COMPARISON; PATTERN RECOGNITION; MOLECULAR FEATURES; STATISTICAL SIGNIFICANCE ID AMINO-ACID SEQUENCES; PROTEIN; SIMILARITIES; ALIGNMENTS; DROSOPHILA; EVOLUTION; FAMILY; GENES AB Score-based measures of molecular-sequence features provide versatile aids for the study of proteins and DNA. They are used by many sequence data base search programs, as well as for identifying distinctive properties of single sequences. For any such measure, it is important to know what can be expected to occur purely by chance. The statistical distribution of high-scoring segments has been described elsewhere. However, molecular sequences will frequently yield several high-scoring segments for which some combined assessment is in order. This paper describes the statistical distribution for the sum of the scores of multiple high-scoring segments and illustrates its application to the identification of possible transmembrane segments and the evaluation of sequence similarity. C1 NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. STANFORD UNIV,DEPT MATH,STANFORD,CA 94305. FU NIGMS NIH HHS [GM39907-02, GM10452-26] NR 41 TC 257 Z9 263 U1 1 U2 11 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 15 PY 1993 VL 90 IS 12 BP 5873 EP 5877 DI 10.1073/pnas.90.12.5873 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LH129 UT WOS:A1993LH12900104 PM 8390686 ER PT J AU RAVUSSIN, E FONTVIEILLE, AM SWINBURN, BA BOGARDUS, C AF RAVUSSIN, E FONTVIEILLE, AM SWINBURN, BA BOGARDUS, C TI RISK-FACTORS FOR THE DEVELOPMENT OF OBESITY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID ENERGY-EXPENDITURE; METABOLIC-RATE; WEIGHT-GAIN; DIETARY-FAT; RESPIRATORY CHAMBER; PIMA-INDIANS; FOOD-INTAKE; CARBOHYDRATE; OXIDATION; HUMANS C1 UNIV AUCKLAND, DEPT COMMUNITY HLTH, AUCKLAND, NEW ZEALAND. RP RAVUSSIN, E (reprint author), NIDDKD, CLIN DIABET & NUTR SECT, 4212 N 16TH ST, PHOENIX, AZ 85016 USA. NR 42 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD JUN 14 PY 1993 VL 683 BP 141 EP 150 PG 10 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LM124 UT WOS:A1993LM12400015 ER PT J AU BEAVEN, MA AF BEAVEN, MA TI HISTAMINE REVISITED - A CITATION-CLASSIC COMMENTARY ON MODIFICATION OF THE ENZYMATIC ISOTOPIC ASSAY OF HISTAMINE AND ITS APPLICATION TO MEASUREMENT OF HISTAMINE IN TISSUES, SERUM AND URINE BY BEAVEN,M.A., JACOBSEN,S., HORAKOVA,Z. SO CURRENT CONTENTS/CLINICAL MEDICINE LA English DT Article ID CALCIUM SIGNAL; 2H3 CELLS RP BEAVEN, MA (reprint author), NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892, USA. NR 8 TC 0 Z9 0 U1 0 U2 1 PU INST SCI INFORM INC PI PHILADELPHIA PA 3501 MARKET ST, PHILADELPHIA, PA 19104 SN 0891-3358 J9 CC/CLIN MED PD JUN 14 PY 1993 IS 24 BP 8 EP 8 PG 1 WC Multidisciplinary Sciences; Social Sciences, Interdisciplinary SC Science & Technology - Other Topics; Social Sciences - Other Topics GA LD653 UT WOS:A1993LD65300001 ER PT J AU RADLERPOHL, A GEBEL, S SACHSENMAIER, C KONIG, H KRAMER, M OEHLER, T STREILE, M PONTA, H RAPP, U RAHMSDORF, HJ CATO, ACB ANGEL, P HERRLICH, P AF RADLERPOHL, A GEBEL, S SACHSENMAIER, C KONIG, H KRAMER, M OEHLER, T STREILE, M PONTA, H RAPP, U RAHMSDORF, HJ CATO, ACB ANGEL, P HERRLICH, P TI THE ACTIVATION AND ACTIVITY CONTROL OF AP-1 (FOS/JUN) SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID PROTEIN-KINASE-C; SIGNAL TRANSDUCTION PATHWAYS; B TRANSCRIPTION FACTOR; GROWTH-FACTOR RECEPTOR; DNA-BINDING PROTEINS; GLUCOCORTICOID RECEPTOR; GENE-EXPRESSION; LEUCINE ZIPPER; FOS-JUN; FUNCTIONAL DISSECTION C1 KERNFORSCHUNGSZENTRUM KARLSRUHE GMBH,INST GENET,POB 3640,W-7500 KARLSRUHE 1,GERMANY. FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. RI Cato, Andrew/H-2071-2013 OI Cato, Andrew/0000-0001-8508-3834 NR 80 TC 48 Z9 48 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 11 PY 1993 VL 684 BP 127 EP 148 DI 10.1111/j.1749-6632.1993.tb32277.x PG 22 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LK215 UT WOS:A1993LK21500012 PM 8317826 ER PT J AU KELLER, H MAHFOUDI, A DREYER, C HIHI, AK MEDIN, J OZATO, K WAHLI, W AF KELLER, H MAHFOUDI, A DREYER, C HIHI, AK MEDIN, J OZATO, K WAHLI, W TI PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS AND LIPID-METABOLISM SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID ACYL-COA OXIDASE; RAT-LIVER; BETA-OXIDATION; AMINO-ACIDS; FATTY-ACIDS; GENE; SUPERFAMILY; MECHANISMS; EXPRESSION; BIOGENESIS C1 MAX PLANCK INST ENTWICKLUNGSBIOL,W-7400 TUBINGEN,GERMANY. NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. RP KELLER, H (reprint author), UNIV LAUSANNE,INST BIOL ANIM,CH-1015 LAUSANNE,SWITZERLAND. RI Wahli, Walter/B-1398-2009 OI Wahli, Walter/0000-0002-5966-9089 NR 40 TC 72 Z9 73 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 11 PY 1993 VL 684 BP 157 EP 173 DI 10.1111/j.1749-6632.1993.tb32279.x PG 17 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LK215 UT WOS:A1993LK21500014 PM 8391237 ER PT J AU CAUDLE, RM AF CAUDLE, RM TI THE DEMONSTRATION OF LONG-LATENCY POTENTIALS IN THE CA1 REGION OF THE RAT HIPPOCAMPAL SLICE SO BRAIN RESEARCH LA English DT Article DE P3; P300; EVOKED POTENTIAL; HIPPOCAMPUS; RAT; CA1 REGION ID ENDOGENOUS POTENTIALS; P300; MEMORY AB Shaffer collateral evoked extracellular DC potentials with latencies greater than 100 ms are demonstrated in the CA1 region of the rat hippocampal slice preparation. The most prominent potential following the population spike is a positive potential peaking between 150 and 400 ms after the stimulus. The amplitude of the potential is approximately two orders of magnitude smaller than the population spike. This potential shares several characteristics with the P300 from electroencephalogram studies of evoked potentials. Thus, it was dubbed the in vitro P3. One of the most distinguishing characteristics of the in vitro P3 is a negative potential that immediately follows it. The negative potential is smaller in amplitude than the in vitro P3, but lasts for several seconds. A similar potential also follows the P300 in electroencephalogram studies. These data suggest that the in vitro P3 is an in vitro version of the long latency evoked potential known as the P300 in electroencephalogram studies. RP CAUDLE, RM (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 30,ROOM B-20,BETHESDA,MD 20892, USA. NR 10 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 11 PY 1993 VL 613 IS 2 BP 247 EP 250 DI 10.1016/0006-8993(93)90905-3 PG 4 WC Neurosciences SC Neurosciences & Neurology GA LH293 UT WOS:A1993LH29300008 PM 8186971 ER PT J AU ARAI, R JACOBOWITZ, DM DEURA, S AF ARAI, R JACOBOWITZ, DM DEURA, S TI ULTRASTRUCTURAL-LOCALIZATION OF CALRETININ IMMUNOREACTIVITY IN LOBULE-V OF THE RAT CEREBELLUM SO BRAIN RESEARCH LA English DT Note DE CALRETININ; CALCIUM-BINDING PROTEIN; CEREBELLUM; GRANULE CELL; PARALLEL FIBER; MOSSY FIBER; PUNCTA-ADHEARENTIA; RAT ID ELECTRON-MICROSCOPIC IMMUNOCYTOCHEMISTRY; CALCIUM-BINDING PROTEIN; IMMUNOHISTOCHEMICAL LOCALIZATION; CALBINDIN-D28K; PEROXIDASE; GLUTAMATE; LIGHT; BRAIN AB Ultrastructural localization of a calcium-binding protein, calretinin, in the cerebellar cortex of the rat was examined with an immunoperoxidase method. The cerebellar lobule V was investigated in detail. In the molecular layer, calretinin immunoreactivity was found in parallel fibers and in their varicosities that formed synapses with unlabeled Purkinje cell dendritic thorns and Golgi cell dendrites. In the granular layer, most granule cells were immunostained for calretinin. Within immunostained granule cells, the labels were found in the cytoplasmic matrix of both the perikaryon and primary dendrite, and in euchromatin patches of the nucleus. Some mossy fiber terminals also stained for calretinin. In the white matter, a few axons were labeled for calretinin and surrounded by unstained myelin sheath. It is suggested that calretinin may play a role at the presynaptic sites of the parallel and mossy fiber terminals. C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. RP ARAI, R (reprint author), FUJITA HLTH UNIV,SCH MED,DEPT ANAT,TOYOAKE,AICHI 47011,JAPAN. NR 19 TC 14 Z9 14 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 11 PY 1993 VL 613 IS 2 BP 300 EP 304 DI 10.1016/0006-8993(93)90915-A PG 5 WC Neurosciences SC Neurosciences & Neurology GA LH293 UT WOS:A1993LH29300018 PM 8186980 ER PT J AU ATACK, JR RAPOPORT, SI VARLEY, CL AF ATACK, JR RAPOPORT, SI VARLEY, CL TI CHARACTERIZATION OF INOSITOL MONOPHOSPHATASE IN HUMAN CEREBROSPINAL-FLUID SO BRAIN RESEARCH LA English DT Note DE INOSITOL MONOPHOSPHATASE; CEREBROSPINAL FLUID; MANIC DEPRESSION; LITHIUM; MAGNESIUM; BISPHOSPHONATE ID BOVINE BRAIN; LITHIUM AB Inositol monophosphatase (IMPase) has been identified and characterized in human lumbar cerebrospinal fluid (CSF). The CSF enzyme has a K(m) for inositol 1-phosphate (Ins(1)P; 0.12 mM), a magnesium dependence (optimum concentration 10 mM) and a sensitivity to inhibition by either the bisphosphonate inhibitor 1-(4-hydroxyphenyloxy)ethane-1,1-bisphosphonic acid (L-690,330) or LiCl (IC50's: 1.3 muM and 1.6 mM, respectively) similar to native human brain and human recombinant enzymes. In CSF, antiserum raised against purified bovine brain IMPase recognised a protein of 30 kDa, identical to that seen in human brain homogenate. It remains to be determined whether CSF IMPase activity may be a useful in vivo marker of CNS phosphatidyl inositol cycle activity in disorders where this signalling pathway may be altered (e.g. manic depression). C1 MERCK SHARP & DOHME LTD,NEUROSCI RES CTR,HARLOW,ENGLAND. NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 12 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 11 PY 1993 VL 613 IS 2 BP 305 EP 308 DI 10.1016/0006-8993(93)90916-B PG 4 WC Neurosciences SC Neurosciences & Neurology GA LH293 UT WOS:A1993LH29300019 PM 8186981 ER PT J AU ARAI, M ARAI, R SASAMOTO, K KANI, K MAEDA, T DEURA, S JACOBOWITZ, DM AF ARAI, M ARAI, R SASAMOTO, K KANI, K MAEDA, T DEURA, S JACOBOWITZ, DM TI APPEARANCE OF CALRETININ-IMMUNOREACTIVE NEURONS IN THE UPPER LAYERS OF THE RAT SUPERIOR COLLICULUS AFTER EYE ENUCLEATION SO BRAIN RESEARCH LA English DT Note DE CALRETININ; CALCIUM-BINDING PROTEIN; SUPERIOR COLLICULUS; EYE ENUCLEATION; RETINAL DEAFFERENTATION; PLASTICITY; IMMUNOHISTOCHEMISTRY; RAT ID DORSAL-ROOT GANGLION; VISUAL-SYSTEM; ALBINO-RATS; PROJECTIONS; CALBINDIN; BRAIN; DEAFFERENTATION; LOCALIZATION; INDUCTION; CELLS AB The effects of retinal deafferentation on a calcium-binding protein, calretinin, in the upper layers (superficial gray layer and optic nerve layer) of the rat superior colliculus were examined. In intact rats and on the ipsilateral side of unilaterally eye-enucleated rats, the superficial gray layer and optic nerve layer contained a few dispersed calretinin-immunoreactive cells. On the contralateral side to the enucleation, the number of immunostained cells in the superficial gray layer and optic nerve layer was increased. These findings suggest that retinal deafferentation results in an increase in contents of calretinin in some cell bodies within the upper layers of the superior colliculus. C1 SHIGA UNIV MED SCI,DEPT ANAT,OTSU,SHIGA 52021,JAPAN. FUJITA HLTH UNIV,SCH MED,DEPT ANAT,TOYOAKE,AICHI,JAPAN. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. RP ARAI, M (reprint author), SHIGA UNIV MED SCI,DEPT OPHTHALMOL,OTSU,SHIGA 52021,JAPAN. NR 32 TC 24 Z9 24 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 11 PY 1993 VL 613 IS 2 BP 341 EP 346 DI 10.1016/0006-8993(93)90924-C PG 6 WC Neurosciences SC Neurosciences & Neurology GA LH293 UT WOS:A1993LH29300027 PM 8186989 ER PT J AU KOONIN, EV AF KOONIN, EV TI A COMMON SET OF CONSERVED MOTIFS IN A VAST VARIETY OF PUTATIVE NUCLEIC ACID-DEPENDENT ATPASES INCLUDING MCM PROTEINS INVOLVED IN THE INITIATION OF EUKARYOTIC DNA-REPLICATION SO NUCLEIC ACIDS RESEARCH LA English DT Article ID ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; BINDING PROTEINS; ATP-BINDING; GENE; SUPERFAMILY; ALIGNMENT; ORIGIN; VIRUS; RECOMBINATION AB A new superfamily of (putative) DNA-dependent ATPases is described that includes the ATPase domains of prokaryotic NtrC-related transcription regulators, MCM proteins involved in the initiation of eukaryotic DNA replication, and a group of uncharacterized bacterial and chloroplast proteins. MCM proteins are shown to contain a modified form of the ATP-binding motif and are predicted to mediate ATP-dependent opening of double-stranded DNA in the replication origins. In a second line of investigation, it is demonstrated that the products of unidentified open reading frames from Marchantia mitochondria and from yeast, and a domain of a baculovirus protein involved in viral DNA replication are related to the superfamily III of DNA and RNA helicases that previously has been known to include only proteins of small viruses. Comparison of the multiple alignments showed that the proteins of the NtrC superfamily and the helicases of superfamily III share three related sequence motifs tightly packed in the ATPase domain that consists of 100 - 150 amino acid residues. A similar array of conserved motifs is found in the family of DnaA-related ATPases. It is hypothesized that the three large groups of nucleic acid-dependent ATPases have similar structure of the core ATPase domain and have evolved from a common ancestor. RP KOONIN, EV (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BLDG 38A,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 56 TC 314 Z9 317 U1 0 U2 7 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD JUN 11 PY 1993 VL 21 IS 11 BP 2541 EP 2547 DI 10.1093/nar/21.11.2541 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LJ612 UT WOS:A1993LJ61200001 PM 8332451 ER PT J AU SAX, CM ILAGAN, JG PIATIGORSKY, J AF SAX, CM ILAGAN, JG PIATIGORSKY, J TI FUNCTIONAL REDUNDANCY OF THE DE-1 AND ALPHA-A-CRYBP1 REGULATORY SITES OF THE MOUSE ALPHA-A-CRYSTALLIN PROMOTER SO NUCLEIC ACIDS RESEARCH LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; TISSUE-SPECIFIC EXPRESSION; LENS-SPECIFIC EXPRESSION; NF-KAPPA-B; CHLORAMPHENICOL ACETYLTRANSFERASE; TRANSGENIC MICE; MAMMALIAN-CELLS; GENE-EXPRESSION; PROTEIN; CHICKEN AB Previous studies have implicated the DE-1 (-111/-106) and alphaA-CRYBP1 (-66/-57) sites for activity of the mouse alphaA-crystallin promoter in transiently transfected lens cells. Here we have used the bacterial chloramphenicol acetyltransferase (CAT) reporter gene to test the functional importance of the putative DE-1 and alphaA-CRYBP1 regulatory elements by site-specific and deletion mutegenesis in stably transformed alphaTN4-1 lens cells and in transgenic mice. FVB/N and C57BL/6 x SJL F2 hybrid transgenic mice were assayed for CAT activiy in the lens, heart, lung, kidney, spleen, liver, cerebrum, and muscle. F0, F1, and F2 mice from multiple lines carrying single mutations of the DE-1 or alphaA-CRYBP1 sites showed high levels of CAT activity in the lens, but not in any of the non-lens tissues. By contrast, despite activity of the wild-type promoter, none of the mutant promoter/CAT constructs were active in the transiently transfected and stably transformed lens cells. The mice carrying transgenes with either site-specific mutations in both the DE-1 and alphaA-CRYBP1 sites or a deletion of the entire DE-1 and part of the alphaA-CRYBP1 site (- 60/ + 46) fused to the CAT gene did not exhibit CAT activity above background in any of the tissues examined, including the lens. Our results thus indicate that the DE-1 and alphaA-CRYBP1 sites are functionally redundant in transgenic mice. Moreover, the present data coupled with previous transfection and transgenic mouse experiments suggest that this functionally redundancy is confined to lens expression within the mouse and is not evident in transiently transfected and stably transformed lens cells, making the cultured lens cells sensitive indicators of functional elements of crystallin genes. RP SAX, CM (reprint author), NEI, MOLEC & DEV BIOL, BLDG 6, ROOM 208, BETHESDA, MD 20892 USA. FU NICHD NIH HHS [N01-HD-0-2911] NR 39 TC 23 Z9 23 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD JUN 11 PY 1993 VL 21 IS 11 BP 2633 EP 2640 DI 10.1093/nar/21.11.2633 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LJ612 UT WOS:A1993LJ61200014 PM 8332460 ER PT J AU SWAMINATHAN, S MALHOTRA, P MANOHAR, CF DHAR, R THIMMAPAYA, B AF SWAMINATHAN, S MALHOTRA, P MANOHAR, CF DHAR, R THIMMAPAYA, B TI ACTIVATION OF A DUAL ADENOVIRUS PROMOTER CONTAINING NONCONSENSUS TATA MOTIFS IN SCHIZOSACCHAROMYCES-POMBE - ROLE OF TATA SEQUENCES IN THE EFFICIENCY OF TRANSCRIPTION SO NUCLEIC ACIDS RESEARCH LA English DT Article ID BOX-BINDING-FACTOR; RNA POLYMERASE-II; FISSION YEAST; SACCHAROMYCES-CEREVISIAE; FUNCTIONAL DOMAINS; TFIID COMPLEX; GENE; PROTEIN; ELEMENTS; INITIATION AB The role of TATA elements in the expression of a mammalian promoter was investigated in the fission yeast Schizosaccharomyces pombe, by studying the human adenovirus E2-early promoter. This is a unique dual promoter with two nonconsensus TATA elements directing transcription from two cap sites, + 1 and - 26. A sequence TTAAGA provides the TATA box function for the + 1 promoter, whereas a sequence TAAATT, with a closer resemblance to the consensus (TATAA/TA) provides this function for the - 26 promoter. Yet, in human cells, the + 1 promoter is transcribed about 20 fold more efficiently than the - 26 promoter. We found that both promoters are transcribed faithfully in S.pombe with start sites identical or close to those found in human cells. Surprisingly, the relative ratio of expression for the + 1 and - 26 promoters was exactly reversed in S.pombe cells. This reversal appeared to be due to the relatively weak binding of S.pombe TATA binding protein to the TTAAGA motif, rather than to its rate of dissociation. Furthermore, we show that in S.pombe, promoter expression correlates well with the nucleotide sequence of the TATA element rather than the context in which it is placed. By contrast, it is the context of the TATA element, rather than its nucleotide sequence that appears to be critical for promoter expression in human cells. Our data suggest the existence of one or more additional factors in human cells that permit the utilization of nonconsensus TATA elements. S.pombe appears to lack these factors. C1 NORTHWESTERN UNIV,SCH MED,ROBERT H LURIE CANC CTR,303 E CHICAGO AVE,CHICAGO,IL 60611. NORTHWESTERN UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,CHICAGO,IL 60611. NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. OI Swaminathan, Sathyamangalam/0000-0002-4388-2248 FU NIAID NIH HHS [AI18029, AI 20156] NR 72 TC 11 Z9 11 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD JUN 11 PY 1993 VL 21 IS 11 BP 2737 EP 2746 DI 10.1093/nar/21.11.2737 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LJ612 UT WOS:A1993LJ61200029 PM 8332470 ER PT J AU DOBRZANSKI, D SHARONI, Y WADA, E BATTEY, J SAUSVILLE, E AF DOBRZANSKI, D SHARONI, Y WADA, E BATTEY, J SAUSVILLE, E TI NEUROMEDIN-B RECEPTOR TRANSFECTED BALB/3T3 CELLS - SIGNAL-TRANSDUCTION AND EFFECTS OF ECTOPIC RECEPTOR EXPRESSION ON CELL-GROWTH SO REGULATORY PEPTIDES LA English DT Article DE BOMBESIN; PHOSPHOLIPASE-C; CALCIUM ION; ARACHIDONATE ID GASTRIN-RELEASING PEPTIDE; SWISS 3T3 CELLS; BOMBESIN-LIKE PEPTIDES; LUNG-CARCINOMA CELLS; PERTUSSIS TOXIN; PHOSPHOLIPASE-C; DNA-SYNTHESIS; ARACHIDONIC-ACID; STIMULATION; INHIBITION AB Bombesin-like peptides including neuromedin B have been proposed as autocrine or paracrine growth factors for carcinomas. To examine signal transduction and regulation of cell growth by NMB, transfectants were created with the rat NMB receptor (NMB-R) gene in BALB/3T3 cells which do not express an endogenous bombesin peptide receptor. The resultant cell line, NMB-8, expresses 800,000 NMB binding sites/cell. Addition of NMB has a biphasic effect on [H-3]thymidine ([H-3]dT) incorporation in confluent and quiescent cells: up to 10 nM of NMB causes a 1.5-3-fold stimulation of [H-3]dT incorporation, but at greater than 10 nM there is inhibition of [H-3]dT incorporation, and at 100 nM of NMB there is inhibition of cell growth. NMB causes protracted increases in intracellular Ca2+, and pertussis toxin (PT)-insensitive phosphatidylinositol (PI) turnover. NMB-mediated increase in membrane phospholipase-C activity is stimulated by guanosine 5'-O-(3-thiotriphosphate). Arachidonate release is also activated by NMB in a PT-insensitive manner. Brief exposure to 12-tetradecanoylphorbol 13-acetate inhibits NMB-mediated PI turnover but not arachidonate release. Thus, in NMB-8 cells, distinct mechanisms govern NMB-mediated phospholipase-C activation and arachidonate release. Also, neuromedin-B is potentially a bifunctional regulator of cell growth. C1 NCI,DIV CANC TREATMENT,BIOL CHEM LAB,37 RM 5D02 NIH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. BEN GURION UNIV NEGEV,SOROKA MED CTR,FAC HLTH SCI,CLIN BIOCHEM UNIT,IL-84105 BEER SHEVA,ISRAEL. NR 32 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD JUN 11 PY 1993 VL 45 IS 3 BP 341 EP 352 DI 10.1016/0167-0115(93)90360-K PG 12 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA LH197 UT WOS:A1993LH19700002 PM 8394594 ER PT J AU ROULEAU, GA MEREL, P LUTCHMAN, M SANSON, M ZUCMAN, J MARINEAU, C HOANGXUAN, K DEMCZUK, S DESMAZE, C PLOUGASTEL, B PULST, SM LENOIR, G BIJLSMA, E FASHOLD, R DUMANSKI, J DEJONG, P PARRY, D ELDRIGE, R AURIAS, A DELATTRE, O THOMAS, G AF ROULEAU, GA MEREL, P LUTCHMAN, M SANSON, M ZUCMAN, J MARINEAU, C HOANGXUAN, K DEMCZUK, S DESMAZE, C PLOUGASTEL, B PULST, SM LENOIR, G BIJLSMA, E FASHOLD, R DUMANSKI, J DEJONG, P PARRY, D ELDRIGE, R AURIAS, A DELATTRE, O THOMAS, G TI ALTERATION IN A NEW GENE ENCODING A PUTATIVE MEMBRANE-ORGANIZING PROTEIN CAUSES NEUROFIBROMATOSIS TYPE-2 SO NATURE LA English DT Article ID BILATERAL ACOUSTIC NEUROFIBROMATOSIS; GRADIENT GEL-ELECTROPHORESIS; HUMAN-CHROMOSOME 22; SUBUNIT NF-H; POLYPOSIS-COLI; DNA FRAGMENTS; MENINGIOMA; TALIN; EZRIN; HOMOLOGY AB Neurofibromatosis type 2 (NF2) is a monogenic dominantly inherited disease predisposing carriers to develop nervous system tumours. To identify the genetic defect, the region between two flanking polymorphic markers on chromosome 22 was cloned and several genes identified. One is the site of germ-line mutations in NF2 patients and of somatic mutations in NF2-related tumours. Its deduced product has homology with proteins at the plasma membrane and cytoskeleton interface, a previously unknown site of action of tumour suppressor genes in humans. C1 MONTREAL GEN HOSP,RES INST,MONTREAL H3G 1A4,QUEBEC,CANADA. INST CURIE,GENET TUMEURS LAB,INSERM,CJF 9201,F-75231 PARIS 05,FRANCE. CEDARS SINAI MED CTR,NEUROGENET LAB,LOS ANGELES,CA 90048. INT AGCY RES CANC,F-69372 LYON,FRANCE. UNIV AMSTERDAM,INST HUMAN GENET,1105 AZ AMSTERDAM,NETHERLANDS. UNIV ERLANGEN NURNBERG,INST HUMAN GENET,W-8520 ERLANGEN,GERMANY. KAROLINSKA INST,DEPT CLIN GENET,S-10401 STOCKHOLM 60,SWEDEN. LAWRENCE LIVERMORE NATL LAB,CTR HUMAN GENOME,LIVERMORE,CA 94550. NCI,CLIN EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP ROULEAU, GA (reprint author), MCGILL UNIV,CTR RECH NEUROSCI,MONTREAL H3A 2T5,QUEBEC,CANADA. OI zucman-rossi, Jessica/0000-0002-5687-0334 NR 43 TC 992 Z9 1009 U1 1 U2 36 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JUN 10 PY 1993 VL 363 IS 6429 BP 515 EP 521 DI 10.1038/363515a0 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LF939 UT WOS:A1993LF93900040 PM 8379998 ER PT J AU CANNON, RO AF CANNON, RO TI CHEST PAIN WITH NORMAL CORONARY ANGIOGRAMS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID ANGINA-PECTORIS; ENDOTHELIAL DYSFUNCTION; ARTERIOGRAMS; FLOW; RESISTANCE RP CANNON, RO (reprint author), NHLBI,BETHESDA,MD 20892, USA. NR 14 TC 25 Z9 27 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUN 10 PY 1993 VL 328 IS 23 BP 1706 EP 1708 DI 10.1056/NEJM199306103282310 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA LF054 UT WOS:A1993LF05400010 PM 8487830 ER PT J AU STLOUIS, ME KAMENGA, M BROWN, C NELSON, AM MANZILA, T BATTER, V BEHETS, F KABAGABO, U RYDER, RW OXTOBY, M QUINN, TC HEYWARD, WL AF STLOUIS, ME KAMENGA, M BROWN, C NELSON, AM MANZILA, T BATTER, V BEHETS, F KABAGABO, U RYDER, RW OXTOBY, M QUINN, TC HEYWARD, WL TI RISK FOR PERINATAL HIV-1 TRANSMISSION ACCORDING TO MATERNAL IMMUNOLOGICAL, VIROLOGICAL, AND PLACENTAL FACTORS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; ACQUIRED IMMUNODEFICIENCY; SEROPOSITIVE MOTHERS; PREGNANT-WOMEN; INFECTION; TYPE-1; INFANTS; CELLS; AIDS; CHORIOAMNIONITIS AB Objective.-To evaluate how maternal and obstetric factors interact to influence mother-to-child human immunodeficiency virus type 1 (HIV-1) transmission. Design.-Prospective, observational cohort study of children born to HIV-infected women to determine child's HIV infection status. The analysis then compared peripartum maternal, placental, and obstetric variables between HIV-1 transmitter and nontransmitter women. Setting.-Two large maternity wards in Kinshasa, Zaire. Participants.-Consecutive sample of 324 HIV-1-infected women at delivery, with 254 HIV-seronegative women followed up as control subjects. Principal Outcome Measures.-HIV infection status of children, to classify each woman as an HIV-1 transmitter or nontransmitter. Results.-The highest transmission risk (TR) was associated with maternal p24 antigenemia (TR, 71 %; relative risk [RR], 3.0; 95% confidence interval [CI], 1.7 to 5.2) and maternal CD8+ lymphocyte counts of at least 1.80 X 10(9)/L (1800/muL) (TR, 50%; RR, 2.2; 95% CI, 1.2 to 4.2). Among women with CD8+ lymphocyte counts of less than 1.80 X 10(9)/L, CD4+ lymphocyte counts of less than 0.60 x 10(9)/L were a risk factor (TR, 29%; RR, 2.2; 95% CI, 1.2 to 4.2). In women with neither high CD8+ nor low CD4+ lymphocyte counts, placental membrane inflammation was associated with perinatal transmission (TR, 40%; RR, 4.2; 95% CI, 1.3 to 13.7). In women with neither p24 antigenemia, high CD8+ or low CD4+ lymphocyte counts, nor placental membrane inflammation, the transmission risk was only 7%. Additional correlates of transmission included maternal anemia and fever, but not maternal sexually transmitted diseases. Conclusions.-Identifiable subgroups of HIV-1-infected women based on maternal and placental characteristics had between a 7% and 71% risk of perinatal HIV-1 transmission. Not only the overall rate of transmission but the impact of different risk factors for transmission appear to vary over the course of HIV infection. C1 PROJET SIDA, KINSHASA, ZAIRE. NIAID, BETHESDA, MD 20892 USA. ARMED FORCES INST PATHOL, WASHINGTON, DC 20306 USA. RP STLOUIS, ME (reprint author), CTR DIS CONTROL & PREVENT, NATL CTR INFECT DIS, DIV HIV AIDS, 1600 CLIFTON RD, MAILSTOP E-50, ATLANTA, GA 30333 USA. RI Quinn, Thomas/A-2494-2010 NR 59 TC 235 Z9 241 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 EI 1538-3598 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 9 PY 1993 VL 269 IS 22 BP 2853 EP 2859 DI 10.1001/jama.269.22.2853 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA LE936 UT WOS:A1993LE93600020 PM 8098783 ER PT J AU BRAUN, MM COTE, TR RABKIN, CS AF BRAUN, MM COTE, TR RABKIN, CS TI TRENDS IN DEATH WITH TUBERCULOSIS DURING THE AIDS ERA SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; UNITED-STATES; INFECTION; EPIDEMIC; MORTALITY; IMPACT AB Objective.-To describe and analyze recent changes in tuberculosis mortality in the United States during the acquired immunodeficiency syndrome (AIDS) epidemic. Design.-We used National Center for Health Statistics multiple-cause mortality data and analyzed deaths with tuberculosis (1980 through 1990) and/or AIDS (1987 through 1990) as an underlying or associated cause. We also categorized the 50 states and the District of Columbia into high (five states), medium (23 states), and low (23 states) AIDS incidence groups and then compared the groups' rates of death with tuberculosis during the period 1980 through 1990. Study Population.-Residents of the United States who died in the period 1980 through 1990. Main Outcome Measures.-Death certificates indicating AIDS and/or tuberculosis. Results.-A bimodal age distribution of persons dying with tuberculosis has emerged concurrent with the AIDS epidemic. A new peak spanning the ages 20 to 49 years accompanies the preexisting peak in the elderly. In 1990, 54.2% (729/1344) of the deaths with tuberculosis in persons 20 to 49 years of age occurred in persons who also had AIDS listed on their death certificates. During the period 1987 through 1990, there was an increasing trend in the proportion of AIDS deaths that also had tuberculosis: 2.3% (353/15 075) in 1987, 2.5% (460/18 649) in 1988, 3.0% (738/24 607) in 1989, and 3.0% (836/27 975) in 1990 (P<.001). Of AIDS deaths in 1990, 1.6% (253/15 565) of whites died with tuberculosis, compared with 4.7% (400/8533) of blacks (P<.001) and 4.7% (172/3666) of Hispanics (P<.001). In the high AIDS incidence states, the rate of death with tuberculosis in persons aged 20 to 49 years rose from 0.61 to 2.82 per 100 000 population in the period 1982 through 1990, an increase of 362%. For this age group in the states with medium and low AIDS incidence, the rates of death with tuberculosis during this period rose 52% and 47% (from 0.44 to 0.67 and from 0.19 to 0.28 per 100 000 population), respectively. The increases in the rate of death with tuberculosis within all three groups and the differences among the groups were all highly statistically significant (P<.001). Conclusion.-The AIDS epidemic has significantly increased the number and rate of tuberculosis deaths in younger adults through 1990, although in this study discrimination of deaths due to tuberculosis from deaths with tuberculosis was not possible. Vigorous efforts to prevent and treat tuberculosis and AIDS are indicated to reverse the trends we have described. C1 NCI,ENVIRONM EPIDEMIOL BRANCH,ENVIRONM STUDIES SECT,BETHESDA,MD 20892. NCI,VIRAL STUDIES SECT,BETHESDA,MD 20892. NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. NR 24 TC 57 Z9 61 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 9 PY 1993 VL 269 IS 22 BP 2865 EP 2868 DI 10.1001/jama.269.22.2865 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA LE936 UT WOS:A1993LE93600022 PM 8497090 ER PT J AU SUMMERS, RW WU, XR FITZGERALD, SC BRENNEMAN, DE VONAGOSTON, D AF SUMMERS, RW WU, XR FITZGERALD, SC BRENNEMAN, DE VONAGOSTON, D TI EXCITATORY AMINO-ACID REGULATION OF THE ENKEPHALIN PHENOTYPE IN MOUSE EMBRYONIC SPINAL-CORD CULTURES SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE ENKEPHALIN; PHENOTYPE; N-METHYL-D-ASPARTATE; DEVELOPMENT; CENTRAL NERVOUS SYSTEM ID NERVE GROWTH-FACTOR; PREPROENKEPHALIN MESSENGER-RNA; NEURONAL SURVIVAL; VISUAL-CORTEX; GLOBUS-PALLIDUS; NMDA RECEPTORS; RAT STRIATUM; SYSTEM; BRAIN; HIPPOCAMPUS AB Expression of the preproenkephalin gene in developing spinal cord-dorsal root ganglia (SC-DRG) cultures was determined by Northern analysis following treatments with different agonists and antagonists of the glutamate receptor. Cultures (10-12 days old) were treated with various concentrations (10(-7)-10(-3) M) of N-methyl-D-aspartate (NMDA), quisqualate, kainic acid (KA), 2-amino-5-phosphonovaleric acid (APV) and 5-methyl-10,11-dihydro-H-5-dibenzo[a, d]cyclohepten-5,10-imine maleate (MK801) either with or without blocking spontaneous electrical activity with 1 muM tetrodotoxin (TTX). In electrically active cultures, treatments with NMDA and KA increased preproenkephalin transcripts (mRNA(ppENK)), showing maximum effects at 1 muM (4-fold and 2-fold, respectively), while treatments with quisqualate and MK801 caused concentration-dependent down-regulation in mRNA(ppENK). The most effective concentrations of NMDA (1 muM) and quisqualate (10 muM) altered mRNA(ppENK) levels within 4 h of treatment and peaked after 24 h for NMDA and 48 h for quisqualate treatment. Co-treatment with APV completely blocked the NMDA-induced rise of mRNA(ppENK). During electrical blockade, none of the concentrations of NMDA tested showed any effect on enkephalin expression, neither could NMDA pre-treatment prevent the TTX-induced down-regulation of mRNA(ppENK). Our results indicate that the activity-dependent establishment of the enkephalin phenotype is modulated through the selective activation of the NMDA-glutamate receptor. C1 NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892. NICHHD,DEV & MOLEC PHARMACOL SECT,BETHESDA,MD 20892. NICHHD,NEUROBIOL SECT,BETHESDA,MD 20892. UNIV IOWA,COLL MED,IOWA CITY,IA 52242. NICHHD,MOLEC CONTROL NEURODIFFERENTIAT,BETHESDA,MD 20892. BEIJING MED UNIV,FIRST TEACHING HOSP,DEPT PEDIAT NEUROL,BEIJING,PEOPLES R CHINA. VET AFFAIRS MED CTR,DEPT INTERNAL MED,IOWA CITY,IA. NR 55 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD JUN 8 PY 1993 VL 73 IS 2 BP 185 EP 192 DI 10.1016/0165-3806(93)90137-Y PG 8 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA LJ389 UT WOS:A1993LJ38900005 ER PT J AU CHRISTODOULOU, D GEORGE, C KEEFER, LK AF CHRISTODOULOU, D GEORGE, C KEEFER, LK TI AN UNUSUAL BI-TRI-BINUCLEAR SANDWICH COMPLEX FORMED IN THE REACTION OF CUCL2 WITH THE ET2N-N2O2- ION SO JOURNAL OF THE CHEMICAL SOCIETY-CHEMICAL COMMUNICATIONS LA English DT Article ID NITRIC-OXIDE; MOLECULAR-STRUCTURE; CRYSTAL-STRUCTURE; LIGANDS; CHEMISTRY; EXCHANGE; ABILITY AB Reaction of the Et2N-N2O2- ligand with Cu(II) ions in methanol produces a mixed complex, shown by X-ray crystallography to consist of simple, alkoxo-bridged bi- and tri-nuclear units held together in a discrete triple-decker array. C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,CHEM SECT,FREDERICK,MD 21702. USN,RES LAB,STRUCT MATTER LAB,WASHINGTON,DC 20375. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 NR 23 TC 28 Z9 28 U1 0 U2 0 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK MILTON ROAD, CAMBRIDGE, CAMBS, ENGLAND CB4 4WF SN 0022-4936 J9 J CHEM SOC CHEM COMM JI J. Chem. Soc.-Chem. Commun. PD JUN 7 PY 1993 IS 11 BP 937 EP 939 DI 10.1039/c39930000937 PG 3 WC Chemistry, Multidisciplinary SC Chemistry GA LG166 UT WOS:A1993LG16600028 ER PT J AU FANG, Y RAND, RP LEIKIN, S KOZLOV, MM AF FANG, Y RAND, RP LEIKIN, S KOZLOV, MM TI CHAIN-MELTING REENTRANT TRANSITION IN BIMOLECULAR LAYERS AT LARGE SEPARATIONS SO PHYSICAL REVIEW LETTERS LA English DT Article ID FORCES AB We have detected a reentrant phase transition within well-separated bimolecular layers of diacylphosphates. The disorder-order-disorder transitions of the hydrocarbon chains can be accounted for on the basis of the electrostatic energy between bilayers and the elastic compressibility energy within bilayers. C1 BROCK UNIV,DEPT BIOL SCI,ST CATHARINES L2S 3A1,ONTARIO,CANADA. NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. FREE UNIV BERLIN,FACHBEREICH PHYS,W-1000 BERLIN 33,GERMANY. RI Leikin, Sergey/A-5518-2008 OI Leikin, Sergey/0000-0001-7095-0739 NR 8 TC 6 Z9 6 U1 0 U2 0 PU AMERICAN PHYSICAL SOC PI COLLEGE PK PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA SN 0031-9007 J9 PHYS REV LETT JI Phys. Rev. Lett. PD JUN 7 PY 1993 VL 70 IS 23 BP 3623 EP 3626 DI 10.1103/PhysRevLett.70.3623 PG 4 WC Physics, Multidisciplinary SC Physics GA LE942 UT WOS:A1993LE94200026 ER PT J AU BHAT, ST VINAYEK, R JENSEN, RT GARDNER, JD AF BHAT, ST VINAYEK, R JENSEN, RT GARDNER, JD TI A NEWLY RECOGNIZED ACTION OF CHOLECYSTOKININ ON PANCREATIC ACINI-RELEASE OF LACTATE-DEHYDROGENASE SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE CHOLECYSTOKININ OCTAPEPTIDE; LACTATE DEHYDROGENASE; (PANCREATIC ACINAR CELL); (RAT) ID GUINEA-PIG PANCREAS; PROTEIN KINASE-C; DISPERSED ACINI; AMYLASE RELEASE; SECRETION; CELLS; PROSTAGLANDIN; SECRETAGOGUES; ANTAGONISTS; GASTRIN AB In the course of examining the actions of the cholecystokinin octapeptide (CCK-8) on pancreatic acini we found that CCK-8 can stimulate release of the large-molecular-weight cytoplasmic protein, lactate dehydrogenase (LDH) by as much as 6-fold. CCK-8-stimulated LDH release is mediated by a CCK-preferring receptor, detectable at 100 pM CCK-8, maximal at 100 nM CCK-8, constant for up to 30 min, reversible, not desensitized, and dependent on oxidative metabolism and incubation temperature but not on calcium in the extracellular medium. This action of CCK-8 is blocked by inhibitors of protein kinases, staurosporine, H-7, H-8 and H-9, but not by calmodulin antagonists, chlorpromazine, trifluoperazine or W-7. This action of CCK-8 on LDH release is not reproduced by TPA, 8Br-cAMP or A23187. Thus, it appears to be mediated by a previously uncharacterized protein kinase or an isoform of protein kinase C that is not maximally stimulated by TPA. C1 NATL INST DIABET & DIGEST & KIDNEY DIS,DIGEST DIS BRANCH,BETHESDA,MD. NR 34 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD JUN 6 PY 1993 VL 1177 IS 2 BP 208 EP 214 DI 10.1016/0167-4889(93)90042-N PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LG443 UT WOS:A1993LG44300014 PM 8499490 ER PT J AU CHAMULITRAT, W JORDAN, SJ MASON, RP SAITO, K CUTLER, RG AF CHAMULITRAT, W JORDAN, SJ MASON, RP SAITO, K CUTLER, RG TI NITRIC-OXIDE FORMATION DURING LIGHT-INDUCED DECOMPOSITION OF PHENYL N-TERT-BUTYLNITRONE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ELECTRON-SPIN RESONANCE; BUTYL-ALPHA-PHENYLNITRONE; SOLUBLE GUANYLATE-CYCLASE; HYDROXYL RADICAL ADDUCT; AQUEOUS-SOLUTIONS; L-ARGININE; TRANSDUCTION MECHANISM; OXIDATIVE DAMAGE; TRAPPING AGENTS; ENZYME-ACTIVITY AB Phenyl N-tert-butylnitrone (PBN) is a spin trap commonly employed in free radical research. PBN has been shown to have adverse and beneficial effects on various biological systems. We report here evidence that photolysis (or even ambient light) decomposes PBN to nitric oxide in aqueous solutions. Non-heme and heme proteins have been employed to form nitrosyl complexes, which were detected using EPR spectroscopy. Concomitantly, nitrite formation was detected after light-induced decomposition of PBN. In addition, we found that tert-nitrosobutane and decomposed PBN caused an activation of guanylate cyclase. We propose a mechanism where PBN is decomposed by light to tert-nitrosobutane. The latter compound is, in turn, decomposed to nitric oxide. This study suggests the possibility that PBN or PBN radical adducts may be sources of nitric oxide in biological environments. When using PBN as a spin trap in biological samples, not only is the trapping of reactive free radicals operative, but nitric oxide produced from PBN decomposition may play an important role in altering biological functions. C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. RP CHAMULITRAT, W (reprint author), NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 47 TC 68 Z9 68 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1993 VL 268 IS 16 BP 11520 EP 11527 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF284 UT WOS:A1993LF28400013 PM 8099352 ER PT J AU NAKAMURA, S AF NAKAMURA, S TI POSSIBLE ROLE OF PHOSPHORYLATION IN THE FUNCTION OF CHICKEN MYOD1 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MUSCLE-SPECIFIC ENHANCER; CREATINE-KINASE GENE; LOOP-HELIX PROTEINS; DNA-BINDING; EXPRESSION VECTORS; TRICHOPLUSIA-NI; CHAIN ENHANCER; MYC HOMOLOGY; REGION; FIBROBLASTS AB Chicken MyoD1 (CMD1), an equivalent to the mouse MyoD1, expressed in chicken skeletal muscle (Lin, Z.Y., Dechesne, C. A., Eldridge, J., and Paterson, B. M. (1989) Genes & Dev. 3, 986-996), was produced in Spodoptera frugiperda (Sf9) cells by Baculovirus expression vector and purified to almost homogeneity. This CMD1 was directly demonstrated to be a phosphoprotein by a P-32-labeling experiment. Phosphoamino acid analysis revealed that only serine residue was phosphorylated. Phosphoamino acid of CMD1 from chick primary culture of 11-day embryonic breast muscle was also serine. Electrophoretic mobility on SDS-polyacrylamide gel electrophoresis of the phosphorylated CMD1 produced in Sf9 cells and that obtained from primary culture of muscle were indistinguishable. Gel retardation and methylation interference assays showed that purified CMD1 bound specifically to the mouse muscle creatine kinase enhancer in combination with the in vitro translated E12. CMD1 alone had almost no affinity to the target DNA. When purified CMD1 was treated with calf intestinal phosphatase, its affinity to the target DNA in combination with E12 was reduced by approximately 5-fold. The affinity recovered at least partially by possible rephosphorylation of CMD1 by kinase(s) contained in wheat germ extract. These results suggested that phosphorylation of CMD1 could be involved in the regulation of muscle differentiation. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 41 TC 7 Z9 7 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1993 VL 268 IS 16 BP 11670 EP 11677 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF284 UT WOS:A1993LF28400034 PM 8389359 ER PT J AU CAMERON, CE GRINDE, B JACQUES, P JENTOFT, J LEIS, J WLODAWER, A WEBER, IT AF CAMERON, CE GRINDE, B JACQUES, P JENTOFT, J LEIS, J WLODAWER, A WEBER, IT TI COMPARISON OF THE SUBSTRATE-BINDING POCKETS OF THE ROUS-SARCOMA VIRUS AND HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PROTEASES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HIV-1 PROTEASE; ASPARTIC PROTEASES; POL POLYPROTEINS; INHIBITOR; RESOLUTION; CLEAVAGE; GAG; COMPLEX; SITE; SPECIFICITY AB A steady state kinetic analysis of the avian myeloblastosis virus/Rous sarcoma virus (AMV/RSV) and human immunodeficiency virus Type 1 (HIV-1) retroviral proteases (PRs) was carried out using a series of 40 peptide substrates that are derivatives of the AMV/RSV nucleocapsid-PR cleavage site. These peptides contain single amino acid substitutions in each of the seven positions of the minimum length substrate required by the PR for specific and efficient cleavage. These peptide substrates are distinguished by the individual enzyme subsites of the AMV/RSV and HIV-1 PRs. The molecular basis for similarities and differences of the individual subsites for both proteases is discussed using steady state kinetic data and modeling based on crystal structures. C1 CASE WESTERN RESERVE UNIV,SCH MED,CLEVELAND,OH 44106. NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,BETHESDA,MD 20892. THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,PHILADELPHIA,PA 19107. FU NCI NIH HHS [CA52047]; NIGMS NIH HHS [GM13628]; PHS HHS [N01 C0 74101] NR 34 TC 42 Z9 42 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1993 VL 268 IS 16 BP 11711 EP 11720 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF284 UT WOS:A1993LF28400040 PM 8389361 ER PT J AU PIATIGORSKY, J HORWITZ, J NORMAN, BL AF PIATIGORSKY, J HORWITZ, J NORMAN, BL TI J1-CRYSTALLINS OF THE CUBOMEDUSAN JELLYFISH LENS CONSTITUTE A NOVEL FAMILY ENCODED IN AT LEAST 3 INTRONLESS GENES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMINO-ACID-SEQUENCE; HEAT-SHOCK PROTEIN; EYE LENS; NUCLEOTIDE-SEQUENCE; HSP70 GENE; CRYSTALLINS; RECRUITMENT; EVOLUTION; IDENTIFICATION; EXPRESSION AB The transparent cellular eye lens of the jellyfish (Tripedalia cystophora) contains three major proteins called J1-, J2-, and J3-crystallins. Here we have isolated cDNAs encoding three novel 37-kDa J1-crystallin polypeptides (J1A, J1B, and J1C) sharing 84-98% identity in amino acid sequence among themselves. Each polypeptide is encoded in a separate gene lacking introns. In contrast to the striking similarity of the coding regions, the 5'- and 3'-untranslated sequences of the three J1-crystallin mRNAs are completely different, consistent with an ancient duplication of their genes. Thermostability experiments showed that J1-crystallins remain soluble at 50-degrees-C, but precipitate at 60-degrees-C, suggesting that these major lens proteins are neither heat shock proteins nor unusually heat-resistant as are many vertebrate crystallins. Although J1 mRNAs appear polyadenylated, no typical polyadenylation signal was detected in the cDNAs. Surprisingly, the only obvious similarities among the 5'-flanking regions of the three J1-crystallin genes are putative TATA boxes and several CAAT sequences, consistent with fewer evolutionary constraints on the regulatory sequences than on the coding sequences of these crystallin genes. C1 UNIV CALIF LOS ANGELES, SCH MED, JULES STEIN EYE INST, LOS ANGELES, CA 90024 USA. RP NEI, MOLEC & DEV BIOL LAB, BLDG 30, RM 201, BETHESDA, MD 20892 USA. NR 43 TC 31 Z9 34 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1993 VL 268 IS 16 BP 11894 EP 11901 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF284 UT WOS:A1993LF28400066 PM 8505315 ER PT J AU AZARYAN, AV WONG, M FRIEDMAN, TC CAWLEY, NX ESTIVARIZ, FE CHEN, HC LOH, YP AF AZARYAN, AV WONG, M FRIEDMAN, TC CAWLEY, NX ESTIVARIZ, FE CHEN, HC LOH, YP TI PURIFICATION AND CHARACTERIZATION OF A PAIRED BASIC RESIDUE-SPECIFIC YEAST ASPARTIC PROTEASE ENCODED BY THE YAP3 GENE - SIMILARITY TO THE MAMMALIAN PRO-OPIOMELANOCORTIN-CONVERTING ENZYME SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LOBE SECRETORY VESICLES; SACCHAROMYCES-CEREVISIAE; ANTERIOR-PITUITARY; INTERMEDIATE; FURIN; KEX2; RAT; TRANSFORMATION; IDENTIFICATION; LOCALIZATION AB Yeast cells express an alternate enzyme encoded by the YAP3 gene which can process pro-alpha-mating factor when this pheromone is overexpressed in KEX2-deficient mutants. The YAP3 gene product is an aspartic protease (YAP3) that cleaves at paired basic residues (Egel-Mittani, M., Flygenring, H. P., and Hansen, M. T. (1990) Yeast 6, 127-137). In this study, the YAP3 gene was overexpressed in the BJ 3501 strain of Saccharomyces cerevisiae. YAP3 was purified to apparent homogeneity using concanavalin A and pepstatin A affinity chromatography. The enzyme was characterized as an M(r) 68,000 glycoprotein with a pH optimum of 4.0-4.5. It was inhibited by pepstatin A and activated by 5 mM Ca2+. YAP3 cleaved at paired basic residues of mouse pro-opiomelanocortin (POMC) to yield adrenocorticotropin (ACTH) and beta-lipotropin (LPH); human beta-LPH to yield beta-endorphin-(1-31), beta-endorphin-(1-29), beta-endorphin-(1-28), gamma-LPH, and beta-melanocyte-stimulating hormone; and bovine N-POMC1-77 to yield gamma3-melanocyte-stimulating hormone. It also cleaved the tetrabasic residues of ACTH1-39 to yield primarily ACTH1-15 and Lys-Arg-corticotropin-like intermediate lobe peptide. The physical properties, pH optimum, and specificity of YAP3 indicate that it is a homologue of the mammalian POMC-converting enzyme (EC 3.4.23.17), a paired basic residue-specific aspartic protease from bovine pituitary intermediate lobe secretory granules (Loh, Y. P., Parish, D. C., and Tuteja, R. (1985) J. Biol. Chem. 260, 7194-7205). C1 NICHHD,DEV NEUROBIOL LAB,CELLULAR NEUROBIOL SECT,BLDG 49,RM 5A38,BETHESDA,MD 20892. NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT BIOCHEM,BETHESDA,MD 20814. NR 31 TC 71 Z9 73 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1993 VL 268 IS 16 BP 11968 EP 11975 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF284 UT WOS:A1993LF28400077 PM 8389368 ER PT J AU DELAHUNTY, MD STAFFORD, FJ YUAN, LC SHAZ, D BONIFACINO, JS AF DELAHUNTY, MD STAFFORD, FJ YUAN, LC SHAZ, D BONIFACINO, JS TI UNCLEAVED SIGNALS FOR GLYCOSYLPHOSPHATIDYLINOSITOL ANCHORING CAUSE RETENTION OF PRECURSOR PROTEINS IN THE ENDOPLASMIC-RETICULUM SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA; DECAY-ACCELERATING FACTOR; PHOSPHATIDYLINOSITOL MEMBRANE ANCHOR; SITE-SPECIFIC MUTAGENESIS; CLEAVAGE ATTACHMENT SITE; CELL ANTIGEN RECEPTOR; QA-2 ANTIGEN; THY-1 GLYCOPROTEIN; MOLECULAR-CLONING; PHOSPHOLIPASE-C AB Glycosylphosphatidylinositol (GPI)-anchored proteins are generally absent from the surface of cells that are defective in GPI biosynthesis. The current study was undertaken to: (a) examine in detail the intracellular localization and fate of precursors of GPI-anchored proteins in cells that fail to add GPI groups and (b) define structural characteristics of the precursor proteins that determine their intracellular localization. By examining GPI-deficient cells, we show that the uncleaved precursor of the GPI-anchored protein, Q7b, is retained in the cisternae of the endoplasmic reticulum (ER) and is largely lost intracellularly with a half-time of 2-4 h. Only a small amount (1-10%) of a proteolytically cleaved form of the protein is secreted into the medium. In cells competent for GPI anchor addition, mutation of the putative cleavage/attachment site for GPI addition in Q7b results in a similar phenotype of ER retention of the uncleaved precursor. An aspartic acid residue (Asp316) within the Q7b GPI anchoring signal, previously found to be essential for GPI anchor addition (Waneck, G. L., Stein, M. E., and Flavell, R. A. (1988) Science 241, 697-699), is also shown to be critical for ER retention. Information leading to ER retention is transferable to another protein by fusion of the GPI anchoring signals from either Q7b or the GPI-anchored form of the IgG Fc receptor type III. Analysis by sedimentation on sucrose gradients shows that Q7b species retained in the ER are multimeric, whereas species that exit the ER are monomeric. This correlation suggests that the presence of an uncleaved signal for GPI anchoring induces changes in the aggregation state of the precursor proteins, which may lead to their retention in the ER. RP DELAHUNTY, MD (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. OI Bonifacino, Juan S./0000-0002-5673-6370 NR 65 TC 71 Z9 71 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1993 VL 268 IS 16 BP 12017 EP 12027 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF284 UT WOS:A1993LF28400084 PM 8505326 ER PT J AU LEE, SC KIM, IG MAREKOV, LN OKEEFE, EJ PARRY, DAD STEINERT, PM AF LEE, SC KIM, IG MAREKOV, LN OKEEFE, EJ PARRY, DAD STEINERT, PM TI THE STRUCTURE OF HUMAN TRICHOHYALIN - POTENTIAL MULTIPLE ROLES AS A FUNCTIONAL EF-HAND-LIKE CALCIUM-BINDING PROTEIN, A CORNIFIED CELL-ENVELOPE PRECURSOR, AND AN INTERMEDIATE FILAMENT-ASSOCIATED (CROSS-LINKING) PROTEIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMINO-ACID-SEQUENCE; HUMAN LORICRIN GENE; HAIR FOLLICLE; EPIDERMAL-KERATINOCYTES; EXPRESSION; MOUSE; CITRULLINE; FILAGGRIN; PEPTIDES; REGION AB Trichohyalin is an intermediate filament-associated protein that associates in regular arrays with keratin intermediate filaments (KIF) of the inner root sheath cells of the hair follicle and the granular layer of the epidermis and is a known substrate of transglutaminases. We have determined the full-length sequence of human trichohyalin by use of RNA-mediated anchored polymerase chain reaction methods and from a genomic clone and analyzed its potential secondary structure. We show here that trichohyalin may have at least three important functions in these cells. The protein of 248 kDa is unusual in that it contains one of the highest contents of charged residues of any protein. Of several defined domains, domains 2-4, 6, and 8 are almost entirely alpha-helical, configured as a series of peptide repeats of varying regularity, and are thought to form a single-stranded alpha-helical rod stabilized by ionic interactions between successive turns of the alpha-helix. Domain 6 is the most regular and may bind KIF directly by ionic interactions. Domains 5 and 7 are less well organized and may introduce folds in the molecule. Thus, human trichohyalin is predicted to be an elongated flexible rod at least 215 nm long and to function as a KIF-associated protein by cross-linking the filaments in loose networks. In addition, trichohyalin is similar to, but several times longer than, involucrin, a known cell envelope constituent, so that together, involucrin and trichohyalin may serve as scaffold proteins in the organization of the cell envelope of these cells or even anchor the cell envelope to the KIF network. Finally, trichohyalin possesses a pair of functional calcium-binding domains of the EF-hand type at its amino terminus that may be involved in its calcium-dependent postsynthetic processing during terminal differentiation. C1 NIAMSD,SKIN BIOL BRANCH,BLDG 6,ROOM 425,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT DERMATOL,CHAPEL HILL,NC 27514. MASSEY UNIV,DEPT PHYS & BIOPHYS,PALMERSTON NORTH,NEW ZEALAND. NR 63 TC 135 Z9 136 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1993 VL 268 IS 16 BP 12164 EP 12176 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF284 UT WOS:A1993LF28400104 PM 7685034 ER PT J AU TAFURI, SR FAMILARI, M WOLFFE, AP AF TAFURI, SR FAMILARI, M WOLFFE, AP TI A MOUSE-Y BOX PROTEIN, MSY1, IS ASSOCIATED WITH PATERNAL MESSENGER-RNA IN SPERMATOCYTES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID OOCYTE-SPECIFIC PROTEINS; 3' UNTRANSLATED REGION; HISTONE-LIKE PROTEINS; BINDING-PROTEINS; XENOPUS OOCYTES; RIBONUCLEOPROTEIN PARTICLES; MAMMALIAN SPERMATOGENESIS; TRANSCRIPTION FACTOR; GENE-EXPRESSION; BASIC DOMAIN AB We have isolated a mouse cDNA clone, which encodes the protein MSY1 (mouse Y box protein 1), a new member of the Y box family of proteins. Northern analysis indicates that MSY1 mRNA accumulates over 100-fold more in testis than in other tissues. Moreover, MSY1 mRNA is developmentally regulated, initially appearing at the pachytene stage of spermatogenesis. This is the stage of maximal transcription and translation in the spermatocyte. In Xenopus laevis, homologous Y box proteins, FRGY1 and FRGY2, positively regulate transcription from promoters containing a Y box (CTGATTGGCCAA). In addition, the germ cell-specific Y box protein FRGY2 binds maternal mRNA within 60-80 S mRNP storage particles and in doing so regulates translation in the developing oocyte and embryo (Smith, L. D., Richter, J. D., and Taylor, M. A. (1984) in Molecular Biology of Development (Davidson, E. R., and Firtel, R. A., eds) pp. 129-141, Alan R. Liss, New York). The MSY1 protein can be isolated from a 60-80 S mRNP fraction of testis which like the frog oocyte contains stored, untranslated mRNAs. Furthermore, cross-linking experiments demonstrate that MSY1 is bound to mRNAs of this fraction. Finally, mobility shift analysis performed using the isolated protein indicates that MSY1 has nucleic acid binding properties similar to those of the FRGY proteins. These data suggest that the mouse Y box protein, MSY1, functions similarly to the FRGY2 protein in regulating the storage and translation of germ cell RNAs. RP TAFURI, SR (reprint author), NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892, USA. NR 59 TC 117 Z9 121 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1993 VL 268 IS 16 BP 12213 EP 12220 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF284 UT WOS:A1993LF28400110 PM 8505341 ER PT J AU PERSECHINI, A JARRETT, HW KOSKKOSICKA, D KRINKS, MH LEE, HG AF PERSECHINI, A JARRETT, HW KOSKKOSICKA, D KRINKS, MH LEE, HG TI ACTIVATION OF ENZYMES BY CALMODULINS CONTAINING INTRAMOLECULAR CROSS-LINKS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE CALMODULIN; MLC KINASE; CALCINEURIN; NAD KINASE; ATPASE, CA(2+)-MG(2+); ENZYME REGULATION ID LIGHT-CHAIN KINASE; BINDING; CALCINEURIN; PROTEINS; BRAIN AB We have reacted calmodulins containing cysteines substituted at positions 3 and 146 or 5 and 146 with bismaleimidohexane (BMH) to generate intramolecularly cross-linked proteins termed BMHCM or BMHCM1, respectively. Reactions were also performed with N-ethylmaleimide (NEM) in place of BMH to generate corresponding S-ethylsuccinimidylated proteins termed NEMCM or NEMCM1. The abilities of these proteins to activate plant NAD kinase, erythrocyte Ca2+-ATPase and bovine brain calcineurin activities were assessed. The BMH- or NEM-reacted proteins activate calcineurin activity as does control calmodulin. K(act) values for Ca2+-ATPase activation by BMHCM and BMHCM1 are increased 10-fold relative to the control value, with no corresponding change in V(max) values. Activation of this enzyme by NEMCM or NEMCM1 is not different from the control. In NAD kinase activation experiments BMHCM and BMHCM1 are associated with a 10 to 20-fold increase in K(act) values and a 60-75% reduction in V(max) values relative to the control. NEMCM1 is not associated with any apparent changes in NAD kinase activation, however, NEMCM is associated with a 10-fold increase in the K(act) value. NEM-reacted calmodulin containing a cysteine only at position 3 is not associated with an increased K(act) value, implying that this change is due to interactions between S-(ethylsuccinimido)cysteines at positions 3 and 146. In conclusion, cross-linking and associated distortions in the structure of calmodulin appear to have little or no effect on activation of calcineurin enzyme activity. However, bending in the central helix and/or steric restrictions associated with cross-linking increase significantly the K(act) value for Ca2+-ATPase and NAD kinase activation, and dramatically reduce maximal activation of NAD kinase activity. C1 UNIV TENNESSEE CTR HLTH SCI,SCH MED,DEPT BIOCHEM,MEMPHIS,TN 38163. JOHNS HOPKINS UNIV,SCH MED,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205. NCI,BIOCHEM LAB,BETHESDA,MD 20892. RP PERSECHINI, A (reprint author), UNIV ROCHESTER,SCH MED,DEPT PHYSIOL,601 ELMWOOD AVE,BOX 642,ROCHESTER,NY 14642, USA. NR 30 TC 14 Z9 14 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD JUN 4 PY 1993 VL 1163 IS 3 BP 309 EP 314 DI 10.1016/0167-4838(93)90167-P PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LG890 UT WOS:A1993LG89000012 PM 8389593 ER PT J AU WELLER, M FINIELSMARLIER, F PAUL, SM AF WELLER, M FINIELSMARLIER, F PAUL, SM TI NMDA RECEPTOR-MEDIATED GLUTAMATE TOXICITY OF CULTURED CEREBELLAR, CORTICAL AND MESENCEPHALIC NEURONS - NEUROPROTECTIVE PROPERTIES OF AMANTADINE AND MEMANTINE SO BRAIN RESEARCH LA English DT Note DE AMANTADINE; MEMANTINE; GLUTAMATE; N-METHYL-D-AMPHETAMINE NEURON; EXCITOTOXICITY; NEUROTOXICITY ID METHYL-D-ASPARTATE; MONOAMINE-DEPLETED RATS; PARKINSONS-DISEASE; ANTAGONISTS; PHENCYCLIDINE; NEUROTOXICITY; INVITRO; POTENT; CORTEX AB Effects of amantadine and memantine on NMDA receptor-mediated glutamate toxicity were studied in cultured cerebellar, cortical and mesencephalic neurons. Both drugs protected cerebellar and cortical neurons against glutamate toxicity, memantine being consistently more effective than amantadine but less effective than MK-801. Glutamate toxicity of dopaminergic neurons in mesencephalic cultures was only mildly attenuated by memantine but was also only incompletely blocked by MK-801. These findings suggest that adamantanamines act by inhibiting NMDA receptor-mediated excitatory neurotransmission. However, since non-NMDA receptors appear to be principal mediators of glutamate toxicity of dopaminergic mesencephalic neurons, adamantanamines may fail to protect the nigrostriatal neurons which specifically degenerate in Parkinson's disease. C1 NATL INST MENTAL HLTH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BLDG 10,ROOM 4N224,BETHESDA,MD 20892. NR 32 TC 69 Z9 69 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 4 PY 1993 VL 613 IS 1 BP 143 EP 148 DI 10.1016/0006-8993(93)90464-X PG 6 WC Neurosciences SC Neurosciences & Neurology GA LG892 UT WOS:A1993LG89200019 PM 8102306 ER PT J AU ADHYA, S AF ADHYA, S TI ECHOLS,HARRISON (1933-1993) - OBITUARY SO CELL LA English DT Item About an Individual RP ADHYA, S (reprint author), NCI,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JUN 4 PY 1993 VL 73 IS 5 BP 833 EP 834 DI 10.1016/0092-8674(93)90263-P PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LF061 UT WOS:A1993LF06100001 PM 8500175 ER PT J AU BLISKA, JB GALAN, JE FALKOW, S AF BLISKA, JB GALAN, JE FALKOW, S TI SIGNAL-TRANSDUCTION IN THE MAMMALIAN-CELL DURING BACTERIAL ATTACHMENT AND ENTRY SO CELL LA English DT Review ID ENTEROPATHOGENIC ESCHERICHIA-COLI; PSEUDOTUBERCULOSIS INVASIN PROTEIN; TISSUE-CULTURE CELLS; MONOCYTE COMPLEMENT RECEPTORS; OUTER-MEMBRANE PROTEIN; YERSINIA-PSEUDOTUBERCULOSIS; EPITHELIAL-CELLS; VIRULENCE PLASMID; HEP-2 CELLS; SALMONELLA-TYPHIMURIUM C1 STANFORD UNIV,MED CTR,SCH MED,DEPT MICROBIOL & IMMUNOL,STANFORD,CA 94305. NIH,NATL INST ALLERGY & INFECT DIS,ROCKY MT LAB,HAMILTON,MT 59840. RP BLISKA, JB (reprint author), SUNY,SCH MED,DEPT MICROBIOL,STONY BROOK,NY 11794, USA. FU NIAID NIH HHS [AI26-195, AI30492]; NIDDK NIH HHS [DK38707] NR 157 TC 288 Z9 291 U1 1 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JUN 4 PY 1993 VL 73 IS 5 BP 903 EP 920 DI 10.1016/0092-8674(93)90270-Z PG 18 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LF061 UT WOS:A1993LF06100008 PM 8500180 ER PT J AU WALKER, JM BOWEN, WD PATRICK, SL WILLIAMS, WE MASCARELLA, SW BAI, X CARROLL, FI AF WALKER, JM BOWEN, WD PATRICK, SL WILLIAMS, WE MASCARELLA, SW BAI, X CARROLL, FI TI A COMPARISON OF (-)-DEOXYBENZOMORPHANS DEVOID OF OPIATE ACTIVITY WITH THEIR DEXTROROTATORY PHENOLIC COUNTERPARTS SUGGESTS ROLE OF SIGMA(2) RECEPTORS IN MOTOR FUNCTION (VOL 231, PG 61, 1993) SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Correction, Addition AB Three novel benzomorphans, (+)-N-benzylnormetazocine, (-)-deoxy-N-benzylnormetazocine, and (-)-deoxypentazocine were tested for their ability to produce circling behavior in rats following intranigral microinjections. Dose studies revealed the following rank order of potency: (-)-deoxypentazocine > (-)-deoxy-N-benzylnormetazocine > (+)-N-benzylnormetazocine. This rank order approximates that for affinities for sigma2 receptors but not sigma1 receptors. It is very unlikely that the effects of the (-)-deoxybenzomorphans were mediated by opiate receptors for the following reasons: (1) consistent with the known requirement for the phenolic hydroxyl group for opiate activity, both (-)-deoxy compounds showed very low affinity for opiate receptors; (2) naloxone (4 mug) co-administered with (-)-deoxy-N-benzylnormetazocine failed to reduce its efficacy; (3) both (-)-deoxy compounds failed to produce marked analgesic effects in the tail flick test following systemic injections of 20 mg/kg s.c. These findings suggest that sigma2 receptors mediate the motor effects of sigma ligands in rats. C1 NIDDKD,MED CHEM LAB,RECEPTOR BIOCHEM & PHARMACOL UNIT,BETHESDA,MD 20892. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. RP WALKER, JM (reprint author), BROWN UNIV,DEPT PSYCHOL,SCHRIER RES LAB,POB 1853,89 WATERMAN ST,PROVIDENCE,RI 02912, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD JUN 4 PY 1993 VL 236 IS 3 BP 495 EP 495 DI 10.1016/0014-2999(93)90491-Y PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LG534 UT WOS:A1993LG53400023 ER PT J AU BRECHBIEL, MW MCMURRY, TJ GANSOW, OA AF BRECHBIEL, MW MCMURRY, TJ GANSOW, OA TI A DIRECT SYNTHESIS OF A BIFUNCTIONAL CHELATING AGENT FOR RADIOLABELING PROTEINS SO TETRAHEDRON LETTERS LA English DT Article ID DTPA AB A convenient synthesis of a bifunctional derivative of the ligand NOTA is described. The synthesis offers advantages over current literature methods for making similar molecules by starting with the easily prepared ortho-amide of 1,4,7-triazacyclononane which can be sequentially alkylated to provide a bifunctional NOTA derivative in 9% yield overall. The replacement of preparative HPLC with simple ion-exchange chromatography provides analytically pure ligand suitable for clinical applications. RP BRECHBIEL, MW (reprint author), NIH,RADIAT ONCOL BRANCH,CHEM SECT,BETHESDA,MD 20892, USA. NR 17 TC 21 Z9 21 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4039 J9 TETRAHEDRON LETT JI Tetrahedron Lett. PD JUN 4 PY 1993 VL 34 IS 23 BP 3691 EP 3694 DI 10.1016/S0040-4039(00)79202-1 PG 4 WC Chemistry, Organic SC Chemistry GA LF898 UT WOS:A1993LF89800009 ER PT J AU HIGGINS, MW ENRIGHT, PL KRONMAL, RA SCHENKER, MB ANTONCULVER, H LYLES, M AF HIGGINS, MW ENRIGHT, PL KRONMAL, RA SCHENKER, MB ANTONCULVER, H LYLES, M TI SMOKING AND LUNG-FUNCTION IN ELDERLY MEN AND WOMEN - THE CARDIOVASCULAR HEALTH STUDY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID FORCED EXPIRATORY VOLUME; PULMONARY-FUNCTION; ADULT-POPULATION; ONE 2ND; MORTALITY; DISEASE; RISK; PREDICTORS; TECUMSEH; CANCER AB Objective.-To investigate relationships between cigarette smoking and pulmonary function in elderly men and women. Design.-Cross-sectional analysis of baseline data from a prospective, population-based study of risk factors, preclinical, and overt cardiovascular and pulmonary disease. Setting.-Defined communities in Forsyth County, North Carolina; Pittsburgh, Pa; Sacramento County, California; and Washington County, Maryland. Population.-A total of 5201 noninstitutionalized men and women 65 years of age and older. Main Outcome Measures.-Pulmonary function; means of forced expiratory volume in 1 second (FEV1) and forced vital capacity and prevalence of low FEV1 levels. Results.-Prevalence of cigarette smoking was 10% to 20% and higher in women than men and in blacks than whites. Forced vital capacity and FEV1 levels were related positively to height and white race and negatively to age and waist girth. Age- and height-adjusted FEV1 means were 23% and 18% lower in male and female current smokers, respectively, than in never smokers but not reduced in never smokers currently living with a smoker. Smokers who quit before age 40 years had FEV1 levels similar to never smokers, but FEV1 levels were lower by 7% and 14% in smokers who quit at ages 40 to 60 years and older than 60 years, respectively. Lung function was related inversely to pack-years of cigarette use. Prevalence rates of impaired lung function were highest in current smokers and lowest in never smokers. Regression coefficients for the smoking variables were smaller in persons without cardiovascular or respiratory conditions than in the total cohort. Conclusions.-Cigarette smoking is associated with reduced pulmonary function in elderly men and women. However, smokers who quit, even after age 60 years, have better pulmonary function than continuing smokers. C1 UNIV ARIZONA,CTR RESP SCI,TUCSON,AZ 85721. CARDIOVAS HLTH STUDY COORDINATING CTR,SEATTLE,WA. UNIV CALIF IRVINE,CALIF COLL MED,IRVINE,CA 92717. UNIV CALIF DAVIS,DIV OCCUPAT & ENVIRONM MED,DAVIS,CA 95616. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT GERIATR MED,WINSTON SALEM,NC 27103. RP HIGGINS, MW (reprint author), NHLBI,FED BLDG,ROOM 2C08,7550 WISCONSIN AVE,BETHESDA,MD 20892, USA. FU PHS HHS [N01-87079, N01-87086] NR 24 TC 78 Z9 80 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 2 PY 1993 VL 269 IS 21 BP 2741 EP 2748 DI 10.1001/jama.269.21.2741 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA LD671 UT WOS:A1993LD67100023 PM 8492399 ER PT J AU SU, TP PAGLIARO, M SCHMIDT, PJ PICKAR, D WOLKOWITZ, O RUBINOW, DR AF SU, TP PAGLIARO, M SCHMIDT, PJ PICKAR, D WOLKOWITZ, O RUBINOW, DR TI NEUROPSYCHIATRIC EFFECTS OF ANABOLIC-STEROIDS IN MALE NORMAL VOLUNTEERS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID ANDROGENIC STEROIDS; MEN; METHYLTESTOSTERONE; MESTEROLONE; DEPENDENCE; HORMONES; STATE AB Objective.-To evaluate the acute effects of anabolic steroids on mood and behavior in male normal volunteers. Design.-A 2-week, double-blind (subject and rater), fixed-order, placebo-controlled crossover trial of methyltestosterone. Setting.-An inpatient research unit at the National Institutes of Health. Subjects.-A volunteer sample of 20 men who were medication free, free of medical and psychiatric illness, not involved in athletic training, and had no prior history of anabolic steroid use. Intervention.-A sequential trial for 3 days each of the following four drug conditions: placebo baseline, low-dose methyltestosterone (40 mg/d), high-dose methyltestosterone (240 mg/d), and placebo withdrawal. Main Outcome Measures.-Mood and behavioral ratings were completed during each drug condition and included both subjective and objective measures. Results.-Significant (P<.05) albeit subtle increases in symptom scores were observed during high-dose methyltestosterone administration compared with baseline in positive mood (euphoria, energy, and sexual arousal), negative mood (irritability, mood swings, violent feelings, and hostility), and cognitive impairment (distractibility, forgetfulness, and confusion). An acute manic episode was observed in one of the 20 subjects, representing a 5% incidence, even under these conservative conditions. An additional subject became hypomanic. Baseline characteristics including family psychiatric history or previous drug abuse did not predict symptom changes. Conclusion.-This is the first placebo-controlled prospective study demonstrating the adverse and activating mood and behavioral effects of anabolic steroids. C1 NIMH,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892. NIH,CTR CLIN,DEPT NURSING,MENTAL HLTH NURSING SERV,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT PSYCHIAT,SAN FRANCISCO,CA 94143. RP SU, TP (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BEHAV ENDOCRINOL SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 3N238,BETHESDA,MD 20892, USA. RI Wolkowitz, Owen/J-6649-2013 OI Wolkowitz, Owen/0000-0003-0655-5042 NR 36 TC 245 Z9 249 U1 0 U2 15 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 2 PY 1993 VL 269 IS 21 BP 2760 EP 2764 DI 10.1001/jama.269.21.2760 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA LD671 UT WOS:A1993LD67100026 PM 8492402 ER PT J AU MAGRATH, I LITVAK, J AF MAGRATH, I LITVAK, J TI CANCER IN DEVELOPING-COUNTRIES - OPPORTUNITY AND CHALLENGE SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Review ID P53 GENE; LYMPHOMA; LEUKEMIA AB Epidemiologic observations indicate that environment and lifestyle are the major determinants of the geographical patterns of cancer. The developing countries, which account for 75% of the world's population, have lower incidence rates of cancer compared with the industrialized nations but bear more than half the global cancer burden. Demographic trends resulting from economic progress (decreasing incidence of infectious diseases, population growth, aging, and urbanization), coupled with increased tobacco consumption and dietary changes, indicate that developing countries will bear a continually increasing proportion of the world's cancer burden and its accompanying demand for the provision of costly treatment programs. Yet the developing countries command only 5% of the world's economic resources, and health care programs are already fully extended and frequently inadequate. Thus, cancer control in the developing countries, including preemptive prevention of the anticipated increases in cancers presently more common in the industrialized nations (e.g., lung, breast, and colon), should include much greater emphasis on cancer prevention than is presently the case. But there is another perspective. The developing countries, with their dramatic contrasts in lifestyles and environments and equally diverse patterns of cancer, provide an unparalleled, and often neglected, opportunity for studies directed toward understanding the mechanisms of environmental carcinogenesis. Such an understanding should eventually lead to the development of novel intervention approaches. Unfortunately, cancer research is much more difficult to conduct in the developing countries because of the lack of population-based registries, poor communication and transportation systems, and deficiencies in infrastructure, financial support, and the training of health professionals. These difficulties could be overcome, to the benefit of all, if the extent of collaboration in cancer research between the developing and industrialized nations were to be greatly expanded. C1 UNIV CHILE,INST UNIV EXCHANGE,SANTIAGO,CHILE. CHILEAN EMBASSY,WASHINGTON,DC. RP MAGRATH, I (reprint author), NCI,CLIN ONCOL PROGRAM,BLDG 10,RM 13N240,BETHESDA,MD 20892, USA. NR 41 TC 82 Z9 93 U1 0 U2 2 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JUN 2 PY 1993 VL 85 IS 11 BP 862 EP 874 DI 10.1093/jnci/85.11.862 PG 13 WC Oncology SC Oncology GA LE279 UT WOS:A1993LE27900011 PM 8492315 ER PT J AU FEUER, EJ WUN, LM BORING, CC FLANDERS, WD TIMMEL, MJ TONG, T AF FEUER, EJ WUN, LM BORING, CC FLANDERS, WD TIMMEL, MJ TONG, T TI THE LIFETIME RISK OF DEVELOPING BREAST-CANCER SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID UNITED-STATES; PROBABILITIES AB Background: The lifetime risk of developing breast cancer in U.S. women, often quoted as one in nine, is a commonly cited cancer statistic. However, many estimates have used cancer rates derived from total rather than the cancer-free population and have not properly accounted for multiple cancers in the same individual. Purpose: Our purpose was to provide a revised method for calculating estimates of the lifetime risk of developing breast cancer and to aid in interpretation of the estimates. Methods: A multiple decrement life table was derived by applying age-specific incidence and mortality rates from cross-sectional data to a hypothetical cohort of women. Incidence, mortality, and population data from 1975-1988 were used, representing the geographic areas of the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program. The incidence rates reflected only the first breast primary cancer; mortality rates reflected causes other than breast cancer. The population denominator used in calculating incidence rates was adjusted to reflect only those women without previously diagnosed breast cancers in the hypothetical cohort. Results: Our calculations showed an overall lifetime risk for developing invasive breast cancer of approximately one in eight with use of 1987-1988 SEER data, although up to age 85, it was still the commonly quoted one in nine. Conclusion: Our estimate was calculated assuming constant age-specific rates derived from 1987-1988 SEER data. Because incidence and mortality rates change over time, conditional risk estimates over the short term (10 or 20 years) may be more reliable. A large portion of the rise in the lifetime risk of breast cancer estimated using 1975-1977 data (one in 10.6) to an estimate using 1987-1988 data (one in eight) may be attributed to 1) early detection of prevalent cases due to increased use of mammographic screening and 2) lower mortality due to causes other than breast cancer. A common misperception is that the lifetime risk estimate assumes that all women live to a particular age (e.g., 85 or 95). In fact, the calculation assumes that women can die from causes other than breast cancer at any possible age. Cutting off the lifetime risk calculation at age 85 assumes that no women develop breast cancer after that age. While the lifetime risk of developing breast cancer rose over the period 1976-1977 to 1987-1988, the lifetime risk of dying of breast cancer increased from one in 30 to one in 28, reflecting generally flat mortality trends. C1 AMER CANC SOC,ATLANTA,GA. EMORY UNIV,DIV EPIDEMIOL,ATLANTA,GA 30322. IMS INC,SILVER SPRING,MD. RP FEUER, EJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,EPN-313,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 20 TC 336 Z9 339 U1 1 U2 4 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JUN 2 PY 1993 VL 85 IS 11 BP 892 EP 897 DI 10.1093/jnci/85.11.892 PG 6 WC Oncology SC Oncology GA LE279 UT WOS:A1993LE27900014 PM 8492317 ER PT J AU PEARSON, JW FOGLER, WE VOLKER, K RIGGS, CW GRUYS, E GROVES, ES WILTROUT, RH LONGO, DL AF PEARSON, JW FOGLER, WE VOLKER, K RIGGS, CW GRUYS, E GROVES, ES WILTROUT, RH LONGO, DL TI RESTORATION OF INTERFERON-ALPHA POTENTIATION OF A RECOMBINANT RICIN-A CHAIN IMMUNOTOXIN FOLLOWING CYTOREDUCTION OF XENOGRAFTS OF ADVANCED OVARIAN-TUMORS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID EXPRESSION; CELLS; CARCINOMA; ANTIGENS; BREAST; CANCER AB Background: We have demonstrated that, in the human ovarian carcinoma cell line (OVCAR-3), recombinant human interferon alpha (rHuIFN-alpha) potentiated in vitro inhibition of protein synthesis by immunotoxins. The antitumor activity of intracavitary immunotoxin administered to nude mice 5 days after tumor cell injection was enhanced by a nontherapeutic dose of rHuIFN-alpha, as evidenced by increased survival time. Purpose: Our purpose was to determine the outcome of treatment with immunotoxin and rHuIFN-alpha in xenografts of more advanced tumors. Methods: At 10 or 15 days after tumor cell injection, nude mice with peritoneal OVCAR-3 xenografts were treated intraperitoneally with immunotoxin or with 454A12 monoclonal antibody (MAb) recombinant ricin A chain (rRA), alone or combined with a nontherapeutic dose of rHuIFN-alpha. The immunotoxin was composed of rRA covalently bound to an anti-CD71 (transferrin receptor) MAb. In other experiments, mice were treated intraperitoneally with cyclophosphamide and cisplatin to reduce tumor size on days 20 and 27 after tumor cell inoculation and then, beginning on day 40, with immunotoxin alone or combined with rHuIFN-alpha. Results: Initiation of treatment 10 days after OVCAR-3 transplantation significantly increased median survival from 41 to 89 days (10% survivors on day 120) with 454A12 MAb rRA alone and to more than 120 days (70% survivors) with 454A12 MAb rRA combined with rHuIFN-alpha. (P<.0001). The increase in survival time between tumor-bearing mice treated with immunotoxin combined with rHuIFN-alpha and those treated with immunotoxin alone was statistically significant (P = .017). In contrast, the 15-day transplant tumors were not curable with immunotoxin therapy (survival, 72 days; 0% survivors) and were refractory to rHuIFN-alpha potentiation (survival, 75 days; 0% survivors). After the second course of chemotherapy to reduce the size of the advanced tumors (day 40), during the ascites cell count nadir, initiation of treatment with 454A12 MAb rRA alone or combined with rHuIFN-alpha resulted in significantly different survival times of 129 and 162 days, respectively (P = .0037). Pathologic examination of surviving mice treated with chemotherapy and 454A12 MAb rRA alone or in combination with rHuIFN-alpha revealed that one (17%) of six mice and 11 (65%) of 17 were tumor free, respectively. Conclusions: The synergy between immunotoxins and IFN-alpha is dependent on tumor burden. These agents are less effective against large tumor burdens (i.e., advanced stage disease), but their beneficial effects re-emerge after cytoreduction by combination chemotherapy. Implications: The ideal setting for testing the efficacy of intracavitary immunotoxin combined with rHuIFN-alpha after front-line chemotherapy is in patients with residual tumor refractory to additional chemotherapy or in those with toxic effects that prevent delivery of effective doses. C1 PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. NCI,FCRDC,DATA MANAGEMENT SERV INC,FREDERICK,MD 21701. CETUS CORP,EMERYVILLE,CA 94608. RP PEARSON, JW (reprint author), NCI,FCRDC,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,BLDG 560,RM 31-93,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01CO-74102] NR 14 TC 4 Z9 4 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JUN 2 PY 1993 VL 85 IS 11 BP 907 EP 912 DI 10.1093/jnci/85.11.907 PG 6 WC Oncology SC Oncology GA LE279 UT WOS:A1993LE27900017 PM 8492319 ER PT J AU TAYLOR, JA SANDLER, DP SHORE, DL AF TAYLOR, JA SANDLER, DP SHORE, DL TI ACUTE MYELOGENOUS LEUKEMIA - RESPONSE SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter C1 WESTAT CORP,DURHAM,NC. RP TAYLOR, JA (reprint author), NIEHS,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC 27709, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JUN 2 PY 1993 VL 85 IS 11 BP 921 EP 921 DI 10.1093/jnci/85.11.921 PG 1 WC Oncology SC Oncology GA LE279 UT WOS:A1993LE27900021 ER PT J AU WILLINGER, M AF WILLINGER, M TI CONCLUDING REMARKS - STATE-OF-THE-ART CONFERENCE ON SIDS, GOTHENBURG SO ACTA PAEDIATRICA LA English DT Editorial Material RP WILLINGER, M (reprint author), NICHHD,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0803-5253 J9 ACTA PAEDIATR JI Acta Paediatr. PD JUN PY 1993 VL 82 SU 389 BP 128 EP 129 DI 10.1111/j.1651-2227.1993.tb12900.x PG 2 WC Pediatrics SC Pediatrics GA LR209 UT WOS:A1993LR20900037 ER PT J AU YANAGISHITA, M AF YANAGISHITA, M TI FUNCTION OF PROTEOGLYCANS IN THE EXTRACELLULAR-MATRIX SO ACTA PATHOLOGICA JAPONICA LA English DT Review DE EXTRACELLULAR MATRIX; PROTEOGLYCANS ID CHONDROITIN SULFATE PROTEOGLYCAN; TRANSFORMING GROWTH FACTOR-BETA-1; SMOOTH-MUSCLE CELLS; HEPARAN-SULFATE; CORE PROTEIN; BINDING PROTEIN; HOMING RECEPTOR; LINK PROTEIN; CHICK-EMBRYO; CARTILAGE AB Proteoglycans are glycosylated proteins which have covalently attached highly anionic glycosaminoglycans. Many forms of proteoglycans are present in virtually all extracellular matrices of connective tissues. The major biological function of proteoglycans derives from the physicochemical characteristics of the glycosaminoglycan component of the molecule, which provides hydration and swelling pressure to the tissue enabling it to withstand compressional forces. This function is best illustrated by the most abundant proteoglycan in cartilage tissues, aggrecan. During the past decade, diverse species of proteoglycans have been identified in many connective tissues, on cell surfaces and in intracellular compartments. These proteoglycans have distinct biological functions apart from their hydrodynamic functions, and their involvement in many aspects of cell and tissue activities has been demonstrated. For example, decorin, which is widely distributed in many connective tissues, may have functions in regulating collagen fibril formation and in modifying the activity of transforming growth factor-beta; perlecan, the major heparan sulfate proteoglycan in the glomerular basement membrane, may play an important role as the major anionic site responsible for the charge selectivity in glomerular filtration. Specific interactions between proteoglycans (through both their glycosaminoglycan and core protein components) and macromolecules in the extracellular matrix are the key factors in the functions of proteoglycans. Exciting biological functions of proteoglycans are now gradually emerging. RP NIDR, BONE RES BRANCH, BETHESDA, MD 20892 USA. NR 72 TC 113 Z9 117 U1 0 U2 28 PU BLACKWELL PUBLISHING ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 0001-6632 J9 ACTA PATHOL JAPON PD JUN PY 1993 VL 43 IS 6 BP 283 EP 293 PG 11 WC Pathology SC Pathology GA LJ563 UT WOS:A1993LJ56300001 PM 8346704 ER PT J AU GRACE, WC AF GRACE, WC TI CORRELATES OF HIV RISK BEHAVIOR AMONG HIV-INFECTED PRISONERS SO ADDICTION LA English DT Letter RP GRACE, WC (reprint author), NIDA,ROOM 11A-33,ROCKVILLE,MD 20857, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0965-2140 J9 ADDICTION JI Addiction PD JUN PY 1993 VL 88 IS 6 BP 836 EP 836 DI 10.1111/j.1360-0443.1993.tb02099.x PG 1 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA LG240 UT WOS:A1993LG24000013 PM 8329976 ER PT J AU ROTH, GS AF ROTH, GS TI ARE FREE-RADICALS CAUSES OR EFFECTS OF AGING - THE ENTROPY THEORY SO AGING-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Letter RP ROTH, GS (reprint author), NIA,FRANCIS SCOTT KEY MED CTR,GERONTOL RES CTR,BALTIMORE,MD 21224, USA. NR 0 TC 4 Z9 7 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-9532 J9 AGING-CLIN EXP RES JI Aging-Clin. Exp. Res. PD JUN PY 1993 VL 5 IS 3 BP 241 EP 242 PG 2 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA LH825 UT WOS:A1993LH82500011 PM 8399470 ER PT J AU BATTJES, RJ HAVERKOS, HW AF BATTJES, RJ HAVERKOS, HW TI COCAINE, AIDS, AND INTRAVENOUS DRUG-USE - FRIEDMAN,SR, LIPTON,DS SO AIDS EDUCATION AND PREVENTION LA English DT Book Review RP BATTJES, RJ (reprint author), NIDA,ROCKVILLE,MD, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0899-9546 J9 AIDS EDUC PREV JI Aids Educ. Prev. PD SUM PY 1993 VL 5 IS 2 BP 178 EP 179 PG 2 WC Education & Educational Research; Public, Environmental & Occupational Health SC Education & Educational Research; Public, Environmental & Occupational Health GA LH415 UT WOS:A1993LH41500011 ER PT J AU BIGGAR, RJ NEEQUAYE, JE NEEQUAYE, AR ANKRABADU, GA LEVINE, PH MANNS, A TAYLOR, M DRUMMOND, J WATERS, D AF BIGGAR, RJ NEEQUAYE, JE NEEQUAYE, AR ANKRABADU, GA LEVINE, PH MANNS, A TAYLOR, M DRUMMOND, J WATERS, D TI THE PREVALENCE OF ANTIBODIES TO THE HUMAN T-LYMPHOTROPIC VIRUS (HTLV) IN GHANA, WEST-AFRICA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID TROPICAL SPASTIC PARAPARESIS; PERIPHERAL-BLOOD; IVORY-COAST; LEUKEMIA; HIV-1; POPULATIONS; LYMPHOMA; ZAIRE AB We conducted a population-based serosurvey of urban areas and rural regions of southern Ghana, West Africa. Subjects (3763) of all ages were enrolled from 25 city and village sites and in studies of groups of special interest. ''Positive'' results were difficult to define because of a high frequency of results that were indeterminate on immunoblotting, the current standard for confirmation of HTLV-I. However, polymerase chain reaction results and HTLV type-specific discriminatory tests proved HTLV-I was present in Ghana. No HTLV-2 positivity was observed. By using strict criteria that considered indeterminate results as negative, the overall prevalence was found to be between 1 and 2% in all areas, with no difference by geographic location. Prevalence rose with age and was higher in adult women than men. However, in substudies of selected populations, we found HTLV prevalence among 124 persons with lymphomas and hematological malignancies was not different from that in the general population. Furthermore, the prevalence in prostitutes was similar to that in the general population and in pregnant women. HTLV-I is present in West Africa, but we were unable to associate HTLV-I seropositivity with malignancy or with prostitution. C1 NCI,BETHESDA,MD 20892. PROGRAM RESOURCES INC,FREDERICK,MD. UNIV GHANA,SCH MED,ACCRA,GHANA. UNIV ALABAMA,SCH MED,BIRMINGHAM,AL 35233. NR 24 TC 18 Z9 18 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JUN PY 1993 VL 9 IS 6 BP 505 EP 511 DI 10.1089/aid.1993.9.505 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LJ320 UT WOS:A1993LJ32000004 PM 8347395 ER PT J AU WEEKS, BS KLOTMAN, ME HOLLOWAY, E STETLERSTEVENSON, WG KLEINMAN, HK KLOTMAN, PE AF WEEKS, BS KLOTMAN, ME HOLLOWAY, E STETLERSTEVENSON, WG KLEINMAN, HK KLOTMAN, PE TI HIV-1 INFECTION STIMULATES T-CELL INVASIVENESS AND SYNTHESIS OF THE 92-KDA TYPE-IV COLLAGENASE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; NECROSIS-FACTOR-ALPHA; HUMAN GLIAL-CELLS; MONONUCLEAR PHAGOCYTES; HTLV-III; HUMAN MACROPHAGES; LANGERHANS CELLS; TISSUE INHIBITOR; TAT PROTEIN; EXPRESSION AB Tissue-specific localization of HIV-1-infected lymphoid cells may contribute to clinical manifestations of AIDS. Therefore we investigated the effect of HIV-1 infection on mechanisms of T lymphocyte invasion, a process required for movement of cells into and out of the circulation. In the present study, we demonstrate that HIV-1-infected human lymphocytes secrete increased amounts of the human 92-kDa type IV collagenase when compared to uninfected lymphocytes. Furthermore, HIV-1-infected lymphocytes degrade the extracellular matrix proteins collagen IV and fibronectin, and they are more invasive through a reconstituted basement membrane when compared to uninfected cells. The addition of either antibody to the 92-kDa collagenase or TIMP-2, a type IV collagenase inhibitor, abolishes invasive activity. These data suggest that HIV-1-infected lymphocytes express phenotypic characteristics that are consistent with an enhanced ability to leave the circulation and to localize in target tissues. Local viral infection or the release of viral proteins, cytokines, or proteolytic enzymes in tissues may contribute to pathogenesis. C1 NIDR,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. RP WEEKS, BS (reprint author), NIH,DEV BIOL LAB,BETHESDA,MD 20892, USA. RI Stetler-Stevenson, William/H-6956-2012; klotman, mary/A-1921-2016 OI Stetler-Stevenson, William/0000-0002-5500-5808; NR 44 TC 38 Z9 38 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JUN PY 1993 VL 9 IS 6 BP 513 EP 518 DI 10.1089/aid.1993.9.513 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LJ320 UT WOS:A1993LJ32000005 PM 8347396 ER PT J AU BRESSLER, P POLI, G JUSTEMENT, JS BISWAS, P FAUCI, AS AF BRESSLER, P POLI, G JUSTEMENT, JS BISWAS, P FAUCI, AS TI GLUCOCORTICOIDS SYNERGIZE WITH TUMOR-NECROSIS-FACTOR-ALPHA IN THE INDUCTION OF HIV EXPRESSION FROM A CHRONICALLY INFECTED PROMONOCYTIC CELL-LINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; LONG TERMINAL REPEAT; NF-KAPPA-B; GENE-EXPRESSION; TRANSCRIPTION; ACTIVATION; HORMONES; ENHANCER; TYPE-1 AB In this study we have investigated the effects of glucocorticoids (GCs) on the expression of human immunodeficiency virus (HIV) in a chronically infected promonocytic cell line, U1. Although no increase in virus production was observed in U1 cells stimulated with physiological concentrations of GC alone, costimulation with dexamethasone plus tumor necrosis factor alpha (TNF-alpha) synergistically enhanced TNF-alpha-dependent HIV expression. Molecular analysis demonstrated that GCs plus TNF-alpha resulted in an accumulation of steady state HIV RNA secondary to either an increase in transcription or an increase in message stability. These findings may be of physiological relevance because GCs are used in the treatment of certain disorders associated with HIV infection and TNF-alpha levels have been reported to be elevated in the plasma and cerebrospinal fluid of certain HIV-infected individuals. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 26 TC 24 Z9 24 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JUN PY 1993 VL 9 IS 6 BP 547 EP 551 DI 10.1089/aid.1993.9.547 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LJ320 UT WOS:A1993LJ32000009 PM 8347399 ER PT J AU METZ, DC BENYA, RV FISHBEYN, VA PISEGNA, JR ORBUCH, M STRADER, DB NORTON, JA JENSEN, RT AF METZ, DC BENYA, RV FISHBEYN, VA PISEGNA, JR ORBUCH, M STRADER, DB NORTON, JA JENSEN, RT TI PROSPECTIVE-STUDY OF THE NEED FOR LONG-TERM ANTISECRETORY THERAPY IN PATIENTS WITH ZOLLINGER-ELLISON SYNDROME FOLLOWING SUCCESSFUL CURATIVE GASTRINOMA RESECTION SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS LA English DT Article ID ACID-SECRETION; OMEPRAZOLE; MANAGEMENT; CIMETIDINE; RANITIDINE; POTENT; US AB A long-term cure is now possible in more than 30% of selected patients with Zollinger-Ellison syndrome who undergo gastrinoma resection. The need, however, for continued gastric acid antisecretory therapy in these patients remains controversial. The current study was designed to determine whether post-operative antisecretory therapy is needed in patients who have undergone successful gastrinoma resection and, if so, to attempt to define criteria with which to identify patients who require therapy. Twenty-eight consecutive patients who had previously undergone curative gastrinoma resection were prospectively studied. When antisecretory therapy was discontinued, 43% (12/28) of these patients developed gastro-oesophageal reflux, diarrhoea, acid-peptic symptoms or endoscopic evidence of acid-peptic disease within 2 weeks and were deemed to have failed a trial of antisecretory drug withdrawal. The remaining 57% (16/28) of patients who successfully discontinued antisecretory therapy were followed for a mean time of 31 months after withdrawal of therapy. Analysis of acid output studies pre-operatively, as well as at the time of drug withdrawal, demonstrated that patients who were unable to discontinue antisecretory therapy exhibited higher pre-operative maximal acid output values and higher basal acid output values at the time of attempted drug withdrawal than patients who were able to discontinue therapy. Despite these findings, there was significant overlap in acid output values between groups so that it was not possible to define specific acid output criteria for successful drug withdrawal. Pre-operative clinical characteristics, such as the presence or absence of gastro-esophageal reflux or acid-peptic disease, or post-operative laboratory values, such as the fasting serum gastrin level, did not correlate with the ability to discontinue antisecretory therapy. We conclude that following successful curative gastrinoma resection, 40% of patients still require antisecretory therapy and that both symptom evaluation as well as upper endoscopy should be used to guide attempted drug withdrawal. Although patients who are not able to discontinue therapy have significantly higher acid output measurements than those who are able to discontinue therapy, neither acid output criteria nor any other laboratory or clinical characteristics are able to predict the need for continued antisecretory therapy in these patients. C1 NIDDKD,DIGEST DIS BRANCH,BLDG 10,ROOM 9C103,BETHESDA,MD 20892. NR 33 TC 23 Z9 23 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0269-2813 J9 ALIMENT PHARM THERAP JI Aliment. Pharmacol. Ther. PD JUN PY 1993 VL 7 IS 3 BP 247 EP 257 PG 11 WC Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Gastroenterology & Hepatology; Pharmacology & Pharmacy GA LJ388 UT WOS:A1993LJ38800002 PM 8364130 ER PT J AU LITTLE, RE WEINBERG, CR AF LITTLE, RE WEINBERG, CR TI RISK-FACTORS FOR ANTEPARTUM AND INTRAPARTUM STILLBIRTH SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ALCOHOL DRINKING; BODY MASS INDEX; FETAL DEATH; LABOR; MATERNAL AGE; PARITY; RACE; SMOKING ID BIRTH-WEIGHT; PREGNANCY; CONSUMPTION; MORTALITY; DRINKING; SMOKING; COFFEE; FETAL; WOMEN AB Data from married women who participated in the 1980 National Natality Survey and the National Fetal Mortality Survey were used for a case-control study of antepartum and intrapartum stillbirth. Risk factors were identified by comparing antepartum deaths and intrapartum deaths to livebirths in separate logistic regression analyses. Risk of antepartum death was increased among black mothers, those having their first delivery, those aged 35 years or more, and those with less education. Smoking cigarettes was associated with increased risk. For intrapartum deaths, total abstention from alcohol during pregnancy was associated with increased risk in the best-fitting logistic model, as was first delivery. Body mass index was logit-linear in both models, with lower body mass index associated with lower risk. While some of these factors have already been associated with stillbirth, others have not; the new associations may reflect the continuum of loss over the gestational period, bias in the study, or clues to mechanisms by which the risk of death, before or during parturition, is increased. C1 NIEHS,DIV BIOMETRY & RISK ASSESSMENT,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC 27709. RP LITTLE, RE (reprint author), NIEHS,DIV BIOMETRY & RISK ASSESSMENT,EPIDEMIOL BRANCH,BOX 12233,MD A3-05,RES TRIANGLE PK,NC 27709, USA. NR 21 TC 77 Z9 81 U1 0 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 1 PY 1993 VL 137 IS 11 BP 1177 EP 1189 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LM337 UT WOS:A1993LM33700002 PM 8322759 ER PT J AU WACHOLDER, S ARMSTRONG, B HARTGE, P AF WACHOLDER, S ARMSTRONG, B HARTGE, P TI VALIDATION STUDIES USING AN ALLOYED GOLD STANDARD SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE BIAS (EPIDEMIOLOGY); BIOMETRY; MISCLASSIFICATION; PROSPECTIVE STUDY; RETROSPECTIVE STUDY ID RELATIVE RISK; MEASUREMENT ERROR; DIET; QUESTIONNAIRE; CANCER; RATES; FOOD AB A key assumption made when using a validation study to correct an estimate of relative risk for bias due to misclassification or measurement error is that the available measure, known to have error but nonetheless used routinely in the main study, is compared to a gold standard measured without error. In most epidemiologic applications, the putative gold standard is in fact measured with error. The effect of the violation of the assumption on the corrected estimate depends on the magnitudes of the errors in the two measures and on their correlation. In particular, when the errors are negatively correlated, independent, or weakly positively correlated, the corrected estimate will tend to overcorrect beyond the true value. C1 MCGILL UNIV,SCH OCCUPAT HLTH,MONTREAL H3A 2T5,QUEBEC,CANADA. RP WACHOLDER, S (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,6130 EXECUT BLVD,EPN 403,ROCKVILLE,MD 20852, USA. NR 17 TC 91 Z9 92 U1 0 U2 3 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 1 PY 1993 VL 137 IS 11 BP 1251 EP 1258 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LM337 UT WOS:A1993LM33700009 PM 8322765 ER PT J AU SINNETT, D WAGSTAFF, J GLATT, K WOOLF, E KIRKNESS, EJ LALANDE, M AF SINNETT, D WAGSTAFF, J GLATT, K WOOLF, E KIRKNESS, EJ LALANDE, M TI HIGH-RESOLUTION MAPPING OF THE GAMMA-AMINOBUTYRIC-ACID RECEPTOR SUBUNIT-BETA-3 AND ALPHA-5 GENE-CLUSTER ON CHROMOSOME-15Q11-Q13, AND LOCALIZATION OF BREAKPOINTS IN 2 ANGELMAN SYNDROME PATIENTS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID PRADER-WILLI SYNDROME; NICOTINIC ACETYLCHOLINE-RECEPTOR; PARENTAL ORIGIN; 15Q DELETIONS; PROXIMAL 15Q; DNA STRANDS; LOCUS; REGION; EXPRESSION; ORGANIZATION AB The gamma-aminobutyric acid (GABA(A)) receptors are a family of ligand-gated chloride channels constituting the major inhibitory neurotransmitter receptors in the nervous system. In order to determine the genomic organization of the GABA(A) receptor beta3 subunit gene (GABRB3) and alpha5 subunit gene (GABRA5) in chromosome 15q11-q13, we have constructed a high-resolution physical map using the combined techniques of field-inversion gel electrophoresis and phage genomic library screening. This map, which covers nearly 1.0 Mb, shows that GABRB3 and GABRA5 are separated by less than 100 kb and are arranged in a head-to-head configuration. GABRB3 encompasses approximately 250 kb, while GABRA5 is contained within 70 kb. This difference in size is due in large part to an intron of 150 kb within GABRB3. We have also identified seven putative CpG islands within a 600-kb interval. Chromosomal rearrangement breakpoints-in one Angelman syndrome (AS) patient with an unbalanced translocation and in another patient with a submicroscopic deletion-are located within the large GABRB3 intron. These findings will facilitate chromosomal walking strategies for cloning the regions disrupted by the DNA rearrangements in these AS patients and will be valuable for mapping new genes to the AS chromosomal region. C1 CHILDRENS HOSP MED CTR,DIV GENET,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA. NIAAA,MOLEC NEUROBIOL SECT,NEUROGENET LAB,ROCKVILLE,MD 20852. FU NINDS NIH HHS [R01NS30628-01]; PHS HHS [P01H018658-11] NR 64 TC 49 Z9 50 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JUN PY 1993 VL 52 IS 6 BP 1216 EP 1229 PG 14 WC Genetics & Heredity SC Genetics & Heredity GA LG133 UT WOS:A1993LG13300023 PM 8389098 ER PT J AU ABASSI, ZA KLEIN, H GOLOMB, E KEISER, HR AF ABASSI, ZA KLEIN, H GOLOMB, E KEISER, HR TI REGULATION OF THE URINARY-EXCRETION OF ENDOTHELIN IN THE RAT SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article DE ENDOTHELIN; ANGIOTENSIN-II; ARGININE VASOPRESSIN; NIFEDIPINE; SARALASIN; DUP753 (LOSARTAN) AB The regulation of the urinary excretion of endothelin (U(ET)V) and its clinical significance has not yet been established. The present study was designed to examine the effect of angiotensin II (A-II), arginine vasopressin (AVP), and nifedipine on U(ET)V. Anesthetized Munich-Wistar rats were infused with low (50 ng/kg/min) and high (500 ng/kg/min) doses of A-II for 30 min. Both doses significantly increased U(ET)V, from nondetectable (ND) levels to 155 +/- 54 (P < .03) and 450 +/- 86 fg/min (P < .001), respectively. This effect was accompanied by a significant increase in urine flow (UV), from 6 +/- 1 to 67 +/- 12 and 89 +/- 10 muL/min, and in mean arterial pressure (MAP), from 139 +/- 4 to 187 +/- 5 and 217 +/- 3 mm Hg. Infusions of A-II with its nonspecific antagonist, saralasin, resulted in a further increase in U(ET)V to 647 +/- 126 and 782 +/- 117 fg/min (P < .002), respectively. However, infusion of A-II with its specific antagonist, losartan, completely blocked its stimulatory effect on U(ET)V. Infusion of AVP, 10 or 100 mU/kg/h, produced increases in MAP, from 134 +/- 3 to 165 +/- 7 and 203 +/- 4 mm Hg, and in UV from 6 +/- 1 to 37 +/- 6 and 97 +/- 17 muL/min, comparable to A-II, but AVP did not have a marked effect on U(ET)V. Infusion of 0.1 or 1.0 mg/kg/h of nifedipine increased U(ET)V, from ND levels to 84 +/- 36 and 146 +/- 40 fg/min (P < .006), respectively, despite a significant decrease in MAP, from 139 +/- 8 to 118 +/-3 and 107 +/- 3 mm Hg (P <.05), respectively. Pretreatment of rats with captopril, 1 mg/kg/h, prevented the nifedipine-induced increase in U(ET)V. Our data suggest that A-II is a major regulator of urinary endothelin excretion. The effect was independent of urinary flow or blood pressure. The effect of nifedipine on U(ET)V was abolished by captopril, suggesting its mediation via reflex activation of the renin-angiotensin axis. RP ABASSI, ZA (reprint author), NHLBI,HYPERTENS ENDOCRINE BRANCH,BLDG 10,ROOM 8C103,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 18 Z9 18 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD JUN PY 1993 VL 6 IS 6 BP 453 EP 457 PN 1 PG 5 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LG134 UT WOS:A1993LG13400001 PM 8343226 ER PT J AU WU, MC AF WU, MC TI ANALYSIS OF BLOOD-PRESSURE VARIABILITY SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article RP WU, MC (reprint author), NHLBI,BIOSTAT RES BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD JUN PY 1993 VL 6 IS 6 SU S BP S198 EP S200 PN 2 PG 3 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LG862 UT WOS:A1993LG86200010 PM 8347318 ER PT J AU KAUPPINEN, T KOGEVINAS, M JOHNSON, E BECHER, H BERTAZZI, PA DEMESQUITA, HBB COGGON, D GREEN, L LITTORIN, M LYNGE, E MATHEWS, J NEUBERGER, M OSMAN, J PANNETT, B PEARCE, N WINKELMANN, R SARACCI, R AF KAUPPINEN, T KOGEVINAS, M JOHNSON, E BECHER, H BERTAZZI, PA DEMESQUITA, HBB COGGON, D GREEN, L LITTORIN, M LYNGE, E MATHEWS, J NEUBERGER, M OSMAN, J PANNETT, B PEARCE, N WINKELMANN, R SARACCI, R TI CHEMICAL-EXPOSURE IN MANUFACTURE OF PHENOXY HERBICIDES AND CHLOROPHENOLS AND IN SPRAYING OF PHENOXY HERBICIDES SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE PHENOXY ACIDS; CHLOROPHENOLS; DIOXINS; OCCUPATIONAL EXPOSURE ID CANCER MORTALITY; WORKERS; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN AB Exposure patterns are reported for manufacturing and sprayer cohorts incorporated in the ''IARC International Register of Workers exposed to Phenoxy Herbicides and Contaminants.'' Information was based on company questionnaires, company reports, plant visits, and serum 2,3,7,8-TCDD measurements. In addition to phenoxy herbicides and chlorophenols, workers in manufacturing plants may have been exposed to raw materials, process chemicals, other agents synthesized or formulated, and impurities of all these agents. Sprayers also had a complex exposure pattern, including phenoxy herbicides and some other pesticides, their carriers and additives, and residues of chemicals formed during manufacture. Occurrence of agents, including dioxins, varied between countries. Biological monitoring and industrial hygiene data were rarely available, most since the late 1970s. Exposure of workers depended mainly on the jobs they performed, but several factors influenced level of exposure. A quantitative exposure classification is not feasible in this study. Semiquantitative exposure estimates may be derived through a critical interpretation of biological monitoring and industrial hygiene data together with individual work histories. C1 NIEHS,CINCINNATI,OH. GERMAN CANC RES CTR,W-6900 HEIDELBERG 1,GERMANY. NATL INST PUBL HLTH & ENVIRONM PROTECT,AMSTERDAM,NETHERLANDS. UNIV MILAN,I-20122 MILAN,ITALY. MRC,ENVIRONM EPIDEMIOL UNIT,SOUTHAMPTON,ENGLAND. ONTARIO HYDRO,TORONTO,ONTARIO,CANADA. LUND UNIV,S-22101 LUND,SWEDEN. DANISH CANC REGISTRY,COPENHAGEN,DENMARK. MENZIES SCH HLTH RES,CASUARINA,AUSTRALIA. INST ENVIRONM HYG,VIENNA,AUSTRIA. HLTH & SAFETY EXECUT,BOOTLE,ENGLAND. WELLINGTON SCH MED,WELLINGTON,NEW ZEALAND. INT AGCY RES CANC,F-69372 LYON,FRANCE. RP KAUPPINEN, T (reprint author), INST OCCUPAT HLTH,DEPT EPIDEMIOL & BIOSTAT,TOPELIUKSENK 41AA,SF-00250 HELSINKI,FINLAND. RI Kogevinas, Manolis/C-3918-2017; bertazzi, pietro alberto/D-5039-2017; OI bertazzi, pietro alberto/0000-0003-3475-2449; Mathews, John/0000-0001-9029-7140 FU NIEHS NIH HHS [1-ES-95267] NR 15 TC 29 Z9 29 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 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD JUN PY 1993 VL 23 IS 6 BP 903 EP 920 DI 10.1002/ajim.4700230607 PG 18 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LD344 UT WOS:A1993LD34400006 PM 8328476 ER PT J AU ROMERO, R BAUMANN, P GOMEZ, R SALAFIA, C RITTENHOUSE, L BARBERIO, D BEHNKE, E COTTON, DB MITCHELL, MD AF ROMERO, R BAUMANN, P GOMEZ, R SALAFIA, C RITTENHOUSE, L BARBERIO, D BEHNKE, E COTTON, DB MITCHELL, MD TI THE RELATIONSHIP BETWEEN SPONTANEOUS RUPTURE OF MEMBRANES, LABOR, AND MICROBIAL INVASION OF THE AMNIOTIC CAVITY AND AMNIOTIC-FLUID CONCENTRATIONS OF PROSTAGLANDINS AND THROMBOXANE-B(2) IN TERM PREGNANCY SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE PROSTAGLANDINS; RUPTURE OF MEMBRANES; LABOR; PARTURITION; INFECTION ID PRETERM LABOR; PREMATURE RUPTURE; HUMAN PARTURITION; PLASMA; INFECTION AB OBJECTIVE: The purpose of this study was to examine the relationship between rupture of membranes, labor, and microbial invasion of the amniotic cavity and amniotic fluid concentrations of eicosanoids in patients with spontaneous rupture of membranes at term. STUDY DESIGN: Amniotic fluid was retrieved by transabdominal amniocentesis from patients with rupture of membranes and patients with intact membranes at term. Studies to determine the microbial state of the amniotic cavity included culture for bacteria and mycoplasmas, Gram stain, amniotic fluid white blood cell count, and Limulus amebocyte lysate. Eicosanoids (prostaglandin E2, prostaglandin F2alpha and its stable metabolite, 6-keto-prostaglandin F1alpha, and thromboxane B2) were determined with sensitive and specific radioimmunoassays validated for human amniotic fluid. Statistical inference was conducted with analysis of variance and linear contrast. RESULTS: (1) Spontaneous rupture of membranes at term was associated with a significant increase in amniotic fluid concentrations of all eicosanoids measured in this study except 6-keto-prostaglandin F1alpha. (2) Early labor in patients with rupture of membranes was associated with a significant increase in the amniotic fluid concentration of all eicosanoids. (3) A significant increase in amniotic fluid eicosanoids in women with microbial invasion of the amniotic cavity could not be documented. CONCLUSIONS: Whereas preterm labor in the absence of microbial invasion of the amniotic cavity is not associated with a significant increase in amniotic fluid concentrations of prostaglandins, a clear increase was documented in women with early labor after spontaneous rupture of membranes. These observations suggest that there are fundamental differences in the biochemistry of term and preterm parturition. C1 NICHHD,PERINATOL BRANCH,BETHESDA,MD 20892. UNIV CONNECTICUT,FARNAM,CT. DANBURY HOSP,DANBURY,CT 06810. HOSP SOTERO DEL RIO,SANTIAGO,CHILE. UNIV UTAH,SALT LAKE CITY,UT 84112. RP ROMERO, R (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,SCH MED,DEPT OBSTET & GYNECOL,4707 ST ANTOINE BLVD,DETROIT,MI 48201, USA. RI Mitchell, Murray/A-8639-2010 OI Mitchell, Murray/0000-0002-6167-7176 NR 25 TC 52 Z9 53 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD JUN PY 1993 VL 168 IS 6 BP 1654 EP 1668 PN 1 PG 15 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA LJ321 UT WOS:A1993LJ32100002 PM 8317506 ER PT J AU HU, ZY EVARTS, RP FUJIO, K MARSDEN, ER THORGEIRSSON, SS AF HU, ZY EVARTS, RP FUJIO, K MARSDEN, ER THORGEIRSSON, SS TI EXPRESSION OF HEPATOCYTE GROWTH-FACTOR AND C-MET GENES DURING HEPATIC DIFFERENTIATION AND LIVER DEVELOPMENT IN THE RAT SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID SCATTER FACTOR; PARTIAL-HEPATECTOMY; INSITU HYBRIDIZATION; EPITHELIAL-CELLS; DNA-SYNTHESIS; OVAL CELLS; TGF-BETA; REGENERATION; RECEPTOR; CARCINOGENESIS AB Hepatocyte growth factor (HGF) is a potent mitogen for mature hepatocytes in vitro. The receptor for HGF has recently been characterized as the product of the proto-oncogene c-met We have examined the possible involvement of HGF in hepatic growth and differentiation in the rat. The experimental systems used were acetylaminofluorene treatment combined with partial hepatectomy to induce proliferation and differentiation of oval cells in adult liver and the pre- and postnatal liver. In the acetylaminofluorene model, Northern blot analysis showed that level of HGF transcripts increased one day after partial hepatectomy, reached a peak by day 6, were maintained at that level until day 13, and then declined, reaching normal level at 20 days. The expression of c-met also increased gradually, reached a peak around 9 to 13 days after partial hepatectomy, at which time oval cell proliferation was most prominent. In the developing liver, an elevated level of HGF transcripts was found between 4 and 21 days after birth. The expression of c-met also slightly increased at the same time. In situ hybridization showed that the transcripts for HGF were localized in desmin-positive Ito cells, whereas the transcripts for c-met were strongly expressed by total cells. We have shown earlier that Ito cells and oval cells proliferate simultaneously and exist in close proximity in the acetylaminofluorene model and that Ito cells are a primary source of growth factors such as transforming growth factor-alpha and acidic fibroblast growth factors. The data presented here suggest that HGF is, in combination with other growth factors, involved in the proliferation and differentiation of oval cells via a paracrine mechanism. RP HU, ZY (reprint author), NCI,EXPTL CARCINOGENESIS LAB,BLDG 37,ROOM 3C28,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 43 TC 149 Z9 152 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JUN PY 1993 VL 142 IS 6 BP 1823 EP 1830 PG 8 WC Pathology SC Pathology GA LF978 UT WOS:A1993LF97800017 PM 8506951 ER PT J AU WILLIAMS, AO FLANDERS, KC SAFFIOTTI, U AF WILLIAMS, AO FLANDERS, KC SAFFIOTTI, U TI IMMUNOHISTOCHEMICAL LOCALIZATION OF TRANSFORMING GROWTH-FACTOR-BETA-1 IN RATS WITH EXPERIMENTAL SILICOSIS, ALVEOLAR TYPE-II HYPERPLASIA, AND LUNG-CANCER SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID INDUCED PULMONARY FIBROSIS; FACTOR-BETA; EXTRACELLULAR-MATRIX; EPITHELIAL-CELLS; TGF-BETA; COLLAGEN-SYNTHESIS; ENDOTHELIAL-CELLS; PROLIFERATION; FIBRONECTIN; CARCINOGENESIS AB Immunohistochemical localization of transforming growth factor-beta1, (TGF-beta1) was studied in the lungs of rats given crystalline silica or ferric oxide by single intratracheal instillation. Ferric oxide elicited no progressive granulomatous reaction, no epithelial hyperplasia, and no lung tumors; no demonstrable reactivity to TGF-beta1 was observed. Silica induced a granulomatous reaction with progressive fibrosis, adjacent alveolar type II hyperplasia, and alveolar carcinomas. Rabbit polyclonal antibodies to synthetic peptides corresponding to the first 30 amino acids of mature TGF-beta1, anti-LC (1-30), and anti-CC (1-30) were used for the localization of intracellular and extracellular TGF-beta1. An antibody to a peptide corresponding to amino acids 266-278 of the TGF-beta1 precursor sequence, anti-Pre (266-278), was used to detect the TGF-beta precursor and the latency-associated peptide. Intracellular mature TGF-beta (anti-LC) was demonstrated in fibroblasts and macrophages located at the periphery of silicotic granulomas and in fibroblasts adjacent to hyperplastic type II cells. Extracellular mature TGF-beta1, was localized in the connective tissue matrix of the granulomas and in the stroma of both hyperplastic type H cells and well-differentiated adenocarcinomas. Immunoreactivity to anti-Pre was localized, intracellularly, in hyperplastic alveolar type II cells and their proliferative lesions adjacent to granulomas, in adenomas, but not in adenocarcinomas. The hyperplastic type II cells appear to be the sites of production and secretion of TGF-beta1, which may regulate their own growth and differentiation and mediate the production of extracellular TGF-beta1-associated matrix. The lack of reactivity to TGF-beta1 precursor in the adeno-carcinomas is consistent with the loss of normal cellular differentiation and function. TGF-beta1 appears to have a pathogenetic role in silica-induced mesenchymal and epithelial lesions. The role of TGF-beta1 and other cytokines in silica-induced carcinogenesis requires further investigation. C1 NCI, EXPTL PATHOL LAB, BLDG 41, ROOM C-105, BETHESDA, MD 20892 USA. NCI, DIV CANC ETIOL, CHEMOPREVENT LAB, BETHESDA, MD 20892 USA. NR 48 TC 75 Z9 80 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JUN PY 1993 VL 142 IS 6 BP 1831 EP 1840 PG 10 WC Pathology SC Pathology GA LF978 UT WOS:A1993LF97800018 PM 8389528 ER PT J AU ZHANG, J HERMAN, EH FERRANS, VJ AF ZHANG, J HERMAN, EH FERRANS, VJ TI DENDRITIC CELLS IN THE HEARTS OF SPONTANEOUSLY HYPERTENSIVE RATS TREATED WITH DOXORUBICIN WITH OR WITHOUT ICRF-187 SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID MEDIATED CYTO-TOXICITY; ADRIAMYCIN-INDUCED AUGMENTATION; (+/-)-1,2-BIS(3,5-DIOXOPIPERAZINYL-1-YL)PROPANE ICRF-187; MONOCLONAL-ANTIBODIES; ANTIGEN EXPRESSION; CARDIOTOXICITY; MACROPHAGE; CANCER; HETEROGENEITY; PRETREATMENT AB Histological and immunohistochemical studies using specific monoclonal antibodies were made to evaluate the severity of the chronic cardiomyopathy and the quantitative changes in interstitial dendritic cells (antigen-presenting cells), T helper lymphocytes, T cytotoxic/suppressor lymphocytes, and macrophages in the hearts of spontaneously hypertensive rats (SHRs) treated with doxorubicin at 1 mg/kg per week for 3, 6, 9 or 12 weeks. In addition, an assessment was made of the modifications of the responses of these cell populations by pretreatment of the SHR with ICRF-187, which protects against doxorubicin cardiotoxicity. The number of interstitial dendritic cells/mm2 of section of left ventricle was similar in saline-treated control SHRs (76 +/- 6) and in those treated with ICRG-187 alone (75 +/- 2) but increased markedly (319 +/- 33) in animals receiving a total cumulative dose of 12 mg/kg doxorubicin. Treatment with ICRF-187 prior to each administration of doxorubicin attenuated in a dose-dependent manner the increase in numbers of dendritic cells induced by doxorubicin (231 +/- 47,174 +/- 11, and 100 +/- 16 cells/mm2) after treatment with 6.25, 12.5, and 25 mg of ICRF-187, respectively. Doxorubicin also induced increases in the numbers of T helper lymphocytes and macrophages but not of T cytotoxic/suppressor lymphocytes. These increases were also attenuated by pretreatment with ICRF-187. These data were interpreted as indicating that doxorubicin cardiotoxicity results in the release of substances that initiate immune reactions involving the antigen-presenting cells of the heart and that such reactions are attenuated by pretreatment with ICRF-187. C1 NHLBI,PATHOL BRANCH,ULTRASTRUCT SECT,BLDG 10,ROOM 2N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. US FDA,DIV RES & TRAINING,LAUREL,MD. NR 34 TC 31 Z9 31 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JUN PY 1993 VL 142 IS 6 BP 1916 EP 1926 PG 11 WC Pathology SC Pathology GA LF978 UT WOS:A1993LF97800027 PM 8506959 ER PT J AU CAROME, MA STRIKER, LJ PETEN, EP MOORE, J YANG, CW STETLERSTEVENSON, WG STRIKER, GE AF CAROME, MA STRIKER, LJ PETEN, EP MOORE, J YANG, CW STETLERSTEVENSON, WG STRIKER, GE TI HUMAN GLOMERULI EXPRESS TIMP-1 MESSENGER-RNA AND TIMP-2 PROTEIN AND MESSENGER-RNA SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GLOMERULOSCLEROSIS; EXTRACELLULAR MATRIX; GENE EXPRESSION; METALLOPROTEINASE; INHIBITOR; COMPETITIVE POLYMERASE CHAIN REACTION ID POLYMERASE CHAIN-REACTION; DEGRADING NEUTRAL PROTEINASE; TISSUE INHIBITOR; MESANGIAL CELLS; METALLOPROTEINASES-2; PURIFICATION; INVITRO; QUANTITATION AB Alterations in the balance between synthesis and degradation of extracellular matrix may result in glomerulosclerosis. The interaction between metalloproteinases and their inhibitors presumably modulates the rate of glomerular matrix degradation. We examined the gene expression of tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 in human glomeruli and TIMP-2 protein in tissue sections. Kidney tissue was obtained from adults undergoing nephrectomy for renal tumor (n = 9) or biopsy for nephrosis and renal failure (n = 1). Glomeruli were microdissected and subjected to reverse transcription. TIMP cDNAs were quantitated by competitive polymerase chain reaction assays. Five nephrectomy specimens had normal glomeruli and four had diffuse glomerulosclerosis. TIMP-1 and TIMP-2 cDNA levels, detected in glomeruli from all patients, were increased fourfold and threefold, respectively, in patients with glomerulosclerosis. The elevated TIMP cDNA levels could not be attributed to an increased number of glomerular cells. TIMP-2 protein was detected within normal and sclerotic glomeruli. In conclusion, both TIMP genes were expressed in normal glomeruli, and their level of expression was increased in glomerulosclerosis associated with renal carcinoma, suggesting that expression of these inhibitors may correlate with the development of sclerosis. C1 NIDDKD,RENAL CELL BIOL SECT,METAB DIS BRANCH,BLDG 10,RM 3N110,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,DEPT MED,SERV NEPHROL,WASHINGTON,DC 20307. WALTER REED ARMY MED CTR,DEPT CLIN INVEST,WASHINGTON,DC 20307. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 33 TC 63 Z9 65 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUN PY 1993 VL 264 IS 6 BP F923 EP F929 PN 2 PG 7 WC Physiology SC Physiology GA LL133 UT WOS:A1993LL13300093 PM 8322893 ER PT J AU FELDER, CC ALBRECHT, FE CAMPBELL, T EISNER, GM JOSE, PA AF FELDER, CC ALBRECHT, FE CAMPBELL, T EISNER, GM JOSE, PA TI CAMP-INDEPENDENT, G-PROTEIN-LINKED INHIBITION OF NA+ H+ EXCHANGE IN RENAL BRUSH-BORDER BY D1 DOPAMINE AGONISTS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE DOPAMINE D1 RECEPTOR; PROXIMAL TUBULES; ADENYLYL CYCLASE; PROTEIN KINASE-A; GUANINE NUCLEOTIDE BINDING PROTEINS; BRUSH-BORDER ID ADENYLATE-CYCLASE; KIDNEY; RECEPTOR; MEMBRANE; LOCALIZATION; SUBUNITS; RAT AB When D1 dopamine agonists are incubated with renal cortical tissue, Na+/H+ exchange activity is inhibited, presumably due to D1 receptor-mediated stimulation of adenylyl cyclase and subsequent increase in protein kinase A activity. Although the role of adenosine 3',5'-cyclic monophosphate (cAMP) and cAMP-dependent protein kinase in the regulation of Na+/H+ exchange activity is well established, receptors functionally coupled to adenylyl cyclase can regulate Na+/H+ exchange activity independently of changes of cAMP accumulation. The current studies were designed to determine whether D1 agonists can inhibit Na+/H+ exchange activity independently of changes of cAMP accumulation and also to determine the role of G proteins in this process. The D1 agonist, fenoldopam, inhibited Na+/H+ exchange activity in a time-related and concentration-dependent manner. The 50% inhibitory concentration was 5-34 muM. Occupation of the renal D1 receptor mediates this action, since the D1 antagonist, SKF 83742, partially blocks the effect. This action, however, was independent of adenylyl cyclase, protein kinase A, and protein kinase C activity. Inhibition of adenylyl cyclase with dideoxyadenosine or inhibition of protein kinase A and C with the isoquinolines N-(2-guanidinoethyl)-5-isoquinolinesulfonamide hydrochloride (H-4) and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) did not block the effect of fenoldopam on the exchanger. The action of fenoldopam is not due to an amiloride-like action on the exchanger, because kinetic analysis of the inhibitory action was noncompetitive and the effect of fenoldopam was time dependent. The process involved G proteins, since guanosine 5'-O-(2-thiodiphosphate) prevented while guanosine 5'-O-(3-thiotriphosphate) increased the inhibitory effect of fenoldopam. C1 GEORGETOWN UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,WASHINGTON,DC 20007. GEORGETOWN UNIV,CHILDRENS MED CTR,DEPT PEDIAT,WASHINGTON,DC 20007. RP FELDER, CC (reprint author), NIMH,PHARMACOL SECT,CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 24 TC 61 Z9 62 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUN PY 1993 VL 264 IS 6 BP F1032 EP F1037 PN 2 PG 6 WC Physiology SC Physiology GA LL133 UT WOS:A1993LL13300109 ER PT J AU HONDA, T ZHOU, ZC GU, ZF KITSUKAWA, Y MROZINSKI, JE JENSEN, RT AF HONDA, T ZHOU, ZC GU, ZF KITSUKAWA, Y MROZINSKI, JE JENSEN, RT TI STRUCTURAL-ANALYSIS OF CGRP RECEPTORS ON GASTRIC SMOOTH-MUSCLE AND PANCREATIC ACINAR-CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CHEMICAL CROSS-LINKING; N-GLYCANASE; GUINEA PIG; DEGLYCOSYLATION; SIALOGLYCOPROTEIN ID GENE-RELATED-PEPTIDE; GUINEA-PIG PANCREAS; CALCITONIN-GENE; BINDING-SITES; HUMAN CEREBELLUM; DISPERSED ACINI; CROSS-LINKING; BRAIN; RAT; CHOLECYSTOKININ AB Calcitonin gene-related peptide (CGRP) immunoreactivity is widely distributed in the central nervous system and gastrointestinal (GI) tract, and specific receptors have been described on many GI tissues. In the present study, we compared CGRP receptors on gastric smooth muscle cells with those on pancreatic acini from guinea pig with the use of chemical cross-linking techniques combined with various enzymatic digestions. I-125-labeled rat CGRP-I demonstrated temperature-dependent saturable binding to both acinar and gastric smooth muscle cell membranes. After binding, membranes were incubated with 1 mM disuccinimidyl suberate (DSS), solubilized with sodium dodecyl sulfate (SDS), and subjected to SDS-polyacrylamide gel electrophoresis. Cross-linked radioactivity was analyzed by autoradiography. A single broad radioactive band [molecular weight (M(r)) 57,000] was seen on cell membranes from both tissues and after cross-linking to intact cells. These bands were not altered by addition of dithiothreitol. This radioactive band was not detected without DSS present or with addition of 10 muM rCGRP-I. rCGRP-I inhibited cross-linking with half-maximal inhibition of 32 nM with membranes from both tissues, and there was a close correlation between its ability to inhibit binding and to inhibit cross-linking. Cross-linking was not inhibited by non-CGRP related peptides. With membranes from both tissues, N-glycanase digestion increased the mobility of the original band. Neuraminidase digestion only slightly increased the mobility of the original band; however, the subsequent addition of O-glycanase showed no additional effect on both membranes. Endoglycosidase H digestion had no effect in either tissue. The present results demonstrate that on both tissues the cell membrane receptor for CGRP is an N-linked sialoglycoprotein. The apparent M(r) of this sialoglycoprotein is 57,000, and this polypeptide does not contain disulfide-linked subunits or O-linked carbohydrates. C1 NIH,DIGEST DIS BRANCH,BLDG 10,RM 9C-103,BETHESDA,MD 20892. NR 38 TC 4 Z9 4 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUN PY 1993 VL 264 IS 6 BP G1142 EP G1152 PN 1 PG 11 WC Physiology SC Physiology GA LL132 UT WOS:A1993LL13200074 ER PT J AU DILISA, F FAN, CZ GAMBASSI, G HOGUE, BA KUDRYASHOVA, I HANSFORD, RG AF DILISA, F FAN, CZ GAMBASSI, G HOGUE, BA KUDRYASHOVA, I HANSFORD, RG TI ALTERED PYRUVATE-DEHYDROGENASE CONTROL AND MITOCHONDRIAL FREE CA2+ IN HEARTS OF CARDIOMYOPATHIC HAMSTERS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE HEART FAILURE; CARDIAC MYOCYTES; TRICARBOXYLATE CYCLE; INDO-1 ID INCREASED CARDIAC WORK; SYRIAN-HAMSTER; CALCIUM-IONS; RAT-HEART; PIG-HEART; HEREDITARY POLYMYOPATHY; ENERGY-METABOLISM; TRANSPORT; MYOCYTES; COMPLEX AB The fraction of total pyruvate dehydrogenase in the active, dephosphorylated form is much lower in the glucose-perfused isolated hearts of two myopathic strains of Syrian hamster (BIO 14.6 and TO-2) than in the hearts of healthy control animals (F1B). The myopathic hearts also develop significantly less pressure under these conditions. Experiments with isolated myocytes from the BIO 14.6 heart reveal that intramitochondrial free Ca2+ ([Ca2+]m), a positive effector of pyruvate dehydrogenase interconversion, rises much less in response to a protocol of increased frequency of electrical stimulation and adrenergic stimulation than does [Ca2+]m in cells from the healthy control animals (viz from 248 +/- 15 to 348 +/- 44 nM in BIO 14.6 vs. from 241 +/- 35 to 830 +/- 124 nM in FIB, at 4 Hz). As the concentration of Ca2+ that produces half-maximal activation of pyruvate dehydrogenase within mitochondria is 650 nM, this difference between strains is likely the mechanism of the altered enzyme interconversion. The lesser response of [Ca2+]m to electrical stimulation in the BIO 14.6 cells probably results mainly from smaller systolic transients in cytosolic free Ca2+ in response to excitation of single myocytes from the BIO 14.6 animal. Lowered values of [Ca2+]m within the range described would compromise not only pyruvate dehydrogenase activity, but also flux through the tricarboxylate cycle in the myopathic heart, owing to the sensitivity of 2-oxoglutarate dehydrogenase to Ca2+. This may explain the decreased activity of oxidative phosphorylation and performance of work in the myopathic heart. C1 NIA,GERONTOL RES CTR,ENERGY METAB & BIOENERGET SECT,CARDIOVASC SCI LAB,4940 EASTERN AVE,BALTIMORE,MD 21224. NR 55 TC 49 Z9 49 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUN PY 1993 VL 264 IS 6 BP H2188 EP H2197 PN 2 PG 10 WC Physiology SC Physiology GA LL133 UT WOS:A1993LL13300054 ER PT J AU LAUGHLIN, MR TAYLOR, J CHESNICK, AS DEGROOT, M BALABAN, RS AF LAUGHLIN, MR TAYLOR, J CHESNICK, AS DEGROOT, M BALABAN, RS TI PYRUVATE AND LACTATE METABOLISM IN THE IN-VIVO DOG HEART SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE OXYGEN CONSUMPTION; REDOX POTENTIAL; MYOCARDIAL METABOLISM; P-31 NUCLEAR MAGNETIC RESONANCE; C-13 NUCLEAR MAGNETIC RESONANCE; PHOSPHOCREATINE; PHOSPHORYLATION POTENTIAL; ADENOSINE 5'-TRIPHOSPHATE; MAGNESIUM; GLUTAMATE; ALANINE; INTRACELLULAR PH ID PERFUSED RAT-HEART; P-31 MAGNETIC-RESONANCE; INTRACELLULAR PH; C-13 NMR; OXYGEN-CONSUMPTION; WORKING HEART; GUINEA-PIG; TRANSPORT; EXTRACTION; LIVER AB Pyruvate increases the phosphorylation potential in perfused heart to a greater extent than the closely correlated substrate L-lactate. Therefore, metabolism of these compounds was studied in the myocardium of intact dogs. Phosphocreatine/ATP was increased 23% at 5.3 mM plasma pyruvate but was not significantly increased by lactate except at the highest concentration (17.5 mM in blood). Calculated [ADP] fell during pyruvate infusion from 51.5 +/- 2.0 to 38.6 +/- 3.3 muM but did not change significantly during lactate infusion. Intracellular free [Mg2+] fell from 705 +/- 53 to 498 +/- 30 muM at the highest pyruvate infusion and from 692 +/- 112 to 417 +/- 19 muM with lactate infusion. Extraction of both substrates was linear at low concentrations, reaching 0.56 mumol lactate.min-1.g wet wt-1 at 17.5 mM blood lactate and 0.58 mumol pyruvate.min-1.g wet wt-1 at 5.3 mM plasma pyruvate. Therefore, lactate uptake was almost five times lower than pyruvate uptake at similar concentrations. Elevated pyruvate (>3 mM) resulted in almost complete inhibition of net lactate uptake. Infused [3-C-13]lactate or -pyruvate gave rise to labeled glutamate and alanine in vivo, but labeled lactate was not visible when [3-C-13]pyruvate was the substrate. The C-13 enrichment of myocardial lactate was similar to alanine and acetyl CoA with infused [3-C-13]lactate but was only one-half that of alanine and acetyl CoA when [3-C-13]-pyruvate was the substrate, indicating a possible inhibition of lactate dehydrogenase. RP LAUGHLIN, MR (reprint author), NHLBI,CARDIAC ENERGET LAB,9000 ROCKVILLE PIKE,BLDG 1,RM B3-07,BETHESDA,MD 20892, USA. RI Balaban, Robert/A-7459-2009 OI Balaban, Robert/0000-0003-4086-0948 NR 50 TC 69 Z9 69 U1 1 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUN PY 1993 VL 264 IS 6 BP H2068 EP H2079 PN 2 PG 12 WC Physiology SC Physiology GA LL133 UT WOS:A1993LL13300039 ER PT J AU CARDOSO, WV STEWART, LG PINKERTON, KE JI, CM HOOK, GER SINGH, G KATYAL, SL THURLBECK, WM PLOPPER, CG AF CARDOSO, WV STEWART, LG PINKERTON, KE JI, CM HOOK, GER SINGH, G KATYAL, SL THURLBECK, WM PLOPPER, CG TI SECRETORY PRODUCT EXPRESSION DURING CLARA CELL-DIFFERENTIATION IN THE RABBIT AND RAT SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CLARA CELL SECRETORY PROTEIN; BRONCHIOLAR DIFFERENTIATION; LUNG DEVELOPMENT ID LUNG MATURATION; PROTEIN; UTEROGLOBIN; LOCALIZATION; EPITHELIUM AB One function of the nonciliated (Clara) cells of bronchiolar epithelium is to synthesize, store, and release small-molecular-mass (6-12 kDa) secretory proteins or Clara cell secretory protein (CCSP). This study compares the emergence of this secretory function during Clara cell differentiation in rabbits and rats. Lungs of fetal and postnatal animals were evaluated by ultrastructural morphometry and immunohistochemistry. Secretory granules were rarely seen in perinatal animals and increased to adult levels of abundance earlier in rats (1 wk postnatal) than in rabbits (3-4 wk). In contrast, rough endoplasmic reticulum was abundant in perinatal animals and decreased with age. Antibodies raised against CCSP revealed little CCSP in fetal animals; however, after birth CCSP increased to adult levels earlier in rats (1 wk postnatal) than in rabbits (3 wk). We conclude that the maturation of Clara cell secretory function 1) occurs postnatally, 2) involves a decrease in biosynthetic organelles, 3) shows close association between CCSP expression and secretory granule abundance, and 4) varies by species in timing and cellular abundance of biosynthetic machinery. C1 UNIV CALIF DAVIS,SCH VET MED,DEPT ANAT & CELL BIOL,DAVIS,CA 95616. NIEHS,RES TRIANGLE PK,NC 27709. UNIV PITTSBURGH,VET ADM MED CTR,PITTSBURGH,PA 15240. UNIV BRITISH COLUMBIA,FAC MED,DEPT PATHOL,VANCOUVER V6T 1W5,BC,CANADA. FU NHLBI NIH HHS [HL-43032] NR 26 TC 33 Z9 33 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUN PY 1993 VL 264 IS 6 BP L543 EP L552 PN 1 PG 10 WC Physiology SC Physiology GA LL132 UT WOS:A1993LL13200082 PM 8333547 ER PT J AU LYNESS, JM CAINE, ED CONWELL, Y KING, DA COX, C AF LYNESS, JM CAINE, ED CONWELL, Y KING, DA COX, C TI DEPRESSIVE SYMPTOMS, MEDICAL ILLNESS, AND FUNCTIONAL STATUS IN DEPRESSED PSYCHIATRIC-INPATIENTS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID PHYSICAL HEALTH AB Objective: There is evidence that both psychiatric (especially affective) and medical illnesses contribute to physical disability. However, the differential contributions of specific psychiatric disorders and of medical pathology to functional status in psychiatric populations have not been studied. The authors therefore examined the contributions of depressive symptoms and medical illness to functional disability in depressed inpatients. Method: This prospective investigation included 109 psychiatric inpatients with DSM-III-R major depression. Regression techniques were used to examine the contribution of demographic variables (age, sex, education), depressive symptom severity (Hamilton Rating Scale for Depression score), psychiatric function (Global Assessment of Functioning Scale score), organ system pathology (Cumulative Illness Rating Scale score), and medical disability (Karnofsky Performance Status Scale score) to overall functional status (Instrumental Activities of Daily Living and Physical Self-Maintenance scores). These relationships were also examined in older and younger subgroups. Results: Greater age, female sex, and illness factors all contributed to poorer functional status. Of the illness factors, psychiatric pathology contributed more to low functional status than did medical illness. The predictive power came specifically from the functionally based measures of psychiatric and medical illness; a quantitative measure of symptoms (Hamilton depression scale) or organ pathology (Cumulative Illness Rating Scale) did not significantly predict overall functional status. Conclusions: Clinicians and researchers should recognize that symptomatic and functional assessments tap related but different domains and that both psychiatric and medical illnesses contribute to overall disability. C1 UNIV ROCHESTER,NIMH,MED CTR,CLIN RES CTR STUDY PSYCHOPATHOL ELDERLY,ROCHESTER,NY 14627. FU NIMH NIH HHS [MH-18911, MH-40381] NR 21 TC 88 Z9 88 U1 1 U2 3 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD JUN PY 1993 VL 150 IS 6 BP 910 EP 915 PG 6 WC Psychiatry SC Psychiatry GA LD843 UT WOS:A1993LD84300011 PM 8494068 ER PT J AU LINN, S CARROLL, M JOHNSON, C FULWOOD, R KALSBEEK, W BRIEFEL, R AF LINN, S CARROLL, M JOHNSON, C FULWOOD, R KALSBEEK, W BRIEFEL, R TI HIGH-DENSITY-LIPOPROTEIN CHOLESTEROL AND ALCOHOL-CONSUMPTION IN UNITED-STATES WHITE AND BLACK ADULTS - DATA FROM NHANES-II SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID CORONARY HEART-DISEASE; CARDIOVASCULAR-DISEASE; RISK-FACTORS; SUBFRACTIONS; MEN; NUTRITION; SMOKING; LIPIDS; HDL AB Objectives. High-density lipoprotein (HDL) cholesterol is known to be positively related to moderate alcohol consumption from studies in selected populations. This study describes the association in a representative sample of the US adult population. Methods. Stratification and multivariate regression analyses were used to examine HDL cholesterol levels and alcohol consumption. Results. Fewer women than men reported consumption of alcohol at any frequency. similar percentages of Whites and Blacks reported alcohol consumption. Age-adjusted mean HDL cholesterol levels were higher among alcohol drinkers than among nondrinkers in all sex-race strata. Mean HDL cholesterol levels of Whites and Blacks of both sexes increased consistently with increased frequency of consumption of beer, wine, and liquor. With age, education, body mass index, smoking, and physical activity controlled for, there were higher age-adjusted HDL cholesterol levels with increasing reported quantities of alcohol consumed. Daily or weekly use of alcohol led to an increase of 5.1 mg/dL in mean HDL cholesterol level, whereas consumption of 1 g of alcohol led to an increase of 0.87 mg/dL. Conclusion. Even if there is a causal association between alcohol consumption and higher HDL cholesterol levels, it is suggested that efforts to reduce coronary heart disease risks concentrate on the cessation of smoking and weight control. C1 NATL CTR HLTH STAT,DIV HLTH EXAMINAT STAT,HYATTSVILLE,MD 20782. NHLBI,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT BIOSTAT,CHAPEL HILL,NC 27514. RP LINN, S (reprint author), RAMBAM MED CTR,CLIN EPIDEMIOL UNIT,HAIFA,ISRAEL. RI Linn, Shai/C-8212-2013 OI Linn, Shai/0000-0001-5471-5034 NR 54 TC 87 Z9 88 U1 1 U2 5 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JUN PY 1993 VL 83 IS 6 BP 811 EP 816 DI 10.2105/AJPH.83.6.811 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LF150 UT WOS:A1993LF15000008 PM 8498617 ER PT J AU ZAGZAG, D MILLER, DC KLEINMAN, GM ABATI, A DONNENFELD, H BUDZILOVICH, GN AF ZAGZAG, D MILLER, DC KLEINMAN, GM ABATI, A DONNENFELD, H BUDZILOVICH, GN TI DEMYELINATING DISEASE VERSUS TUMOR IN SURGICAL NEUROPATHOLOGY - CLUES TO A CORRECT PATHOLOGICAL DIAGNOSIS SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE DEMYELINATION; MULTIPLE SCLEROSIS; TUMEFACTIVE LESION; CENTRAL NERVOUS SYSTEM ID MULTIPLE-SCLEROSIS; COMPUTED-TOMOGRAPHY; CORPUS-CALLOSUM; CEREBRAL-TUMOR; BRAIN-TUMOR; GLIOMA; CT AB Clinical presentations as well as radiological and histopathological findings in biopsies from patients with multiple sclerosis (MS) or other demyelinating disorders of the central nervous system are sometimes misleading, resulting in an erroneous diagnosis of brain or spinal cord tumor. We report 17 patients who presented with symptoms mimicking those of brain (14 cases) or spinal cord (three cases) tumors. Computerized tomography or magnetic resonance imaging studies or both were interpreted as consistent with a tumor in each case. All patients underwent surgery, and all 17 pathological specimens were eventually diagnosed as showing demyelinating disease, usually consistent with MS. In each case we examined a variety of histological features and immunohistochemical studies and addressed their relative importance in considering the diagnosis of MS. All cases showed perivascular lymphocytic inflammation with variable amounts of macrophage infiltration, necrosis, and edema. The hypercellularity of the lesions and the presence of atypical reactive astrocytes with mitotic figures were the disturbing features that might have led to the erroneous diagnosis of an astrocytic neoplasm. Immunohistochemistry for astrocytic (glial fibrillary acidic protein) and macrophage (HAM-56) markers are helpful in evaluating biopsies. Our results emphasize the need to perform special stains (i.e., for myelin and axons) that demonstrate myelin loss and relative preservation of axons and allow a correct diagnosis. C1 ST VINCENTS MED CTR NEW YORK,DEPT NEUROL,NEW YORK,NY. BRIDGEPORT HOSP,DEPT PATHOL,BRIDGEPORT,CT 06610. ST VINCENTS MED CTR NEW YORK,DEPT PATHOL,NEW YORK,NY. NCI,DEPT PATHOL,BETHESDA,MD 20892. RP ZAGZAG, D (reprint author), NYU MED CTR,DEPT PATHOL,DIV NEUROPATHOL,550 1ST AVE,NEW YORK,NY 10016, USA. NR 24 TC 100 Z9 109 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD JUN PY 1993 VL 17 IS 6 BP 537 EP 545 DI 10.1097/00000478-199306000-00001 PG 9 WC Pathology; Surgery SC Pathology; Surgery GA LD355 UT WOS:A1993LD35500001 PM 8333553 ER PT J AU DEWOLFPEETERS, C JAFFE, ES AF DEWOLFPEETERS, C JAFFE, ES TI CENTROCYTIC LYMPHOMA - REPLY SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Letter C1 NCI,BETHESDA,MD 20892. RP DEWOLFPEETERS, C (reprint author), UNIV HOSP ST RAPHAEL,B-3000 LOUVAIN,BELGIUM. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD JUN PY 1993 VL 17 IS 6 BP 641 EP 641 PG 1 WC Pathology; Surgery SC Pathology; Surgery GA LD355 UT WOS:A1993LD35500018 ER PT J AU LANZARO, GC OSTROVSKA, K HERRERO, MV LAWYER, PG WARBURG, A AF LANZARO, GC OSTROVSKA, K HERRERO, MV LAWYER, PG WARBURG, A TI LUTZOMYIA-LONGIPALPIS IS A SPECIES COMPLEX - GENETIC-DIVERGENCE AND INTERSPECIFIC HYBRID STERILITY AMONG 3 POPULATIONS SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID SAND FLIES DIPTERA; VISCERAL LEISHMANIASIS; PSYCHODIDAE; DISPERSAL AB The sand fly Lutzomyia longipalpis is the vector of Leishmania donovani chagasi in Latin America. An analysis of genetic variability at 27 enzyme coding loci among three laboratory populations of Lu. longipalpis revealed substantial genetic polymorphism. Levels of genetic distance between all pairwise comparisons of colonies were very high, and consistent with those previously reported among separate species in the genus Lutzomyia. Between 7% and 22% of the loci studied were diagnostic for any two of the colony populations. Experimental hybridization between colonies resulted in the production of sexually sterile male progeny. Our results provide strong evidence that Lu. longipalpis exists in nature as a complex of at least three distinct species. The possible effects of colonization on the genetic makeup of laboratory populations is considered in extending our results to natural populations. C1 WALTER REED ARMY MED CTR,WALTER REED ARMY INST RES,DEPT ENTOMOL,WASHINGTON,DC 20307. UNIV NACL,SCH VET MED,TROP DIS RES PROGRAM,HEREDIA,COSTA RICA. RP LANZARO, GC (reprint author), NIAID,MALARIA RES LAB,BLDG 4,BETHESDA,MD 20892, USA. NR 25 TC 121 Z9 122 U1 0 U2 1 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD JUN PY 1993 VL 48 IS 6 BP 839 EP 847 PG 9 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA LR003 UT WOS:A1993LR00300016 PM 8333579 ER PT J AU HIRSCHFELD, S JAROSINSKI, P AF HIRSCHFELD, S JAROSINSKI, P TI DRUG-INTERACTION OF TERFENADINE AND CARBAMAZEPINE SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP HIRSCHFELD, S (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JUN 1 PY 1993 VL 118 IS 11 BP 907 EP 908 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA LD252 UT WOS:A1993LD25200021 PM 8480971 ER PT J AU PAGE, WF KURTZKE, JF MURPHY, FM NORMAN, JE AF PAGE, WF KURTZKE, JF MURPHY, FM NORMAN, JE TI EPIDEMIOLOGY OF MULTIPLE-SCLEROSIS IN UNITED-STATES VETERANS .5. ANCESTRY AND THE RISK OF MULTIPLE-SCLEROSIS SO ANNALS OF NEUROLOGY LA English DT Article AB Self-reported ancestry data for the U.S. population from the 1980 decennial census and multiple sclerosis (MS) risk data derived from a large series of World War 11 white male veterans with MS and matched controls were aggregated on a state level and analyzed to determine the relationship between ancestry and MS risk. A significant portion of the state-by-state variation in MS risk is explainable statistically by differences in ancestry among state populations, even when geographic latitude is included in analyses. In the main, Swedish and other Scandinavian ancestry is most consistently associated with places with increased MS risk. In some analyses, Italian, French, and (to a lesser extent) Scottish ancestries are also associated with increased risk, whereas English and Dutch ancestries are each associated with decreased risk, but most of these non-Scandinavian correlations may reflect predominantly geography per se. These findings provide evidence that ancestry of the resident population, a confounded measure of genetic susceptibility and cultural environment, is part of the complicated picture of MS as a disease of place. C1 NATL ACAD SCI,INST MED,WASHINGTON,DC 20418. VET AFFAIRS MED CTR,NEUROL SERV,WASHINGTON,DC. NHLBI,BETHESDA,MD 20892. RP PAGE, WF (reprint author), MED FOLLOW UP AGCY,2101 CONSTITUT AVE NW,WASHINGTON,DC 20418, USA. NR 13 TC 41 Z9 41 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JUN PY 1993 VL 33 IS 6 BP 632 EP 639 DI 10.1002/ana.410330612 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA LE987 UT WOS:A1993LE98700011 PM 8498844 ER PT J AU CARRASQUILLO, JA REYNOLDS, JC BUNN, PA FOON, KA SHUKE, N SCHROFF, RW MULSHINE, JL PERENTESIS, P SZYMENDERA, J HOROWITZ, M LARSON, SM AF CARRASQUILLO, JA REYNOLDS, JC BUNN, PA FOON, KA SHUKE, N SCHROFF, RW MULSHINE, JL PERENTESIS, P SZYMENDERA, J HOROWITZ, M LARSON, SM TI PHARMACOKINETICS OF IN-111 T101 (ANTI-CD5) MONOCLONAL-ANTIBODY IN PATIENTS WITH CUTANEOUS T-CELL LYMPHOMA SO ANTIBODY IMMUNOCONJUGATES AND RADIOPHARMACEUTICALS LA English DT Article ID CHRONIC LYMPHOCYTIC-LEUKEMIA; CARCINOEMBRYONIC ANTIGEN; RADIOLABELED ANTIBODIES; TUMOR-LOCALIZATION; CANCER-PATIENTS; SEZARY SYNDROME; MELANOMA; CARCINOMA; RADIOIMMUNODETECTION; MODULATION AB The pharmacokinetics of In-111 T101, an anti-CD5 murine monoclonal antibody, were studied in 11 patients. The T101 was labeled with In-111 using a modification of the mixed anhydride method. Each patient received the content of one kit (5 mCi and 1 mg) injected alone (five patients) or mixed and co-injected with 9 mg (three patients) or 49 mg (three patients) of unlabeled T101. Dose dependent differences in biodistribution in normal organs were observed. The liver, spleen and bone marrow were sites of prominent accumulation at all dose levels. Higher doses of T101 resulted in less accumulation of In-111 in these sites and prolongation of the blood pool retention. Visualization of tumors was seen at all dose levels and did not appear to be dose dependent. These studies indicate that dose is an important determinant of T101 pharmacokinetics. C1 NCI,DEPT NUCL MED,BETHESDA,MD 20892. NCI,WARREN G MAGNUSON CLIN CTR,NAVY MED ONCOL BRANCH,BETHESDA,MD 20892. NCI,CLIN ONCOL & BIOL RESPONSE MODIFERS PROGRAM,BETHESDA,MD 20892. RI Carrasquillo, Jorge/E-7120-2010; OI Carrasquillo, Jorge/0000-0002-8513-5734 NR 36 TC 1 Z9 1 U1 0 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0892-7049 J9 ANTIBODY IMMUNOCONJ JI Antib. Immunoconjug. Radiopharm. PD SUM PY 1993 VL 6 IS 2 BP 111 EP 126 PG 16 WC Immunology; Radiology, Nuclear Medicine & Medical Imaging SC Immunology; Radiology, Nuclear Medicine & Medical Imaging GA LF159 UT WOS:A1993LF15900002 ER PT J AU KOVACS, JA POWELL, F VOELLER, D ALLEGRA, CJ AF KOVACS, JA POWELL, F VOELLER, D ALLEGRA, CJ TI INHIBITION OF PNEUMOCYSTIS-CARINII DIHYDROPTEROATE SYNTHETASE BY PARA-ACETAMIDOBENZOIC ACID - POSSIBLE MECHANISM OF ACTION OF ISOPRINOSINE IN HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID LIPID-SOLUBLE ANTIFOLATE; TOXOPLASMA-GONDII; INOSINE PRANOBEX; EFFICACY; TRIMETREXATE; SYNTHASE AB Isoprinosine has been reported to decrease progression to AIDS, primarily by preventing Pneumocystis carinii pneumonia (PCP), in human immunodeficiency virus-infected patients, but the mechanism of action is unknown. para-Acetamidobenzoic acid (PAcBA), one component of isoprinosine, is structurally related to para-aminobenzoic acid (PABA), a precursor of de novo folate synthesis. This pathway is known to be important for P. carinii because sulfonamides, which are effective anti-P. carinii agents, inhibit incorporation of PABA into folate precursors by the enzyme dihydropteroate synthetase (DHPS). Inhibition of P. carinii DHPS by PAcBA was investigated by using two assays. In short-term cultures of P. carinii from rats, [H-3]PABA incorporation into reduced folates was inhibited by both isoprinosine (mean +/- standard error 50% inhibitory concentration [IC50], 20 +/- 8.4 muM) and PAcBA free acid (IC50, 240 +/- 100 muM); a soluble PAcBA salt was more potent than PAcBA free acid alone (IC50, 29 +/- 48 muM). The activity of PAcBA free acid was confirmed in a cell-free DHPS inhibition assay (IC50, 120 +/- 120 muM). Inosine and dimethylaminopropanol, two other components of isoprinosine, were poor inhibitors of PABA incorporation (IC50, > 1,000 muM). PAcBA free acid also showed activity in inhibiting the DHPS of Toxoplasma gondii, but was a poor inhibitor of the DHPSs of Escherichia coli and Saccharomyces cerevisiae. In a rat model of PCP, the PAcBA salt administered intraperitoneally demonstrated no activity against established PCP either alone or when used in combination with trimethoprim; the lack of efficacy in this model may be due to the rapid metabolism of the drug. Prevention of PCP by PaCBA through inhibition of P. carinii DHPS may explain the activity of isoprinosine in decreasing the progression to AIDS in human immunodeficiency virus-infected patients. C1 NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20892. RP KOVACS, JA (reprint author), NCI,CTR CLIN,DEPT CRIT CARE MED,BETHESDA,MD 20892, USA. NR 18 TC 6 Z9 6 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JUN PY 1993 VL 37 IS 6 BP 1227 EP 1231 PG 5 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA LF135 UT WOS:A1993LF13500004 PM 7687120 ER PT J AU WALSH, TJ STANDIFORD, HC REBOLI, AC JOHN, JF MULLIGAN, ME RIBNER, BS MONTGOMERIE, JZ GOETZ, MB MAYHALL, CG RIMLAND, D STEVENS, DA HANSEN, SL GERARD, GC RAGUAL, RJ AF WALSH, TJ STANDIFORD, HC REBOLI, AC JOHN, JF MULLIGAN, ME RIBNER, BS MONTGOMERIE, JZ GOETZ, MB MAYHALL, CG RIMLAND, D STEVENS, DA HANSEN, SL GERARD, GC RAGUAL, RJ TI RANDOMIZED DOUBLE-BLINDED TRIAL OF RIFAMPIN WITH EITHER NOVOBIOCIN OR TRIMETHOPRIM-SULFAMETHOXAZOLE AGAINST METHICILLIN-RESISTANT STAPHYLOCOCCUS-AUREUS COLONIZATION - PREVENTION OF ANTIMICROBIAL RESISTANCE AND EFFECT OF HOST FACTORS ON OUTCOME SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID NASAL CARRIAGE; HOSPITAL OUTBREAK; UNITED-STATES; INFECTIONS; MUPIROCIN; ERADICATION; EFFICACY; THERAPY; HEMODIALYSIS; PROPHYLAXIS AB Methicillin-resistant Staphylococcus aureus (MRSA) is a major pathogen in hospitals. Current antimicrobial regimens for eradicating colonizing strains are not well defined and are often complicated by the emergence of resistance. The combination of novobiocin plus rifampin in vitro and in vivo was found to prevent the emergence of resistant populations of initially susceptible strains of MRSA, particularly resistance to rifampin. We therefore studied, in a randomized, double-blind, multicenter comparative trial, the combination of novobiocin plus rifampin versus trimethoprim-sulfamethoxazole (T/S) plus rifampin in order to determine the efficacy of each regimen in eradicating MRSA colonization and to further characterize the host factors involved in the response to this antimicrobial therapy. Among the 126 individuals enrolled in the study, 94 (80 patients; 14 hospital personnel) were evaluable. Among the 94 evaluable subjects, no significant demographic or medical differences existed between the two treatment groups. Successful clearance of the colonizing MRSA strains was achieved in 30 of 45 (67%) subjects receiving novobiocin plus rifampin, whereas successful clearance was achieved in 26 of 49 (53%) subjects treated with T/S plus rifampin (P = 0.18). The emergence of resistance to rifampin developed more frequently in 14% (7 of 49) of subjects treated with T/S plus rifampin than in 2% (1 of 45) of subjects treated with novobiocin plus rifampin (P = 0.04). Restriction endonuclease studies of large plasmid DNA demonstrated that the same strain was present at pretherapy and posttherapy in most refractory cases (24 of 29 [83%] subjects). Among the 56 successfully treated subjects, clearance of MRSA was age dependent: 29 of 36 (80%) subjects in the 18- to 49-year-old age group, 19 of 35 (54%) subjects in the 50- to 69-year-old age group, and 8 of 23 (35%) in the 70- to 94-year-old age group (P < 0.01). Clearance was also site dependent; culture-positive samples from wounds were related to a successful outcome in only 22 (48%) of 46 subjects, whereas culture-positive samples from sites other than wounds (e.g., nares, rectum, and sputum) were associated with a success rate of 34 of 48 (71%) subjects (P = 0.02). Foreign bodies in wounds did not prevent the eradication of MRSA by either regimen. T/S plus rifampin was less effective in clearing pressure wounds compared with other wounds, whereas novobiocin plus rifampin was equally effective in clearing both pressure and other wounds. There were no significant differences in toxicity between the two regimens. Thus, the combination of novobiocin plus rifampin, in comparison with T/S plus rifampin, was more effective in preventing the emergence of resistance to rifampin and demonstrated a trend toward greater activity in clearing the MRSA carrier state. The response to either combination depended on host factors, particularly age and the site of MRSA colonization. C1 BALTIMORE VET AFFAIRS MED CTR,INFECT DIS SECT,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. MED UNIV S CAROLINA,CHARLESTON,SC 29425. NCI,BETHESDA,MD 20892. VET AFFAIRS MED CTR,CHARLESTON,SC 29425. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. ASHEVILLE VET AFFAIRS MED CTR,ASHEVILLE,NC 28805. DUKE UNIV,MED CTR,DURHAM,NC 27710. RANCHO LOS AMIGOS MED CTR,DOWNEY,CA 90242. UNIV CALIF LOS ANGELES,SEPULVEDA VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. VIRGINIA COMMONWEALTH UNIV MED COLL VIRGINIA,RICHMOND,VA 23219. VET AFFAIRS MED CTR,DECATUR,GA 30033. EMORY UNIV,SCH MED,ATLANTA,GA 30322. SANTA CLARA VALLEY MED CTR,SAN JOSE,CA 95128. STANFORD UNIV,SCH MED,CALIF INST MED RES,SAN JOSE,CA 94305. UPJOHN CO,KALAMAZOO,MI 49001. OI Goetz, Matthew/0000-0003-4542-992X NR 56 TC 88 Z9 89 U1 3 U2 7 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JUN PY 1993 VL 37 IS 6 BP 1334 EP 1342 PG 9 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA LF135 UT WOS:A1993LF13500022 PM 8328783 ER PT J AU BARR, R AF BARR, R TI SUCCESSFUL AGING - PERSPECTIVES FROM THE BEHAVIORAL-SCIENCES - BALTES,PB, BALTES,MM SO APPLIED COGNITIVE PSYCHOLOGY LA English DT Book Review RP BARR, R (reprint author), NATL INST AGING,BETHESDA,MD, USA. NR 2 TC 1 Z9 1 U1 1 U2 6 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0888-4080 J9 APPL COGNITIVE PSYCH JI Appl. Cogn. Psychol. PD JUN PY 1993 VL 7 IS 3 BP 272 EP 274 DI 10.1002/acp.2350070311 PG 3 WC Psychology, Experimental SC Psychology GA LH716 UT WOS:A1993LH71600010 ER PT J AU KNECHT, KT MASON, RP AF KNECHT, KT MASON, RP TI INVIVO SPIN-TRAPPING OF XENOBIOTIC FREE-RADICAL METABOLITES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID TERT-BUTYL-NITRONE; PERFUSED RAT-LIVER; CARBON-TETRACHLORIDE METABOLISM; LIPID-PEROXIDATION INVIVO; ISOLATED HEPATOCYTES; IRON OVERLOAD; RESONANCE INVESTIGATIONS; SOYBEAN LIPOXYGENASE; CATALYZED OXIDATION; HALOTHANE C1 NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,DEPT PHARMACOL,HEPATOBIOL & TOXICOL LAB,CHAPEL HILL,NC 27599. FU NIAAA NIH HHS [NIAAA AA-03624] NR 119 TC 81 Z9 81 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JUN PY 1993 VL 303 IS 2 BP 185 EP 194 DI 10.1006/abbi.1993.1272 PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LG146 UT WOS:A1993LG14600002 PM 8390216 ER PT J AU HIRAIWA, M SOEDA, S MARTIN, BM FLUHARTY, AL HIRABAYASHI, Y OBRIEN, JS KISHIMOTO, Y AF HIRAIWA, M SOEDA, S MARTIN, BM FLUHARTY, AL HIRABAYASHI, Y OBRIEN, JS KISHIMOTO, Y TI THE EFFECT OF CARBOHYDRATE REMOVAL ON STABILITY AND ACTIVITY OF SAPOSIN-B SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID SPHINGOLIPID ACTIVATOR PROTEIN-1; METACHROMATIC LEUKODYSTROPHY; SULFATASE ACTIVATOR; LYSOSOMAL STORAGE; MESSENGER-RNA; HUMAN-LIVER; DEFICIENCY; SAP-1; LOCALIZATION; SPECIFICITY C1 UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92093. NIMH,CLIN NEUROSCI BRANCH,MOLEC NEUROGENET SECT,BETHESDA,MD 20892. LANTERMAN DEV CTR,UCLA MRRC RES GRP,POMONA,CA 91769. INST PHYS & CHEM RES,INT FRONTIER RES SYST,WAKO 35101,JAPAN. FU NINDS NIH HHS [NS-08682, NS-13559, NS-22655] NR 34 TC 41 Z9 42 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JUN PY 1993 VL 303 IS 2 BP 326 EP 331 DI 10.1006/abbi.1993.1291 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LG146 UT WOS:A1993LG14600021 PM 8099782 ER PT J AU KNECHT, KT THURMAN, RG MASON, RP AF KNECHT, KT THURMAN, RG MASON, RP TI ROLE OF SUPEROXIDE AND TRACE TRANSITION-METALS IN THE PRODUCTION OF ALPHA-HYDROXYETHYL RADICAL FROM ETHANOL BY MICROSOMES FROM ALCOHOL DEHYDROGENASE-DEFICIENT DEERMICE SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID LIPID-PEROXIDATION; POLYMORPHONUCLEAR LEUKOCYTES; CARBON-TETRACHLORIDE; IRON MOBILIZATION; HYDROGEN-PEROXIDE; PARA-NITROPHENOL; OXYGEN RADICALS; RAT HEPATOCYTES; TREATED RATS; OXIDATION C1 UNIV N CAROLINA,DEPT PHARMACOL,HEPATOBIOL & TOXICOL LAB,CHAPEL HILL,NC 27599. RP KNECHT, KT (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU NIAAA NIH HHS [NIAAA (AA-03624]; NIEHS NIH HHS [ES07126] NR 41 TC 67 Z9 68 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JUN PY 1993 VL 303 IS 2 BP 339 EP 348 DI 10.1006/abbi.1993.1293 PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LG146 UT WOS:A1993LG14600023 PM 8390220 ER PT J AU LEONARD, HL SWEDO, SE LENANE, MC RETTEW, DC HAMBURGER, SD BARTKO, JJ RAPOPORT, JL AF LEONARD, HL SWEDO, SE LENANE, MC RETTEW, DC HAMBURGER, SD BARTKO, JJ RAPOPORT, JL TI A 2-YEAR TO 7-YEAR FOLLOW-UP-STUDY OF 54 OBSESSIVE-COMPULSIVE CHILDREN AND ADOLESCENTS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID CLOMIPRAMINE TREATMENT; EXPRESSED EMOTION; DISORDER; CHILDHOOD; EXPOSURE; DESIPRAMINE; NEUROSIS AB Objective: Due to the generally poor prognosis previously reported for patients with obsessive-compulsive disorder (OCD), this report systematically assessed the outcome of patients who had had access to new psychopharmacologic treatments to determine whether there had been any long-term gains and if there were any predictors of outcome. Designs: Prospective follow-up study of a cohort of consecutive pediatric patients with OCD who had participated in controlled treatment (clomipramine hydrochloride) trials and then received a variety of interim treatments. Patients: Fifty-four children and adolescents were reevaluated 2 to 7 years (mean, 3.4 +/- 1.0 years) after initial clomipramine treatment. Information for 48 (89%) of the patients was from direct interview and for the remaining six (1,1%) from at least two sources. Results: On follow-up, 23 of the subjects (43%) still met diagnostic criteria for OCD, and only three (6%) could be considered in true remission. Thirty-eight subjects (70%) were taking psychoactive medication at the time of follow-up. Although OCD symptoms continued, the group as a whole was significantly improved at follow-up, with only 10 subjects (19%) rated as unchanged or worse. A worse OCD outcome score at follow-up was predicted in a stepwise multiple regression by (1) more severe OCD symptoms score after 5 weeks of clomipramine therapy, (2) lifetime history of a tic disorder, and (3) presence of parental Axis I psychiatric diagnosis (R2=.31, P<.01). Conclusions: With new treatments available, most patients with pediatric OCD can expect significant longterm improvements but not complete remission. This study supports previous reports of the chronicity and intractability of the disorder, as there still remained a significant subgroup of subjects who exhibited continued morbidity despite multiple interventions. C1 NIMH,DIV APPL & SERV RES,BETHESDA,MD 20895. RP LEONARD, HL (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20895, USA. NR 49 TC 268 Z9 273 U1 1 U2 16 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUN PY 1993 VL 50 IS 6 BP 429 EP 439 PG 11 WC Psychiatry SC Psychiatry GA LF796 UT WOS:A1993LF79600002 PM 8498877 ER PT J AU GORDON, CT STATE, RC NELSON, JE HAMBURGER, SD RAPOPORT, JL AF GORDON, CT STATE, RC NELSON, JE HAMBURGER, SD RAPOPORT, JL TI A DOUBLE-BLIND COMPARISON OF CLOMIPRAMINE, DESIPRAMINE, AND PLACEBO IN THE TREATMENT OF AUTISTIC DISORDER SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; CHILDREN; FENFLURAMINE; SEROTONIN; HALOPERIDOL; DYSKINESIA; FLUOXETINE; DOPAMINE; TARDIVE; DRUGS AB Objective: To determine whether clomipramine hydro chloride, a serotonin reuptake blocker with unique anti-obsessional properties, is differentially effective for obsessive-compulsive and stereotyped motor behaviors in autistic disorder compared with placebo and with the noradrenergic tricyclic antidepressant agent, desipramine hydrochloride. Design: Following a 2-week, single-blind placebo washout phase, 12 autistic subjects completed a 10-week, double-blind, crossover comparison of clomipramine and placebo, and 12 different subjects completed a similar comparison of clomipramine and desipramine. Setting: Outpatient clinic. Patients: A referral sample of 30 male and female autistic patients were enrolled, and 24 completed the study. Measures: Key outcome measures were the Autism Relevant Subscale of the Children's Psychiatric Rating Scale, the Modified Comprehensive Psychopathological Rating Scale-Obsessive-Compulsive Disorder Subscale, and the Clinical Global Impressions Scale. Results: Clomipramine was superior to both placebo and desipramine on ratings of autistic symptoms (including stereotypies), anger, and compulsive, ritualized behaviors (P<.05), with no differences between desipramine and placebo. Clomipramine was equal to desipramine and both tricyclic agents were superior to placebo for amelioration of hyperactivity. Conclusion: Biological links between compulsions and stereotyped, repetitive behaviors in autistic disorder should be explored. RP GORDON, CT (reprint author), NIMH,CHILD PSYCHIAT BRANCH,ROOM 6N240,BLDG 10,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 42 TC 249 Z9 255 U1 5 U2 12 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUN PY 1993 VL 50 IS 6 BP 441 EP 447 PG 7 WC Psychiatry SC Psychiatry GA LF796 UT WOS:A1993LF79600003 PM 8498878 ER PT J AU WINOKUR, G CORYELL, W KELLER, M ENDICOTT, J AKISKAL, H AF WINOKUR, G CORYELL, W KELLER, M ENDICOTT, J AKISKAL, H TI A PROSPECTIVE FOLLOW-UP OF PATIENTS WITH BIPOLAR AND PRIMARY UNIPOLAR AFFECTIVE-DISORDER SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID MANIC-DEPRESSIVE ILLNESS; HETEROGENEITY; PREDICTORS; INTERVIEW; FAMILY AB Objective: As part of the National Institute of Mental Health Collaborative Study of the Psychobiology of Depression, the comparative course of manic depressive (bipolar) and primary unipolar patients was assessed. Design: Systematic evaluation using structured instruments every 6 months for a period of 5 years with the recording of remissions, new episodes, and subsequent hospitalizations. Patients: The number of subjects varied somewhat depending on the analyses conducted. For a comparison of course in bipolar patients and unipolar patients, 148 bipolars were compared with 172 unipolar patients. Results: Both unipolar and bipolar patients were more likely to have episodes if they had episodes prior to index admission. Likewise, prior hospitalizations predicted multiple hospitalizations in follow-up. Chronicity was significantly more prevalent among unipolar depressives but in both unipolar and bipolar patients, chronicity diminished over time. Bipolar patients were more likely than unipolar patients to have multiple episodes at the 2-year and 5-year follow-ups. In bipolar patients, there was no difference in the number of episodes in folloW-Up between males and females but in unipolar patients, females were significantly more likely to have subsequent hospitalizations and episodes than males. Treatment variables did not relate to these differences. A family history of mania or schizoaffective mania predicted multiple episodes in bipolar patients but not in primary unipolar depressives. A family history of all affective illness (mania, schizoaffective mania, bipolar II illness, and depression) did not predict a multiple-episode course-in either bipolar or unipolar illness. In unipolar patients, the independent variables leading to multiple-episode course in follow-up are being female, an early age of onset, and prior episodes. Conclusions: As a result of this systematic follow-up study, new data add to the distinction between bipolar and primary unipolar patients both as regards number of episodes in follow-up and also as regards risk factors that are associated with the multiple-episode course. C1 NIMH,COLLABORAT PROGRAM PSYCHOBIOL DEPRESS CLIN STUDIES,BETHESDA,MD 20892. FU NIMH NIH HHS [R01 MH051415] NR 25 TC 207 Z9 208 U1 2 U2 5 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUN PY 1993 VL 50 IS 6 BP 457 EP 465 PG 9 WC Psychiatry SC Psychiatry GA LF796 UT WOS:A1993LF79600005 PM 8498880 ER PT J AU SCHMIDT, PJ GROVER, GN RUBINOW, DR AF SCHMIDT, PJ GROVER, GN RUBINOW, DR TI ALPRAZOLAM IN THE TREATMENT OF PREMENSTRUAL-SYNDROME - A DOUBLE-BLIND, PLACEBO-CONTROLLED TRIAL SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID DYSPHORIA AB Objective: To evaluate the efficacy of alprazolam in the treatment of premenstrual syndrome. Design: A randomized, double-blind, placebo-controlled, crossover trial of alprazolam during eight menstrual cycles. Setting: Outpatient clinic at the National Institute of Mental Health, Bethesda, Md. Participants: Twenty-two women with prospectively confirmed premenstrual syndrome entered this study. All subjects were either self-referred or were referred by their physicians. All reported having regular menstrual cycle lengths, were taking no medication, and were free of current or recent medical or psychiatric illness. Two subjects did not complete the trial. Intervention: Participants were assigned to receive alprazolam or placebo as follows: cycle 1, 0.25 mg of alprazolam or placebo three times daily beginning on menstrual cycle day 16; cycle 2, 0.50 mg of alprazolam or placebo three times daily according to the regimen during the first cycle; cycles 3 and 4, 0.75 mg of alprazolam or placebo three times daily from menstrual cycle day 16 and continued throughout the fourth menstrual cycle to evaluate the efficacy of relatively long-term (approximately 6 weeks) treatment with alprazolam. Main Outcome Measures: Daily self-report symptoms ratings were completed during the entire study period. Results: We observed no significant differences in the severity of premenstrual symptom ratings during alprazolam administration compared with placebo on any scale except the Beck Depression Inventory Scale. The Beck Depression Inventory ratings demonstrated a statistically (F1,19=7.1, P<.05), but not clinically, significant improvement in depressive symptoms during alprazolam administration compared with placebo. Conclusion: Our findings do not support alprazolam as a uniformly effective treatment for the symptoms of premenstrual syndrome. RP SCHMIDT, PJ (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BLDG 10,ROOM 3N238,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 19 TC 63 Z9 63 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUN PY 1993 VL 50 IS 6 BP 467 EP 473 PG 7 WC Psychiatry SC Psychiatry GA LF796 UT WOS:A1993LF79600006 PM 8498881 ER PT J AU WEHR, TA AF WEHR, TA TI CAN ANTIDEPRESSANTS INDUCE RAPID-CYCLING SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter ID ILLNESS; THERAPY RP WEHR, TA (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,ROOM 4S-239,BLDG 10,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 6 TC 20 Z9 20 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUN PY 1993 VL 50 IS 6 BP 495 EP 496 PG 2 WC Psychiatry SC Psychiatry GA LF796 UT WOS:A1993LF79600010 PM 8498885 ER PT J AU REHAK, NN OERTEL, YC HERP, A CHIANG, BT CSAKO, G AF REHAK, NN OERTEL, YC HERP, A CHIANG, BT CSAKO, G TI BIOCHEMICAL-ANALYSIS OF THYROID CYST FLUID OBTAINED BY FINE-NEEDLE ASPIRATION SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID MALIGNANT LESIONS; CANCER; BIOPSY; NODULE; THYROGLOBULIN; DILEMMA; SERUM AB Despite the relatively ready availability of thyroid cyst fluid specimens, little has been published on their biochemical composition. We measured the concentrations of 18 analytes in thyroid cyst fluid specimens from benign (n=17) and malignant (n=3) lesions and in homogenates of normal thyroid tissue (n=5). The concentrations of an additional five analytes were measured in selected cyst fluid specimens only. Compared with normal human serum specimens, we found that in thyroid cyst fluid specimens the activities of acid phosphatase, aspartate aminotransferase, amylase, and lactate dehydrogenase, and the concentrations of iron and total bilirubin were highly increased. The concentration of glucose was low. The gross appearance of the fluids and the presence of certain analytes were consistent with a hemorrhagic origin of most of the benign and malignant cyst fluid specimens. Other biochemical markers, however, indicated colloidlike features and/or an admixture of thyroid tissue components to the cyst fluid. Although we have limited data for cyst fluid specimens from malignant thyroid lesions, we found no evidence that the results of any of the common biochemical tests would distinguish benign from malignant lesions. C1 GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,DEPT PATHOL,WASHINGTON,DC 20052. NEW YORK MED COLL,DEPT BIOCHEM & MOLEC BIOL,VALHALLA,NY 10595. RP REHAK, NN (reprint author), NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT CLIN PATHOL,BLDG 10,BETHESDA,MD 20892, USA. NR 38 TC 12 Z9 12 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD JUN PY 1993 VL 117 IS 6 BP 625 EP 630 PG 6 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA LF306 UT WOS:A1993LF30600018 PM 8503736 ER PT J AU HONG, HL YANG, RSH BOORMAN, GA AF HONG, HL YANG, RSH BOORMAN, GA TI ENHANCEMENT OF MYELOTOXICITY INDUCED BY REPEATED IRRADIATION IN MICE EXPOSED TO A MIXTURE OF GROUNDWATER CONTAMINANTS SO ARCHIVES OF TOXICOLOGY LA English DT Article DE CHEMICAL MIXTURES; GROUNDWATER CONTAMINANTS; IRRADIATION; MYELOTOXICITY; MICE; SYNERGISM; ENHANCEMENT ID BENZENE METABOLITES; CHEMICAL-MIXTURES; STEM-CELLS; TOXICOLOGY AB As part of a program on the toxicology of chemical mixtures at the National Institute of Environmental Health Sciences/National Toxicology Program (NIEHS/NTP), hematopoietic functions were studied in female B6C3F1 mice treated with 0, 1%, and 5% of a chemical mixture stock of 25 groundwater contaminants in drinking water for 31.5 weeks. The toxicologic interaction between continuous exposure to groundwater contaminants and stress induced by multiple irradiation on hematopoiesis was investigated. For those mice receiving both the chemical mixture and irradiation, the exposure to the former was continuous throughout the 31.5-week experimental period, whereas whole body irradiations (4 times at 200 rads/each) were carried out at 7-week intervals with the first one at 3.5 weeks. Myelotoxicity assessment was made by determining the number of granulocyte-macrophage progenitor cells (CFU-GM) 1 week after each irradiation and also at 6 weeks following irradiation as a measure of recovery from stress. Non-irradiated mice treated with 5% chemical mixture solution showed suppression of CFU-GM after 15.5 weeks and became progressively more affected (only 70% of controls by 31.5 weeks of treatment). The population of CFU-GM in mice treated with 5% chemical mixture for 4.5 weeks plus irradiation (I week after first irradiation) was only 22% of the non-irradiated vehicle control group. This combined (i. e., chemical mixture plus irradiation) suppression of CFU-GM intensified after repeated irradiation until the number of CFU-GM was only 10.7% following the fourth irradiation at 25.5 weeks. Thus, irradiation caused a significant reduction in CFU-GMs in all mice but the effects were more pronounced in mice treated with a chemical mixture. In the chemical mixture pretreated mice, the hematopoietic cells were depressed more by multiple irradiation, and the recovery was delayed as compared to non-irradiated control. Furthermore, even at 1% mixture stock level (the lowest concentration tested), when all routine hematologic or conventional toxicologic endpoints appeared to be normal, an enhancement of radiation injury to hematopoiesis was detected. It is suggested that a residual. subclinical, bone marrow effect of the chemical Mixture renders the mice more sensitive to subsequent irradiation-induced injury and also prolongs the recovery of mice following multiple irradiation. These findings suggest that long-term exposure to highly contaminated driking water may render a population more susceptible to subsequent hematopoietic stress. C1 COLORADO STATE UNIV,DEPT ENVIRONM HLTH,FT COLLINS,CO 80523. RP HONG, HL (reprint author), NIEHS,CHEM CARCINOGENESIS BRANCH,RES TRIANGLE PK,NC 27709, USA. NR 35 TC 4 Z9 4 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-5761 J9 ARCH TOXICOL JI Arch. Toxicol. PD JUN PY 1993 VL 67 IS 5 BP 358 EP 364 DI 10.1007/BF01973708 PG 7 WC Toxicology SC Toxicology GA LJ890 UT WOS:A1993LJ89000011 PM 8368945 ER PT J AU SCHREINER, PJ MORRISETT, JD SHARRETT, AR PATSCH, W TYROLER, HA WU, K HEISS, G AF SCHREINER, PJ MORRISETT, JD SHARRETT, AR PATSCH, W TYROLER, HA WU, K HEISS, G TI LIPOPROTEIN[A] AS A RISK FACTOR FOR PRECLINICAL ATHEROSCLEROSIS SO ARTERIOSCLEROSIS AND THROMBOSIS LA English DT Article DE LIPOPROTEIN[A]; ATHEROSCLEROSIS; B-MODE ULTRASONOGRAPHY; RACE ID CORONARY HEART-DISEASE; B-MODE ULTRASOUND; APOLIPOPROTEIN-B; FAMILIAL HYPERCHOLESTEROLEMIA; CEREBROVASCULAR-DISEASE; MYOCARDIAL-INFARCTION; SERUM LIPOPROTEIN(A); LP(A) CONCENTRATIONS; ARTERY DISEASE; PLASMA AB Elevated mean levels of lipoprotein[a] (Lp[a]) have been associated with symptomatic cardiovascular diseases such as clinically manifest myocardial infarction (MI), coronary artery disease, restenosis of coronary artery vein grafts after bypass, and a family history of MI. Associations of Lp[a] with arterial wall thickening in asymptomatic individuals previously have not been addressed and are evaluated in this report among participants of the Atherosclerosis Risk in Communities (ARIC) Study. Intima-media wall thickening in the extracranial carotid arteries was assessed noninvasively with B-mode ultrasonography; Lp[a] was measured as its total protein component. Individuals with wall thickening greater-than-or-equal-to 90th percentile of the population maximum far-wall thickness were pair matched to participants < 75th percentile of wall thickness by race, gender, center, 10-year age group, and time of examination. These selection criteria yielded 492 matched pairs, with 395 white pairs and 97 black pairs. The mean Lp[a] protein level for all black participants was 174.6 mug/mL compared with 77.8 mug/mL for whites. Conditional logistic regression analysis for the association of Lp[a] with case-control status yielded a statistically significant prevalence odds ratio (OR) estimate of 1.49, based on a I-SD difference in Lp[a] protein, after adjusting for age, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, fibrinogen, hypertension, and cigarette smoking. None of these risk factors significantly altered the OR, in agreement with reports that Lp[a] is unaffected by environmental influences. In addition, no differential effect of Lp[a] protein on case-control status (effect modification) was observed by race, gender, low-density lipoprotein cholesterol, or fibrinogen in this population. We conclude that Lp[a] is an independent risk factor for intima-media carotid thickening in individuals free of prevalent cardiovascular disease. Further investigation of racial effects may benefit from a population-based analysis that includes additional black participants as well as from elucidation of apolipoprotein[a] polymorph differences between races and degree of wall thickening. C1 METHODIST HOSP,DEPT MED,HOUSTON,TX 77030. METHODIST HOSP,ATHEROSCLEROSIS CLIN LAB,HOUSTON,TX 77030. NHLBI,DECA,ARIC PROJECT OFF,BETHESDA,MD 20892. UNIV TEXAS,SCH MED,HOUSTON,TX 77025. RP SCHREINER, PJ (reprint author), UNIV N CAROLINA,DEPT EPIDEMIOL,CB 7400 MCGAVRAN GREENBERG HALL,CHAPEL HILL,NC 27599, USA. RI Wu, Kenneth Kun-Yu/B-1070-2010 FU NHLBI NIH HHS [1-HC-55019] NR 49 TC 107 Z9 110 U1 1 U2 4 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1049-8834 J9 ARTERIOSCLER THROMB JI Arterioscler. Thromb. PD JUN PY 1993 VL 13 IS 6 BP 826 EP 833 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LF156 UT WOS:A1993LF15600008 PM 8499402 ER PT J AU BERMAN, CM RASMUSSEN, KLR SUOMI, SJ AF BERMAN, CM RASMUSSEN, KLR SUOMI, SJ TI REPRODUCTIVE CONSEQUENCES OF MATERNAL-CARE PATTERNS DURING ESTRUS AMONG FREE-RANGING RHESUS-MONKEYS SO BEHAVIORAL ECOLOGY AND SOCIOBIOLOGY LA English DT Article ID MOTHER-OFFSPRING CONFLICT; MACACA-MULATTA; BIRTH INTERVALS; VERVET MONKEYS; CAYO-SANTIAGO; FERTILITY; MACAQUES; BEHAVIOR; AGE; INVESTMENT AB We examined the hypothesis that among free-ranging rhesus monkeys (Macaca mulatta), maternal care patterns during estrus influence chances of conception independently of variation in the timing of the postpartum resumption of mating. We observed 24 multiparous mothers and their infants before and during the 1990 mating season. When mothers resumed mating, they abruptly sought less contact with their infants. Infants responded by increasing the rates with which they emitted distress calls and attempted to make nipple contact. High levels of maternal rejection and low levels of maternal nipple contact initiation during the mother's first estrus were associated with low suckling frequencies and high chances of conception. Although demanding infants had some success in gaining access to the nipples of reluctant mothers during estrus, mothers' chances of conception were unrelated to measures of infant demand or distress calling. Individual differences in maternal behavior regulating access to the nipple during estrus were unrelated to those shown previously. During estrus, mothers appeared to regulate nipple contact according to their infant's age and perhaps other factors related to its vulnerability. C1 NICHHD, COMPARAT ETHOL LAB, POOLESVILLE, MD 20837 USA. RP BERMAN, CM (reprint author), SUNY Buffalo, DEPT ANTHROPOL, BUFFALO, NY 14261 USA. NR 51 TC 19 Z9 19 U1 1 U2 4 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0340-5443 J9 BEHAV ECOL SOCIOBIOL JI Behav. Ecol. Sociobiol. PD JUN PY 1993 VL 32 IS 6 BP 391 EP 399 PG 9 WC Behavioral Sciences; Ecology; Zoology SC Behavioral Sciences; Environmental Sciences & Ecology; Zoology GA LJ908 UT WOS:A1993LJ90800005 ER PT J AU ROBINSON, JK CRAWLEY, JN AF ROBINSON, JK CRAWLEY, JN TI INTRAVENTRICULAR GALANIN IMPAIRS DELAYED-NONMATCHING-TO-SAMPLE PERFORMANCE IN RATS SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID CHOLINERGIC RECEPTOR BLOCKADE; CENTRAL NERVOUS-SYSTEM; BASAL FOREBRAIN COMPLEX; SHORT-TERM-MEMORY; ALZHEIMERS-DISEASE; NUCLEUS BASALIS; NEUROMODULATORY SYSTEMS; VENTRAL HIPPOCAMPUS; PLACE NAVIGATION; ORGANIC AMNESIA AB Galanin is a neuroactive peptide that coexists with acetylcholine in the basal forebrain region. Galanin inhibits cholinergic functions in vitro and in vivo and has been shown to impair performance in some memory tasks. The present study compared the effects of galanin with the effects of scopolamine (a muscarinic antagonist) and ketamine and MK-801 (both NMDA receptor antagonists) on performance of an operant, spatial, delayed nonmatching-to-sample task in rats. Choice accuracy was impaired in a dose-dependent but delay-independent manner by galanin, scopolamine, and MK-801 but was not systematically influenced by ketamine. Measures of session duration, trials completed, discrimination accuracy, perseveration, within-trial error distribution, and operant lever pressing were also analyzed. These results support observations that galanin disrupts performance in memory tasks requiring delayed responding but that the disruption is not specific to mnemonic capabilities. RP ROBINSON, JK (reprint author), NIMH,EXPTL THERAPEUT BRANCH,BEHAV NEUROPHARMACOL UNIT,BLDG 10,ROOM 4N214,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 89 TC 67 Z9 68 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7044 J9 BEHAV NEUROSCI JI Behav. Neurosci. PD JUN PY 1993 VL 107 IS 3 BP 458 EP 467 DI 10.1037/0735-7044.107.3.458 PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA LH023 UT WOS:A1993LH02300006 PM 7687133 ER PT J AU MICHIEL, D AF MICHIEL, D TI CHEMOKINES - THE MISSING LINK SO BIO-TECHNOLOGY LA English DT Editorial Material RP MICHIEL, D (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 0733-222X J9 BIO-TECHNOL JI Bio-Technology PD JUN PY 1993 VL 11 IS 6 BP 739 EP 739 DI 10.1038/nbt0693-739 PG 1 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA LE975 UT WOS:A1993LE97500027 PM 7763678 ER PT J AU THOMPSON, KS VINSON, CR FREIRE, E AF THOMPSON, KS VINSON, CR FREIRE, E TI THERMODYNAMIC CHARACTERIZATION OF THE STRUCTURAL STABILITY OF THE COILED-COIL REGION OF THE BZIP TRANSCRIPTION FACTOR GCN4 SO BIOCHEMISTRY LA English DT Note ID DNA-BINDING DOMAIN; LEUCINE ZIPPER; CALORIMETRIC DETERMINATION; PROTEINS; C/EBP; RECOGNITION; ENERGETICS; TRANSITION; EXCHANGE AB The thermal stability of a 56 amino acid fragment of GCN4 has been studied by high-sensitivity differential scanning calorimetry and circular dichroism spectroscopy. This fragment contains the leucine zipper and part of the basic region. The thermal unfolding of GCN4-56 is a reversible process and can be well represented by a reaction of the form N2 <-> 2U, indicating that the unfolding of the leuzine zipper is a two-state process in which the helices are only stable when they are in the coiled-coil conformation. As expected, the transition temperature is concentration dependent. At pH 7.06 and a protein concentration of 5 X 10(-4) M the transition temperature is close to 70-degrees-C while at 5 X 10(-6) M it is close to 50-degrees-C. The enthalpy change for unfolding is 31.5 kcal mol-1 at 70-degrees-C. Since the isolated helices are unstable, interactions at the interface between the two helices play a key role in the stabilization of the native dimer. These interactions primarily involve the burial of apolar surface from the solvent (hydrophobic effect) and electrostatic interactions. Structural thermodynamic calculations have permitted a dissection of the magnitude of the various contributions to the total Gibbs free energy of stabilization. C1 JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,CTR BIOCALORIMETRY,BALTIMORE,MD 21218. NCI,BIOCHEM LAB,BETHESDA,MD 20892. FU NCRR NIH HHS [RR04328] NR 34 TC 175 Z9 175 U1 2 U2 10 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JUN 1 PY 1993 VL 32 IS 21 BP 5491 EP 5496 DI 10.1021/bi00072a001 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF063 UT WOS:A1993LF06300001 PM 8504069 ER PT J AU POST, K GUO, JH KALMAN, E UCHIDA, T CROUCH, RJ LEVIN, JG AF POST, K GUO, JH KALMAN, E UCHIDA, T CROUCH, RJ LEVIN, JG TI A LARGE DELETION IN THE CONNECTION SUBDOMAIN OF MURINE LEUKEMIA-VIRUS REVERSE-TRANSCRIPTASE OR REPLACEMENT OF THE RNASE-H DOMAIN WITH ESCHERICHIA-COLI RNASE-H RESULTS IN ALTERED POLYMERASE AND RNASE-H ACTIVITIES SO BIOCHEMISTRY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; AVIAN-MYELOBLASTOSIS VIRUS; DEPENDENT DNA-POLYMERASE; HIV-1 RIBONUCLEASE-H; TUMOR-VIRUSES; MUTATIONAL ANALYSIS; ENDONUCLEASE; EXPRESSION; EXONUCLEASE; MECHANISM AB The functional relationship between the polymerase and RNase H domains of reverse transcriptase (RT) was investigated by studying the activities of AKR murine leukemia virus (MuLV) enzymes. In addition to the wild type, an RNase H-minus RT missing the entire RNase H domain and two other mutants having abnormal polymerase:RNase H ratios were expressed. These mutants include (i) a chimeric protein in which the MuLV RNase H domain was replaced by the entire Escherichia coli RNase H sequence and (ii) an RT with a 126 amino acid deletion in a region analogous to the ''connection'' subdomain in the p66 subunit of human immunodeficiency virus type 1 RT (Kohlstaedt, L. A., Wang, J., Friedman, J. M., Rice, P. A., & Steitz, T. A. (1992) Science 256, 1783-1790). With the wild-type RT, the major RNase H cleavage reaction was coordinated with DNA synthesis and occurred at a position corresponding to 15 nucleotides from the 3'-terminus of the DNA primer. Additional cleavages closer to the 5'-end of the RNA were explained in terms of a model relating binding of the RNA.DNA hybrid substrate and enzyme structure. The chimeric RT behaved like E. coli RNase H, exhibited 300-fold higher RNase H activity than wild-type RT, and was limited in its ability to synthesize DNA. Qualitative and quantitative changes in the polymerase and RNase H activities of the deletion mutant were also observed. The RNase H domain appeared to function independently of the polymerase domain, supporting the idea that the proper spatial relationship between the two active centers was disrupted by the mutation. Taken together, our results indicate that alteration of the normal polymerase:RNase H ratio can have profound effects on both polymerase and RNase H cleavage activities, as expected for an enzyme with two interdependent domains. C1 NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. MITSUBISHI KASEI INST LIFE SCI,MACHIDA,TOKYO 194,JAPAN. NR 59 TC 37 Z9 37 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JUN 1 PY 1993 VL 32 IS 21 BP 5508 EP 5517 DI 10.1021/bi00072a004 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF063 UT WOS:A1993LF06300004 PM 7684924 ER PT J AU SHER, T YI, HF MCBRIDE, OW GONZALEZ, FJ AF SHER, T YI, HF MCBRIDE, OW GONZALEZ, FJ TI CDNA CLONING, CHROMOSOMAL MAPPING, AND FUNCTIONAL-CHARACTERIZATION OF THE HUMAN PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR SO BIOCHEMISTRY LA English DT Article ID COA OXIDASE GENE; BETA-OXIDATION; MAMMALIAN-CELLS; HUMAN GENOME; RAT; LIVER; DNA; EXPRESSION; NAFENOPIN; MARMOSET AB The human peroxisome proliferator activated receptor (hPPAR) was cloned from a human liver cDNA library. The cDNA exhibited 85% and 91% DNA and deduced amino acid sequence identity with mouse PPAR (mPPAR), respectively. The hPPAR gene was mapped on human chromosome 22 slightly telomeric to a linkage group of six genes and genetic markers that are located in the general region 22q12q-q13.1. Cotransfection assays of mouse Hepa 1 cells were used to roughly compare the ability of hPPAR- and mPPAR-expressed cDNAs to trans-activate the acyl CoA oxidase (ACO) PPAR response element located 5' upstream to the minimal thymidine kinase promoter driving the expression of the chloramphenicol acetyl transferase (CAT) reporter gene. Both receptors elicited a response with the prototypical peroxisome proliferators nafenopin, clofibrate, and WY-14,643. Moreover, using cotransfection assays in which the CAT reporter plasmid contained the CYP4A6 gene response element rather than the ACO element, it was shown that hPPAR is capable of very efficently trans-activating a second PPAR response element. These results indicate that the PPAR is present in humans in a form that is functional and can trans-activate response elements derived from two different genes, the rat ACO and the rabbit CYP4A6. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. RP SHER, T (reprint author), NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 40 TC 399 Z9 404 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JUN 1 PY 1993 VL 32 IS 21 BP 5598 EP 5604 DI 10.1021/bi00072a015 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF063 UT WOS:A1993LF06300015 PM 7684926 ER PT J AU KWONG, CH MALECH, HL ROTROSEN, D LETO, TL AF KWONG, CH MALECH, HL ROTROSEN, D LETO, TL TI REGULATION OF THE HUMAN NEUTROPHIL NADPH OXIDASE BY RHO-RELATED G-PROTEINS SO BIOCHEMISTRY LA English DT Article ID CHRONIC GRANULOMATOUS-DISEASE; GTP-BINDING PROTEIN; CELL-FREE SYSTEM; CYTOSOLIC COMPONENT; MOLECULAR-CLONING; AMINO-ACIDS; ACTIVATION; RAS; PURIFICATION; MACROPHAGES AB Superoxide production by phagocytic white blood cells requires the assembly of an NADPH oxidase from membrane and cytosolic proteins. Recombinant cytosolic proteins p47phox and p67phox and neutrophil membranes were used to purify a third cytosolic component that is necessary and sufficient for cell-free reconstitution of NADPH oxidase. The component was isolated as a complex of rho-GDP dissociation inhibitor (rho-GDI) and two members of the rho subfamily of ras-related guanine nucleotide binding proteins, rac2 and CDC42Hs. Oxidase reconstitution with these pure cytosolic proteins was unaffected by GTPgammaS but was inhibited by GDPbetaS, suggesting that the active complex contained endogenous bound GTP. Direct binding of rho-GDI to the GTPgammaS-bound forms of these G-proteins was demonstrated by gel filtration following exchange with radiolabeled guanine nucleotide. rho-GDI was shown to be nonessential for cell-free oxidase reconstitution in experiments that compared the activities of pure recombinant forms of these G-proteins. Recombinant rac augmented superoxide production, while recombinant CDC42Hs, which shares 70% amino acid sequence identity with rac, did not. Three highly conserved regions of rac1 and rac2 were noted as markedly divergent in CDC42Hs. It is proposed that one or more of these regions of rac may be involved in the specific interaction of rac with the other NADPH oxidase protein(s). C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 38 TC 96 Z9 100 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JUN 1 PY 1993 VL 32 IS 21 BP 5711 EP 5717 DI 10.1021/bi00072a029 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF063 UT WOS:A1993LF06300029 PM 8504089 ER PT J AU SMITH, SS NEWMAN, JP EVANS, A PICKENS, R WYDEVEN, J UHL, GR NEWLIN, DB AF SMITH, SS NEWMAN, JP EVANS, A PICKENS, R WYDEVEN, J UHL, GR NEWLIN, DB TI COMORBID PSYCHOPATHY IS NOT ASSOCIATED WITH INCREASED D(2)-DOPAMINE RECEPTOR TAQI-A OR TAQI-B GENE MARKER FREQUENCIES IN INCARCERATED SUBSTANCE-ABUSERS SO BIOLOGICAL PSYCHIATRY LA English DT Note ID ANTISOCIAL PERSONALITY; SEVERE ALCOHOLISM; DRUG-ABUSE; DISORDERS; ALLELES; LOCUS C1 NIDA, ADDICT RES CTR, BALTIMORE, MD USA. OAKHILL CORRECT INST, OREGON, WI USA. RP SMITH, SS (reprint author), UNIV WISCONSIN, DEPT PSYCHOL, 1202 W JOHNSON ST, MADISON, WI 53706 USA. NR 28 TC 14 Z9 14 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 EI 1873-2402 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD JUN 1 PY 1993 VL 33 IS 11-12 BP 845 EP 848 DI 10.1016/0006-3223(93)90028-C PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LP448 UT WOS:A1993LP44800013 PM 8104042 ER PT J AU BAILER, AJ PORTIER, CJ AF BAILER, AJ PORTIER, CJ TI AN INDEX OF TUMORIGENIC POTENCY SO BIOMETRICS LA English DT Article DE CARCINOGENICITY; POTENCY ESTIMATION; TUMOR INCIDENCE ID ANIMAL CARCINOGENESIS EXPERIMENTS; CHRONOLOGICAL SUPPLEMENT; BIOASSAYS; DATABASE; MORTALITY; RANKING; HAZARDS; TESTS AB A new index of tumorigenic potency is derived using a survival-adjusted quantal response estimator given by Bailer and Portier (1988, Biometrics 44, 417-431). The small-sample bias and mean squared error properties of this estimator are explored using computer simulations of animal carcinogenicity experiments and are compared to the characteristics of the TD50, an estimator proposed by Sawyer et al. (1984, Biometrics 40, 27-40). It is observed that this new index tends to have smaller bias and mean squared error relative to the TD50 over varying shapes of the tumor onset distribution. levels of tumor lethality, and levels of treatment lethality. C1 NIEHS,STAT & BIOMATH BRANCH,RES TRIANGLE PK,NC 27709. RP BAILER, AJ (reprint author), MIAMI UNIV,DEPT MATH & STAT,OXFORD,OH 45056, USA. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 13 TC 6 Z9 6 U1 0 U2 2 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD JUN PY 1993 VL 49 IS 2 BP 357 EP 365 DI 10.2307/2532549 PG 9 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA LN254 UT WOS:A1993LN25400003 PM 8369372 ER PT J AU BAKER, SG WAX, Y PATTERSON, BH AF BAKER, SG WAX, Y PATTERSON, BH TI REGRESSION-ANALYSIS OF GROUPED SURVIVAL-DATA - INFORMATIVE CENSORING AND DOUBLE SAMPLING SO BIOMETRICS LA English DT Article DE COMPETING RISKS; DEPENDENT CENSORING; EM ALGORITHM; LOGISTIC REGRESSION ID COMPETING RISKS; MODEL; VARIABLES AB To analyze grouped survival data subject to informative censoring, we propose the following two-part model: a logistic regression model for the hazard tor failure, given covariates, and a logistic regression model for the hazard for informative censoring. given time of failure and covariates. We fit the model to survival data arising from a double sampling design: In a full follow-up (FF) sample subjects are followed after censoring, and in a partial follow-up (PF) sample subjects are not followed after censoring. We illustrate the methodology using data from a study of wound infection in which patients in the PF sample are censored by release from the hospital, whereas patients in the FF sample are followed after hospital release. We discuss identifiability when there is only a PF sample. We also consider how the allocation between the PF and FF samples affects the precision of estimates. C1 HEBREW UNIV JERUSALEM,DEPT STAT,IL-91905 JERUSALEM,ISRAEL. RP BAKER, SG (reprint author), NCI,EPN 344,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 30 TC 24 Z9 24 U1 0 U2 2 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD JUN PY 1993 VL 49 IS 2 BP 379 EP 389 DI 10.2307/2532551 PG 11 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA LN254 UT WOS:A1993LN25400005 PM 8369374 ER PT J AU DINSE, GE AF DINSE, GE TI EVALUATING CONSTRAINTS THAT ALLOW SURVIVAL-ADJUSTED INCIDENCE ANALYSES IN SINGLE-SACRIFICE STUDIES SO BIOMETRICS LA English DT Article DE ANIMAL EXPERIMENT; CARCINOGENESIS BIOASSAY; CONSTANT RISK DIFFERENCE; CONSTANT RISK RATIO; ED(01) STUDY; INCIDENCE; LETHALITY; OCCULT TUMOR; SACRIFICE; SURVIVAL ID ANIMAL TUMORIGENICITY DATA; ED01 AB Ideally, analyses of tumor incidence data from long-term animal experiments should allow the incidence rates to vary with age, without restricting tumor lethality, without requiring data on cause of death, and without assuming independence of competing risks. This article focuses on nonparametric methods that not only satisfy these conditions. but also accommodate studies having just one sacrifice time, by constraining the effects of age on one of the three functions used to characterize the likelihood. Several constrained analyses were evaluated using data on over 18,000 mice from the ED01 study. Of the five constraints considered. only the assumption of constant differences between the death rates for animals with and without the tumor of interest produced reasonable results across a wide range of tumor lethalities. RP DINSE, GE (reprint author), NIEHS,STAT & BIOMATH BRANCH,A3-03,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 10 TC 12 Z9 12 U1 0 U2 1 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD JUN PY 1993 VL 49 IS 2 BP 399 EP 407 DI 10.2307/2532553 PG 9 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA LN254 UT WOS:A1993LN25400007 PM 8369376 ER PT J AU RUSSEKCOHEN, E SIMON, RM AF RUSSEKCOHEN, E SIMON, RM TI QUALITATIVE INTERACTIONS IN MULTIFACTOR STUDIES SO BIOMETRICS LA English DT Article DE ANALYSIS OF VARIANCE; CLINICAL TRIALS; CROSSOVER INTERACTION; LINEAR MODELS ID LINEAR INEQUALITIES; TESTS; HYPOTHESES AB In clinical trials qualitative interaction or crossover interaction is said to occur when one treatment is superior for some sets of patients and the alternative treatment is superior for other subsets. Here we propose a definition of no qualitative interaction with respect to a single continuous covariate which implies that one treatment is superior to the other treatment over a prespecified range of the covariate. Further, in studies involving patients cross-classified by two or more prognostic factors, we define a marginal qualitative interaction with respect to a treatment factor and a prognostic factor by averaging in some sense over the remaining prognostic factors. In some situations, the methodology of Gail and Simon (1985, Biometrics 41, 361-372) is shown to be appropriate. Their procedure assumes independent estimates of treatment effect for each subset of patients and this may not be appropriate for the generalizations we propose. Therefore, we generalize the procedure of Gail and Simon to the case of two correlated estimates of treatment effect, providing a table of critical values. Results for one-sided tests for the case of J correlated estimates are also obtained. We also present an example illustrating our procedure. C1 NCI,BIOMETR RES BRANCH,BETHESDA,MD 20892. RP RUSSEKCOHEN, E (reprint author), UNIV MARYLAND,DEPT ANIM SCI,COLL PK,MD 20742, USA. NR 18 TC 10 Z9 10 U1 0 U2 2 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD JUN PY 1993 VL 49 IS 2 BP 467 EP 477 DI 10.2307/2532559 PG 11 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA LN254 UT WOS:A1993LN25400013 PM 8369382 ER PT J AU PARK, T DAVIS, CS AF PARK, T DAVIS, CS TI A TEST OF THE MISSING DATA MECHANISM FOR REPEATED CATEGORICAL-DATA SO BIOMETRICS LA English DT Article DE LONGITUDINAL DATA; MISSING DATA; REPEATED MEASURES DESIGN; WALD TEST STATISTIC; WEIGHTED LEAST SQUARES ID GENERALIZED LINEAR-MODELS; LONGITUDINAL DATA AB Due to the occurrence of missing observations, longitudinal data are rarely balanced and complete. Weighted least squares analyses described by Grizzle, Starmer, and Koch (1969, Biometrics 25, 489-504) have been developed for the analysis of incomplete longitudinal categorical data [Stanish, Gillings, and Koch (1978, Biometrics 34, 305-317); Woolson and Clarke (1984. Journal of the Royal Statistical Society, Series A 147, 87-99)]. However, all these analyses have assumed that missing observations are missing completely at random in the sense of Rubin (1976. Biometrika 63, 581-592). When the occurrence of missing observations is related to the unobserved response values, these analyses may result in biased results. In this paper, we develop a simple and practical test of the missing mechanism in incomplete repeated categorical data. The proposed test is an extension of the test of Little (1988, Journal of the American Statistical Association 83, 1198-1202) and uses a test criterion given in general form by Wald. The test is illustrated using data from a longitudinal investigation of obesity in school-age children. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BIOMETRY & MATH STAT BRANCH,BETHESDA,MD 20892. UNIV IOWA,DEPT PREVENT MED & ENVIRONM HLTH,IOWA CITY,IA 52242. FU NIMH NIH HHS [MH46011] NR 16 TC 20 Z9 21 U1 0 U2 3 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD JUN PY 1993 VL 49 IS 2 BP 631 EP 638 DI 10.2307/2532576 PG 8 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA LN254 UT WOS:A1993LN25400030 PM 8369395 ER PT J AU WEINBERG, CR WACHOLDER, S AF WEINBERG, CR WACHOLDER, S TI PROSPECTIVE ANALYSIS OF CASE-CONTROL DATA UNDER GENERAL MULTIPLICATIVE-INTERCEPT RISK MODELS SO BIOMETRIKA LA English DT Article DE CASE-CONTROL STUDY; CHOICE-BASED SAMPLING; COHORT STUDY; EPIDEMIOLOGY; EXPECTATION-MAXIMIZATION, EM ALGORITHM; RETROSPECTIVE STUDY ID EM ALGORITHM AB We show that, under a general multiplicative-intercept model for risk, case-control data can be analyzed by maximum likelihood as if they had arisen prospectively, up to an unidentifiable multiplicative constant which depends on the relative sampling fractions. This generalizes earlier work of Anderson (1972, 1979), by showing that not only the point estimates but also the standard errors based on the observed information matrix are correct when the prospective likelihood is maximized. Likelihood ratio testing is also valid under this broad class of risk models. Data on disease status from a much larger cohort are shown to add no information to the estimation of the covariate-related parameters. C1 NCI,ROCKVILLE,MD 20852. RP WEINBERG, CR (reprint author), NIEHS,STAT & BIOMATH BRANCH,MD A3-03,PO 12233,RES TRIANGLE PK,NC 27709, USA. NR 10 TC 50 Z9 50 U1 1 U2 5 PU BIOMETRIKA TRUST PI LONDON PA UNIV COLLEGE LONDON GOWER ST-BIOMETRIKA OFFICE, LONDON, ENGLAND WC1E 6BT SN 0006-3444 J9 BIOMETRIKA JI Biometrika PD JUN PY 1993 VL 80 IS 2 BP 461 EP 465 DI 10.1093/biomet/80.2.461 PG 5 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA LZ065 UT WOS:A1993LZ06500020 ER PT J AU KOVACS, T PABUCCUOGLU, A LESIAK, K TORRENCE, PF AF KOVACS, T PABUCCUOGLU, A LESIAK, K TORRENCE, PF TI FLUORODEOXY SUGAR ANALOGS OF 2',5'-OLIGOADENYLATES AS PROBES OF HYDROGEN-BONDING IN ENZYMES OF THE 2-5A SYSTEM SO BIOORGANIC CHEMISTRY LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; BIOLOGICAL-ACTIVITY; PROTEIN-SYNTHESIS; 2',5'-PHOSPHODIESTERASE ACTIVITY; OLIGONUCLEOTIDE SUBSTRATE; GLYCOGEN-PHOSPHORYLASE; PENULTIMATE POSITION; 2-5A-DEPENDENT RNASE; MONOCLONAL-ANTIBODY; CORDYCEPIN ANALOGS C1 NIDDKD,MED CHEM LAB,BIOMED CHEM SECT,BLDG 8,ROOM B2A02,BETHESDA,MD 20892. NR 69 TC 25 Z9 25 U1 2 U2 10 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0045-2068 J9 BIOORG CHEM JI Bioorganic Chem. PD JUN PY 1993 VL 21 IS 2 BP 192 EP 208 DI 10.1006/bioo.1993.1017 PG 17 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA LJ286 UT WOS:A1993LJ28600004 ER PT J AU LEE, JW MARQUEZ, VE LEWIN, NE KAZANIETZ, MG BAHADOR, A BLUMBERG, PM AF LEE, JW MARQUEZ, VE LEWIN, NE KAZANIETZ, MG BAHADOR, A BLUMBERG, PM TI CONFORMATIONALLY CONSTRAINED ANALOGS OF DIACYLGLYCEROL (DAG) .3. INTERACTION OF ALPHA-ALKYL-GAMMA-LACTONES WITH PROTEIN-KINASE-C (PK-C) SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID TUMOR PROMOTERS; ACTIVATION AB Enantiomeric 2-Alkyl-3-O-acyl-gamma-lactones designed as rigid analogues of 1,2-diacylglycerol (DAG) were synthesized and evaluated as inhibitors of [20-H-3]-phorbol-12,13-dibutyrate binding to protein kinase C (PK-C). The most potent compound (2c) displayed a binding affinity below 1 muM and, consistent with a DAG binding mode, activity was associated with only one enantiomeric form. C1 NCI, DIV CANC TREATMENT, DEV THERAPEUT PROGRAM, MED CHEM LAB, BETHESDA, MD 20892 USA. NCI, CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB, BETHESDA, MD 20892 USA. NR 13 TC 12 Z9 12 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0960-894X EI 1464-3405 J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD JUN PY 1993 VL 3 IS 6 BP 1101 EP 1106 DI 10.1016/S0960-894X(00)80295-4 PG 6 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA LH321 UT WOS:A1993LH32100024 ER PT J AU LEE, J MARQUEZ, VE LEWIN, NE BAHADOR, A KAZANIETZ, MG BLUMBERG, PM AF LEE, J MARQUEZ, VE LEWIN, NE BAHADOR, A KAZANIETZ, MG BLUMBERG, PM TI CONFORMATIONALLY CONSTRAINED ANALOGS OF DIACYLGLYCEROL (DAG) .4. INTERACTION OF ALPHA-ALKYLIDENE-GAMMA-LACTONES WITH PROTEIN-KINASE-C (PK-C) SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article AB Isomeric alpha-alkylidene-gamma-lactones with a C-14 chain were synthesized and evaluated as inhibitors of phorbol ester binding to protein kinase C (PK-C). While the Z-isomer 3 was the most potent inhibitor (K(i) = 0.2 muM), the stereochemistry at the alpha-position of the lactone appears to have only a modest effect in modulating PK-C binding. The same appears to be true for both isomeric alpha-alkyl-gamma-lactones which were obtained by catalytic hydrogenation of the unsaturated lactones. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NR 5 TC 10 Z9 10 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD JUN PY 1993 VL 3 IS 6 BP 1107 EP 1110 DI 10.1016/S0960-894X(00)80296-6 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA LH321 UT WOS:A1993LH32100025 ER PT J AU SMOLEN, P RINZEL, J SHERMAN, A AF SMOLEN, P RINZEL, J SHERMAN, A TI WHY PANCREATIC-ISLETS BURST BUT SINGLE BETA-CELLS DO NOT - THE HETEROGENEITY HYPOTHESIS SO BIOPHYSICAL JOURNAL LA English DT Article ID INDUCED ELECTRICAL-ACTIVITY; B-CELLS; INSULIN RELEASE; GLUCOSE; MOUSE; OSCILLATIONS; CHANNEL; CURRENTS; CALCIUM; CLUSTERS AB Previous mathematical modeling of beta cell electrical activity has involved single cells or, recently, clusters of identical cells. Here we model clusters of heterogeneous cells that differ in size, channel density, and other parameters. We use gap-junctional electrical coupling, with conductances determined by an experimental histogram. We find that, for reasonable parameter distributions, only a small proportion of isolated beta cells will burst when uncoupled, at any given value of a glucose-sensing parameter. However, a coupled, heterogeneous cluster of such cells, if sufficiently large (approximately 125 cells), will burst synchronously. Small clusters of such cells will burst only with low probability. In large clusters, the dynamics of intracellular calcium compare well with experiments. Also, these clusters possess a dose-response curve of increasing average electrical activity with respect to a glucose-sensing parameter that is sharp when the cluster is coupled, but shallow when the cluster is decoupled into individual cells. This is in agreement with comparative experiments on cells in suspension and islets. RP SMOLEN, P (reprint author), NIDDKD,MATH RES BRANCH,BETHESDA,MD 20892, USA. NR 37 TC 105 Z9 105 U1 0 U2 5 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JUN PY 1993 VL 64 IS 6 BP 1668 EP 1680 PG 13 WC Biophysics SC Biophysics GA LJ216 UT WOS:A1993LJ21600005 PM 8369400 ER PT J AU ZHOU, HX AF ZHOU, HX TI BROWNIAN DYNAMICS STUDY OF THE INFLUENCES OF ELECTROSTATIC INTERACTION AND DIFFUSION ON PROTEIN-PROTEIN ASSOCIATION KINETICS SO BIOPHYSICAL JOURNAL LA English DT Article ID CYTOCHROME-C PEROXIDASE; NON-SIMPLE MOLECULES; ORIENTATION CONSTRAINTS; GENERAL THEORY; SIMULATION AB A unified model is presented for protein-protein association processes that are under the influences of electrostatic interaction and diffusion (e.g., protein oligomerization, enzyme catalysis, electron and energy transfer). The proteins are modeled as spheres that bear point charges and undergo translational and rotational Brownian motion. Before association can occur the two spheres have to be aligned properly to form a reaction complex via diffusion. The reaction complex can either go on to form the product or it can dissociate into the separate reactants through diffusion. The electrostatic interaction, like diffusion, influences every step except the one that brings the reaction complex into the product. The interaction potential is obtained by extending the Kirkwood-Tanford protein model (Tanford, C., and J. G. Kirkwood. 1957. J. Am. Chem. Soc. 79:5333-5339) to two charge-embedded spheres and solving the consequent equations under a particular basis set. The time-dependent association rate coefficient is then obtained through Brownian dynamics simulations according an algorithm developed earlier (Zhou, H.-X. 1990. J. Phys. Chem. 94:8794-8800). This method is applied to a model system of the cytochrome c and cytochrome c peroxidase association process and the results confirm the experimental dependence of the association rate constant on the solution ionic strength. An important conclusion drawn from this study is that when the product is formed by very specific alignment of the reactants, as is often the case, the effect of the interaction potential is simply to scale the association rate constant by a Boltzmann factor. This explains why mutations in the interface of the reaction complex have strong influences on the association rate constant whereas those away from the interface have minimal effects. It comes about because the former mutations change the interaction potential of the reaction complex significantly and the latter ones do not. RP ZHOU, HX (reprint author), NIDDKD,BETHESDA,MD 20892, USA. RI Zhou, Huan-Xiang/M-5170-2016 OI Zhou, Huan-Xiang/0000-0001-9020-0302 NR 44 TC 105 Z9 105 U1 0 U2 14 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JUN PY 1993 VL 64 IS 6 BP 1711 EP 1726 PG 16 WC Biophysics SC Biophysics GA LJ216 UT WOS:A1993LJ21600009 PM 8396447 ER PT J AU JOSHI, A JEANG, KT AF JOSHI, A JEANG, KT TI REDUCTION IN GROWTH TEMPERATURE MINIMIZES INSTABILITY OF LARGE PLASMIDS CONTAINING HIV-1 PROVIRAL GENOMES SO BIOTECHNIQUES LA English DT Note C1 NIAID,MOLEC MICROBIOL LAB,BLDG 4,ROOM 306,BETHESDA,MD 20892. RI Jeang, Kuan-Teh/A-2424-2008 NR 4 TC 9 Z9 9 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD JUN PY 1993 VL 14 IS 6 BP 880 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LF326 UT WOS:A1993LF32600002 PM 8333948 ER PT J AU DEBATIN, KM GOLDMAN, CK WALDMANN, TA KRAMMER, PH AF DEBATIN, KM GOLDMAN, CK WALDMANN, TA KRAMMER, PH TI APO-1-INDUCED APOPTOSIS OF LEUKEMIA-CELLS FROM PATIENTS WITH ADULT T-CELL LEUKEMIA SO BLOOD LA English DT Article ID MONOCLONAL-ANTIBODY; INTERLEUKIN-2 RECEPTOR; CLONAL ELIMINATION; LYMPHOMA VIRUS; DEATH; MECHANISM; SELECTION; THERAPY; TAC C1 UNIV HEIDELBERG,CHILDRENS HOSP,ONCOL IMMUNOL SECT,W-6900 HEIDELBERG,GERMANY. NCI,METAB BRANCH,BETHESDA,MD 20892. RP DEBATIN, KM (reprint author), GERMAN CANC RES CTR,DIV IMMUNOGENET,NEUENHEIMERFELD 280,W-6900 HEIDELBERG,GERMANY. RI Debatin, Klaus-Michael/J-9704-2014 OI Debatin, Klaus-Michael/0000-0002-8397-1886 NR 32 TC 138 Z9 140 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD JUN 1 PY 1993 VL 81 IS 11 BP 2972 EP 2977 PG 6 WC Hematology SC Hematology GA LF065 UT WOS:A1993LF06500018 PM 7684622 ER PT J AU BRASILNETO, JP VALLSSOLE, J PASCUALLEONE, A CAMMAROTA, A AMASSIAN, VE CRACCO, R MACCABEE, P CRACCO, J HALLETT, M COHEN, LG AF BRASILNETO, JP VALLSSOLE, J PASCUALLEONE, A CAMMAROTA, A AMASSIAN, VE CRACCO, R MACCABEE, P CRACCO, J HALLETT, M COHEN, LG TI RAPID MODULATION OF HUMAN CORTICAL MOTOR OUTPUTS FOLLOWING ISCHEMIC NERVE BLOCK SO BRAIN LA English DT Article ID MAGNETIC BRAIN-STIMULATION; SPINAL-CORD INJURY; COIL STIMULATION; CORTEX; REORGANIZATION; PATHWAYS; CONNECTIONS; PLASTICITY; LESIONS; MUSCLES AB The amplitudes of motor evoked potentials to transcranial magnetic stimulation from muscles immediately proximal to a temporarily anaesthetized (Bier's block) human forearm increase in minutes after the onset of anaesthesia and return to control values after the anaesthesia subsides. In order to determine the level at which the early modulation of human motor outputs takes place, we recorded maximal H reflexes, peripheral M responses, motor evoked potentials to transcranial magnetic stimulation, and motor evoked potentials to transcranial electrical stimulation and spinal electrical stimulation from a muscle immediately proximal to a limb segment made ischaemic by a pneumatic tourniquet. The amplitudes of motor evoked potentials to transcranial magnetic stimulation, but not to transcranial electrical stimulation and spinal electrical stimulation, were larger during ischaemia, implying that the site of change was in the motor cortex. The maximal H/M ratios were unaffected by ischaemia, indicating that alpha-motor neuron excitability to segmental la inputs remained unchanged. The map of cortical representation areas for this muscle obtained with transcranial magnetic stimulation was also enlarged. Taken together, our findings suggest that the temporary removal by ischaemic nerve block of myelinated afferent inputs reduces inhibition at the motor cortical level and that this disinhibition is responsible for the increased excitability of the corticospinal system. C1 NINCDS, MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT, HUMAN CORT PHYSIOL UNIT,BLDG 10, BETHESDA, MD 20892 USA. SUNY HLTH SCI CTR, DEPT PHYSIOL, BROOKLYN, NY USA. SUNY HLTH SCI CTR, DEPT NEUROL, BROOKLYN, NY USA. RI Pascual-Leone, Alvaro/G-6566-2011; Brasil-Neto, Joaquim/A-1171-2009 NR 36 TC 244 Z9 247 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0006-8950 J9 BRAIN JI Brain PD JUN PY 1993 VL 116 BP 511 EP 525 DI 10.1093/brain/116.3.511 PN 3 PG 15 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA LK837 UT WOS:A1993LK83700002 PM 8513390 ER PT J AU MILLAR, DB THOMAS, JR PACHECO, ND ROLLWAGEN, FM AF MILLAR, DB THOMAS, JR PACHECO, ND ROLLWAGEN, FM TI NATURAL-KILLER-CELL CYTOTOXICITY AND T-CELL PROLIFERATION IS ENHANCED BY AVOIDANCE-BEHAVIOR SO BRAIN BEHAVIOR AND IMMUNITY LA English DT Article ID LYMPHOCYTE-PROLIFERATION; IMMUNE-RESPONSE; INDUCED MODULATION; PERIPHERAL-BLOOD; BETA-ENDORPHIN; TUMOR-GROWTH; STRESS; SYSTEM; RATS; SUPPRESSION C1 NIMH,CTR NEUROSCI,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. USN,MED RES INST,ENTER DIS PROGRAM,BETHESDA,MD 20889. RP MILLAR, DB (reprint author), USN,MED RES INST,THERMAL STRESS PROGRAM,MS-11,BETHESDA,MD 20889, USA. NR 48 TC 23 Z9 23 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0889-1591 J9 BRAIN BEHAV IMMUN JI Brain Behav. Immun. PD JUN PY 1993 VL 7 IS 2 BP 144 EP 153 DI 10.1006/brbi.1993.1016 PG 10 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA LJ034 UT WOS:A1993LJ03400004 PM 8347896 ER PT J AU SAVAGE, PJ SAAD, MF AF SAVAGE, PJ SAAD, MF TI INSULIN AND ATHEROSCLEROSIS - VILLAIN, ACCOMPLICE, OR INNOCENT BYSTANDER SO BRITISH HEART JOURNAL LA English DT Editorial Material ID BLOOD-PRESSURE; RISK-FACTORS; CARDIOVASCULAR-DISEASE; GLUCOSE-TOLERANCE; HEART-DISEASE; RESISTANCE; HYPERTENSION; OBESITY; HYPERINSULINEMIA; MORTALITY C1 UNIV SO CALIF,SCH MED,DEPT MED,DIV DIABET,LOS ANGELES,CA 90033. RP SAVAGE, PJ (reprint author), NHLBI,DIV CLIN APPLICAT,EPIDEMIOL & BIOMETRY PROGRAM,BETHESDA,MD 20892, USA. NR 41 TC 23 Z9 23 U1 1 U2 1 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-0769 J9 BRIT HEART J JI Br. Heart J. PD JUN PY 1993 VL 69 IS 6 BP 473 EP 475 PG 3 WC Cardiac & Cardiovascular Systems; History & Philosophy Of Science SC Cardiovascular System & Cardiology; History & Philosophy of Science GA LG264 UT WOS:A1993LG26400001 PM 8343309 ER PT J AU BOUZAS, EA FREIDLIN, V PARRY, DM ELDRIDGE, R KAISERKUPFER, MI AF BOUZAS, EA FREIDLIN, V PARRY, DM ELDRIDGE, R KAISERKUPFER, MI TI LENS OPACITIES IN NEUROFIBROMATOSIS-2 - FURTHER SIGNIFICANT CORRELATIONS SO BRITISH JOURNAL OF OPHTHALMOLOGY LA English DT Article ID LISCH NODULES; TYPE-2; ASSOCIATION; HAMARTOMA AB This prospective study of 96 individuals from 29 families with neurofibromatosis 2, 49 of whom were affected, confirms in an extended series the previously reported association between posterior subcapsular/capsular cataract and neurofibromatosis 2. Posterior subcapsular/capsular cataracts were found in 36 (80%) of the 45 affected individuals (four individuals were excluded from statistical analyses). In addition, the association of peripheral cortical lens opacities with neurofibromatosis 2 was found to be statistically significant. Seventeen of the patients with neurofibromatosis 2 (37.8%) had peripheral cortical cataracts in comparison with none of the unaffected family members (p<0.0001). In three patients peripheral cortical opacities were present despite the absence of posterior subcapsular/capsular cataracts. These findings support the inclusion of cortical cataracts of early onset, in addition to posterior subcapsular/capsular cataracts, in the diagnostic criteria of neurofibromatosis 2. C1 NEI,NIH 10-1ON226,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NINCDS,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 15 TC 32 Z9 32 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-1161 J9 BRIT J OPHTHALMOL JI Br. J. Ophthalmol. PD JUN PY 1993 VL 77 IS 6 BP 354 EP 357 DI 10.1136/bjo.77.6.354 PG 4 WC Ophthalmology SC Ophthalmology GA LF501 UT WOS:A1993LF50100008 PM 8318482 ER PT J AU ALDAMLUJI, S KRSMANOVIC, LZ CATT, KJ AF ALDAMLUJI, S KRSMANOVIC, LZ CATT, KJ TI HIGH-AFFINITY UPTAKE OF NORADRENALINE IN POSTSYNAPTIC NEURONS SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE CATECHOLAMINES; NORADRENALINE; UPTAKE; AMINE TRANSPORT; POSTSYNAPTIC NEURONS ID CORTICOTROPIN-RELEASING-FACTOR; VASCULAR SMOOTH-MUSCLE; ISOLATED RAT-HEART; PARAVENTRICULAR NUCLEUS; HYPOTHALAMIC NEURONS; METHODOLOGICAL CONSIDERATIONS; ALPHA-1-ADRENERGIC RECEPTOR; VASOPRESSIN NEURONS; MOLECULAR-CLONING; SUPRAOPTIC NUCLEI AB 1 Neurotransmitters released from nerve endings are inactivated by re-uptake into the presynaptic nerve terminals and possibly into neighbouring glial cells. While analysing the functional properties of alpha1-adrenoceptors in the hypothalamus, we observed a high-affinity uptake process for noradrenaline in postsynaptic peptidergic neurones. 2 In primary hypothalamic cell cultures and in a hypothalamic neuronal cell line, [H-3]-prazosin bound with high affinity and was displaced by unlabelled prazosin in concentrations of 10(-10) to 10(-7) M. However, at concentrations of unlabelled prazosin above 10(-7) M, there was a paradoxical increase in apparent [H-3]-prazosin binding. 3 Methoxamine, an alpha1-adrenoceptor ligand that is not subject to significant neuronal uptake, displaced [H-3]-prazosin but did not cause the paradoxical increase in the apparent binding of [H-3]-prazosin. Cooling the cells to 4-degrees-C reduced the total amount of prazosin associated with the cells; under these conditions, methoxamine almost completely inhibited [H-3]-prazosin binding to the cells. 4 In the presence of desipramine (DMI), unlabelled prazosin displaced [H-3]-prazosin as before, but no paradoxical increase in apparent binding was seen above 10(-7) M. 5 The paradoxical increase of [H-3]-prazosin binding was not observed in membrane preparations of hypothalamic neurones. These findings indicated that the paradoxical increase in apparent [H-3]-prazosin binding was due to a cellular uptake process that becomes evident at high concentrations of the ligand. 6 DMI (10(-5) M) had no effect on the specific binding of [H-3]-prazosin. The presence of alpha1-adrenoceptors was confirmed by binding of [I-125]-HEAT, but [H-3]-idazoxan (an alpha2- ligand) did not bind to the cells. 7 The uptake of prazosin obeyed the Michaelis-Menten model, with similar K(m) and V(max) values in both types of cultures. 8 Noradrenaline was taken up with high affinity by both types of cultures. (+/-)-[H-3]-noradrenaline uptake was reduced by DMI and by excluding sodium from the medium, indicating that this process has some of the properties of uptake1. (+/-)-[H-3]-noradrenaline uptake in the cell line was unaffected by testosterone. 9 The measured uptake of (-)-noradrenaline in the cell line was considerably increased by blockade of catechol-O-methyl-transferase and monoamine oxidase, suggesting that (-)-noradrenaline is metabolized to lipophilic products that escape across the plasma membrane. 10 Studies in rats, in which the noradrenaline isomer 6-hydroxydopamine was used, suggested that the postsynaptic uptake process is operative in hypothalamic CRH and vasopressin neurones in vivo. 11 The K(m) for (-)-noradrenaline was within the range for the high affinity uptake1 process in noradrenergic neurones. Uptake takes place in concentrations at which noradrenaline activates alpha1-adrenoceptors. Removal of noradrenaline from the vicinity of the receptors may prevent desensitization, thus maintaining the responsiveness of postsynaptic neurones to the actions of the neurotransmitter. RP ALDAMLUJI, S (reprint author), NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLD 10,ROOM 5N214,BETHESDA,MD 20892, USA. NR 58 TC 21 Z9 21 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD JUN PY 1993 VL 109 IS 2 BP 299 EP 307 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LE287 UT WOS:A1993LE28700005 PM 8358534 ER PT J AU CHIKANZA, IC PETROU, P CHROUSOS, G KINGSLEY, G PANAYI, GS AF CHIKANZA, IC PETROU, P CHROUSOS, G KINGSLEY, G PANAYI, GS TI EXCESSIVE AND DYSREGULATED SECRETION OF PROLACTIN IN RHEUMATOID-ARTHRITIS - IMMUNOPATHOGENETIC AND THERAPEUTIC IMPLICATIONS SO BRITISH JOURNAL OF RHEUMATOLOGY LA English DT Article DE CHRONIC OSTEOMYELITIS; DIURNAL RHYTHM; SURGERY; INFLAMMATION ID PITUITARY-HORMONES; LYMPHOCYTE-T; DISEASE; RATS; BROMOCRIPTINE; CYCLOSPORINE; ACTIVATION; RECEPTORS; BINDING C1 UNITED MED & DENT SCH GUYS & ST THOMAS HOSP,DIV MED,RHEUMATOL UNIT,GUYS CAMPUS,ST THOMAS ST,LONDON SE1 9RT,ENGLAND. ORSZAGOS REUMA,FIZIOTERAPIAS INT,BUDAPEST,HUNGARY. NICHHD,BETHESDA,MD 20892. NR 31 TC 78 Z9 78 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0263-7103 J9 BRIT J RHEUMATOL JI Br. J. Rheumatol. PD JUN PY 1993 VL 32 IS 6 BP 445 EP 448 PG 4 WC Rheumatology SC Rheumatology GA LF190 UT WOS:A1993LF19000003 PM 8508278 ER PT J AU ZHENG, W SHU, XO MCLAUGHLIN, JK CHOW, WH GAO, YT BLOT, WJ AF ZHENG, W SHU, XO MCLAUGHLIN, JK CHOW, WH GAO, YT BLOT, WJ TI OCCUPATIONAL PHYSICAL-ACTIVITY AND THE INCIDENCE OF CANCER OF THE BREAST, CORPUS UTERI, AND OVARY IN SHANGHAI SO CANCER LA English DT Article DE BREAST CANCER; ENDOMETRIAL CANCER; PHYSICAL ACTIVITY; OCCUPATION; OVARIAN CANCER ID ENDOMETRIAL CANCER; COLORECTAL-CANCER; DIETARY FACTORS; COLON CANCER; EPIDEMIOLOGY; RISK; EXERCISE; SUBSITE AB Background. A sedentary life style has been consistently associated with an increased risk of colon cancer, but the evidence for its association with breast and other gynecologic cancers is limited. Methods. Occupational information for 3783 incident patients with cancer (breast, 2736; corpus uteri, 452; and ovary, 595) whose disease was diagnosed during the period 1980-1984 was compared with 1982 census data on employment in Shanghai urban areas. The standardized incidence ratios (SIR) of these cancers were estimated for each occupational group classified by job titles and physical activity levels. Results. A significantly increased incidence of breast cancer was found among professionals (SIR = 158), government officials (SIR = 131), and clerical workers (SIR = 143); the incidence was reduced among service workers (SIR = 87) and craftsmen (SIR = 91). Occupational physical activity, as measured by sitting time and energy expenditure, was inversely related to breast cancer incidence, with SIR of 127-131 for inactive jobs (sedentary or low-energy expenditure) and 79-93 for active jobs (long periods of standing or high energy expenditure). Similar associations, although to a lesser extent, were also seen for cancer of the corpus uteri and ovary. Conclusions. Women with low physical activity occupations had an increased incidence of cancer of the breast, corpus uteri, and ovary; the incidence was reduced among women with high-activity jobs. These findings were consistent with observations from earlier studies and provided further evidence that physical activity may lower the risk of these female hormone-dependent cancers. C1 SHANGHAI CANC INST,DEPT EPIDEMIOL,SHANGHAI,PEOPLES R CHINA. NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. NR 25 TC 112 Z9 114 U1 2 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JUN 1 PY 1993 VL 71 IS 11 BP 3620 EP 3624 DI 10.1002/1097-0142(19930601)71:11<3620::AID-CNCR2820711125>3.0.CO;2-S PG 5 WC Oncology SC Oncology GA LE419 UT WOS:A1993LE41900024 PM 8490910 ER PT J AU DOLAN, ME PEGG, AE BISER, ND MOSCHEL, RC ENGLISH, HF AF DOLAN, ME PEGG, AE BISER, ND MOSCHEL, RC ENGLISH, HF TI EFFECT OF O6-BENZYLGUANINE ON THE RESPONSE TO 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA IN THE DUNNING-R3327G MODEL OF PROSTATIC-CANCER SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article ID MAMMALIAN O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE; ALKYLATING-AGENTS; CROSS-LINKING; HUMAN-CELLS; DNA; TUMOR; SENSITIVITY; PROTEIN; N-METHYL-N'-NITRO-N-NITROSOGUANIDINE; CHLOROETHYLNITROSOUREA AB The DNA-repair protein O6-alkylguanine-DNA alkyltransferase is known to protect tumor cells from the antitumor effects of carmustine (BCNU). This repair protein was inactivated in Copenhagen rat prostate tumors by treatment with O6-benzylguanine in attempts to increase the effectiveness of BCNU therapy. The alkyltransferase activity in the liver, kidney, lung, and prostate of Copenhagen rats was 66, 37, 65, and 122 fmol/mg protein, respectively. The activity in the Dunning R3327G rat prostate tumor was found to be 129 and 126 fmol/mg protein from intact and castrated animals, respectively. The level of this protein remained low in the tissues and tumors of rats for up to 24 h and slowly began to rise at 36 h following an i.p. injection of 80 mg/kg O6-benzylguanine. Animal survival and body weight as well as tumor volumes were monitored in rats bearing prostate tumors in the flank area that had received no treatment, O6-benzylguanine alone, BCNU alone (5.5-60 mg/kg), or 80 mg/kg O6-benzylguanine 1 h prior to BCNU (5.5 mg/kg). When O6-benzylguanine was combined with BCNU therapy, there was a regression in tumor growth that was not observed in animals treated with an equal dose of BCNU alone. A similar regression in tumor growth was observed in animals treated with a higher dose of BCNU alone (45 mg/kg); however, this regimen was more toxic than O6-benzylguanine plus BCNU (5.5 mg/kg) as determined by animal weight loss. The mean weight loss observed in animals treated with BCNU alone and in those given the combination was 24% and 6%, respectively. Histopathology revealed that animals receiving either BCNU alone or the combination had a decrease in all types of bone marrow cells, a loss of intestinal crypts, and a decreased number of lymphocytes in the spleen. The enhancement of the antitumor effect on BCNU by pretreatment with O6-benzylguanine supports a role for this therapy in the treatment of prostate cancer. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. PENN STATE UNIV,MILTON S HERSHEY MED CTR,COLL MED,DEPT MED,HERSHEY,PA 17033. PENN STATE UNIV,MILTON S HERSHEY MED CTR,COLL MED,DEPT CELLULAR & MOLEC PHYSIOL,HERSHEY,PA 17033. PENN STATE UNIV,MILTON S HERSHEY MED CTR,COLL MED,DEPT PHARMACOL,HERSHEY,PA 17033. RP DOLAN, ME (reprint author), UNIV CHICAGO,MED CTR,DIV HEMATOL ONCOL,5841 S MARYLAND AVE,BOX MC2115,CHICAGO,IL 60637, USA. FU NCI NIH HHS [P01 CA40011, CA47228, CA57725] NR 29 TC 40 Z9 40 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD JUN PY 1993 VL 32 IS 3 BP 221 EP 225 DI 10.1007/BF00685839 PG 5 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA LB238 UT WOS:A1993LB23800010 PM 8500228 ER PT J AU SPARBER, AG BILLERSPARBER, K AF SPARBER, AG BILLERSPARBER, K TI IMMUNOTHERAPY AND NEUROPSYCHIATRIC TOXICITY - NURSING CLINICAL MANAGEMENT CONSIDERATIONS SO CANCER NURSING LA English DT Article DE NEUROPSYCHIATRIC TOXICITY; IMMUNOTHERAPY ID RECOMBINANT INTERLEUKIN-2 AB Ensuring the safety of patients who receive immunotherapy is an essential element of nursing care. Communicating changes in mental status to the medical team is important feedback for modifying or discontinuing the cycle of immunotherapy. These observations are even more crucial if neuropsychiatric toxicity (NPT) has been exhibited in a previous cycle of treatment. If nurses are aware of associative factors of NPT they can be more alert for emerging cognitive dysfunction. Early intervention will also mean the nurse will take additional measures to ensure patient safety, such as suggesting possible pharmacological alternatives and closer observation, and encouraging family members to help with orientation. The nurse can further assist by helping alleviate the patient's or family's feelings of helplessness by assuring them that the NPT will begin to subside once treatment has been terminated. RP SPARBER, AG (reprint author), NIH,CTR CLIN,RM 7D55,2 E,BETHESDA,MD 20892, USA. NR 15 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0162-220X J9 CANCER NURS JI Cancer Nurs. PD JUN PY 1993 VL 16 IS 3 BP 188 EP 192 PG 5 WC Oncology; Nursing SC Oncology; Nursing GA LK628 UT WOS:A1993LK62800004 PM 8348526 ER PT J AU CHISHOLM, LG BERMAN, AR DECARVALHO, M GORRELL, CR AF CHISHOLM, LG BERMAN, AR DECARVALHO, M GORRELL, CR TI CANCER-CHEMOTHERAPY - ALTERNATIVE ADMINISTRATION ROUTES SO CANCER NURSING LA English DT Article RP CHISHOLM, LG (reprint author), NIH,CTR CLIN,DEPT NURSING,BETHESDA,MD 20892, USA. NR 11 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0162-220X J9 CANCER NURS JI Cancer Nurs. PD JUN PY 1993 VL 16 IS 3 BP 237 EP 246 PG 10 WC Oncology; Nursing SC Oncology; Nursing GA LK628 UT WOS:A1993LK62800010 ER PT J AU RAO, CV RIVENSON, A KATIWALLA, M KELLOFF, GJ REDDY, BS AF RAO, CV RIVENSON, A KATIWALLA, M KELLOFF, GJ REDDY, BS TI CHEMOPREVENTIVE EFFECT OF OLTIPRAZ DURING DIFFERENT STAGES OF EXPERIMENTAL COLON CARCINOGENESIS INDUCED BY AZOXYMETHANE IN MALE F344 RATS SO CANCER RESEARCH LA English DT Article ID GLUTATHIONE S-TRANSFERASES; 5-(2-PYRAZINYL)-4-METHYL-1,2-DITHIOL-3-THIONE OLTIPRAZ; HEPATIC TUMORIGENESIS; PROTECTION; METABOLISM; CANCER; DITHIOLTHIONES; ANTIOXIDANTS; METHYLATION; ETHOXYQUIN AB Oltipraz [5-(2-pyrazinyl)-4-methyl-1,2-dithiole-3-thione], a substituted 1.2-dithiole-3-thione, protects against the acute and chronic toxicities of many xenobiotics and prevents chemically induced carcinogenicity in several target organs of rodents. The effects of dietary oltipraz, fed during the initiation and postinitiation stages, on azoxymethane-induced colon carcinogenesis and on the levels of several detoxifying enzymes, namely, glutathione S-transferase, NAD(P)H:quinone reductase. and UDP-glucurinyl transferase activities, were studied in male F344 rats. At 5 weeks of age, groups of animals were fed the control diet (modified AIN-76A diet) or a diet containing 200 ppm (40% maximum tolerated dose) of oltipraz. At 7 weeks of age, all animals except those in the vehicle (normal saline solution)-treated groups were given two weekly s.c. injections of azoxymethane at a dose of 15 mg/kg body weight. Three days after the second injection of azoxymethane. the groups of animals fed the oltipraz diet were transferred to the control diet (termed the initiation period) and the groups of animals receiving the control diet were transferred to the oltipraz diet (termed the postinitiation period). All groups were continued on this regimen until the termination of the experiment at 52 weeks after the carcinogen treatment. Intestinal tumors were evaluated histopathologically using routine procedures. Liver, colonic mucosa, and tumors were analyzed for glutathione S-transferase, NAD(P)H:quinone reductase, and UDP-glucurinyl transferase activities. The results indicate that oltipraz administered during the initiation stage significantly inhibited the incidence and multiplicity of invasive adenocarcinomas of the colon (P < 0.001), as well as the multiplicity of invasive and noninvasive adenocarcinomas (P < 0.01). Feeding of oltipraz during the postinitiation phase completely suppressed the formation of invasive adenocarcinomas (P < 0.0001) and significantly inhibited the formation of noninvasive and total adenocarcinomas, as well as the multiplicity (tumors/tumor-bearing animal, P < 0.001). Furthermore, oltipraz significantly suppressed the tumor volume when administered during the initiation phase (>80%) or the postinitiation (>93%) phase. Animals fed the oltipraz diet during the postinitiation stage showed increased levels of glutathione S-transferase, NAD(P)H:quinone reductase, and UDP-glucurinyl transferase activities (2-6-fold). Although the precise mechanism by which oltipraz inhibits colon tumor initiation and/or promotion remains to be elucidated, it is likely that the effect during the initiation stage may be due to an alteration of carcinogen metabolism. C1 AMER HLTH FDN,DIV NUTR CARCINOGENESIS,1 DANA RD,VALHALLA,NY 10595. AMER HLTH FDN,DIV PATHOL,VALHALLA,NY 10595. NCI,CHEMOPREVENT BRANCH,DIV CANC CONTROL & PREVENT,BETHESDA,MD 20892. RI Chinthalapally, Rao/B-3633-2010 FU NCI NIH HHS [CA 17613] NR 37 TC 82 Z9 83 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 1 PY 1993 VL 53 IS 11 BP 2502 EP 2506 PG 5 WC Oncology SC Oncology GA LE026 UT WOS:A1993LE02600011 PM 8495412 ER PT J AU SZALLASI, Z KRSMANOVIC, L BLUMBERG, PM AF SZALLASI, Z KRSMANOVIC, L BLUMBERG, PM TI NONPROMOTING 12-DEOXYPHORBOL 13-ESTERS INHIBIT PHORBOL 12-MYRISTATE 13-ACETATE INDUCED TUMOR PROMOTION IN CD-1 MOUSE SKIN SO CANCER RESEARCH LA English DT Article ID PROTEIN-KINASE-C; ORNITHINE DECARBOXYLASE; ESTER; BRYOSTATIN-1; HYPERPLASIA; ACTIVATOR AB Prostratin and 12-deoxyphorbol 13-phenylacetate (dPP) form a new class of protein kinase C activators of unique biological activity. Although they bind to and activate protein kinase C, in mouse skin they either fail to induce typical phorbol ester (PMA) effects (e.g., hyperplasia) or induce only partial response (e.g., inflammation). Furthermore, pretreatment with these agents inhibits a range of PMA induced effects (acute and chronic hyperplasia, inflammation, etc.) These observations suggested that prostratin and dPP would function as inhibitors of phorbol ester tumor promotion. Here we verify that prediction. We report that both compounds reduced both the average number of papillomas and the tumor incidence in a tumor promotion schedule in CD-1 mouse skin, in which each PMA application was preceded by 12-deoxyphorbol 13-monoester pretreatment. The highest dose of prostratin used (2.56 mumol or 1 mg/pretreatment) caused a 96% (23-fold) reduction in the average number or papillomas with a decrease of tumor incidence from 97 to 40%. The highest dose of dPP used (21.4 nmol or 10 mug/pretreatment) induced an 86% (7-fold) reduction in the average number of papillomas with a 53% reduction of tumor incidence from 100 to 47%. The inhibitory effect was dose dependent. The dose causing 50% inhibition was 11 nmol/pretreatment for prostratin and 0.8 nmol/pretreatment for dPP. Maximal inhibition of tumor promotion was accompanied by a block of epidermal hyperplasia; however, significant inhibition of tumor induction was observed at doses without any apparent effect on the PMA induced hyperplasia. C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. BIOCON,ROCKVILLE,MD 20850. NR 30 TC 68 Z9 70 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 1 PY 1993 VL 53 IS 11 BP 2507 EP 2512 PG 6 WC Oncology SC Oncology GA LE026 UT WOS:A1993LE02600012 PM 8495413 ER PT J AU BERG, SL SAVARESE, DMF BALIS, FM DENICOFF, AM HILLIG, M OSHAUGHNESSY, JA POPLACK, DG COWAN, KH AF BERG, SL SAVARESE, DMF BALIS, FM DENICOFF, AM HILLIG, M OSHAUGHNESSY, JA POPLACK, DG COWAN, KH TI PHARMACOKINETICS OF PIROXANTRONE IN A PHASE-I TRIAL OF PIROXANTRONE AND GRANULOCYTE-COLONY-STIMULATING FACTOR SO CANCER RESEARCH LA English DT Article ID ANTHRAPYRAZOLE; OXANTRAZOLE; AGENTS AB Piroxantrone is an anthrapyrazole derivative with broad antitumor activity in vitro. In previous phase I trials, the dose-limiting toxicity of this agent was myelosuppression. Therefore, a phase I and pharmacokinetic study of a 1-h infusion of piroxantrone in combination with granulocyte-colony stimulating factor was conducted. In this article, we report the results of the pharmacokinetic analysis. Thirty-seven patients were studied over a dosage range of 150 to 555 mg/m2. The plasma elimination of piroxantrone was biexponential with a mean (+/- SD) t1/2alpha of 3.2 +/- 2.7 min and a mean (+/- SD) t1/2beta of 82 +/- 92 min. Clearance was 840 +/- 230 ml/min/m2. A limited sampling strategy was developed to allow the estimation of total drug exposure (area under the plasma concentration-time curve) from the plasma piroxantrone concentrations at 30, 60, and 120 min after the start of the infusion. The pharmacokinetic behavior of a presumed piroxantrone metabolite not previously described in plasma was also characterized. Based on in vitro cytotoxicity studies with partially purified extract of this compound, we do not believe that it contributes to the antitumor effects of piroxantrone at the concentrations observed in plasma. Finally. piroxantrone elimination was linear over the nearly 4-fold dose range studied, indicating that when dose adjustments are made. systemic drug exposure will remain predictable. C1 NCI,MED BRANCH,BETHESDA,MD 20892. RP BERG, SL (reprint author), NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 14 TC 5 Z9 5 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 1 PY 1993 VL 53 IS 11 BP 2587 EP 2590 PG 4 WC Oncology SC Oncology GA LE026 UT WOS:A1993LE02600025 PM 7684320 ER PT J AU ELESPURU, RK SAAVEDRA, JE KOVATCH, RM LIJINSKY, W AF ELESPURU, RK SAAVEDRA, JE KOVATCH, RM LIJINSKY, W TI EXAMINATION OF ALPHA-CARBONYL DERIVATIVES OF NITROSODIMETHYLAMINE AND ETHYLNITROSOMETHYLAMINE AS PUTATIVE PROXIMATE CARCINOGENS SO CARCINOGENESIS LA English DT Article ID N-NITROSO-COMPOUNDS; MUTAGENS; LIVER; RATS AB Metabolites produced by enzymic oxidation are believed to be responsible for the mutagenicity and carcinogenicity of N-nitrosamines. Although alpha-hydroxy compounds are often considered, a related and more stable oxidation product, the alpha-carbonyl compound, was studied here. The alpha-carbonyl derivatives of nitrosodimethylamine (NDMA) and ethylnitrosomethylamine (oxidized at either the methyl or the ethyl group) were synthesized. The derivatives were methylnitrosoformamide (MNFA), ethylnitrosoformamide (ENFA) and methylnitrosoacetamide (MNAA). These compounds were then studied as potential toxic, mutagenic and carcinogenic intermediates. All three compounds were very potent directly acting mutagens to Salmonella typhimurium TA1535. Mutational Fingerprints in Escherichia coli of MNFA and ENFA (but not MNAA) matched those produced by S(N)1-type methylating and ethylating compounds respectively. The latter results indicate that the two alkylnitrosoformamides could be intermediates in the mutagenicity of the parent nitrosamines. In animal studies the putative metabolite MNFA was more acutely toxic than NDMA in F344 rats. In chronic experiments with MNFA in F344 rats and Syrian golden hamsters, tumors of the forestomach were induced by oral administration in most animals (except female hamsters) within 8 months. The properties of these oxidized derivatives of N-nitrosamines are consistent with expectations for proximate carcinogenic intermediates. C1 US FDA,MOLEC BIOL BRANCH,HFZ-113,5600 FISHERS LANE,ROCKVILLE,MD 20857. FREDERICK CANC RES & DEV CTR,ABI,BASIC RES PROGRAM,FREDERICK,MD 21701. FU NCI NIH HHS [N01-CO-74101] NR 22 TC 8 Z9 8 U1 0 U2 0 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 JUN PY 1993 VL 14 IS 6 BP 1189 EP 1193 DI 10.1093/carcin/14.6.1189 PG 5 WC Oncology SC Oncology GA LG261 UT WOS:A1993LG26100019 PM 8508506 ER PT J AU RUTTNER, Z LIGETI, L REINLIB, L HINES, K MCLAUGHLIN, AC AF RUTTNER, Z LIGETI, L REINLIB, L HINES, K MCLAUGHLIN, AC TI MONITORING OF INTRACELLULAR FREE CALCIUM IN PERFUSED-RAT-LIVER SO CELL CALCIUM LA English DT Article ID RABBIT HEARTS; FLUORESCENCE; TRANSIENTS; ISCHEMIA; INDO-1; FURA-2; CA-2+; CELLS; HEPATOCYTES; SECRETION AB Fluorescent calcium indicators have been widely used to assess cytoplasmic calcium concentration in cells. To examine the role of calcium ions on different physiological functions (e.g. in case of liver; bile secretion, glucose metabolism, etc.) there is a need for whole organ studies. We have developed a technique to estimate intracellular free calcium changes in perfused rat liver. Krebs-Henseleit perfused livers were loaded with 7 muM or 35 muM indo-1/AM. An area 3 mm in diameter and approximately 300 mum in depth was illuminated at 340 nm. Fluorescence was monitored with photomultiplier tubes at 3 wavelengths (400 nm for Ca-bound dye, 504 nm for free dye and 464 nm for NADH). The viability of liver preparations was assessed by measurement of the concentrations of lactate dehydrogenase and alanine aminotransferase in the effluent Loading of the livers with 7 muM indo-1/AM via the portal vein resulted in a 5-fold increase of fluorescence at 400 nm. However the dye 'leaked' out of the liver with a half-time of 18 min. Probenecid (a specific anion carrier blocker) inhibited loss of dye in a dose dependent fashion (2.5-10 mM). Transient calcium elevations were observed in response to vasopressin (5-50 nM) at physiological levels, ethanol (0.3-0.8 M) and the calcium ionophore, ionomycin. Certain limitations were apparent with this approach: (1) it was necessary to use an anion carrier blocker to maintain a relatively steady dye concentration; (2) endogenous NADH fluorescence interfered with the calcium signal; and (3) absolute values of calcium concentration could not be determined. C1 SEMMELWEIS UNIV MED, SCH MED, EXPTL RES DEPT, H-1085 BUDAPEST 8, HUNGARY. SEMMELWEIS UNIV MED, DEPT PHYSIOL 2, H-1085 BUDAPEST 8, HUNGARY. NHLBI, BETHESDA, MD 20892 USA. RP NIAAA, MEMBRANE BIOCHEM & BIOPHYS LAB, 12501 WASHINGTON AVE, ROCKVILLE, MD 20852 USA. NR 33 TC 10 Z9 10 U1 0 U2 1 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0143-4160 EI 1532-1991 J9 CELL CALCIUM JI Cell Calcium PD JUN PY 1993 VL 14 IS 6 BP 465 EP 472 DI 10.1016/0143-4160(93)90005-Q PG 8 WC Cell Biology SC Cell Biology GA LJ772 UT WOS:A1993LJ77200005 PM 8358770 ER PT J AU SHI, D NIKODIJEVIC, O JACOBSON, KA DALY, JW AF SHI, D NIKODIJEVIC, O JACOBSON, KA DALY, JW TI CHRONIC CAFFEINE ALTERS THE DENSITY OF ADENOSINE, ADRENERGIC, CHOLINERGIC, GABA, AND SEROTONIN RECEPTORS AND CALCIUM CHANNELS IN MOUSE-BRAIN SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article DE CAFFEINE; ADENOSINE RECEPTORS; ADRENERGIC RECEPTORS; CHOLINERGIC RECEPTORS; SEROTONIN RECEPTORS; GABA RECEPTORS; CALCIUM CHANNELS; DOPAMINE RECEPTORS; NMDA RECEPTORS ID CENTRAL-NERVOUS-SYSTEM; RAT CEREBRAL-CORTEX; ADENYLATE CYCLASE SYSTEM; BINDING-SITES; UP-REGULATION; A1-ADENOSINE RECEPTORS; DOPAMINE-RECEPTORS; TREATED RATS; THEOPHYLLINE; EXPOSURE AB 1. Chronic ingestion of caffeine by male NIH strain mice alters the density of a variety of central receptors. 2. The density of cortical A1 adenosine receptors is increased by 20%, while the density of striatal A2A adenosine receptors is unaltered. 3. The densities of cortical beta1 and cerebellar beta2 adrenergic receptors are reduced by ca. 25%, while the densities of cortical alpha1 and alpha2 adrenergic receptors are not significantly altered. Densities of striatal D1 and D2 dopaminergic receptors are unaltered. The densities of cortical 5 HT1 and 5 HT2 serotonergic receptors are increased by 26-30%. Densities of cortical muscarinic and nicotinic receptors are increased by 40-50%. The density of cortical benzodiazepine-binding sites associated with GABA(A) receptors is increased by 65%, and the affinity appears slightly decreased. The density of cortical MK-801 sites associated with NMDA-glutaminergic receptors appear unaltered. 4. The density of cortical nitrendipine-binding sites associated with calcium channels is increased by 18%. 5. The results indicate that chronic ingestion of caffeine equivalent to about 100 mg/kg/day in mice causes a wide range of biochemical alterations in the central nervous system. RP SHI, D (reprint author), NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892, USA. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999] NR 59 TC 87 Z9 87 U1 0 U2 5 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD JUN PY 1993 VL 13 IS 3 BP 247 EP 261 DI 10.1007/BF00733753 PG 15 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA LY375 UT WOS:A1993LY37500005 PM 8242688 ER PT J AU JHAPPAN, C STAHLE, C WOLFF, M MERLINO, G PASTAN, I AF JHAPPAN, C STAHLE, C WOLFF, M MERLINO, G PASTAN, I TI AN EPIDERMAL GROWTH-FACTOR RECEPTOR PROMOTER CONSTRUCT SELECTIVELY EXPRESSES IN THE THYMUS AND SPLEEN OF TRANSGENIC MICE SO CELLULAR IMMUNOLOGY LA English DT Article ID EPITHELIAL-CELLS; GENE-EXPRESSION; PROTO-ONCOGENE; RETINOIC ACID; FACTOR-ALPHA; NURSE CELLS; TRANSCRIPTION; IDENTIFICATION; SEQUENCES; BETA RP JHAPPAN, C (reprint author), NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 41 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD JUN PY 1993 VL 149 IS 1 BP 99 EP 106 DI 10.1006/cimm.1993.1139 PG 8 WC Cell Biology; Immunology SC Cell Biology; Immunology GA LJ146 UT WOS:A1993LJ14600009 PM 8513514 ER PT J AU BRISTOL, LA DURUM, SK EISENBERG, SP AF BRISTOL, LA DURUM, SK EISENBERG, SP TI DIFFERENTIAL REGULATION OF GROUP-A STREPTOCOCCAL PEPTIDOGLYCAN POLYSACCHARIDE (PG-APS)-STIMULATED MACROPHAGE PRODUCTION OF IL-1 BY RAT STRAINS SUSCEPTIBLE AND RESISTANT TO PG-APS-INDUCED ARTHRITIS SO CELLULAR IMMUNOLOGY LA English DT Article ID INTERLEUKIN-1 RECEPTOR ANTAGONIST; TRANSFORMING GROWTH-FACTOR; LYMPHOCYTE ACTIVATING FACTOR; MURAMYL DIPEPTIDE; IL-1-BETA PRODUCTION; ACUTE-INFLAMMATION; HUMAN-MONOCYTES; FACTOR-BETA; CELLS; EXPRESSION C1 NIAAA,ADAMHA,PHYSIOL & PHARMACOL STUDIES LAB,ROCKVILLE,MD 20852. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. SYNERGEN INC,BOULDER,CO 80301. NR 46 TC 13 Z9 13 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD JUN PY 1993 VL 149 IS 1 BP 130 EP 143 DI 10.1006/cimm.1993.1142 PG 14 WC Cell Biology; Immunology SC Cell Biology; Immunology GA LJ146 UT WOS:A1993LJ14600012 PM 8513508 ER PT J AU YUSUF, S GARG, R AF YUSUF, S GARG, R TI DESIGN, RESULTS, AND INTERPRETATION OF RANDOMIZED, CONTROLLED TRIALS IN CONGESTIVE-HEART-FAILURE AND LEFT-VENTRICULAR DYSFUNCTION SO CIRCULATION LA English DT Article DE CLINICAL TRIALS; HEART FAILURE; CARDIOVASCULAR DISEASE ID CLINICAL-TRIALS; MYOCARDIAL-INFARCTION; ORAL MILRINONE; MORTALITY; DISEASE; THERAPY AB This article discusses how randomized trials can be designed in patients with heart failure and left ventricular dysfunction to provide reliable answers regarding various interventions. Most previous trials have been limited by their small size, short duration, and restricted entry of highly selected patients, leading to unconvincing answers. The effects of treatment on surrogate end points (e.g., exercise tolerance, arrhythmia suppression) do not necessarily correlate with the ability of an intervention to reduce mortality or morbidity. Therefore, promising results obtained on surrogate end points should be complemented by data from further studies using clinical outcomes. Recent experiences from major trials in heart failure and other cardiovascular diseases indicate that if such trials are large, they are likely to provide reliable information on clinically important outcomes even if only limited data are collected on individual subjects. The results of some of the larger trials are summarized, and their implications for both study design and clinical applications are discussed. C1 NHLBI, DIV EPIDEMIOL & CLIN APPLICAT, CLIN TRIALS BRANCH, BETHESDA, MD 20892 USA. RP YUSUF, S (reprint author), MCMASTER UNIV, HAMILTON GEN HOSP, MCMASTER CLIN, DIV CARDIOL, 2ND FLOOR, HAMILTON L8S 4L8, ONTARIO, CANADA. NR 33 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0009-7322 EI 1524-4539 J9 CIRCULATION JI Circulation PD JUN PY 1993 VL 87 IS 6 SU 7 BP 115 EP 121 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LG180 UT WOS:A1993LG18000021 ER PT J AU TOWBIN, JA HEJTMANCIK, JF BRINK, P GELB, B ZHU, XM CHAMBERLAIN, JS MCCABE, ERB SWIFT, M AF TOWBIN, JA HEJTMANCIK, JF BRINK, P GELB, B ZHU, XM CHAMBERLAIN, JS MCCABE, ERB SWIFT, M TI X-LINKED DILATED CARDIOMYOPATHY - MOLECULAR-GENETIC EVIDENCE OF LINKAGE TO THE DUCHENNE MUSCULAR-DYSTROPHY (DYSTROPHIN) GENE AT THE XP21 LOCUS SO CIRCULATION LA English DT Article DE DYSTROPHIN; CARDIOMYOPATHY; DUCHENNE MUSCULAR DYSTROPHY ID FAMILIAL HYPERTROPHIC CARDIOMYOPATHY; POLYMERASE CHAIN-REACTION; CYSTIC-FIBROSIS GENE; CARDIAC-MUSCLE; ABNORMAL MITOCHONDRIA; DINUCLEOTIDE REPEAT; SKELETAL-MUSCLE; DNA; IDENTIFICATION; POLYMORPHISMS AB Background. X-linked cardiomyopathy (XLCM) is a rapidly progressive primary myocardial disorder presenting in teenage males as congestive heart failure. Manifesting female carriers have later onset (fifth decade) and slower progression. The purpose of this study was to localize the XLCM gene locus in two families using molecular genetic techniques. Methods and Results. Linkage analysis using 60 X-chromosome-specific DNA markers was performed in a previously reported large XLCM pedigree and a smaller new pedigree. Two-point and multipoint linkage was calculated using the LINKAGE computer program package. Deletion analysis included multiplex polymerase chain reaction (PCR). Dystrophin protein was evaluated by Western blotting with N-terminal and C-terminal dystrophin antibody. Linkage of XLCM to the centromeric portion of the dystrophin or Duchenne muscular dystrophy (DMD) locus at Xp21 was demonstrated with combined maximum logarithm of the scores of +4.33, theta = 0 with probe XJ1.1 (DXS206) using two-point linkage and +4.81 at XJ1.1 with multipoint linkage analysis. LOD scores calculated using other proximal DMD genomic and cDNA probes and polymerase chain reaction polymorphisms supported linkage. No deletions were observed. Abnormalities of cardiac dystrophin were shown by Western blotting with N-terminal dystrophin antibody, whereas skeletal muscle dystrophin was normal, suggesting primary involvement of the DMD gene with preferential involvement of cardiac muscle. Conclusions. XLCM is due to an abnormality within the centromeric half of the dystrophin genomic region in heart. This abnormality could be due to 1) a point mutation in the 5' region of the DMD coding sequence preferentially affecting cardiac function, 2) a cardiac-specific promoter mutation that alters expression in this tissue, 3) splicing abnormalities, resulting in an abnormal cardiac protein, or 4) deletion mutations undetectable by Southern and multiplex polymerase chain reaction analysis. C1 BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. BAYLOR COLL MED,INST MOLEC GENET,HOUSTON,TX 77030. NEI,MECH OPHTHALMOL DIS LAB,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT MED,CHAPEL HILL,NC 27514. RP TOWBIN, JA (reprint author), BAYLOR COLL MED,DEPT PEDIAT,HOUSTON,TX 77030, USA. FU NHLBI NIH HHS [5-K08-HL-02485]; NICHD NIH HHS [3-R01-HD22563] NR 62 TC 322 Z9 329 U1 0 U2 6 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JUN PY 1993 VL 87 IS 6 BP 1854 EP 1865 PG 12 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LG175 UT WOS:A1993LG17500008 PM 8504498 ER PT J AU YUSUF, S TEO, K WOODS, K AF YUSUF, S TEO, K WOODS, K TI INTRAVENOUS MAGNESIUM IN ACUTE MYOCARDIAL-INFARCTION - AN EFFECTIVE, SAFE, SIMPLE, AND INEXPENSIVE INTERVENTION SO CIRCULATION LA English DT Editorial Material ID RANDOMIZED TRIALS; SULFATE; HEART; REPERFUSION; CALCIUM; IONS; PROTECTION; MORTALITY; DISEASE; MG-2+ C1 NHLBI,CLIN TRIALS BRANCH,BETHESDA,MD 20892. MCMASTER UNIV,DIV CARDIOL,HAMILTON L8S 4L8,ONTARIO,CANADA. UNIV ALBERTA,EDMONTON T6G 2E1,ALBERTA,CANADA. LEICESTER ROYAL INFIRM,LEICESTER LE2 7LX,ENGLAND. NR 34 TC 57 Z9 61 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 JUN PY 1993 VL 87 IS 6 BP 2043 EP 2046 PG 4 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LG175 UT WOS:A1993LG17500030 PM 8504519 ER PT J AU ZWEIG, MH AF ZWEIG, MH TI ROC PLOTS DISPLAY TEST ACCURACY, BUT ARE STILL LIMITED BY THE STUDY DESIGN SO CLINICAL CHEMISTRY LA English DT Letter ID EFFICACY RP ZWEIG, MH (reprint author), NIH,DEPT CLIN PATHOL,CLIN CHEM SERV,BLDG 10,RM 2C407,BETHESDA,MD 20892, USA. NR 3 TC 12 Z9 12 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD JUN PY 1993 VL 39 IS 6 BP 1345 EP 1346 PG 2 WC Medical Laboratory Technology SC Medical Laboratory Technology GA LF992 UT WOS:A1993LF99200039 PM 7684958 ER PT J AU HITRI, A OCONNOR, DA COHEN, JM KEULER, DJ DEUTSCH, SI AF HITRI, A OCONNOR, DA COHEN, JM KEULER, DJ DEUTSCH, SI TI DIFFERENTIATION BETWEEN MK-801-INDUCED AND APOMORPHINE-INDUCED STEREOTYPED BEHAVIORS IN MICE SO CLINICAL NEUROPHARMACOLOGY LA English DT Review DE MK-801; APOMORPHINE; STEREOTYPED BEHAVIOR; MOUSE ID APPARENT ANXIOLYTIC PROPERTIES; POTENT ANTICONVULSANT; AUTOMATED MEASUREMENT; 10-IMINE MK-801; PHENCYCLIDINE; RATS; STIMULATION; ACTIVATION; SUBSTANCE; BRAIN AB The ability of phencyclidine (PCP) to model schizophreniform psychosis is believed to be related to its ability to produce both hypoglutamatergia and hyperdopaminergia. As such, identification of PCP-stimulated behaviors may be important for the development of animal models of schizophrenia. In this study, MK-801 {(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cycloheptane-5,10-imine maleate}, a high-affinity PCP analogue, was administered to mice in order to stimulate ''PCP behaviors.'' These PCP behaviors were compared with behaviors stimulated by apomorphine, a dopamine agonist. Stereotyped behavior was assessed by both visual observations and automated measurements. Visual observations showed highly intense gnawing and sniffing in apomorphine-treated mice and the absence of gnawing in MK-801-treated mice. Automated stereotypic measures showed that, compared with vehicle-treated controls, there were frequent dissociations between MK-801 and apomorphine. Conceivably, a compound that attenuates PCP-stimulated behaviors while sparing apomorphine-stimulated behaviors would possess both antipsychotic efficacy and be devoid of undesirable side effects associated with dopamine blockade. C1 GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20007. DEPT VET AFFAIRS,VET ADM NIDA RES UNIT,WASHINGTON,DC 20422. RP HITRI, A (reprint author), DEPT VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,50 IRVING ST NW,WASHINGTON,DC 20422, USA. NR 35 TC 18 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-5664 J9 CLIN NEUROPHARMACOL JI Clin. Neuropharmacol. PD JUN PY 1993 VL 16 IS 3 BP 220 EP 236 DI 10.1097/00002826-199306000-00006 PG 17 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA LC343 UT WOS:A1993LC34300006 PM 8504439 ER PT J AU DEUTSCH, SI HITRI, A AF DEUTSCH, SI HITRI, A TI MEASUREMENT OF AN EXPLOSIVE BEHAVIOR IN THE MOUSE, INDUCED BY MK-801, A PCP ANALOG SO CLINICAL NEUROPHARMACOLOGY LA English DT Note DE MK-801; PHENCYCLIDINE; POPPING; MOUSE; PSYCHOSIS ID D-ASPARTATE RECEPTOR; NMDA ANTAGONIST; RAT-BRAIN; GLYCINE; PHENCYCLIDINE; CHANNEL; DRUGS; MICE AB MK-801, a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor complex that binds with high-affinity to the phencyclidine (PCP) binding site, stimulated an outbred strain of NIH Swiss mice to display discrete episodes of explosive jumping behavior, designated as ''popping.'' The episodes of this behavior were characterized with respect to their dose dependency, latency, and duration. The number of mice displaying this behavior increased with increasing doses of MK-801. The intensity of the popping behavior was sensitive to dose-dependent inhibition by haloperidol, a conventional antipsychotic medication, and clozapine, an atypical antipsychotic medication. In view of PCP's ability to precipitate a schizophreniform psychosis in humans, the behavior may serve as a useful preclinical paradigm for the screening of potentially novel antipsychotic medications. C1 DEPT VET AFFAIRS MED CTR,VET ADM NIDA RES UNIT,WASHINGTON,DC 20007. GEORGETOWN UNIV,DEPT PSYCHIAT,WASHINGTON,DC 20007. RP DEUTSCH, SI (reprint author), DEPT VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,50 IRVING ST NW,WASHINGTON,DC 20422, USA. NR 14 TC 31 Z9 31 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-5664 J9 CLIN NEUROPHARMACOL JI Clin. Neuropharmacol. PD JUN PY 1993 VL 16 IS 3 BP 251 EP 257 DI 10.1097/00002826-199306000-00009 PG 7 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA LC343 UT WOS:A1993LC34300009 PM 8504442 ER PT J AU SAAVEDRADELGADO, AM METCALFE, DD AF SAAVEDRADELGADO, AM METCALFE, DD TI SEAFOOD TOXINS SO CLINICAL REVIEWS IN ALLERGY LA English DT Review ID FISH; CIGUATERA; DINOFLAGELLATE; SHELLFISH; OUTBREAKS C1 NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BLDG 10,RM 11C210,BETHESDA,MD 20892. CTR DRUG EVALUAT & RES,DIV ONCOL & PULM DRUG PROD,ROCKVILLE,MD. NR 51 TC 5 Z9 5 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0731-8235 J9 CLIN REV ALLERG JI Clin. Rev. Allergy PD SUM PY 1993 VL 11 IS 2 BP 241 EP 260 PG 20 WC Allergy SC Allergy GA LU469 UT WOS:A1993LU46900006 PM 8221511 ER PT J AU DASANAYAKE, AP CAUFIELD, PW CUTTER, GR STILES, HM AF DASANAYAKE, AP CAUFIELD, PW CUTTER, GR STILES, HM TI TRANSMISSION OF MUTANS STREPTOCOCCI TO INFANTS FOLLOWING SHORT-TERM APPLICATION OF AN IODINE-NAF SOLUTION TO MOTHERS DENTITION SO COMMUNITY DENTISTRY AND ORAL EPIDEMIOLOGY LA English DT Article DE STREPTOCOCCUS-MUTANS; INCIDENCE, GROWTH AND DEVELOPMENT, DRUG EFFECTS; IODINE, THERAPEUTIC USE; SODIUM FLUORIDE; THERAPEUTIC USE; DENTITION, DRUG EFFECTS, MICROBIOLOGY; MOTHERS; EPIDEMIOLOGY ID DENTAL-CARIES; PREVENTIVE MEASURES; CHILDREN; LACTOBACILLI; INFECTION; MOUTHS; FAMILY; DECAY AB In a randomized clinical trial, six applications of an I2-NaF or a placebo solution were administered to the mothers' dentition at the time of tooth emergence of her infant, to evaluate its effect on transmission of mutans streptococci (MS) to the infant. MS and other bacterial levels were periodically monitored in 48 mother-infant pairs until the child's third birthday. There were significant reductions in maternal salivary MS (P = 0.04), lactobacilli (P = 0.04), total streptococci (P = 0.002), and total cultivable organisms (P = 0.004) immediately following treatment. In children, 3-yr incidence of MS colonization and the time of acquisition of MS or the caries experience did not differ significantly between the two groups. We conclude that short-term application of I2-NaF to the maternal dentition of predentate infants significantly lowers MS, lactobacilli, total streptococci, and total cultivable bacteria in mothers' saliva, but does not influence the incidence and the time of acquisition of MS or the caries experience in children. C1 UNIV ALABAMA,SCH DENT,BIRMINGHAM,AL 35294. NIDR,BETHESDA,MD 20892. RP DASANAYAKE, AP (reprint author), UNIV ALABAMA,SCH PUBL HLTH,DEPT EPIDEMIOL,BIRMINGHAM,AL 35294, USA. FU NIDCR NIH HHS [N01-DE-42552] NR 37 TC 24 Z9 25 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0301-5661 J9 COMMUNITY DENT ORAL JI Community Dentist. Oral Epidemiol. PD JUN PY 1993 VL 21 IS 3 BP 136 EP 142 DI 10.1111/j.1600-0528.1993.tb00738.x PG 7 WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health GA LL429 UT WOS:A1993LL42900005 PM 8348786 ER PT J AU SALAMON, P WOOTTON, JC KONOPKA, AK HANSEN, LK AF SALAMON, P WOOTTON, JC KONOPKA, AK HANSEN, LK TI ON THE ROBUSTNESS OF MAXIMUM-ENTROPY RELATIONSHIPS FOR COMPLEXITY DISTRIBUTIONS OF NUCLEOTIDE-SEQUENCES SO COMPUTERS & CHEMISTRY LA English DT Article; Proceedings Paper CT 2ND INTERNATIONAL WORKSHOP ON OPEN PROBLEMS OF COMPUTATIONAL MOLECULAR BIOLOGY CY JUL 19-AUG 02, 1992 CL TELLURIDE SUMMER RES CTR, TELLURIDE, CO HO TELLURIDE SUMMER RES CTR AB Given a functionally equivalent set of natural nucleotide sequences, the distribution of local compositional complexity among all subsequences of this set appears to be as random as possible consistent with the mean complexity of such subsequences. The robustness of this relationship and its possible causes have been explored by means of (1) dynamic simulations based on models of biased substitution mutations, (2) equilibrium models incorporating known mononucleotide probabilities, and (3) extension of the analyses, previously carried out on short oligonucleotides, to much larger subsequences. The maximum entropy effect evidently follows from almost any mechanism for substitution mutation dynamics that incorporates a systematic bias toward low-complexity. The effect is only partially explained by unequal mononucleotide probabilities. The complexity distributions for larger subsequences of length range 40-120 nucleotides show novel regularity of structure ('feathering') that is not yet explained. C1 NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. NCI,DCBRC,FREDERICK,MD 21702. TECH UNIV DENMARK,INST ELECTR,CONNECT,DK-2800 LYNGBY,DENMARK. RP SALAMON, P (reprint author), SAN DIEGO STATE UNIV,DEPT MATH SCI,SAN DIEGO,CA 92182, USA. RI Hansen, Lars/E-3174-2013 NR 24 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 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD JUN PY 1993 VL 17 IS 2 BP 135 EP 148 DI 10.1016/0097-8485(93)85005-W PG 14 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA LX571 UT WOS:A1993LX57100005 ER PT J AU WOOTTON, JC FEDERHEN, S AF WOOTTON, JC FEDERHEN, S TI STATISTICS OF LOCAL COMPLEXITY IN AMINO-ACID-SEQUENCES AND SEQUENCE DATABASES SO COMPUTERS & CHEMISTRY LA English DT Article ID PROTEINS; DNA; IDENTIFICATION; DROSOPHILA AB Protein sequences contain surprisingly many local regions of low compositional complexity. These include different types of residue clusters, some of which contain homopolymers, short period repeats or aperiodic mosaics of a few residue types. Several different formal definitions of local complexity and probability are presented here and are compared for their utility in algorithms for localization of such regions in amino acid sequences and sequence databases. The definitions are:-(1) those derived from enumeration a priori by a treatment analogous to statistical mechanics, (2) a log likelihood definition of complexity analogous to informational entropy, (3) multinomial probabilities of observed compositions, (4) an approximation resembling the chi2 statistic and (5) a modification of the coefficient of divergence. These measures, together with a method based on similarity scores of self-aligned sequences at different offsets, are shown to be broadly similar for first-pass, approximate localization of low-complexity regions in protein sequences, but they give significantly different results when applied in optimal segmentation algorithms. These comparisons underpin the choice of robust optimization heuristics in an algorithm, SEG, designed to segment amino acid sequences fully automatically into subsequences of contrasting complexity. After the abundant low-complexity segments have been partitioned from the Swissprot database, the remaining high-complexity sequence set is adequately approximated by a first-order random model. RP NIH, NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BLDG 38A, 8N805, BETHESDA, MD 20894 USA. NR 27 TC 414 Z9 424 U1 1 U2 9 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD JUN PY 1993 VL 17 IS 2 BP 149 EP 163 DI 10.1016/0097-8485(93)85006-X PG 15 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA LX571 UT WOS:A1993LX57100006 ER PT J AU CLAVERIE, JM STATES, DJ AF CLAVERIE, JM STATES, DJ TI INFORMATION ENHANCEMENT METHODS FOR LARGE-SCALE SEQUENCE-ANALYSIS SO COMPUTERS & CHEMISTRY LA English DT Article ID CAENORHABDITIS-ELEGANS; GENERAL-METHOD; SEARCH; TAGS AB The improved efficiency of similarity search programs and the affordability of even faster computers allow studies where whole sequence databases can be the target of various comparisons with increasingly larger or numerous query sequences. However, the usefulness of those ''brute force'' methods now becomes limited by the time it takes an experienced scientist to sift the biologically relevant matches from overwhelming, albeit ''statistically significant'' outputs. The discrepancy between statistical vs biological significance has different causes: erroneous database entries, repetitive sequence elements, and the ubiquity of low complexity segments with biased composition. We present two masking methods (programs XNU and XBLAST) capable of eliminating most of the irrelevant outputs in a variety of large scale sequence analysis situations: global ''all against all'' database comparisons. massive partial cDNA sequencing (EST), positional cloning and genomic data analysis. RP NIH, NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20894 USA. NR 25 TC 95 Z9 97 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD JUN PY 1993 VL 17 IS 2 BP 191 EP 201 DI 10.1016/0097-8485(93)85010-A PG 11 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA LX571 UT WOS:A1993LX57100010 ER PT J AU MICHAELS, GS TAYLOR, R HAGSTROM, R PRICE, M OVERBEEK, R AF MICHAELS, GS TAYLOR, R HAGSTROM, R PRICE, M OVERBEEK, R TI SEARCHING FOR GENOMIC ORGANIZATIONAL MOTIFS - EXPLORATIONS OF THE ESCHERICHIA-COLI CHROMOSOME SO COMPUTERS & CHEMISTRY LA English DT Article; Proceedings Paper CT 2ND INTERNATIONAL WORKSHOP ON OPEN PROBLEMS OF COMPUTATIONAL MOLECULAR BIOLOGY CY JUL 19-AUG 02, 1992 CL TELLURIDE SUMMER RES CTR, TELLURIDE, CO HO TELLURIDE SUMMER RES CTR ID TRANSLATION INITIATION; TRANSFER-RNA; DNA; ALIGNMENT; BINDING; SITES AB Understanding the coordinated control of gene expression is a central goal for much of the work in molecular biology. In order to understand how the mechanics of these control systems operate at the genome level, the data for the genetic organization of the model organism in question needs to be accessible. In previous work, we developed an integrated database to support analysis of the Escherichia coli genome. That system provided a pidgin English query facility, rudimentary pattern matching capabilities, and the ability to rapidly extract answers to a wide variety of questions about the organization of the E. coli genome. We have used a parser/grammar approach to identify the chromosomal positions of all of the mapped tRNA genes to be found in the aligned sequence fragments. Also, we have used this integrated data set to explore the global organization of the E. coli chromosome. We have begun to develop regulation classifications based on the arrangements of control features in relation to specific genetic control components. For example, using the individual DNA sequences for 111 known transcriptional promoters as a the starting position for analysis, we have identified the relative positions of potential control sites for 47 different procaryotic transcription factors, sigma factor 70 binding sites, and potential ribosome binding sites that occur within the region -500 to +500 bases upstream or downstream of the anchor position (the first base of the sequence feature). We have defined local descriptions for regulation based on the cross-correlated control features revealed through these analyses. C1 ARGONNE NATL LAB,DIV MATH & COMP SCI,ARGONNE,IL 60439. RP MICHAELS, GS (reprint author), NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892, USA. RI Price, Morgan/A-1266-2009 NR 23 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD JUN PY 1993 VL 17 IS 2 BP 209 EP 217 DI 10.1016/0097-8485(93)85012-2 PG 9 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA LX571 UT WOS:A1993LX57100012 ER PT J AU KONOPKA, AK AF KONOPKA, AK TI COMPUTATIONAL MOLECULAR-BIOLOGY - FROM SEQUENCE RESEARCH TO SOFTWARE-DEVELOPMENT - EDITORIAL SO COMPUTERS & CHEMISTRY LA English DT Editorial Material RP KONOPKA, AK (reprint author), NCI,DCBDC,BLDG 1052,ROOM 237,FREDERICK,MD 21702, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD JUN PY 1993 VL 17 IS 2 BP R5 EP R6 DI 10.1016/0097-8485(93)85001-S PG 2 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA LX571 UT WOS:A1993LX57100001 ER PT J AU BORNSTEIN, MH AF BORNSTEIN, MH TI THE CULTURAL-CONTEXT OF INFANCY, VOL 2, MULTICULTURAL AND INTERDISCIPLINARY APPROACHES TO PARENT-INFANT RELATIONS - NUGENT,JK, LESTER,BM, BRAZELTON,TB SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review ID PSYCHOLOGY RP BORNSTEIN, MH (reprint author), NICHHD,BETHESDA,MD 20892, USA. NR 8 TC 0 Z9 0 U1 0 U2 1 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD JUN PY 1993 VL 38 IS 6 BP 616 EP 618 PG 3 WC Psychology, Multidisciplinary SC Psychology GA LF232 UT WOS:A1993LF23200041 ER PT J AU BERENDES, HW LEE, YJ AF BERENDES, HW LEE, YJ TI THE 1953 CLINICAL-TRIAL OF DIETHYLSTILBESTROL DURING PREGNANCY - COULD IT HAVE STOPPED DES USE SO CONTROLLED CLINICAL TRIALS LA English DT Article RP BERENDES, HW (reprint author), NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,6100 EXECUTIVE BLVD,ROOM 7B05,BETHESDA,MD 20892, USA. NR 9 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD JUN PY 1993 VL 14 IS 3 BP 179 EP 182 DI 10.1016/0197-2456(93)90001-T PG 4 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LJ693 UT WOS:A1993LJ69300001 PM 8339548 ER PT J AU GAIL, MH BYAR, DP PECHACEK, TF CORLE, DK AF GAIL, MH BYAR, DP PECHACEK, TF CORLE, DK TI ASPECTS OF STATISTICAL DESIGN FOR THE COMMUNITY INTERVENTION TRIAL FOR SMOKING CESSATION (COMMIT) (VOL 13, PG 6, 1992) SO CONTROLLED CLINICAL TRIALS LA English DT Correction, Addition C1 NCI,CLIN TRIALS SECT,ROCKVILLE,MD 20892. RP GAIL, MH (reprint author), NCI,EPIDEMIOL METHODS SECT,6130 EXECUTIVE BLVD,EPN 403,ROCKVILLE,MD 20892, USA. NR 2 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD JUN PY 1993 VL 14 IS 3 BP 253 EP 254 DI 10.1016/0197-2456(93)90010-B PG 2 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LJ693 UT WOS:A1993LJ69300009 ER PT J AU ROELKE, ME MARTENSON, JS OBRIEN, SJ AF ROELKE, ME MARTENSON, JS OBRIEN, SJ TI THE CONSEQUENCES OF DEMOGRAPHIC REDUCTION AND GENETIC DEPLETION IN THE ENDANGERED FLORIDA PANTHER SO CURRENT BIOLOGY LA English DT Review ID FREE-RANGING CHEETAHS; FELIS-CONCOLOR-CORYI; DNA; POPULATIONS; DIVERSITY; EJACULATE; AFRICAN; LIONS; KINSHIP C1 FLORIDA GAME & FRESHWATER FISH COMMISS,WILDLIFE RES LAB,GAINESVILLE,FL 32601. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 88 TC 206 Z9 215 U1 8 U2 84 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD JUN PY 1993 VL 3 IS 6 BP 340 EP 350 DI 10.1016/0960-9822(93)90197-V PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LL958 UT WOS:A1993LL95800003 PM 15335727 ER PT J AU OBRIEN, SJ AF OBRIEN, SJ TI COMPARATIVE BIOLOGY - THE GENOMICS GENERATION SO CURRENT BIOLOGY LA English DT Article RP OBRIEN, SJ (reprint author), NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702, USA. NR 15 TC 5 Z9 5 U1 1 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD JUN PY 1993 VL 3 IS 6 BP 395 EP 397 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LL958 UT WOS:A1993LL95800018 ER PT J AU KING, LB ASHWELL, JD AF KING, LB ASHWELL, JD TI SIGNALING FOR DEATH OF LYMPHOID-CELLS SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID MATURE T-CELLS; MONOCLONAL-ANTIBODY; CYCLOSPORINE-A; ACTIVATION; APOPTOSIS; BCL-2; THYMOCYTES; RECEPTOR; ANTIGEN; STIMULATION AB The induction of programmed cell death in lymphocytes is a common response to a wide variety of physiological and pharmacological stimuli. While there is still much to be learned about the transmembrane signals that lead to programmed cell death, progress has been made in identifying new cell surface molecules (e.g. APO-1/Fas) that may regulate the physiological induction of lymphocyte death, molecules whose expression inhibits apoptosis (e.g. Bcl-2), and the antagonism of activation-induced cell death in T-cell hybridomas and thymocytes by members of the steroid receptor superfamily. RP KING, LB (reprint author), NCI,ROOM 1B-40,BLDG 10,BETHESDA,MD 20892, USA. NR 58 TC 81 Z9 82 U1 0 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD JUN PY 1993 VL 5 IS 3 BP 368 EP 373 DI 10.1016/0952-7915(93)90055-W PG 6 WC Immunology SC Immunology GA LH451 UT WOS:A1993LH45100008 PM 7688515 ER PT J AU APASOV, S REDEGELD, F SITKOVSKY, M AF APASOV, S REDEGELD, F SITKOVSKY, M TI CELL-MEDIATED CYTOTOXICITY - CONTACT AND SECRETED FACTORS SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID LYMPHOCYTE-T ACTIVATION; CLASS-I PROTEIN; EXTRACELLULAR ATP; EFFECTOR FUNCTIONS; DNA FRAGMENTATION; TARGET-CELLS; LYSIS; GRANULES; BINDING; PERFORIN AB The list of cells with cytotoxic potential now may include small resting T cells, but the exact nature of 'lethal hit delivery' by cytotoxic T lymphocytes remains elusive. Cell-mediated cytotoxicity by cytotoxic T lymphocytes is a complex, multistep process which seems likely to be mediated by several different pathways. Recent experimental evidence for the functioning of a novel cytotoxic mechanism through a target cell's surface receptor illustrates and emphasizes the necessity to study the interactions of cytotoxic T lymphocytes and target cells as a whole. Progress is evident in the description of molecular requirements for triggering cytotoxicity, cell-cell contacts and the regulation of the effector responses of cytotoxic T lymphocytes by extracellular, intracellular and granular proteins. Extracellular Ca2+-dependent secretion of perforin and protease(s) may explain several aspects of cellular cytotoxicity, whereas the apoptosis-mediating cell surface Fas protein is now implicated in Ca2+-independent cytotoxicity. RP APASOV, S (reprint author), NIAID,IMMUNOL LAB,ROOM 11N-311,BLDG 10,BETHESDA,MD 20892, USA. RI Redegeld, Frank/O-6534-2016 OI Redegeld, Frank/0000-0001-8830-7960 NR 72 TC 61 Z9 61 U1 0 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD JUN PY 1993 VL 5 IS 3 BP 404 EP 410 DI 10.1016/0952-7915(93)90060-6 PG 7 WC Immunology SC Immunology GA LH451 UT WOS:A1993LH45100013 PM 7688517 ER PT J AU KARP, JE MERZ, WG DICK, JD AF KARP, JE MERZ, WG DICK, JD TI MANAGEMENT OF INFECTIONS IN NEUTROPENIC PATIENTS - ADVANCES IN THERAPY AND PREVENTION SO CURRENT OPINION IN INFECTIOUS DISEASES LA English DT Article AB The principles guiding the empiric antibiotic therapy for fever and infection in the granulocytopenic host have remained constant since they were formulated over two decades ago. In brief, the absence or impairment of a localizing inflammatory response resulting from granulocytopenia, plus lack of rapid diagnostic tests to identify causative organisms, necessitates the prompt implementation of broad-spectrum antibiotics against potential pathogens. Today, however, there are new options due to advances in three major areas: an expanding therapeutic armamentarium in terms of both broad and targeted coverage; an increasing capacity to define the specific drug susceptibility profiles of diverse organisms in a clinically relevant fashion; and the advent of hematopoietic and immune system biomodulators. As a result, the strategies for prevention, diagnosis, and therapy for infections in the granulocytopenic host are continually being refined. We can now begin to tailor our interventions to address the particular infecting pathogens and the specific host characteristics as determined by the pathogenesis of the underlying disease and the defects induced by antitumor therapy. RP KARP, JE (reprint author), NCI,9000 ROCKVILLE PIKE,BLDG 31,ROOM 11A27,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0951-7375 J9 CURR OPIN INFECT DIS JI Curr. Opin. Infect. Dis. PD JUN PY 1993 VL 6 IS 3 BP 405 EP 411 PG 7 WC Infectious Diseases SC Infectious Diseases GA LF349 UT WOS:A1993LF34900015 ER PT J AU GORBALENYA, AE KOONIN, EV AF GORBALENYA, AE KOONIN, EV TI HELICASES - AMINO-ACID-SEQUENCE COMPARISONS AND STRUCTURE-FUNCTION-RELATIONSHIPS SO CURRENT OPINION IN STRUCTURAL BIOLOGY LA English DT Article ID EXCISION REPAIR GENE; EARLY TRANSCRIPTION FACTOR; SITE-DIRECTED MUTAGENESIS; CONSERVED LYSINE RESIDUE; PUTATIVE RNA HELICASES; TERMINATION FACTOR-RHO; ESCHERICHIA-COLI REP; ATP-BINDING SEQUENCE; DNA HELICASE; SACCHAROMYCES-CEREVISIAE AB DNA and RNA helicases are ubiquitous enzymes that mediate the nucleoside-triphosphate-dependent unwinding of nucleic acid duplexes, a necessary step in genome replication, expression, recombination and repair. All proteins with demonstrated helicase activity contain the purine nucleoside-triphosphate-binding pattern; subsets of helicases possess additional conserved motifs. Three large superfamilies and two smaller families of helicases are described. Experimental results support the value of the conserved motifs for prediction of structure and function of the helicases. Some of these motifs can be used as reliable identifiers of the respective groups of helicases in database searches. The two largest helicase superfamilies share similar patterns of seven conserved sequence motifs, some of which are separated by long poorly conserved spacers. Helicase motifs appear to be organized in a core domain which provides the catalytic function, whereas optional inserts and amino- and carboxy-terminal sequences may comprise distinct domains with diverse accessory roles. C1 NIH, NATL CTR BIOTECHNOL INFORMAT,NATL LIBRARY MED, BLDG 38A,8600 ROCKVILLE PIKE, BETHESDA, MD 20894 USA. RUSSIAN ACAD MED SCI, MOSCOW, RUSSIA. RI Gorbalenya, Alexander/J-4818-2012 OI Gorbalenya, Alexander/0000-0002-4967-7341 NR 95 TC 884 Z9 902 U1 7 U2 49 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0959-440X EI 1879-033X J9 CURR OPIN STRUC BIOL JI Curr. Opin. Struct. Biol. PD JUN PY 1993 VL 3 IS 3 BP 419 EP 429 DI 10.1016/S0959-440X(05)80116-2 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LU406 UT WOS:A1993LU40600017 ER PT J AU TESSAROLLO, L TSOULFAS, P MARTINZANCA, D GILBERT, DJ JENKINS, NA COPELAND, NG PARADA, LF AF TESSAROLLO, L TSOULFAS, P MARTINZANCA, D GILBERT, DJ JENKINS, NA COPELAND, NG PARADA, LF TI TRKC, A RECEPTOR FOR NEUROTROPHIN-3, IS WIDELY EXPRESSED IN THE DEVELOPING NERVOUS-SYSTEM AND IN NONNEURONAL TISSUES SO DEVELOPMENT LA English DT Article DE TRKC; TYROSINE KINASE; NEURAL DEVELOPMENT; NEUROTROPHIN; NT-3; MOUSE NERVOUS SYSTEM ID TYROSINE KINASE RECEPTOR; AFFINITY NGF RECEPTOR; GROWTH-FACTOR FAMILY; MOLECULAR-CLONING; PROTOONCOGENE PRODUCT; GLYCINE RECEPTOR; PROTO-ONCOGENE; MOUSE; GENE; MEMBER AB The Trk family of tyrosine kinases encodes receptors for nerve growth factor-related neurotrophins. Here we present a developmental expression study of trkC, which encodes a receptor for neurotrophin-3 (NT-3). Like the related genes, trk and trkB, trkC is expressed primarily in neural lineages although the pattern is complex and includes non-neuronal cells. Direct comparison with trk and trkB developmental expression patterns permits the following observations. (1) trkC is expressed in novel neural tissues where other Trk genes are silent. (2) Some tissues appear to coexpress trkB and trkC receptors in the embryo and in the adult. (3) trkC expression can be detected in the gastrulating embryo. These data provide insights into the role of Trk-family receptors and nerve growth factor-related neurotrophins during development and suggest that, in addition to regulating neuronal survival and differentiation, the neurotrophin/Trk receptor system may have broader physiological effects. Finally, interspecific mouse backcrosses have been used to map the location of each of the Trk genes on mouse chromosomes. Alignment with available chromosomal maps identify possible linkage between the Trk genes and known neurological mutations. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,MOLEC EMBRYOL SECT,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RI Parada, luis/B-9400-2014; OI Tsoulfas, Pantelis/0000-0003-1974-6366 FU NCI NIH HHS [N01-CO-74101] NR 76 TC 255 Z9 256 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 JUN PY 1993 VL 118 IS 2 BP 463 EP 475 PG 13 WC Developmental Biology SC Developmental Biology GA LH327 UT WOS:A1993LH32700014 PM 8223273 ER PT J AU ONISTO, M GARBISA, S CAENAZZO, C FREDA, MP DIFRANCESCO, C NITTI, D LIOTTA, LA STETLERSTEVENSON, WG AF ONISTO, M GARBISA, S CAENAZZO, C FREDA, MP DIFRANCESCO, C NITTI, D LIOTTA, LA STETLERSTEVENSON, WG TI REVERSE TRANSCRIPTION-POLYMERASE CHAIN-REACTION PHENOTYPING OF METALLOPROTEINASES AND INHIBITORS INVOLVED IN TUMOR MATRIX INVASION SO DIAGNOSTIC MOLECULAR PATHOLOGY LA English DT Article DE MATRIX METALLOPROTEINASES; POLYMERASE CHAIN REACTION; TISSUE INHIBITORS OF METALLOPROTEINASES ID BASEMENT-MEMBRANE COLLAGEN; IV COLLAGENASE; MESSENGER-RNA; CELL-LINES; MR 72,000; INTERSTITIAL COLLAGENASE; CANCER METASTASIS; TISSUE INHIBITOR; EXPRESSION; TIMP-2 AB The matrix metalloproteinase enzymes have been implicated in tumor invasion and metastasis by a series of correlative immunohistochemical studies. In addition, direct evidence for the role of these enzymes in this pathologic process comes from studies using specific metalloproteinase inhibitors to block tumor invasion and metastasis formation, both in vitro and in vivo. Synthetic oligonucleotide primers for four metalloproteinases (MMP-1, MMP-2, MMP-9, MMP-10) and their tissue inhibitors (TIMP-1, TIMP-2) were selected, synthesized, and optimized in the reverse transcriptase-polymerase chain reaction (RT-PCR) to study the qualitative profile of these enzymes and inhibitors in cultured human tumor cells and tumor tissues. These primers are specific and generate unique amplification products for each appropriate enzyme and inhibitor. Slight enhancement in the amplification of cDNA products was achieved by adding dimethylsulfoxide to the reaction mixture, but commercial enhancement reagents were ineffective. Using this RT-PCR method, cDNA amplification was successful with RNA from as few as 20 cultured tumor cells. The RT-PCR analysis was done on three invasive human colon adenocarcinomas and their paired adjacent normal mucosa. The results show MMP-1 and MMP-2 products in all three tumors, and MMP-2 detected in one of the three normal mucosa samples; TIMP-2 expression was present in two of three patients and awaits quantitative assessment of RT-PCR products. C1 UNIV PADUA,INST HISTOL & GEN EMBRYOL,PADUA,ITALY. UNIV PADUA,DEPT SURG PATHOL 1,PADUA,ITALY. NCI,PATHOL LAB,BETHESDA,MD 20892. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 32 TC 49 Z9 50 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1052-9551 J9 DIAGN MOL PATHOL JI Diagn. Mol. Pathol. PD JUN PY 1993 VL 2 IS 2 BP 74 EP 80 DI 10.1097/00019606-199306000-00002 PG 7 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Pathology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Pathology GA MC151 UT WOS:A1993MC15100002 PM 8269280 ER PT J AU HENNINGFIELD, JE STAPLETON, JM BENOWITZ, NL GRAYSON, RF LONDON, ED AF HENNINGFIELD, JE STAPLETON, JM BENOWITZ, NL GRAYSON, RF LONDON, ED TI HIGHER LEVELS OF NICOTINE IN ARTERIAL THAN IN VENOUS-BLOOD AFTER CIGARETTE-SMOKING SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE NICOTINE; SMOKING; ARTERIAL AB We examined differences between arterial and venous concentrations of nicotine in human subjects. Shortly after smoking a cigarette, levels of nicotine in arterial plasma were more than double those in venous plasma. The time course of the rise in arterial nicotine levels and the magnitude of the arteriovenous difference varied considerably among subjects. For some subjects, arterial nicotine concentrations after one cigarette were similar to venous concentrations typically observed after 20 cigarettes and were nearly 10 times greater than venous concentrations. Our findings have implications for understanding the high degree of addictiveness and cardiovascular toxicity of smoked forms of drugs. C1 SAN FRANCISCO GEN HOSP,DEPT MED,MED SERV,CLIN PHARMACOL UNIT,SAN FRANCISCO,CA 94110. JOHNS HOPKINS MED INST,DEPT ANESTHESIOL,BALTIMORE,MD 21205. RP HENNINGFIELD, JE (reprint author), NIDA,ADDICT RES CTR,CLIN PHARMACOL BRANCH,POB 5180,BALTIMORE,MD 21224, USA. NR 21 TC 249 Z9 252 U1 0 U2 4 PU ELSEVIER SCI 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 JUN PY 1993 VL 33 IS 1 BP 23 EP 29 DI 10.1016/0376-8716(93)90030-T PG 7 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA LP035 UT WOS:A1993LP03500004 PM 8370337 ER PT J AU KORACH, KS AF KORACH, KS TI SURPRISING PLACES OF ESTROGENIC ACTIVITY SO ENDOCRINOLOGY LA English DT Editorial Material ID PHENOL RED RP KORACH, KS (reprint author), NIH,BETHESDA,MD 20892, USA. OI Korach, Kenneth/0000-0002-7765-418X NR 15 TC 63 Z9 63 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JUN PY 1993 VL 132 IS 6 BP 2277 EP 2278 DI 10.1210/en.132.6.2277 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LE170 UT WOS:A1993LE17000001 PM 8504730 ER PT J AU WETSEL, WC ERALY, SA WHYTE, DB MELLON, PL AF WETSEL, WC ERALY, SA WHYTE, DB MELLON, PL TI REGULATION OF GONADOTROPIN-RELEASING-HORMONE BY PROTEIN KINASE-A AND KINASE-C IN IMMORTALIZED HYPOTHALAMIC NEURONS SO ENDOCRINOLOGY LA English DT Article ID MEDIAN-EMINENCE; INTRACELLULAR PATHWAYS; CELLULAR-REGULATION; PHORBOL ESTER; ESTROUS-CYCLE; GNRH NEURONS; LHRH NEURONS; RAT-BRAIN; SECRETION; GENE AB As major signal transduction cascades, the protein kinase-A and -C (PKA and PKC) pathways have been implicated in the regulation of GnRH synthesis and secretion in the hypothalamus. We have investigated the roles of these pathways in the regulation of GnRH transcription, mRNA levels, propeptide processing, and secretion in GT1-7 cells, a mouse hypothalamic GnRH neuronal cell line. Forskolin, which activates adenylate cyclase to raise cAMP levels, had no effect on GnRH mRNA levels at 10 muM, but induced c-fos mRNA at 30 min. An activator of PKC, 12-O-tetradecanoylphorbol-13-acetate (TPA; 100 nm), also induced c-fos at 30 min, but produced a progressive decline in GnRH mRNA, resulting in a 70% decrease by 16 h. Coadministration of 10 nM TPA and 20 muM of a PKC inhibitor, NPC 15437 [2,6-diamino-N-([1-(1-oxotridecyl)2-piperidinyl]methyl)hexanamide], prevented c-fos induction, but did not antagonize GnRH repression. Instead, the inhibitor itself reduced GnRH mRNA levels by 56% at 16 h (with no effect on c-fos mRNA). Thus, since extended exposure to TPA can down-regulate PKC, suppression of GnRH mRNA by TPA may be due to decreased PKC activity, indicating a role for PKC in the maintenance of the GnRH gene expression (a role that is unlikely to involve c-fos). In transient transfections, the transcriptional activity from 3 kilobases of GnRH 5'-flanking sequence was repressed 2-fold by either 100 nm TPA or 20 muM NPC 15437 at 24 h, demonstrating that suppression of GnRH mRNA is at least, in part, at the level of transcription. In contrast, both TPA (100 nm) and forskolin (10 muM) stimulated secretion. Enhancement of GnRH secretion by TPA was robust and rapid (2.5 min), while the response to forskolin was relatively delayed (2 h). Over a 24-h period, unstimulated cells released primarily unprocessed prohormone, whereas forskolin and TPA stimulated the secretion of processed products. These data indicate that PKC and PKA may influence propeptide processing and/or the route of GnRH secretion. These data demonstrate that the PKA and PKC pathways regulate GnRH at the multiple levels of transcription, pro-GnRH processing, and GnRH secretion. C1 UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,DEPT REPROD MED,LA JOLLA,CA 92093. RP WETSEL, WC (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,POB 12233,BLDG 101,C4-07,RES TRIANGLE PK,NC 27709, USA. FU NICHD NIH HHS [P50 HD012303, R01 HD072754]; NIDDK NIH HHS [DK-44838, R01 DK044838] NR 57 TC 106 Z9 107 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JUN PY 1993 VL 132 IS 6 BP 2360 EP 2370 DI 10.1210/en.132.6.2360 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LE170 UT WOS:A1993LE17000013 PM 8504741 ER PT J AU RONDINONE, CM RODBARD, D BAKER, ME AF RONDINONE, CM RODBARD, D BAKER, ME TI ALDOSTERONE STIMULATES DIFFERENTIATION OF MOUSE 3T3-L1 CELLS INTO ADIPOCYTES SO ENDOCRINOLOGY LA English DT Article ID LIPOPROTEIN-LIPASE ACTIVITY; 11-BETA-HYDROXYSTEROID DEHYDROGENASE; MINERALOCORTICOID RECEPTOR; GLYCEROPHOSPHATE DEHYDROGENASE; GLUCOCORTICOID RECEPTOR; ADIPOSE CONVERSION; RAT-KIDNEY; BINDING; INVITRO; TISSUE AB We find that 1-10 nM aldosterone can induce differentiation of 3T3-L1 cells into adipose cells as evaluated by microscopic accumulation of fat droplets and quantitative measurement of triglycerides and of glycerol-3-phosphate dehydrogenase, an enzyme specific for adipocyte differentiation. Moreover, the aldosterone antagonist ZK91587 inhibits aldosterone- but not glucocorticoid-mediated differentiation of 3T3-L1 cells. Steroid binding assays with 3T3-L1 cells indicate the presence of specific binding sites for aldosterone. We conclude that there is an aldosterone receptor-mediated pathway for terminal differentiation of 3T3-L1 cells into adipose cells. Receptors for aldosterone have also been found in a variety of cells that do not function to regulate sodium and potassium transport. The aldosterone receptor may have a role in regulation expression of genes involved in differentiation of these cells. C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. OI Baker, Michael/0000-0003-4387-3269 NR 37 TC 65 Z9 65 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JUN PY 1993 VL 132 IS 6 BP 2421 EP 2426 DI 10.1210/en.132.6.2421 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LE170 UT WOS:A1993LE17000020 PM 8504747 ER PT J AU PARK, KS SOHN, DH VEECH, RL SONG, BJ AF PARK, KS SOHN, DH VEECH, RL SONG, BJ TI TRANSLATIONAL ACTIVATION OF ETHANOL-INDUCIBLE CYTOCHROME-P450 (CYP2E1) BY ISONIAZID SO EUROPEAN JOURNAL OF PHARMACOLOGY-ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY SECTION LA English DT Article DE ETHANOL-INDUCIBLE CYTOCHROME-P450; ISONIAZID; TRANSLATIONAL ACTIVATION ID LIVER MICROSOMAL CYTOCHROME-P-450; RAT-LIVER; N-NITROSODIMETHYLAMINE; GROWTH-HORMONE; ISOZYME 3A; ACETONE; INDUCTION; METABOLISM; SUBSTRATE; ACID AB The molecular mechanism of ethanol-inducible cytochrome P450(CYP2E1) induction by isoniazid was studied and compared to that of pyridine, an inducer of CYP2E1. Aniline hydroxylase and immunoreactive CYP2E1 protein were significantly induced by isoniazid without or with only slight activation of other cytochromes P450. In contrast, pyridine increased the activities of a broad range of P450s. The effects of two structural analogs of isoniazid, isonicotinamide and isonicotinic acid were also tested and found to have a markedly decreased ability to induce CYP2E1. The induction of CYP2E1 by isoniazid was not accompanied by an increased level of CYP2E1 mRNA, and was completely blocked by pretreatment with cycloheximide or sodium fluoride, inhibitors of mRNA translation. These data thus suggest that CYP2E1 induction by isoniazid is due to activation of CYP2E1 mRNA translation and that the hydrazide group on the pyridine ring of isoniazid is important both in the selective induction of CYP2E1 and for magnitude of effect. C1 NIAAA,METAB & MOLEC BIOL LAB,12501 WASHINGTON AVE,ROCKVILLE,MD 20852. NR 39 TC 58 Z9 59 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0926-6917 J9 EUR J PHARM-ENVIRON JI Eur. J. Pharmacol.-Environ. Toxicol. Pharmacol. Sect. PD JUN 1 PY 1993 VL 248 IS 1 BP 7 EP 14 DI 10.1016/0926-6917(93)90019-M PG 8 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA LH887 UT WOS:A1993LH88700002 PM 8339754 ER PT J AU WISTOW, G AF WISTOW, G TI POSSIBLE TETRAMER-BASED QUATERNARY STRUCTURES FOR ALPHA-CRYSTALLINS AND SMALL HEAT-SHOCK PROTEINS SO EXPERIMENTAL EYE RESEARCH LA English DT Letter ID MOLECULAR-WEIGHT; BOVINE RP WISTOW, G (reprint author), NEI,LMDB,MOLEC STRUCT & FUNCT SECT,BETHESDA,MD 20892, USA. NR 30 TC 87 Z9 87 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JUN PY 1993 VL 56 IS 6 BP 729 EP 732 DI 10.1006/exer.1993.1090 PG 4 WC Ophthalmology SC Ophthalmology GA LG268 UT WOS:A1993LG26800011 PM 8595815 ER PT J AU HESTDAL, K JACOBSEN, SEW RUSCETTI, FW LONGO, DL BOONE, TC KELLER, JR AF HESTDAL, K JACOBSEN, SEW RUSCETTI, FW LONGO, DL BOONE, TC KELLER, JR TI INCREASED GRANULOPOIESIS AFTER SEQUENTIAL ADMINISTRATION OF TRANSFORMING GROWTH-FACTOR-BETA-1 AND GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE GRANULOPOIESIS; TGF-BETA; GM-CSF ID HEMATOPOIETIC PROGENITOR CELLS; BONE-MARROW CULTURES; FACTOR-BETA; GM-CSF; FACTOR-I; INTERLEUKIN-3; PROLIFERATION; INVITRO; MICE; PURIFICATION AB Transforming growth factor-beta 1 (TGF-beta 1) is an inhibitor of the growth and differentiation of immature hematopoietic progenitors in vitro; however, we have demonstrated that TGF-beta 1 can promote granulopoiesis in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) in vitro. We therefore examined the effect of the combined administration of TGF-1 beta and GM-CSF in vivo. First, TGF-beta 1 enhanced the specific binding of GM-CSF (2.0-fold) on bone marrow cells, reaching a maximum 40 hours after injection, while the specific binding of interleukin-3 (IL-3) was unaffected. Using GM-CSF-specific binding to determine the optimal regimen for cytokine administration in vivo, we found that the administration of TGF-beta 1 and GM-CSF in sequence increased myelopoiesis. Total numbers of colony-forming units-granulocyte/macrophage (CFU-GM) and myeloblasts per femur were increased above the level obtained with the simultaneous injection of TGF-beta 1 plus GM-CSF, GMCSF alone or TGF-beta 1 alone. Further, the sequential administration of TGF-beta 1 and GM-CSF resulted in enhanced numbers of mature granulocytes in both the bone marrow and peripheral blood. In contrast, the sequential combination of TGF-beta 1 and GM-CSF did not enhance the numbers or increase the recovery of erythroid cells in the bone marrow. These results show that TGF-beta 1 in vivo as in vitro has a multifunctional effect on bone marrow progenitors, and by using an optimal combination of TGF-beta 1 and GM-CSF in vivo, one can selectively increase both the central and peripheral granulopoietic compartments. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD. AMGEN INC,THOUSAND OAKS,CA 91320. FU PHS HHS [N01-C0-74102] NR 35 TC 19 Z9 19 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JUN PY 1993 VL 21 IS 6 BP 799 EP 805 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA MW611 UT WOS:A1993MW61100013 PM 8500577 ER PT J AU SNYDERWINE, EG NOUSO, K SCHUT, HAJ AF SNYDERWINE, EG NOUSO, K SCHUT, HAJ TI EFFECT OF 3-METHYLCHOLANTHRENE INDUCTION ON THE DISTRIBUTION AND DNA ADDUCTION OF 2-AMINO-3-METHYLIMIDAZO[4,5-F]QUINOLINE (IQ) IN F344 RATS SO FOOD AND CHEMICAL TOXICOLOGY LA English DT Article ID BORNE CARCINOGEN 2-AMINO-3,8-DIMETHYLIMIDAZO<4,5-F>QUINOXALINE; FOOD MUTAGEN 2-AMINO-1-METHYL-6-PHENYLIMIDAZO<4,5-B>PYRIDINE; HETEROCYCLIC AMINES; METABOLIC-ACTIVATION; CYTOCHROME-P-450 ENZYMES; LIVER; BINDING; MICE; IDENTIFICATION; QUINOLINE AB 3-Methylcholanthrene (3MC) is a potent inducer of the cytochrome P450IA family of enzymes that catalyses the metabolic activation of the food mutagen/carcinogen 2-amino-3-methylimidazo-[4,5-f]quinoline (IQ). We have examined the effect of pretreatment with 3MC on the distribution and DNA adduct formation of IQ in male Fischer F344 rats. 3 hr after a single dose of [C-14]IQ (10 mg/kg body weight, by gavage), the level of radioactivity in extrahepatic tissues was 30-70% less in 3MC-pretreated rats than in vehicle control rats. Although the level of radioactivity in the liver did not change after 3MC pretreatment, IQ-DNA adduct levels, measured by the P-32-postlabelling method, were 60% lower in the livers of 3MC-pretreated rats than those of control rats, and 83-97% lower in extrahepatic tissues such as the kidneys, colon, small intestine, bladder, heart and lung. IQ-DNA adducts in the testes and brain were found in control rats but were not detected in 3MC-pretreated rats. The rate of removal of IQ-DNA adducts from the livers of control and 3MC-pretreated animals was the same from 3 to 48 hr. At 48 hr, the adduct level in 3MC-pretreated rats remained lower than that seen in the control rats. The data suggest that 3MC induction of the P450IA family of cytochromes in vivo results in an increased rate of IQ detoxification. C1 MED COLL OHIO,DEPT PATHOL,TOLEDO,OH 43699. RP SNYDERWINE, EG (reprint author), NCI,DIV CANC ETIOL,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 42 TC 17 Z9 17 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0278-6915 J9 FOOD CHEM TOXICOL JI Food Chem. Toxicol. PD JUN PY 1993 VL 31 IS 6 BP 415 EP 423 DI 10.1016/0278-6915(93)90156-S PG 9 WC Food Science & Technology; Toxicology SC Food Science & Technology; Toxicology GA LK341 UT WOS:A1993LK34100003 PM 8514213 ER PT J AU VINSON, CR HAI, TW BOYD, SM AF VINSON, CR HAI, TW BOYD, SM TI DIMERIZATION SPECIFICITY OF THE LEUCINE ZIPPER-CONTAINING BZIP MOTIF ON DNA-BINDING - PREDICTION AND RATIONAL DESIGN SO GENES & DEVELOPMENT LA English DT Article DE BZIP; C EBP FAMILY; ATF CREB FAMILY; DNA-BINDING PROTEINS; DIMERIZATION SPECIFICITY ID TRANSCRIPTIONAL ACTIVATOR PROTEIN; COILED-COIL; FOS; JUN; C/EBP; FAMILY; GCN4; EXPRESSION; HETERODIMERS; POLYMERASE AB We propose an interhelical salt bridge rule to explain the dimerization specificity between the two amphipathic alpha-helices in the leucine zipper structure. Using the bZIP class of DNA-binding proteins as a model system, we predicted and designed novel dimerization partners. We predicted that ATF4, a member of the ATF/CREB family of transcription factors, would preferentially form heterodimers with IGEBP1, a member of the C/EBP family. We also predicted that neither ATF4 nor IGEBP1 would form heterodimers with DBP, a member of the C/EBP superfamily. These predictions were verified using a gel mobility-shift assay. To further test the value of this interhelical salt bridge rule, we modified the bZIP protein C/EBP attempting to design molecules that would form preferentially heterodimers with C/EBP or molecules that would not interact with C/EBP. These designed molecules behaved as predicted. Therefore, we conclude that this interhelical salt bridge rule is useful in understanding the dimerization specificity of bZIP proteins. In addition, we suggest that this rule could be used to design novel ''dominant-negative'' molecules to specifically inhibit the function of target leucine zipper proteins in vivo. C1 OHIO STATE UNIV,DEPT MED BIOCHEM,COLUMBUS,OH 43210. OHIO STATE UNIV,OHIO STATE BIOTECHNOL CTR,COLUMBUS,OH 43210. RP VINSON, CR (reprint author), NCI,BIOCHEM LAB,BETHESDA,MD 20892, USA. RI Hai, Tsonwin/H-4480-2011 OI Hai, Tsonwin/0000-0003-4510-0315 NR 42 TC 277 Z9 277 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD JUN PY 1993 VL 7 IS 6 BP 1047 EP 1058 DI 10.1101/gad.7.6.1047 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA LF509 UT WOS:A1993LF50900011 PM 8504929 ER PT J AU SLIM, R LEPASLIER, D COMPAIN, S LEVILLIERS, J OUGEN, P BILLAULT, A DONOHUE, SJ KLEIN, DC MINTZ, L BERNHEIM, A COHEN, D WEISSENBACH, J PETIT, C AF SLIM, R LEPASLIER, D COMPAIN, S LEVILLIERS, J OUGEN, P BILLAULT, A DONOHUE, SJ KLEIN, DC MINTZ, L BERNHEIM, A COHEN, D WEISSENBACH, J PETIT, C TI CONSTRUCTION OF A YEAST ARTIFICIAL CHROMOSOME CONTIG SPANNING THE PSEUDOAUTOSOMAL REGION AND ISOLATION OF 25 NEW SEQUENCE-TAGGED SITES SO GENOMICS LA English DT Article ID HUMAN SEX-CHROMOSOMES; DNA-SEQUENCES; GENE; LINKAGE; MAP; DELETIONS; LIBRARY; XP22.3; LOCUS C1 INST PASTEUR,UNITE GENET MOLEC HUMAINE,CNRS,URA 1445,25 RUE DR ROUX,F-75724 PARIS 15,FRANCE. CTR ETUD POLYMORPHISME HUMAIN,F-75010 PARIS,FRANCE. NICHHD,NEUROENDOCRINOL SECT,DEV NEUROBIOL LAB,BETHESDA,MD 20892. INST GUSTAVE ROUSSY,CYTOGENET & GENET ONCOL LAB,CNRS,URA 1158,F-94805 VILLEJUIF,FRANCE. NR 48 TC 26 Z9 26 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JUN PY 1993 VL 16 IS 3 BP 691 EP 697 DI 10.1006/geno.1993.1249 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA LF828 UT WOS:A1993LF82800020 PM 8100802 ER PT J AU LI, K CHRISTIANO, AM COPELAND, NG GILBERT, DJ CHU, ML JENKINS, NA UITTO, J AF LI, K CHRISTIANO, AM COPELAND, NG GILBERT, DJ CHU, ML JENKINS, NA UITTO, J TI CDNA CLONING AND CHROMOSOMAL MAPPING OF THE MOUSE TYPE-VII COLLAGEN GENE (COL7A1) - EVIDENCE FOR RAPID EVOLUTIONARY DIVERGENCE OF THE GENE SO GENOMICS LA English DT Article ID BULLOUS PEMPHIGOID ANTIGEN; LINKAGE MAP; EXPRESSION C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT DERMATOL,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT BIOCHEM & MOLEC BIOL,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON INST MOLEC MED,MOLEC DERMATOL SECT,PHILADELPHIA,PA 19107. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FU NCPDCID CDC HHS [NCI N01-C074101]; NIAMS NIH HHS [P01-AR38923, T32-AR7567] NR 33 TC 20 Z9 22 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JUN PY 1993 VL 16 IS 3 BP 733 EP 739 DI 10.1006/geno.1993.1255 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA LF828 UT WOS:A1993LF82800026 PM 8325648 ER PT J AU GOLDMUNTZ, EA REMMERS, EF ZHA, HB CASH, JM MATHERN, P CROFFORD, LJ WILDER, RL AF GOLDMUNTZ, EA REMMERS, EF ZHA, HB CASH, JM MATHERN, P CROFFORD, LJ WILDER, RL TI GENETIC-MAP OF 12 POLYMORPHIC LOCI ON RAT CHROMOSOME-1 SO GENOMICS LA English DT Note RP GOLDMUNTZ, EA (reprint author), NIAMSD,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD 20892, USA. RI Crofford, Leslie/J-8010-2013 NR 17 TC 26 Z9 26 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JUN PY 1993 VL 16 IS 3 BP 761 EP 764 DI 10.1006/geno.1993.1261 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA LF828 UT WOS:A1993LF82800032 PM 8100804 ER PT J AU SAKAI, A MAKINO, T KATO, Y KATO, T MOTOYAMA, S SAITO, S IIZUKA, R NOZAWA, S AF SAKAI, A MAKINO, T KATO, Y KATO, T MOTOYAMA, S SAITO, S IIZUKA, R NOZAWA, S TI A UTERINE MUSCLE CONTRACTILE SUBSTANCE OBTAINED FROM A HUMAN PLACENTAL CDNA LIBRARY SO GYNECOLOGICAL ENDOCRINOLOGY LA English DT Article DE PLACENTA; CDNA; UTERINE CONTRACTION; OXYTOCIN AB A cDNA clone coding for an oxytocin-like substance was prepared from a human placental cDNA library. using oxytocin antiserum. The cDNA size was approximately 900 bp. A mammalian expression vector containing the cDNA was constructed and transfected into Chinese hamster ovary (CHO) cells. The expression of immunoreactivity to oxytocin antiserum was observed by radioimmunoassay. The cultured medium of the transfected cells was assayed for uterine muscle contractile bioactivity using a Magnus apparatus. Bioactivity was eliminated by incubation with oxytocin antiserum. Thus, the cDNA done, screened with oxytocin antibody, is surmised to code for an oxytocin-like activity, but the nucleotide and amino acid sequences responsible for the biological activity remain to be clarified. RP SAKAI, A (reprint author), NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP PI CARNFORTH LANCASHIRE PA CASTERTON HALL, CARNFORTH LANCASHIRE, ENGLAND LA6 2LA SN 0951-3590 J9 GYNECOL ENDOCRINOL JI Gynecol. Endocrinol. PD JUN PY 1993 VL 7 IS 2 BP 77 EP 82 DI 10.3109/09513599309152484 PG 6 WC Endocrinology & Metabolism; Obstetrics & Gynecology SC Endocrinology & Metabolism; Obstetrics & Gynecology GA LN121 UT WOS:A1993LN12100001 PM 8213230 ER PT J AU KALUZNY, AD LACEY, LM WARNECKE, R HYNES, DM MORRISSEY, J FORD, L SONDIK, E AF KALUZNY, AD LACEY, LM WARNECKE, R HYNES, DM MORRISSEY, J FORD, L SONDIK, E TI PREDICTING THE PERFORMANCE OF A STRATEGIC ALLIANCE - AN ANALYSIS OF THE COMMUNITY CLINICAL ONCOLOGY PROGRAM SO HEALTH SERVICES RESEARCH LA English DT Article DE STRATEGIC ALLIANCE; CLINICAL TRIALS NETWORKS; ACCRUAL TO TREATMENT PROTOCOLS ID ADOPTION; SIZE AB Objective. This study is designed to examine the effects of environment and structure of the Community Clinical Oncology Program (CCOP) on performance as measured by patient accrual to National Cancer Institute (NCI)-approved treatment protocols. Data Sources/Study Setting. Data and analysis are part of a larger evaluation of the NCI Community Clinical Oncology Program during its second funding cycle, June 1987-May 1990. Data, taken from primary and secondary sources, included a survey of selected informants in CCOPs and research bases, CCOP grant applications, CCOP annual progress reports, and site visits to a subsample of CCOPs (N = 20) and research bases (N = 5). Accrual data were obtained from NCI records. Study Design. Analysis involved three complementary sets of factors: the local health care resources environment available to the CCOP, the larger policy environment as reflected by the relationship of the CCOP to selected research bases and the NCI, and the operational structure of the CCOP itself. A hierarchical model examined the separate and cumulative effects of local and policy environment and structure on performance. Principal Findings. Other things equal, the primary predictors of treatment accrual were (1) the larger policy environment, as measured by the attendance of nurses at research base meetings; and (2) operational structure, as measured by the number and character of components within participating CCOPs and the number of hours per week worked by data managers. These factors explained 73 percent of the total variance in accrual performance. Conclusions. Findings suggest criteria for selecting the types of organizations to participate in the alliance, as well as for establishing guidelines for managing such alliances. A future challenge is to determine the extent to which factors predicting accrual to cancer treatment clinical trials are equally important as predictors of accrual to cancer prevention and control trials. C1 UNIV ILLINOIS,SURVEY RES LAB,CHICAGO,IL 60680. DUKE UNIV,DEPT MED,DURHAM,NC 27706. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. VET AFFAIRS MED CTR,DURHAM,NC. NCI,COMMUNITY ONCOL & REHABIL BRANCH,BETHESDA,MD 20892. RP KALUZNY, AD (reprint author), UNIV N CAROLINA,CECIL G SHEPS CTR HLTH SERV RES,CB 7590,725 AIRPORT RD,CHAPEL HILL,NC 27599, USA. NR 30 TC 21 Z9 21 U1 0 U2 4 PU HEALTH ADMINISTRATION PRESS PI MELROSE PARK PA C/O FOUNDATION AMER COLL HEALTHCARE EXECUTIVES 1951 CORNELL AVE, MELROSE PARK, IL 60160 SN 0017-9124 J9 HEALTH SERV RES JI Health Serv. Res. PD JUN PY 1993 VL 28 IS 2 BP 159 EP 182 PG 24 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA LH648 UT WOS:A1993LH64800002 PM 8514498 ER PT J AU ALTER, HJ SHIH, JWK AF ALTER, HJ SHIH, JWK TI PROBABLE VISUALIZATION OF THE ELUSIVE HEPATITIS-C VIRUS SO HEPATOLOGY LA English DT Note RP ALTER, HJ (reprint author), NIH,DEPT TRANSFUS MED,BETHESDA,MD 20892, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 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 JUN PY 1993 VL 17 IS 6 BP 1164 EP 1166 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LJ985 UT WOS:A1993LJ98500032 PM 8390396 ER PT J AU YU, QS LUO, WM LI, YQ BROSSI, A AF YU, QS LUO, WM LI, YQ BROSSI, A TI PROGRESS TOWARDS A PRACTICAL TOTAL SYNTHESIS OF CALABAR ALKALOIDS - TOTAL SYNTHESIS OF (-)-ESERMETHOLE AND (-)-PHYSOVENOL METHYL-ETHER FROM (3S)-1,3-DIMETHYL-3-CARBOXYMETHYL-5-METHOXYOXINDOLE SO HETEROCYCLES LA English DT Article ID ANTICHOLINESTERASE ACTIVITY; CARBAMATE ANALOGS; (-)-PHYSOSTIGMINE; (+)-PHYSOSTIGMINE; (+)-PHYSOVENINE; PHYSOSTIGMINE; OXINDOLES AB Chemical resolution of the oxindoleacetic acid (7) with brucine in water yielded the acid (7a) of (3S)-absolute configuration. Acid (7a), in using conventional methods, was converted into nitrile (8a), lactone (9a) and amides (10a), and (11a) respectively. Amide (10a), on reduction with LAH in refluxing THF, directly yielded (-)-esermethole (12a), and amide (11a) similarly gave (-)-N1-benzylnoresermethole (13a). Reduction of ester (6a) with LAH in refluxing THF yielded (-)-physovenol methyl ether (14a). C1 GEORGETOWN UNIV,DEPT CHEM,WASHINGTON,DC 20057. NIDDKD,BETHESDA,MD 20892. RP YU, QS (reprint author), ACAD SINICA,SHANGHAI INST ORGAN CHEM,345 LINGLING LU,SHANGHAI 200032,PEOPLES R CHINA. NR 23 TC 31 Z9 31 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0385-5414 J9 HETEROCYCLES JI Heterocycles PD JUN 1 PY 1993 VL 36 IS 6 BP 1279 EP 1285 PG 7 WC Chemistry, Organic SC Chemistry GA LC821 UT WOS:A1993LC82100011 ER PT J AU OSHAUGHNESSY, JA COWAN, KH WILSON, W BRYANT, G GOLDSPIEL, B GRESS, R NIENHUIS, AW DUNBAR, C SORRENTINO, B STEWART, FM MOEN, R FOX, M LEITMAN, S AF OSHAUGHNESSY, JA COWAN, KH WILSON, W BRYANT, G GOLDSPIEL, B GRESS, R NIENHUIS, AW DUNBAR, C SORRENTINO, B STEWART, FM MOEN, R FOX, M LEITMAN, S TI PILOT-STUDY OF HIGH-DOSE ICE (IFOSFAMIDE, CARBOPLATIN, ETOPOSIDE) CHEMOTHERAPY AND AUTOLOGOUS BONE-MARROW TRANSPLANT (ABMT) WITH NEOR-TRANSDUCED BONE-MARROW AND PERIPHERAL-BLOOD STEM-CELLS IN PATIENTS WITH METASTATIC BREAST-CANCER SO HUMAN GENE THERAPY LA English DT Article ID MEDIATED GENE-TRANSFER; HEMATOPOIETIC PROGENITOR CELLS; CHRONIC MYELOID-LEUKEMIA; ADENOSINE-DEAMINASE; EXPRESSION; COMBINATION; CULTURE; INVITRO; INTERLEUKIN-6; SURVIVAL C1 NIH,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. UNIV VIRGINIA,CHARLOTTESVILLE,VA 22903. GENET THERAPY INC,GAITHERSBURG,MD. NHLB,BETHESDA,MD. RP OSHAUGHNESSY, JA (reprint author), NCI,BETHESDA,MD 20892, USA. NR 71 TC 12 Z9 12 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD JUN PY 1993 VL 4 IS 3 BP 331 EP 354 DI 10.1089/hum.1993.4.3-331 PG 24 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA LH389 UT WOS:A1993LH38900011 PM 8338880 ER PT J AU MAEKAWA, M SUDO, K KITAJIMA, M MATSUURA, Y LI, SSL KANNO, T AF MAEKAWA, M SUDO, K KITAJIMA, M MATSUURA, Y LI, SSL KANNO, T TI ANALYSIS OF A GENETIC MUTATION IN AN ELECTROPHORETIC VARIANT OF THE HUMAN LACTATE DEHYDROGENASE-B(H) SUBUNIT SO HUMAN GENETICS LA English DT Article ID DNA; DEFICIENCY; AMPLIFICATION; HEART AB An electrophoretic variant of the lactate dehydrogenase (LDH)-B(H) subunit was discovered in a patient with diabetes mellitus. His LDH activity in serum was slightly lower than normal and the LDH isozyme pattern showed an abnormal migration indicating an LDH-B subunit variant of the fast type. The LDH containing the variant subunit revealed a decreased heat stability. DNA analysis of the variant allele detected a base substitution, an A to G transition, at codon 6 (AAA-->GAA). The mutation resulted in the replacement of a lysine by a glutamic acid (K6E). The change may cause the heat instability and affect the net charge of the variant subunit, resulting in an electrophoretic LDH-B subunit variant of the fast type. C1 JIKEI UNIV, DAISAN HOSP, SCH MED, DEPT LAB MED, KOMAE 201, JAPAN. FUJITSU LTD, MINATO KU, TOKYO 105, JAPAN. NIEHS, GENET LAB, RES TRIANGLE PK, NC 27709 USA. RP MAEKAWA, M (reprint author), HAMAMATSU UNIV SCH MED, DEPT LAB MED, HAMAMATSU, SHIZUOKA 431-31, JAPAN. NR 25 TC 12 Z9 14 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD JUN PY 1993 VL 91 IS 5 BP 423 EP 426 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA LK457 UT WOS:A1993LK45700003 PM 8314553 ER PT J AU SCHMIDT, L LI, H WEI, MH LERMAN, MI ZBAR, B TORY, K AF SCHMIDT, L LI, H WEI, MH LERMAN, MI ZBAR, B TORY, K TI 6 DINUCLEOTIDE MICROSATELLITE POLYMORPHISMS ON HUMAN CHROMOSOME-3 SO HUMAN MOLECULAR GENETICS LA English DT Article C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. RP SCHMIDT, L (reprint author), NCI,PROGRAM RESOURCES INC,DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. NR 5 TC 9 Z9 9 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. PD JUN PY 1993 VL 2 IS 6 BP 817 EP 818 DI 10.1093/hmg/2.6.817 PG 2 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA LH892 UT WOS:A1993LH89200036 PM 8353502 ER PT J AU LI, H SCHMIDT, L WEI, MH HUSTAD, T LERMAN, MI ZBAR, B TORY, K AF LI, H SCHMIDT, L WEI, MH HUSTAD, T LERMAN, MI ZBAR, B TORY, K TI 3 TETRAMERIC REPEAT POLYMORPHISMS ON HUMAN CHROMOSOME-3 - D3S1349, D3S1350, D3S1351 SO HUMAN MOLECULAR GENETICS LA English DT Article C1 NCI,PROGRAM RESOURCES INC,DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,IMMUNOL LAB,FREDERICK,MD 21702. NR 3 TC 4 Z9 4 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. PD JUN PY 1993 VL 2 IS 6 BP 819 EP 819 DI 10.1093/hmg/2.6.819 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA LH892 UT WOS:A1993LH89200037 PM 8353503 ER PT J AU MOSS, N STONE, MC SMITH, JB AF MOSS, N STONE, MC SMITH, JB TI FERTILITY AMONG CENTRAL-AMERICAN REFUGEES AND IMMIGRANTS IN BELIZE SO HUMAN ORGANIZATION LA English DT Article DE CENTRAL AMERICA; FAMILY PLANNING; FERTILITY; MIGRATION; REFUGEES AB This study describes how international migration, including refugee status, affects both child spacing and awareness of and interest in family planning. Guatemalan, Salvadoran, and Belizean women with children under six years of age (n = 133) were interviewed in a survey conducted in 1989 in three settlements in Belize, Central America that have a high proportion of refugees and economic immigrants. Migration was characterized by women's nationality, residency status, and length of time in Belize. Over half of the women were interested in family planning, and two-thirds of them had discussed family planning with their spouses. Among women interested in family planning, 62% could spontaneously mention a method of contraception; the pill and sterilization were each mentioned by a quarter of these women. The women had a median age of 28 years, averaged 4.5 live births, and wanted 1.5 additional children. There was no effect of migration on fertility, but when mother's age, parity, and available acreage were controlled for, refugees wanted twice as many additional children as permanent residents or those without legal residency (p < .003). The latter had shorter intervals from migration to next birth (p < .02). Referral to family health services when women immigrants and refugees register at entry is recommended, as are culturally and linguistically appropriate services available for all women. C1 UNIV TEXAS,DEPT ANTHROPOL,AUSTIN,TX 78712. RP MOSS, N (reprint author), NIAID,CTR POPULAT RES,DEMOG & BEHAV SCI BRANCH,BETHESDA,MD 20892, USA. NR 21 TC 3 Z9 3 U1 0 U2 2 PU SOC APPLIED ANTHROPOLOGY PI OKLAHOMA CITY PA BUSINESS OFFICE BOX 24083, OKLAHOMA CITY, OK 73124 SN 0018-7259 J9 HUM ORGAN JI Hum. Organ. PD SUM PY 1993 VL 52 IS 2 BP 186 EP 193 PG 8 WC Anthropology; Social Sciences, Interdisciplinary SC Anthropology; Social Sciences - Other Topics GA LC968 UT WOS:A1993LC96800008 ER PT J AU GAFFEY, MJ FRIERSON, HF MEDEIROS, LJ WEISS, LM AF GAFFEY, MJ FRIERSON, HF MEDEIROS, LJ WEISS, LM TI THE RELATIONSHIP OF EPSTEIN-BARR-VIRUS TO INFECTION-RELATED (SPORADIC) AND FAMILIAL HEMOPHAGOCYTIC SYNDROME AND SECONDARY (LYMPHOMA-RELATED) HEMOPHAGOCYTOSIS - AN INSITU HYBRIDIZATION STUDY SO HUMAN PATHOLOGY LA English DT Article DE HEMOPHAGOCYTIC SYNDROME; HISTIOCYTOSIS; EPSTEIN-BARR VIRUS; INSITU HYBRIDIZATION ID ANGIOCENTRIC IMMUNOPROLIFERATIVE LESIONS; HISTIOCYTIC MEDULLARY RETICULOSIS; MALIGNANT HISTIOCYTOSIS; LYMPHOHISTIOCYTOSIS; MONONUCLEOSIS; PROLIFERATIONS; SPECTRUM; TISSUES C1 NCI,BETHESDA,MD 20892. CITY HOPE NATL MED CTR,DUARTE,CA 91010. RP GAFFEY, MJ (reprint author), UNIV VIRGINIA,HLTH SCI CTR,DEPT PATHOL,BOX 214,CHARLOTTESVILLE,VA 22908, USA. NR 39 TC 54 Z9 55 U1 0 U2 0 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 JUN PY 1993 VL 24 IS 6 BP 657 EP 667 DI 10.1016/0046-8177(93)90247-E PG 11 WC Pathology SC Pathology GA LF598 UT WOS:A1993LF59800015 PM 8389318 ER PT J AU ABASSI, ZA KLEIN, H COX, J KEISER, HR AF ABASSI, ZA KLEIN, H COX, J KEISER, HR TI BRADYKININ DOES NOT MODULATE THE NATRIURETIC RESPONSE TO ATRIAL-NATRIURETIC-FACTOR IN RATS WITH AORTOCAVAL FISTULA SO HYPERTENSION LA English DT Article; Proceedings Paper CT 46TH ANNUAL FALL CONF AND SCIENTIFIC SESSION OF THE COUNCIL FOR HIGH BLOOD PRESSURE RESEARCH CY SEP 29-OCT 02, 1992 CL CLEVELAND, OH SP COUNCIL HIGH BLOOD PRESSURE RES DE ATRIAL NATRIURETIC FACTOR; BRADYKININ; HEART FAILURE, CONGESTIVE; FISTULA; RENAL FUNCTION ID EXPERIMENTAL HEART-FAILURE; PEPTIDE; SODIUM AB Rats with aortocaval fistula, an experimental model of congestive heart failure (CHF), display two distinct patterns of sodium excretion: some rats develop marked sodium retention and worsening edema with urinary excretion of sodium (U(Na)V) < 200 muEq per 24 hours, i.e., uncompensated CHF, whereas in others sodium balance rapidly returns to normal (U(Na)V > 1,400 muEq per 24 hours), i.e., compensated CHF. Similar patterns of sodium excretion are found in patients with CHF. The mechanisms underlying these responses are not fully understood. The present study was designed to assess whether bradykinin plays a role in the compensatory response to CHF. Infusions of either 10 or 50 mug/ kg per minute of synthetic atrial natriuretic factor (ANF)8-33 into sham-operated control animals produced significant increases in urine flow and fractional excretion of sodium (FE(Na)). Infusions of ANF at the same doses into rats with compensated CHF increased FE(Na) from 0.11+/-0.03% to a maximum of 6.10+/-1.30%, whereas the rise in FE(Na) in animals with uncompensated CHF was significantly reduced (0.05+/-0.01% to 0.59+/-0.18%) compared with sham-operated controls (0.23+/-0.05% to 8.32+/-1.0%) or the group with compensated CHF. Treatment of the compensated rats with the bradykinin antagonist HOE-140 (D-Arg,[Hyp3,Thi5,D-Tic7, Oic8]-bradykinin) given at a rate of 100 nmol/ kg per hour did not affect their renal response to the ANF. In addition, infusion of the bradykinin antagonist alone into compensated rats with aortocaval fistula had no significant effect on their basal urinary flow rate or sodium excretion during the infusion. These findings indicate that kinins do not modulate either the natriuretic response to ANF or basal sodium excretion in rats with compensated CHF. RP ABASSI, ZA (reprint author), NHLBI,HYPERTENS ENDOCRINE BRANCH,BLDG 10,RM 8C103,BETHESDA,MD 20892, USA. NR 23 TC 4 Z9 4 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JUN PY 1993 VL 21 IS 6 BP 966 EP 970 PN 2 PG 5 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LF394 UT WOS:A1993LF39400017 PM 8505108 ER PT J AU CARSON, RE YAN, Y DAUBEWITHERSPOON, ME FREEDMAN, N BACHARACH, SL HERSCOVITCH, P AF CARSON, RE YAN, Y DAUBEWITHERSPOON, ME FREEDMAN, N BACHARACH, SL HERSCOVITCH, P TI AN APPROXIMATION FORMULA FOR THE VARIANCE OF PET REGION-OF-INTEREST VALUES SO IEEE TRANSACTIONS ON MEDICAL IMAGING LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; COMPUTED-TOMOGRAPHY AB An approximation formula for the variance of Positron Emission Tomography (PET) region-of-interest (ROI) values has been developed, implemented, and evaluated. This formula does not require access to the original projection data and is therefore convenient for routine use. The formula was derived by applying successive approximations to the filtered-backprojection reconstruction algorithm. ROI variance is estimated from the product of mean pixel variance within the region and a term accounting for the intercorrelation of all pixel pairs inside the region. The formula accounts for radioactivity distribution, attenuation, randoms, scatter, deadtime, detector normalization, scan length, decay, and reconstruction filter. The algorithm was tested by comparison to the exact ROI variance as calculated with Huesman's algorithm. Tests with scan data from phantoms, animals, and humans obtained on the Scanditronix PC2048-15B tomograph showed the approximation formula to be accurate to within +/-10 percent. C1 NIH,DEPT NUCL MED,BETHESDA,MD 20892. POSITRON CORP,HOUSTON,TX 77084. RP CARSON, RE (reprint author), NIH,DEPT POSITRON EMISS TOMOG,BETHESDA,MD 20892, USA. RI Carson, Richard/H-3250-2011 OI Carson, Richard/0000-0002-9338-7966 NR 14 TC 67 Z9 67 U1 0 U2 1 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 0278-0062 J9 IEEE T MED IMAGING JI IEEE Trans. Med. Imaging PD JUN PY 1993 VL 12 IS 2 BP 240 EP 250 DI 10.1109/42.232252 PG 11 WC Computer Science, Interdisciplinary Applications; Engineering, Biomedical; Engineering, Electrical & Electronic; Imaging Science & Photographic Technology; Radiology, Nuclear Medicine & Medical Imaging SC Computer Science; Engineering; Imaging Science & Photographic Technology; Radiology, Nuclear Medicine & Medical Imaging GA LV990 UT WOS:A1993LV99000011 PM 18218411 ER PT J AU UMLAUF, SW BEVERLY, B KANG, SM BRORSON, K TRAN, AC SCHWARTZ, RH AF UMLAUF, SW BEVERLY, B KANG, SM BRORSON, K TRAN, AC SCHWARTZ, RH TI MOLECULAR REGULATION OF THE IL-2 GENE - RHEOSTATIC CONTROL OF THE IMMUNE-SYSTEM SO IMMUNOLOGICAL REVIEWS LA English DT Review ID T-CELL CLONES; ANTIGEN-PRESENTING CELLS; LYMPHOKINE MESSENGER-RNA; HUMAN LYMPHOCYTES-T; INTERLEUKIN-2 GENE; COSTIMULATORY SIGNAL; MONOCLONAL-ANTIBODIES; RECEPTOR OCCUPANCY; ACTIVATION PATHWAY; C-JUN C1 NIH,CELLULAR & MOLEC IMMUNOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. ANERGEN INC,REDWOOD CITY,CA 94063. CELL GENESYS INC,FOSTER CITY,CA 94404. UNIV CALIF SAN FRANCISCO,SCH MED,DEPT SURG,SAN FRANCISCO,CA 94143. US FDA,BETHESDA,MD 20892. NR 68 TC 62 Z9 63 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0105-2896 J9 IMMUNOL REV JI Immunol. Rev. PD JUN PY 1993 VL 133 BP 177 EP 197 DI 10.1111/j.1600-065X.1993.tb01516.x PG 21 WC Immunology SC Immunology GA LR370 UT WOS:A1993LR37000010 PM 8225366 ER PT J AU WALDMANN, TA AF WALDMANN, TA TI THE IL-2/IL-2 RECEPTOR SYSTEM - A TARGET FOR RATIONAL IMMUNE INTERVENTION (REPRINTED FROM TRENDS IN PHARMACOLOGICAL SCIENCES, VOL 14, PG 159-164, 1993) SO IMMUNOLOGY TODAY LA English DT Reprint ID T-CELL LEUKEMIA; CARDIAC ALLOGRAFT SURVIVAL; AFFINITY INTERLEUKIN-2 RECEPTORS; TAC MONOCLONAL-ANTIBODY; RECOMBINANT INTERLEUKIN-2; HUMANIZED ANTIBODY; IL-2 RECEPTOR; BETA-CHAIN; CROSS-LINKING; KILLER-CELLS AB The expression of interleukin 2 (IL-2), induction of its multisubunit receptor and subsequent interplay of this ligand with its receptor are pivotal events in T-cell activation. Our present understanding of the normal IL-2/IL-2R system and of disorders in this network in disease opens the possibility for more specific immune intervention. Thomas Waldmann discusses the clinical application of IL-2, agents that inhibit IL-2 synthesis and action, and how the anti-IL-2 receptor-directed therapy provides a novel perspective for prevention of allograft rejection and for treatment of graft versus host disease, select autoimmune disorders and certain neoplastic diseases. RP WALDMANN, TA (reprint author), NCI, BETHESDA, MD 20892 USA. NR 60 TC 172 Z9 185 U1 1 U2 4 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD JUN PY 1993 VL 14 IS 6 BP 264 EP 270 DI 10.1016/0167-5699(93)90043-K PG 7 WC Immunology SC Immunology GA LL461 UT WOS:A1993LL46100007 PM 8397768 ER PT J AU YARCHOAN, R MITSUYA, H BRODER, S AF YARCHOAN, R MITSUYA, H BRODER, S TI CHALLENGES IN THE THERAPY OF HIV-INFECTION (REPRINTED FROM TRENDS IN PHARMACOLOGICAL SCIENCES, VOL 14, PG 196-202, 1993) SO IMMUNOLOGY TODAY LA English DT Reprint ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; CD4+ T-CELLS; REVERSE-TRANSCRIPTASE; ANTIRETROVIRAL THERAPY; PERIPHERAL-BLOOD; ZIDOVUDINE AZT; LYMPHOCYTES-T; BONE-MARROW; TYPE-1 AB Drugs that inhibit HIV replication have been shown to have clinical utility in patients with HIV infection. However, the immunological improvement induced by available anti-HIV therapies in patients with AIDS is incomplete and transient. Explanations for this may include immunological barriers to complete reconstitution, low therapeutic indices of the available drugs, and the development of viral resistance. An understanding of these processes may provide important leads for the development of improved therapy for AIDS. C1 NCI, OFF DIRECTOR, BETHESDA, MD 20892 USA. RP YARCHOAN, R (reprint author), NCI, MED BRANCH, BLDG 10, RM 12N 226, BETHESDA, MD 20892 USA. NR 59 TC 20 Z9 20 U1 0 U2 2 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD JUN PY 1993 VL 14 IS 6 BP 303 EP 309 DI 10.1016/0167-5699(93)90050-U PG 7 WC Immunology SC Immunology GA LL461 UT WOS:A1993LL46100014 PM 8397771 ER PT J AU GOMEZ, DE HARTZLER, JL CORBITT, RH NASON, AM THORGEIRSSON, UP AF GOMEZ, DE HARTZLER, JL CORBITT, RH NASON, AM THORGEIRSSON, UP TI IMMUNOMAGNETIC SEPARATION AS A FINAL PURIFICATION STEP OF LIVER ENDOTHELIAL-CELLS SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL LA English DT Article DE MONKEY LIVER ENDOTHELIUM; IMMUNOISOLATION; CULTURE ID LOW-DENSITY LIPOPROTEIN; RAT-LIVER; LANGERHANS CELLS; HIGH-YIELD; KUPFFER; BEADS; ANTIBODIES; PARTICLES; CULTURE; BLOOD AB We describe a fast and reproducible method that can be used as a final step in obtaining pure populations of liver endothelial cells. This method employs endothelial cell specific lectin covalently bound to magnetic polystyrene beads (Dynabeads). Evonymus europaeus agglutinin (EEA)-coated Dynabeads were used to purify monkey liver endothelium from Percoll gradient separated nonparenchymal cells. EEA-coated beads were also successfully used to purify monkey aortic endothelial cells. The endothelial cells grew to confluence as a cobblestonelike monolayer, expressed Factor VIII related antigen, and incorporated acetylated-low density lipoprotein. The magnetic beads seemed not to modify the normal properties of the isolated endothelium, thus facilitating their use in experimental studies. This immunomagnetic separation technique may be applicable for purification of endothelial cells from a wide variety of tissue sources. RP GOMEZ, DE (reprint author), NCI,DIV CANC ETIOL,OFF DIRECTOR,9000 ROCKVILLE PIKE,BLDG 37,ROOM 2D-02,BETHESDA,MD 20892, USA. OI Gomez, Daniel E/0000-0002-8629-0787 NR 31 TC 13 Z9 13 U1 1 U2 2 PU SOC IN VITRO BIOLOGY PI UPPER MARLBORO PA 9315 LARGO DR W #255, UPPER MARLBORO, MD 20774-4755 SN 1071-2690 J9 IN VITRO CELL DEV-AN JI In Vitro Cell. Dev. Biol.-Anim. PD JUN PY 1993 VL 29A IS 6 BP 451 EP 455 PG 5 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA LM383 UT WOS:A1993LM38300006 PM 8392507 ER PT J AU KAARTINEN, L NETTESHEIM, P ADLER, KB RANDELL, SH AF KAARTINEN, L NETTESHEIM, P ADLER, KB RANDELL, SH TI RAT TRACHEAL EPITHELIAL-CELL DIFFERENTIATION IN-VITRO SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL LA English DT Article DE COLLAGEN; DIFFERENTIATION; KERATIN; MUCIN; RETINOIDS; TRANSGLUTAMINASE ID SERUM-FREE MEDIUM; ACID-INDUCED EXPRESSION; RETINOIC ACID; TISSUE TRANSGLUTAMINASE; BIOCHEMICAL-CHARACTERIZATION; EPIDERMAL TRANSGLUTAMINASE; SQUAMOUS DIFFERENTIATION; CLONAL PROLIFERATION; GENE-EXPRESSION; GROWTH-FACTORS AB In vitro culture conditions enabling rat tracheal epithelial (RTE) cells to differentiate to mucociliary, mucous, or squamous phenotypes are described. Medium composition for rapid cell growth to confluence in membrane insert cultures was determined, and the effects of major modifiers of differentiation were tested. Retinoic acid (RA), collagen gel substratum, and an air-liquid interface at the level of the cell layer were required for expression of a mucociliary phenotype which most closely approximated the morphology of the tracheal epithelium in vivo. Large quantities of high molecular weight, hyaluronidase-resistant glycoconjugates, most likely mucin glycoproteins, were produced in the presence of RA when the cells were grown with or without a collagen gel and in submerged as well as in interface cultures. However, extensive ciliagenesis was dependent on the simultaneous presence of RA, collagen gel, and an air-liquid interface. When RA was omitted from the media, the cells became stratified squamous and developed a cornified apical layer in air-liquid interface cultures. This phenotype was accompanied by loss of transglutaminase (TGase) type II and keratin 18 and expression of the squamous markers TGase type I and keratin 13. The ability to modulate RTE cell phenotypes in culture will facilitate future studies investigating molecular regulation of tracheal cell proliferation, differentiation, and function. C1 NIEHS,PULM PATHOBIOL,POB 12233,LPP,MD D2-01,RES TRIANGLE PK,NC 27709. COLL VET MED,DEPT PHARMACOL & TOXICOL,SF-00581 HELSINKI,FINLAND. N CAROLINA STATE UNIV,COLL VET MED,DEPT ANAT PHYSIOL SCI & RADIOL,RALEIGH,NC 27606. NR 43 TC 121 Z9 122 U1 0 U2 0 PU SOC IN VITRO BIOLOGY PI UPPER MARLBORO PA 9315 LARGO DR W #255, UPPER MARLBORO, MD 20774-4755 SN 1071-2690 J9 IN VITRO CELL DEV-AN JI In Vitro Cell. Dev. Biol.-Anim. PD JUN PY 1993 VL 29A IS 6 BP 481 EP 492 PG 12 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA LM383 UT WOS:A1993LM38300011 PM 7687243 ER PT J AU SCHAUER, DB FALKOW, S AF SCHAUER, DB FALKOW, S TI ATTACHING AND EFFACING LOCUS OF A CITROBACTER-FREUNDII BIOTYPE THAT CAUSES TRANSMISSIBLE MURINE COLONIC HYPERPLASIA SO INFECTION AND IMMUNITY LA English DT Article ID ENTEROPATHOGENIC ESCHERICHIA-COLI; MAMMALIAN-CELLS; GENETIC-LOCUS; ADHERENCE; DIARRHEA; PROTEIN; EXPRESSION; INFECTION; INVASIN; PLASMID AB Citrobacter freundii biotype 4280 produces attaching and effacing (AE) lesions in the large intestine of laboratory mice and is the causative agent of transmissible murine colonic hyperplasia. AE lesions are also produced by enteropathogenic Escherichia coli in humans. Southern analysis revealed that biotype 4280, but not 20 other strains of C. freundii, contained DNA homologous to the eae (E. coli attaching and effacing) gene which is necessary for AE activity by enteropathogenic E. coli in vitro. We have cloned and determined the nucleotide sequence of the C. freundii eae homolog. Our findings suggest that the eae locus of C. freundii biotype 4280 is necessary for AE activity and has a role in the pathogenesis of transmissible murine colonic hyperplasia. C1 NIAID,ROCKY MT LAB,HAMILTON,MT 59840. STANFORD UNIV,MED CTR,SCH MED,DEPT MICROBIOL & IMMUNOL,STANFORD,CA 94305. FU NIAID NIH HHS [AI26195] NR 32 TC 164 Z9 166 U1 0 U2 5 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 JUN PY 1993 VL 61 IS 6 BP 2486 EP 2492 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LE498 UT WOS:A1993LE49800030 PM 8500884 ER PT J AU MARCONI, RT KONKEL, ME GARON, CF AF MARCONI, RT KONKEL, ME GARON, CF TI VARIABILITY OF OSP GENES AND GENE-PRODUCTS AMONG SPECIES OF LYME-DISEASE SPIROCHETES SO INFECTION AND IMMUNITY LA English DT Article ID POLYMERASE CHAIN-REACTION; BORRELIA-BURGDORFERI DNA; TICKS; MICE; POLYMORPHISMS; HYBRIDIZATION; PROTECTION; PROTEINS; STRAINS AB A comparison of the osp operon in 24 Lyme disease isolates, including representatives from each of the three established species, Borrellia burgdorferi, Borrelia garinii, and group VS461, was conducted. Several properties were assessed to determine whether the variability observed in this operon was reflective of the species of the isolate. At the transcriptional level, start site and Northern (RNA) blot analyses were conducted. B. garinii and VS461 group isolates were found to possess an untranslated leader sequence 6 nucleotides longer than that observed in B. burgdorferi isolates. By Northern blot analyses all Lyme disease isolates, except the B. garinii isolate VS102, were found to produce a polycistronic full-length ospAB message. Isolate VS102 produced a truncated message lacking the ospB portion of the transcript. Southern blot analyses suggest that the deletion occurred at the DNA level and was not due to a posttranscriptional event. Analysis of the outer surface proteins by two-dimensional gel electrophoresis demonstrated that the OspB isoelectric points were variable, with the OspB of B. garinii isolates exhibiting a pronounced acidic shift. The reactivity of different isolates to OspA and -B monoclonal antibodies and to a hyperimmune anti-ospAB serum was also variable. The results presented here demonstrate genotypic and phenotypic heterogeneity in the osp operon at both the inter- and intraspecies levels. The results have implications concerning the use of the osp genes or their gene products in the development of a Lyme disease vaccine, as diagnostic markers of Lyme disease, and in subtyping of Lyme disease isolates. RP MARCONI, RT (reprint author), NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840, USA. NR 40 TC 70 Z9 70 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 JUN PY 1993 VL 61 IS 6 BP 2611 EP 2617 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LE498 UT WOS:A1993LE49800048 PM 8500899 ER PT J AU CHANOCK, RM CROWE, JE MURPHY, BR BURTON, DR AF CHANOCK, RM CROWE, JE MURPHY, BR BURTON, DR TI HUMAN MONOCLONAL-ANTIBODY FAB FRAGMENTS CLONED FROM COMBINATORIAL LIBRARIES - POTENTIAL USEFULNESS IN PREVENTION AND/OR TREATMENT OF MAJOR HUMAN VIRAL DISEASES SO INFECTIOUS AGENTS AND DISEASE-REVIEWS ISSUES AND COMMENTARY LA English DT Review DE HUMAN MONOCLONAL VIRAL ANTIBODIES; FAB FRAGMENTS; PHAGE SURFACE EXPRESSION; FILAMENTOUS PHAGE; PASSIVE IMMUNIZATION; IMMUNOTHERAPY ID RESPIRATORY SYNCYTIAL VIRUS; CENTRAL-NERVOUS-SYSTEM; LYMPHOCYTIC CHORIOMENINGITIS VIRUS; INTRAVENOUS IMMUNE GLOBULIN; COTTON RATS; IMMUNODEFICIENCY-VIRUS; MEDIATED CLEARANCE; PHAGE SURFACES; T-CELLS; INFECTION AB Currently, there is increased interest in the use of human viral antibodies for prophylaxis and therapy because recent advances in molecular immunology have made it possible to generate large numbers of human monoclonal antibodies of desired specificity and functional activity in short order. The strategy, developed particularly at The Scripps Research Institute and at Cambridge University is based on antigen selection of such antibodies from combinatorial libraries that express Fabs on the surface of filamentous DNA bacteriophage. Fabs or their whole immunoglobulin derivatives that exhibit high avidity for the selecting antigen and high neutralizing activity for the corresponding virus have been identified, and many of these human monoclonal antibodies should prove to be useful in prophylaxis or therapy of presently uncontrolled, medically important human viral diseases. C1 SCRIPPS RES INST, LA JOLLA, CA USA. RP CHANOCK, RM (reprint author), NIAID, INFECT DIS LAB, BLDG 7, ROOM 100, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. RI Crowe, James/B-5549-2009 OI Crowe, James/0000-0002-0049-1079 NR 51 TC 32 Z9 32 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1056-2044 J9 INFECT AGENT DIS JI Infect. Agents Dis.-Rev. Issues Comment. PD JUN PY 1993 VL 2 IS 3 BP 118 EP 131 PG 14 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MG712 UT WOS:A1993MG71200002 PM 8173784 ER PT J AU GAZZINELLI, RT DENKERS, EY SHER, A AF GAZZINELLI, RT DENKERS, EY SHER, A TI HOST-RESISTANCE TO TOXOPLASMA-GONDII - MODEL FOR STUDYING THE SELECTIVE INDUCTION OF CELL-MEDIATED-IMMUNITY BY INTRACELLULAR PARASITES SO INFECTIOUS AGENTS AND DISEASE-REVIEWS ISSUES AND COMMENTARY LA English DT Review DE CELL-MEDIATED IMMUNITY; TOXOPLASMA GONDII; INTERFERON-GAMMA; TUMOR NECROSIS FACTOR-ALPHA; OPPORTUNISTIC INFECTION ID TUMOR-NECROSIS-FACTOR; CD8+ T-CELLS; RETROVIRUS-INDUCED IMMUNODEFICIENCY; NATURAL-KILLER-CELLS; IFN-GAMMA; LYMPHOCYTES-T; DEFICIENCY SYNDROME; CHRONIC INFECTION; MACROPHAGE ACTIVATION; INDEPENDENT PATHWAY AB Cell-mediated immunity (CMI) provides a major host defense against infectious disease and malignancy. Nevertheless, the mechanisms underlying the induction of CMI remain poorly understood and this lack of knowledge remains an important impasse in the design of rationally based vaccines and immunotherapies. Toxoplasma gondii is an intracellular pathogen that, as part of its normal life cycle, induces a potent CMI response leading to host resistance. Studies on the interaction of this parasite with the immune system therefore provide a unique approach for identifying events that selectively lead to the triggering of host-protective CMI. In addition, this knowledge may provide new strategies for immunotherapy of opportunistic infections in immunodeficient hosts. RP GAZZINELLI, RT (reprint author), NIAID, PARASIT DIS LAB, IMMUNOL & CELL BIOL SECT, BLDG 4, ROOM 126, BETHESDA, MD 20892 USA. NR 79 TC 108 Z9 112 U1 0 U2 7 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 1056-2044 J9 INFECT AGENT DIS JI Infect. Agents Dis.-Rev. Issues Comment. PD JUN PY 1993 VL 2 IS 3 BP 139 EP 149 PG 11 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MG712 UT WOS:A1993MG71200004 PM 7909708 ER PT J AU WITEBSKY, FG CONVILLE, PS AF WITEBSKY, FG CONVILLE, PS TI THE LABORATORY DIAGNOSIS OF MYCOBACTERIAL DISEASES SO INFECTIOUS DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; CHROMATOGRAPHY-MASS SPECTROMETRY; LINKED IMMUNOSORBENT-ASSAY; TUBERCULOUS MENINGITIS; PULMONARY TUBERCULOSIS; GAS-CHROMATOGRAPHY; BLOOD CULTURE; AVIUM COMPLEX; LIQUID-CHROMATOGRAPHY; CEREBROSPINAL-FLUID RP WITEBSKY, FG (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,MICROBIOL SERV,BLDG 10,BETHESDA,MD 20892, USA. NR 79 TC 5 Z9 6 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0891-5520 J9 INFECT DIS CLIN N AM JI Infect. Dis. Clin. North Am. PD JUN PY 1993 VL 7 IS 2 BP 359 EP 376 PG 18 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LK347 UT WOS:A1993LK34700011 PM 8345173 ER PT J AU SETTE, A SIDNEY, J GAETA, FCA APPELLA, E COLON, SM DELGUERCIO, MF GUERY, JC ADORINI, L AF SETTE, A SIDNEY, J GAETA, FCA APPELLA, E COLON, SM DELGUERCIO, MF GUERY, JC ADORINI, L TI MHC CLASS-II MOLECULES BIND INDISCRIMINATELY SELF AND NON-SELF PEPTIDE HOMOLOGS - EFFECT ON THE IMMUNOGENICITY OF NON-SELF PEPTIDES SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE BETA(2)-MICROGLOBULIN; MHC BINDING; SELF NON-SELF DISCRIMINATION; T-CELL REPERTOIRE ID T-CELL RECOGNITION; ANTIGEN PRESENTATION; SELECTION; COMPLEXES; PROTEIN; IA; COMPETITION; REPERTOIRE; LYSOZYME; THYMUS AB Synthetic peptides spanning the entire sequence of both human and mouse beta2-Microglobulin (beta2M) have been tested for their capacity to bind to three different mouse (I-A(d), I-E(d), and I-A(k)) or human (DR1, DR2, and DR5) class II molecules. The results demonstrate that class II molecules do not discriminate between self and non-self peptides. When the immunogenicity of the human beta2M peptides was measured by their ability to prime H-2d mice for in vitro T cell proliferation, it was found that peptides incapable of binding class II molecules in vitro were also non-immunogenic in vivo. Interestingly, however, several binders, including the human beta2M peptide 1 - 16, the best binder in this series to la(d) molecules, were found to be non-immunogenic. Since the corresponding mouse beta2M peptide 1 - 16 was also capable of binding to Ia(d) molecules, this suggested that lack of responsiveness to the non-self peptide could arise either from central or peripheral tolerance induced by the self homolog. Alternatively, lack of responsiveness could arise from other mechanisms, such as negative selection by other non-homolog sequences or lack of suitable T cell receptor genes. To discriminate between these possibilities, H-2d mice with disrupted beta2M genes were immunized with the human beta2M peptide 1 - 16. This peptide also failed to prime for T cell responsiveness in beta2M-negative mice, suggesting that a hole in the T cell repertoire for this antigen was not mediated by negative selection or peripheral tolerance induced by self beta2M peptides. C1 NCI,BETHESDA,MD 20892. SANDOZ LTD,PRECLIN RES,CH-4002 BASEL,SWITZERLAND. ROCHE MILANO RIC,I-20132 MILAN,ITALY. RP SETTE, A (reprint author), CYTEL CORP,3525 JOHN HOPKINS COURT,SAN DIEGO,CA 92121, USA. RI GUERY, Jean-Charles/G-1452-2013 OI GUERY, Jean-Charles/0000-0003-4499-3270 FU NIAID NIH HHS [AI18634] NR 28 TC 13 Z9 13 U1 0 U2 2 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 JUN PY 1993 VL 5 IS 6 BP 631 EP 638 DI 10.1093/intimm/5.6.631 PG 8 WC Immunology SC Immunology GA LJ998 UT WOS:A1993LJ99800009 PM 8347557 ER PT J AU SCHOLNICK, EK FRIEDMAN, SL AF SCHOLNICK, EK FRIEDMAN, SL TI PLANNING IN CONTEXT - DEVELOPMENTAL AND SITUATIONAL CONSIDERATIONS SO INTERNATIONAL JOURNAL OF BEHAVIORAL DEVELOPMENT LA English DT Article ID PERCEIVED CONTROL; CHILDREN; SKILL; TOWER; MODEL; TASK AB An analysis of the components of planning is presented that incorporates problem representation, goal selection, a decision to plan, strategy choice, strategy execution, and monitoring. We argue that which components are required and which developmental changes are triggered or revealed depend on the planning task. We present analyses of three tasks typically used to study planning: the Tower of Hanoi; errand scheduling; and story comprehension. We argue that the performance on the Tower of Hanoi task reflects representational and monitoring demands, and that story comprehension depends strongly on social comprehension and monitoring. Because many everyday plans like running errands have prepackaged components and take place in a less controllable environment, affective and attributional components affect most strongly the choice of goals, decision to plan, and strategy choice. We then speculate on the course of development of each processing component and the complex interplay of cognition, beliefs, attitudes, and motivation in assembling and implementing plans to handle different tasks. Finally, we consider changes across the life span in the kinds of plans that are generated. C1 NICHHD,BETHESDA,MD 20892. RP SCHOLNICK, EK (reprint author), UNIV MARYLAND,DEPT PSYCHOL,COLL PK,MD 20742, USA. NR 43 TC 34 Z9 35 U1 0 U2 2 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE, EAST SUSSEX, ENGLAND BN3 2FA SN 0165-0254 J9 INT J BEHAV DEV JI Int. J. Behav. Dev. PD JUN PY 1993 VL 16 IS 2 BP 145 EP 167 PG 23 WC Psychology, Developmental SC Psychology GA LJ757 UT WOS:A1993LJ75700003 ER PT J AU COTTAM, DW REES, RC AF COTTAM, DW REES, RC TI REGULATION OF MATRIX METALLOPROTEINASES - THEIR ROLE IN TUMOR INVASION AND METASTASIS SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Review DE MELANOMA; METASTASIS; METALLOPROTEINASES; CYTOKINES ID GROWTH-FACTOR-BETA; COLONY-STIMULATING FACTOR; ERYTHROID-POTENTIATING ACTIVITY; PROCOLLAGENASE MESSENGER-RNA; HUMAN-LUNG FIBROBLASTS; HUMAN TISSUE INHIBITOR; NECROSIS FACTOR-ALPHA; GENE-EXPRESSION; IV COLLAGENASE; PLASMINOGEN-ACTIVATOR AB In order for tumor cells to colonise secondary organs and tissues it is necessary for them to be able to complete all the essential steps of the metastatic cascade. We discuss here some of the important aspects of this process, highlighting those events likely to be important in the control of tumor cell invasion. The expression of matrix metalloproteinases (MMP) capable of degrading tissue matrix or basement membranes, constitutes an important feature of tumor cell escape from the primary neoplasm and entry into/ colonisation of the secondary body site. In particular, the balance between MMP and protease inhibitor expression will determine the invasive capacity of a cancer cell. The molecular control of gene expression, together with the molecules important in regulating the production of proteinases and their inhibitors is complex, and the important facets of these pathways are discussed. Cytokines, particularly tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1) and transforming growth factor-beta (TGF-beta), play a crucial role in modulating MMP-2 and MMP-9 expression, and these, together with other regulatory cytokines constitute an important mechanism whereby the tumor cells can increase their invasive potential through the secretion of proteases. C1 UNIV SHEFFIELD, SCH MED, FAC CANC STUDIES, SHEFFIELD S10 2RX, S YORKSHIRE, ENGLAND. NCI, DIV CANC ETIOL, BETHESDA, MD 20892 USA. NR 179 TC 125 Z9 125 U1 0 U2 2 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 JUN PY 1993 VL 2 IS 6 BP 861 EP 872 PG 12 WC Oncology SC Oncology GA LC863 UT WOS:A1993LC86300001 PM 21573639 ER PT J AU NORMANNO, N QI, CF GULLICK, WJ PERSICO, G YARDEN, Y WEN, DZ PLOWMAN, G KENNEY, N JOHNSON, G KIM, N BRANDT, R MARTINEZLACACI, I DICKSON, RB SALOMON, DS AF NORMANNO, N QI, CF GULLICK, WJ PERSICO, G YARDEN, Y WEN, DZ PLOWMAN, G KENNEY, N JOHNSON, G KIM, N BRANDT, R MARTINEZLACACI, I DICKSON, RB SALOMON, DS TI EXPRESSION OF AMPHIREGULIN, CRIPTO-1, AND HEREGULIN-ALPHA IN HUMAN BREAST-CANCER CELLS SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE BREAST CANCER; CRIPTO; EPIDERMAL GROWTH FACTOR; AMPHIREGULIN; HEREGULIN-ALPHA ID GROWTH-FACTOR-ALPHA; MESSENGER RIBONUCLEIC-ACID; EPITHELIAL-CELLS; TRANSGENIC MICE; MAMMARY-GLAND; LINE MCF-7; TGF-ALPHA; GENE; OVEREXPRESSION; TRANSFORMATION AB Cripto-1 (CR-1), amphiregulin (AR), and heregulin alpha (HRGalpha) are three recently discovered epidermal growth factor (EGF)-related peptides. The expression of these proteins was determined in MCF-7, ZR-75-1, T-47D, SK-BR-3, MDA-MB-231, MDA-MB-468, and Hs-578T human breast cancer cell lines using reverse transcriptase-polymerase chain reaction (RT-PCR), Northern blotting, and immunocytochemistry (ICC). The expression of CR-1 mRNA was detected by RT-PCR in all of the breast cancer cell lines. AR mRNA was detected by Northern blot analysis in MCF-7, ZR-75-1, T-47D, MDA-MB-231, and MDA-MB-468 cells while HRGalpha mRNA was expressed in only MDA-MB-231 and Hs-578T cells. All estrogen receptor-positive cell lines were found to express AR mRNA, and estrogen was able to induce AR mRNA expression in estrogen-depleted MCF-7 cells. CR-1 and AR proteins could be immunocytochemically detected in the breast cancer cell lines that were expressing CR-1 and AR mRNA using monospecific rabbit polyclonal antibodies. The anti-CR-1 antibody was also used to examine 26 human primary breast carcinomas by ICC for CR-1 expression. Seventy-five percent of the carcinomas were found to express the CR-1 protein while the adjacent non-involved breast epithelium was negative. These data demonstrate that CR-1, AR, and HRGalpha are coexpressed in human breast cancer cells and suggest that these three EGF-related peptides might perform a role in the autocrine growth regulation of human breast carcinoma cells. C1 NCI,TUMOR GROWTH FACTOR SECT,TUMOR IMMUNOL & BIOL LAB,BLDG 10,BETHESDA,MD 20892. HAMMERSMITH HOSP,IMPERIAL CANC RES FUND,MOLEC ONCOL LAB,LONDON W12 0HS,ENGLAND. INT INST GENET & BIOPHYS,I-80125 NAPLES,ITALY. WEIZMANN INST SCI,DEPT CHEM IMMUNOL,IL-76100 REHOVOT,ISRAEL. AMGEN INC,THOUSAND OAKS,CA 91320. BRISTOL MYERS SQUIBB CO,INST PHARMACEUT,SEATTLE,WA 98121. US FDA,DIV CYTOKINE BIOL,BETHESDA,MD 20892. GEORGETOWN UNIV,LOMBARDI CANC RES CTR,WASHINGTON,DC. RI PLOWMAN, Greg/E-2012-2011; YARDEN, YOSEF/K-1467-2012; OI Normanno, Nicola/0000-0002-7158-2605 NR 54 TC 66 Z9 66 U1 1 U2 1 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 JUN PY 1993 VL 2 IS 6 BP 903 EP 911 PG 9 WC Oncology SC Oncology GA LC863 UT WOS:A1993LC86300007 PM 21573645 ER PT J AU KING, H AF KING, H TI ENTRY DENIED, EXCLUSION AND THE CHINESE COMMUNITY IN AMERICA, 1882-1943 - CHANG,SC SO INTERNATIONAL MIGRATION REVIEW LA English DT Book Review C1 GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20057. RP KING, H (reprint author), NCI,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU CENTER MIGRATION STUD PI STATEN ISL PA 209 FLAGG PLACE, STATEN ISL, NY 10304 SN 0197-9183 J9 INT MIGR REV JI Int. Migr. Rev. PD SUM PY 1993 VL 27 IS 2 BP 434 EP 435 DI 10.2307/2547137 PG 2 WC Demography SC Demography GA LV545 UT WOS:A1993LV54500013 ER PT J AU LIN, LR CARPER, D YOKOYAMA, T REDDY, VN AF LIN, LR CARPER, D YOKOYAMA, T REDDY, VN TI THE EFFECT OF HYPERTONICITY ON ALDOSE REDUCTASE, ALPHAB-CRYSTALLIN, AND ORGANIC OSMOLYTES IN THE RETINAL-PIGMENT EPITHELIUM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE HUMAN RETINAL PIGMENT EPITHELIUM; HYPERTONIC STRESS; ALDOSE REDUCTASE; ALPHAB-CRYSTALLIN; ORGANIC OSMOLYTES ID NON-LENTICULAR TISSUES; MESSENGER-RNA; B-CRYSTALLIN; EXTRACELLULAR NACL; MEDULLARY CELLS; LENS; EXPRESSION; PROTEIN; RAT; ACCUMULATION AB Purpose. Aldose reductase (AR), an enzyme implicated in diabetic complications of ocular tissues, has been suggested to play a physiologic role in kidney and, possibly, other tissues by elevating the organic osmolytes in conditions of heightened extracellular tonicity. Hypertonicity has been shown to induce AR and alpha(B)-crystallin in some cells. To examine if similar mechanisms are operating in the retinal pigment epithelium (RPE), another target tissue of diabetic complications, we studied the effect of hypertonic media on the induction of AR, alpha(B)-crystallin, myoinositol, taurine, and other free amino acids. Methods. Human RPE cells were cultured in normal and hypertonic media containing 150 mmol/I NaCl or 200 mmol/l cellobiose in combination with 30 mmol/l galactose from 0-8 days. Western blot analysis with antibodies were used to measure the expression of AR and alpha(B)-crystallin. Hybridization of northern blots using AR and alpha(B)-crystallin complementary DNA probes were employed for the measurement of the respective messenger RNA for these proteins. Changes in the levels of myoinositol, galactitol, taurine, and other free amino acids were determined biochemically. Results. AR and alpha(B)-crystallin messenger RNA levels rose 16-fold and 4-fold, respectively, when human RPE cells were cultured for 3 days in media supplemented with either 150 mmol/I NaCl or 200 mmol/l cellobiose. AR and alpha(B)-Crystallin protein levels also increased significantly, as seen by western blots. Consistent with the increased AR, galactitol accumulated to a greater extent when human RPE cells were grown in media containing 30 mmol/l galactose plus 150 mmol/l NaCl compared with cells grown in 30 mmol/l galactose alone. An 11-fold increase in cellular myoinositol and a 1.4-fold increase in taurine was observed in cells exposed to hypertonic media. Conclusions. These findings suggest that human RPE cells are responsive to hypertonic stress by elevating AR activity and use intracellular organic solutes in an interactive manner to help regulate intracellular tonicity. C1 OAKLAND UNIV,EYE RES INST,ROCHESTER,MI 48309. NEI,BETHESDA,MD 20892. FU NEI NIH HHS [EY 00484, EY 05230] NR 41 TC 36 Z9 36 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JUN PY 1993 VL 34 IS 7 BP 2352 EP 2359 PG 8 WC Ophthalmology SC Ophthalmology GA LF867 UT WOS:A1993LF86700027 PM 8505217 ER PT J AU SCOTT, WW LETHBRIDGECEJKU, M REICHLE, R WIGLEY, FM TOBIN, JD HOCHBERG, MC AF SCOTT, WW LETHBRIDGECEJKU, M REICHLE, R WIGLEY, FM TOBIN, JD HOCHBERG, MC TI RELIABILITY OF GRADING SCALES FOR INDIVIDUAL RADIOGRAPHIC FEATURES OF OSTEOARTHRITIS OF THE KNEE - THE BALTIMORE-LONGITUDINAL-STUDY-OF-AGING ATLAS OF KNEE OSTEOARTHRITIS SO INVESTIGATIVE RADIOLOGY LA English DT Article DE CLASSIFICATION; OSTEOARTHRITIS; RADIOLOGY; KNEES ID OSTEO-ARTHRITIS; HAND; PROGRESSION AB RATIONALE AND OBJECTIVES. The authors present an atlas of individual radiographic features of osteoarthritis of the knee and evaluate the inter- and intra-reader reliability of trained readers using this atlas. METHODS. Four trained readers graded 30 standing anterior-posterior knee radiographs for eight selected features of osteoarthritis (medial and lateral osteophytes, joint space narrowing, and sclerosis; osteophytes of the tibial spines and chondrocalcinosis) as well as the Kellgren-Lawrence global scale. Inter- and intra-reader reliability were calculated using intraclass correlation coefficients. RESULTS. For all features except sclerosis and osteophytes of the tibial spines, inter-reader reliability ranged from 0.63 to 0.83, whereas intra-reader reliability ranged from 0.82 to 0.95. CONCLUSION. Using this atlas, trained readers are reliable in measuring the presence and severity of individual radiographic features of osteoarthritis of the knee. This atlas should be useful in clinical and epidemiologic studies of osteoarthritis of the knee. C1 UNIV MARYLAND,SCH MED,DEPT PHYS & ELECT ENGN,DIV RHEUMATOL & CLIN IMMUNOL,PROFESSIONAL BLDG,BALTIMORE,MD 21201. JOHNS HOPKINS UNIV,SCH MED,DEPT RADIOL,SKELETAL RADIOL SECT,BALTIMORE,MD 21205. UNIV MARYLAND,SCH MED,DEPT EPIDEMIOL & PREVENT MED,BALTIMORE,MD 21201. NIA,GERONTOL RES CTR,APPL PHYSIOL SECT,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV MOLEC & CLIN RHEUMATOL,BALTIMORE,MD 21205. NR 21 TC 85 Z9 85 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD JUN PY 1993 VL 28 IS 6 BP 497 EP 501 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LG812 UT WOS:A1993LG81200004 PM 8320066 ER PT J AU LINDBERG, DAB HUMPHREYS, BL AF LINDBERG, DAB HUMPHREYS, BL TI PATIENT RECORDS SO ISSUES IN SCIENCE AND TECHNOLOGY LA English DT Editorial Material C1 NATL COORDINAT OFF,BETHESDA,MD. RP LINDBERG, DAB (reprint author), NATL LIB MED,BETHESDA,MD, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0748-5492 J9 ISSUES SCI TECHNOL JI Issues Sci. Technol. PD SUM PY 1993 VL 9 IS 4 BP 19 EP 20 PG 2 WC Engineering, Multidisciplinary; Engineering, Industrial; Multidisciplinary Sciences; Social Issues SC Engineering; Science & Technology - Other Topics; Social Issues GA LM539 UT WOS:A1993LM53900019 ER PT J AU INOUYE, S AF INOUYE, S TI MOLECULAR EPIDEMIOLOGY OF VIRUS-INFECTION - AN OVERVIEW SO JAPANESE JOURNAL OF MEDICAL SCIENCE & BIOLOGY LA English DT Article; Proceedings Paper CT 3rd NIH Symposium on Genome Diagnosis and Molecular Epidemiology of Viral Diseases CY MAY 21, 1993 CL TOKYO, JAPAN SP NIH RP INOUYE, S (reprint author), NIH,DEPT EPIDEMIOL,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU NATL INST HEALTH PI TOKYO PA C/O JPN J MED SCI BIOL, 23-1, TOYAMA 1-CHOME, SHINJUKU-KU, TOKYO 162, JAPAN SN 0021-5112 J9 JPN J MED SCI BIOL JI Jpn. J. Med. Sci. Biol. PD JUN PY 1993 VL 46 IS 3 BP 142 EP 142 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MN367 UT WOS:A1993MN36700004 ER PT J AU HONDO, R AF HONDO, R TI MOLECULAR EPIDEMIOLOGY OF HERPESVIRUS-INFECTION SO JAPANESE JOURNAL OF MEDICAL SCIENCE & BIOLOGY LA English DT Article; Proceedings Paper CT 3rd NIH Symposium on Genome Diagnosis and Molecular Epidemiology of Viral Diseases CY MAY 21, 1993 CL TOKYO, JAPAN SP NIH RP HONDO, R (reprint author), NIH,DEPT MICROBIOL,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL INST HEALTH PI TOKYO PA C/O JPN J MED SCI BIOL, 23-1, TOYAMA 1-CHOME, SHINJUKU-KU, TOKYO 162, JAPAN SN 0021-5112 J9 JPN J MED SCI BIOL JI Jpn. J. Med. Sci. Biol. PD JUN PY 1993 VL 46 IS 3 BP 143 EP 144 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MN367 UT WOS:A1993MN36700005 ER PT J AU MATSUURA, Y AF MATSUURA, Y TI MOLECULAR-BIOLOGY AND EPIDEMIOLOGY OF HEPATITIS-C VIRUS SO JAPANESE JOURNAL OF MEDICAL SCIENCE & BIOLOGY LA English DT Article; Proceedings Paper CT 3rd NIH Symposium on Genome Diagnosis and Molecular Epidemiology of Viral Diseases CY MAY 21, 1993 CL TOKYO, JAPAN SP NIH RP MATSUURA, Y (reprint author), NIH,DEPT VIROL 2,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL INST HEALTH PI TOKYO PA C/O JPN J MED SCI BIOL, 23-1, TOYAMA 1-CHOME, SHINJUKU-KU, TOKYO 162, JAPAN SN 0021-5112 J9 JPN J MED SCI BIOL JI Jpn. J. Med. Sci. Biol. PD JUN PY 1993 VL 46 IS 3 BP 145 EP 146 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MN367 UT WOS:A1993MN36700006 ER PT J AU TAKEBE, Y AF TAKEBE, Y TI IDENTIFICATION OF 2 DISTINCT HIV-1 SUBTYPES IN THAILAND AND THEIR OCCURRENCE IN JAPAN SO JAPANESE JOURNAL OF MEDICAL SCIENCE & BIOLOGY LA English DT Article; Proceedings Paper CT 3rd NIH Symposium on Genome Diagnosis and Molecular Epidemiology of Viral Diseases CY MAY 21, 1993 CL TOKYO, JAPAN SP NIH RP TAKEBE, Y (reprint author), NIH,AIDS RES CTR,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU NATL INST HEALTH PI TOKYO PA C/O JPN J MED SCI BIOL, 23-1, TOYAMA 1-CHOME, SHINJUKU-KU, TOKYO 162, JAPAN SN 0021-5112 J9 JPN J MED SCI BIOL JI Jpn. J. Med. Sci. Biol. PD JUN PY 1993 VL 46 IS 3 BP 146 EP 149 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA MN367 UT WOS:A1993MN36700007 ER PT J AU KATOW, S AF KATOW, S TI GENOME DIAGNOSIS OF FETAL RUBELLA INFECTION AND IDENTIFICATION OF RUBELLA VACCINE STRAINS USED IN JAPAN SO JAPANESE JOURNAL OF MEDICAL SCIENCE & BIOLOGY LA English DT Article; Proceedings Paper CT 3rd NIH Symposium on Genome Diagnosis and Molecular Epidemiology of Viral Diseases CY MAY 21, 1993 CL TOKYO, JAPAN SP NIH RP KATOW, S (reprint author), NIH,DEPT VIRUS DIS & VACCINE CONTROL,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL INST HEALTH PI TOKYO PA C/O JPN J MED SCI BIOL, 23-1, TOYAMA 1-CHOME, SHINJUKU-KU, TOKYO 162, JAPAN SN 0021-5112 J9 JPN J MED SCI BIOL JI Jpn. J. Med. Sci. Biol. PD JUN PY 1993 VL 46 IS 3 BP 150 EP 152 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA MN367 UT WOS:A1993MN36700009 ER PT J AU YAMADA, A AF YAMADA, A TI MOLECULAR EPIDEMIOLOGY OF MUMPS-VIRUS SO JAPANESE JOURNAL OF MEDICAL SCIENCE & BIOLOGY LA English DT Article; Proceedings Paper CT 3rd NIH Symposium on Genome Diagnosis and Molecular Epidemiology of Viral Diseases CY MAY 21, 1993 CL TOKYO, JAPAN SP NIH RP YAMADA, A (reprint author), NIH,DEPT VIRUS DIS & VACCINE CONTROL,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL INST HEALTH PI TOKYO PA C/O JPN J MED SCI BIOL, 23-1, TOYAMA 1-CHOME, SHINJUKU-KU, TOKYO 162, JAPAN SN 0021-5112 J9 JPN J MED SCI BIOL JI Jpn. J. Med. Sci. Biol. PD JUN PY 1993 VL 46 IS 3 BP 152 EP 152 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MN367 UT WOS:A1993MN36700010 ER PT J AU NEROME, K AF NEROME, K TI EVOLUTIONARY MECHANISMS OF INFLUENZA-VIRUSES - HOST SEGREGATION AND CHANGES IN PATHOLOGY SO JAPANESE JOURNAL OF MEDICAL SCIENCE & BIOLOGY LA English DT Article; Proceedings Paper CT 3rd NIH Symposium on Genome Diagnosis and Molecular Epidemiology of Viral Diseases CY MAY 21, 1993 CL TOKYO, JAPAN SP NIH ID HEMAGGLUTININ; SWINE RP NEROME, K (reprint author), NIH,DEPT VIROL 1,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU NATL INST HEALTH PI TOKYO PA C/O JPN J MED SCI BIOL, 23-1, TOYAMA 1-CHOME, SHINJUKU-KU, TOKYO 162, JAPAN SN 0021-5112 J9 JPN J MED SCI BIOL JI Jpn. J. Med. Sci. Biol. PD JUN PY 1993 VL 46 IS 3 BP 153 EP 154 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MN367 UT WOS:A1993MN36700011 ER PT J AU LAYNE, SP DEMBO, M SPOUGE, JL GELDERBLOM, HR RENZ, H MERGES, MJ NARA, PL AF LAYNE, SP DEMBO, M SPOUGE, JL GELDERBLOM, HR RENZ, H MERGES, MJ NARA, PL TI FACTORS REGULATING THE SPONTANEOUS INACTIVATION OF HIV AND ITS SUSCEPTIBILITY TO NEUTRALIZATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA USA. LOS ALAMOS NATL LAB, LOS ALAMOS, NM 87544 USA. NATL LIB MED, BETHESDA, MD 20209 USA. ROBERT KOCH INST, W-1000 BERLIN 65, GERMANY. NCI, FREDERICK, MD 21701 USA. RI Dembo, Micah/C-2755-2013 NR 0 TC 0 Z9 0 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. PD JUN PY 1993 VL 6 IS 6 BP 704 EP 704 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100164 ER PT J AU MERGES, M LAYNE, S MOORE, J FIESER, G COPELAND, T NARA, P AF MERGES, M LAYNE, S MOORE, J FIESER, G COPELAND, T NARA, P TI DETERMINING BIOLOGICALLY RELEVANT NEUTRALIZATION PARAMETERS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 THROUGH PHYSICOCHEMICAL ANALYSIS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Meeting Abstract C1 NCI, FCRDC, DCE, LTCB, VBU, FREDERICK, MD USA. UNIV CALIF LOS ANGELES, MED CTR, LOS ANGELES, CA USA. AARON DIAMOND AIDS RES CTR, NEW YORK, NY USA. SCRIPPS RES INST, LA JOLLA, CA USA. ADV BIOSCI LABS INC, LMVC, FREDERICK, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. PD JUN PY 1993 VL 6 IS 6 BP 709 EP 709 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100184 ER PT J AU SPOUGE, JL LAYNE, SP DEMBO, M NARA, PL AF SPOUGE, JL LAYNE, SP DEMBO, M NARA, PL TI SINGLE-HIT ANTIBODY KINETICS - THE RESOLUTION OF A PARADOX AND ITS IMPLICATIONS FOR VACCINE DEVELOPMENT SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Meeting Abstract C1 NLM, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20894 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90024 USA. LANL, BIOPHYS GRP, LOS ALAMOS, NM 87545 USA. NCI, FCRF, LTCB, VIRUS BIOL SECT, FREDERICK, MD 21702 USA. RI Dembo, Micah/C-2755-2013 NR 0 TC 0 Z9 0 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. PD JUN PY 1993 VL 6 IS 6 BP 710 EP 710 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100189 ER PT J AU CONLEY, S LAYNE, S RAINA, J MOORE, J NARA, P AF CONLEY, S LAYNE, S RAINA, J MOORE, J NARA, P TI A PERSPECTIVE ON ELISA BASED QUANTITATIVE HIV-1 GP120 AND P-24 ASSAYS - CURRENT APPLICATIONS, LIMITATIONS AND POTENTIAL SOLUTIONS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Meeting Abstract C1 AMER BIOTECHNOL INC, CAMBRIDGE, MA USA. AARON DIAMOND AIDS RES CTR, NEW YORK, NY USA. NCI, FCRDC, PRI DYNCORP, BLDP, BETHESDA, MD 20892 USA. UNIV CALIF LOS ANGELES, MED CTR, LOS ANGELES, CA USA. NCI, FCRDC, DCE, LTCB, VBU, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. PD JUN PY 1993 VL 6 IS 6 BP 729 EP 729 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100265 ER PT J AU GUTEKUNST, KA KASHANCHI, F BRADY, JN BEDNARIK, DP AF GUTEKUNST, KA KASHANCHI, F BRADY, JN BEDNARIK, DP TI TRANSCRIPTION OF THE HIV-1 LTR IS REGULATED BY THE DENSITY OF DNA CPG METHYLATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE CPG; HIV; LATENCY; LONG TERMINAL REPEAT; METHYLATION; TRANSCRIPTION ID HUMAN-IMMUNODEFICIENCY-VIRUS; LONG TERMINAL REPEAT; TRANS-ACTIVATION; GENE-EXPRESSION; TAR RNA; INHIBITS TRANSCRIPTION; INCUBATION PERIOD; LOOP SEQUENCE; PROTEIN; BINDING AB Transcription from the HIV-1 tong terminal repeat (LTR) was shown to be inhibited by DNA CpG methylation both in vivo and in vitro. Enzymatic methylation of CpG sites localized within the LTR decreased the transcription of the CAT reporter gene, chloramphenicol acetyltransferase, as assayed by the transient expression of this gene in tissue culture. The inhibitory effect could be initially overcome, in trans, by the transactivator tat. As a function of time. the presence of tat had no observable effect on transcription, within the limits of detection sensitivity, suggesting that the level of basal transcription was reduced to very low levels. This effect is suggestive of the involvement of cellular CpG methylation-dependent inhibitory factors which have been characterized by other laboratories. These data imply that transactivation is reduced to low levels after longer periods of time when the DNA template is sparsely methylated. The transcriptional inhibitory process may involve proteins such as MeCP which may interact with methylated DNA more slowly and/or weakly. Conversely, densely methylated DNA was transcriptionally repressed immediately which suggests the rapid/strong association of the cellular inhibitory factor(s). The transcriptional inhibitory effect was also observed in an in vitro transcription run-off system. These data suggest that the methylation-mediated inhibition of transcription is directly affected by CpG methylation density and may involve other factors. C1 CTR DIS CONTROL,RETROVIRUS DIS BRANCH,ATLANTA,GA 30333. NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 42 TC 25 Z9 26 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 JUN PY 1993 VL 6 IS 6 BP 541 EP 549 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100001 PM 8496786 ER PT J AU EYSTER, ME DIAMONDSTONE, LS LIEN, JM EHMANN, WC QUAN, S GOEDERT, JJ AF EYSTER, ME DIAMONDSTONE, LS LIEN, JM EHMANN, WC QUAN, S GOEDERT, JJ TI NATURAL-HISTORY OF HEPATITIS-C VIRUS-INFECTION IN MULTITRANSFUSED HEMOPHILIACS - EFFECT OF COINFECTION WITH HUMAN-IMMUNODEFICIENCY-VIRUS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HEPATITIS-C; HIV; HEMOPHILIA; LIVER DISEASE; HEPATIC FAILURE ID NON-B-HEPATITIS; CHRONIC LIVER-DISEASE; NON-A; ANTIBODY; TRANSFUSION; COHORT; AIDS AB The objective of this prospective cohort study was to describe the natural history of hepatitis C virus (HCV) infection and the effect of human immunodeficiency virus (HIV) on the clinical manifestations of HCV liver disease. Two hundred twenty-three hemophiliacs were followed in a comprehensive care setting with periodic clinical and laboratory evaluations. Dates of HIV seroconversion were determined retrospectively from frozen sera. HCV assays were performed by a ''second generation'' four-antigen recombinant immunoblot assay (RIBA 2). Liver failure was found after a latency period of 10 to 20 years in 9% of multitransfused HCV-positive/HIV-positive adult hemophiliacs without an AIDS-defining opportunistic infection or malignancy. Lymphocytopenia, decreased CD4 counts, and, possibly, thrombocytopenia were associated with liver failure which appeared to be accelerated by HIV disease and its treatment. This form of severe liver disease is being seen with increasing frequency among multi-transfused persons with hemophilia who are coinfected with HCV and HIV. C1 PENN STATE SCH MED,DEPT MED,DIV HEMATOL,HERSHEY,PA. NCI,VIRAL EPIDEMIOL SECT,ROCKVILLE,MD. CHIRON CORP,EMERYVILLE,CA. FU NCI NIH HHS [N01-CP-85649] NR 47 TC 426 Z9 431 U1 0 U2 5 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 JUN PY 1993 VL 6 IS 6 BP 602 EP 610 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100009 PM 8098752 ER PT J AU FAUCI, AS AF FAUCI, AS TI IMMUNOPATHOGENESIS OF HIV-INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; TUMOR NECROSIS FACTOR; B-CELL ACTIVATION; CD3/T-CELL RECEPTOR COMPLEX; T-CELLS; GERMINAL-CENTERS; SAN-FRANCISCO; HTLV-III/LAV; EXPRESSION; AIDS RP FAUCI, AS (reprint author), NIAID,9000 ROCKVILLE PIKE,BLDG 31,ROOM 7A-03,BETHESDA,MD 20892, USA. NR 62 TC 59 Z9 60 U1 0 U2 2 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 JUN PY 1993 VL 6 IS 6 BP 655 EP 662 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100020 PM 8098755 ER PT J AU BLAESE, RM MULLEN, C ISHII, H ANDERSON, WF RAM, Z OLDFIELD, E CULVER, K AF BLAESE, RM MULLEN, C ISHII, H ANDERSON, WF RAM, Z OLDFIELD, E CULVER, K TI GENE-THERAPY FOR IMMUNODEFICIENCY AND CANCER SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NINCDS,NHLBI,NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 669 EP 669 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100023 ER PT J AU LISZIEWICZ, J SMYTHE, J SUN, D LUSSO, P HALL, L GALLO, RC REITZ, MS AF LISZIEWICZ, J SMYTHE, J SUN, D LUSSO, P HALL, L GALLO, RC REITZ, MS TI POTENTIAL APPLICATION OF GENE-THERAPY TO HIV-1 INFECTION .1. INHIBITION OF TAT FUNCTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 670 EP 670 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100028 ER PT J AU MORGAN, RA RAGHEB, J GALLO, RC ANDERSON, WF AF MORGAN, RA RAGHEB, J GALLO, RC ANDERSON, WF TI GENE-THERAPY FOR AIDS - INVITRO AND INVIVO PROTECTION OF PRIMARY PBL FROM INFECTION BY HIV SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 670 EP 670 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100030 ER PT J AU SMYTHE, JA SUN, D REITZ, M THOMSON, M GALLO, R LISZIEWICZ, J AF SMYTHE, JA SUN, D REITZ, M THOMSON, M GALLO, R LISZIEWICZ, J TI POTENTIAL APPLICATION OF GENE-THERAPY TO HIV-1 INFECTION .2. TRANSDOMINANT HIV-1 GAG MUTANTS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 670 EP 670 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100029 ER PT J AU SCHLOM, J KANTOR, J ABRAMS, S IRVINE, K AF SCHLOM, J KANTOR, J ABRAMS, S IRVINE, K TI DEVELOPMENT OF A RECOMBINANT VACCINIA-CARCINOEMBRYONIC ANTIGEN (CEA) VACCINE FOR IMMUNOTHERAPY OF HUMAN CARCINOMA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 671 EP 671 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100033 ER PT J AU WALDMANN, TA GOLDMAN, CK TOP, L GANSOW, O KASTENSPORTES, C ROESSLER, E ZAKNOEN, S WHITE, J HORAK, I CARRASQUILLO, JA REYNOLDS, JC NELSON, DL AF WALDMANN, TA GOLDMAN, CK TOP, L GANSOW, O KASTENSPORTES, C ROESSLER, E ZAKNOEN, S WHITE, J HORAK, I CARRASQUILLO, JA REYNOLDS, JC NELSON, DL TI THE TREATMENT OF HTLV-I-ASSOCIATED ADULT T-CELL LEUKEMIA (ATL) WITH GENETICALLY ENGINEERED MONOCLONAL-ANTIBODIES ARMED WITH RADIONUCLIDES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Carrasquillo, Jorge/E-7120-2010 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. PD JUN PY 1993 VL 6 IS 6 BP 671 EP 671 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100031 ER PT J AU KOVACS, JA AF KOVACS, JA TI ADVANCES IN THE MANAGEMENT OF AIDS-RELATED OPPORTUNISTIC INFECTIONS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIH,CC,CCMD,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 672 EP 672 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100035 ER PT J AU LI, G LISZIEWICZ, J SUN, D ZON, G GALLO, RC KLOTMAN, ME AF LI, G LISZIEWICZ, J SUN, D ZON, G GALLO, RC KLOTMAN, ME TI HIV-I REV-REV RESPONSIVE ELEMENT INTERACTION AS A TARGET FOR ANTIVIRAL THERAPY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 APPL BIOSYST INC,FOSTER CITY,CA 94404. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 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. PD JUN PY 1993 VL 6 IS 6 BP 672 EP 672 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100038 ER PT J AU LISZIEWICZ, J SUN, D KLOTMAN, M AGRAWAL, S ZAMECNICK, P GALLO, RC AF LISZIEWICZ, J SUN, D KLOTMAN, M AGRAWAL, S ZAMECNICK, P GALLO, RC TI OLIGONUCLEOTIDES PHOSPHOROTHIOATES FOR HIV-1 THERAPY - INVITRO MODEL FOR TREATMENT SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 WORCESTER FDN EXPT BIOL,SHREWSBURY,MA. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 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. PD JUN PY 1993 VL 6 IS 6 BP 672 EP 672 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100036 ER PT J AU KAGEYAMA, S IVERSEN, P ZON, G MITSUYA, H AF KAGEYAMA, S IVERSEN, P ZON, G MITSUYA, H TI DIFFERENTIAL ANTIVIRAL ACTIVITY OF A PHOSPHOROTHIOATE ANTI-REV ANTISENSE OLIGODEOXYNUCLEOTIDE AGAINST HIV-1 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,MED PROGRAM,EXPTL RETROVIROL SECT,BETHESDA,MD 20892. ABI THERAPEUT,FOSTER CITY,CA. UNIV NEBRASKA,OMAHA,NE 68182. 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. PD JUN PY 1993 VL 6 IS 6 BP 673 EP 673 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100039 ER PT J AU NAGY, K YOUNG, M GOTTE, D OROSZLAN, S AF NAGY, K YOUNG, M GOTTE, D OROSZLAN, S TI PREVENTION OF PRIMARY HIV-1 INFECTION BY SUBSTRATE BASED PROTEINASE-INHIBITORS AND TRUNCATED SUBSTRATES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,BRP,ABL,LMVC,FREDERICK,MD 21701. 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. PD JUN PY 1993 VL 6 IS 6 BP 673 EP 673 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100041 ER PT J AU TUDORWILLIAMS, G AF TUDORWILLIAMS, G TI CLINICAL-SIGNIFICANCE OF HIV-1 INVITRO RESISTANCE TO ZIDOVUDINE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 674 EP 674 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100045 ER PT J AU YARCHOAN, R LIETZAU, JA BRAWLEY, O NGUYEN, BY MITSUYA, H PLUDA, JM WYVILL, KM BRODER, S AF YARCHOAN, R LIETZAU, JA BRAWLEY, O NGUYEN, BY MITSUYA, H PLUDA, JM WYVILL, KM BRODER, S TI THERAPY OF AIDS OR SYMPTOMATIC HIV-INFECTION WITH SIMULTANEOUS OR ALTERNATING REGIMENS OF AZT AND DDI SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 674 EP 674 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100043 ER PT J AU RAPPAPORT, J WONGSTAAL, F OJWANG, JO LOONEY, DJ FRANKS, R RICHARDSON, MW HAMPEL, A NOTKINS, AL KLOTMAN, PE AF RAPPAPORT, J WONGSTAAL, F OJWANG, JO LOONEY, DJ FRANKS, R RICHARDSON, MW HAMPEL, A NOTKINS, AL KLOTMAN, PE TI HIV-1 TARGETED HAIRPIN RIBOZYME - ANTIVIRAL EFFECTS AND POTENTIAL APPLICATION TO GENE-THERAPY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,DEPT MED,WASHINGTON,DC 20052. NIDR,LOM,LDB,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. VET ADM MED CTR,SAN DIEGO,CA 92161. NO ILLINOIS UNIV,DEPT BIOL SCI,DE KALB,IL 60115. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 675 EP 675 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100047 ER PT J AU LANE, HC AF LANE, HC TI IMMUNOLOGICAL APPROACHES TO THE THERAPY OF PATIENTS WITH HIV-1 INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 676 EP 676 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100052 ER PT J AU PINCUS, SH AF PINCUS, SH TI ANTI-HIV IMMUNOTOXINS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 677 EP 677 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100057 ER PT J AU BERZOFSKY, JA SHIRAI, M NAKAGAWA, Y PENDLETON, CD HOUGHTEN, RA YOKOMURO, K GERMAIN, RN TAKAHASHI, H AF BERZOFSKY, JA SHIRAI, M NAKAGAWA, Y PENDLETON, CD HOUGHTEN, RA YOKOMURO, K GERMAIN, RN TAKAHASHI, H TI PROMISCUITY FOR MHC AND INDUCTION OF BROAD CROSS-REACTIVITY FOR HIV-1 ISOLATES OF A DOMINANT CTL DETERMINANT OF THE HIV-1 ENVELOPE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NIPPON MED COLL,TOKYO 113,JAPAN. TORREY PINES INST,SAN DIEGO,CA. 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. PD JUN PY 1993 VL 6 IS 6 BP 678 EP 678 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100061 ER PT J AU ROBERTGUROFF, M MULDOON, R STERN, T ALDRICH, K LOUIE, A GROGG, D WHITESCHARF, M POTTS, B GALLO, RC REITZ, MS AF ROBERTGUROFF, M MULDOON, R STERN, T ALDRICH, K LOUIE, A GROGG, D WHITESCHARF, M POTTS, B GALLO, RC REITZ, MS TI THE HIV-1 V3 LOOP CONFORMATION AND ITS GP120 CONTEXT ARE BOTH IMPORTANT FOR NEUTRALIZATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. REPLIGEN CORP,CAMBRIDGE,MA. 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. PD JUN PY 1993 VL 6 IS 6 BP 679 EP 679 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100063 ER PT J AU ARTHUR, LO BESS, JW SOWDER, RC GORELICK, RJ BENVENISTE, RE CHERMANN, JC HENDERSON, LE AF ARTHUR, LO BESS, JW SOWDER, RC GORELICK, RJ BENVENISTE, RE CHERMANN, JC HENDERSON, LE TI BETA-2-MICROGLOBULIN IS BOUND TO HIV-1 AND SIV, AND ANTIBODIES TO BETA-2-MICROGLOBULIN INHIBIT INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 PRI DYNCORP,IAIDS VACCINE PROGRAM,NCI FCRDC,FREDERICK,MD. UNITE RECH RETROVIRUS & MALAD ASSOCIEES,MARSEILLE,FRANCE. NCI,VIRAL CARCINOGENESIS LAB,BETHESDA,MD 20892. RI Bess, Jr., Julian/B-5343-2012 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. PD JUN PY 1993 VL 6 IS 6 BP 680 EP 680 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100067 ER PT J AU NATUK, RJ ROBERTGUROFF, M CHANDA, PK CHENGALVALA, M MURTY, K LUBECK, MD DAVIS, AR MIZUTANI, S WILHELM, J HJORTH, R LEE, SG EICHBERG, JW WADE, MS GALLO, RC HUNG, PP AF NATUK, RJ ROBERTGUROFF, M CHANDA, PK CHENGALVALA, M MURTY, K LUBECK, MD DAVIS, AR MIZUTANI, S WILHELM, J HJORTH, R LEE, SG EICHBERG, JW WADE, MS GALLO, RC HUNG, PP TI ADENO-HIV RECOMBINANT VACCINES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 WYETH AYERST RES,DIV BIOTECHNOL & MICROBIOL,POB 8299,PHILADELPHIA,PA 19101. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. SW FDN BIOMED RES,SAN ANTONIO,TX 78227. 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. PD JUN PY 1993 VL 6 IS 6 BP 681 EP 681 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100071 ER PT J AU HAIGWOOD, NL ELAMAD, Z CHIN, SM STEIMER, KS JENNINGS, M GARDNER, M HIRSCH, VM JOHNSON, PR AF HAIGWOOD, NL ELAMAD, Z CHIN, SM STEIMER, KS JENNINGS, M GARDNER, M HIRSCH, VM JOHNSON, PR TI CHARACTERIZATION OF GROUP-SPECIFIC ANTIBODIES GENERATED BY LENTIVIRUS INFECTION OR SUBUNIT IMMUNIZATION IN PRIMATES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 CHIRON CORP,EMERYVILLE,CA. UNIV CALIF DAVIS,DAVIS,CA 95616. NIAID,LID,ROCKVILLE,MD. OHIO STATE UNIV,COLUMBUS,OH 43210. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 684 EP 684 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100084 ER PT J AU BALOTTA, C LUSSO, P COCCHI, F GALLO, RC REITZ, MS AF BALOTTA, C LUSSO, P COCCHI, F GALLO, RC REITZ, MS TI VARIATION IN THE BIOLOGICAL PROPERTIES OF HIV-1 ENVELOPE CHIMERAS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,LTCB,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 686 EP 686 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100092 ER PT J AU REITZ, MS LORI, F HALL, L MICHAELS, F LUSSO, P MARKHAM, P POPOVIC, M GALLO, RC AF REITZ, MS LORI, F HALL, L MICHAELS, F LUSSO, P MARKHAM, P POPOVIC, M GALLO, RC TI CHARACTERIZATION OF MACROPHAGE-COMPETENT BIOLOGICALLY-ACTIVE MOLECULAR CLONES OF HIV-1 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,LTCB,BETHESDA,MD 20892. ADV BIOSCI LAB,KENSINGTON,MD 20895. 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. PD JUN PY 1993 VL 6 IS 6 BP 686 EP 686 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100091 ER PT J AU BARILLARI, G HOLMES, A GENDELMAN, R BUONAGURO, L GALLO, RC ENSOLI, B AF BARILLARI, G HOLMES, A GENDELMAN, R BUONAGURO, L GALLO, RC ENSOLI, B TI THE RGD MOTIF AND THE INTEGRIN RECEPTORS ARE INVOLVED IN THE VASCULAR CELL-GROWTH AND ADHESION PROPERTIES OF EXTRACELLULAR HIV-1 TAT PROTEIN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 1 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 JUN PY 1993 VL 6 IS 6 BP 688 EP 688 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100102 ER PT J AU ENSOLI, B ALBINI, A BARILLARI, G BUONAGURO, L GALLO, RC AF ENSOLI, B ALBINI, A BARILLARI, G BUONAGURO, L GALLO, RC TI RELEASE AND ANGIOGENIC PROPERTIES OF EXTRACELLULAR HIV-1 TAT PROTEIN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 688 EP 688 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100100 ER PT J AU LUNARDIISKANDAR, Y AYUB, J GILL, P ZEMAN, RA LAM, HH CHANNAVAJJALA, L GALLO, RC SAXINGER, WC AF LUNARDIISKANDAR, Y AYUB, J GILL, P ZEMAN, RA LAM, HH CHANNAVAJJALA, L GALLO, RC SAXINGER, WC TI EVIDENCE FOR HIV-1 TAT RECEPTOR EXPRESSION IN KAPOSI-SARCOMA (KS) CELL STRAINS AND KS(Y-1) CELL-LINE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,LTCB,DCE,BETHESDA,MD 20892. USC,SCH MED,LOS ANGELES,CA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 688 EP 688 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100101 ER PT J AU LUNARDIISKANDAR, Y LAM, HH GILL, P BRYANT, J ZEMAN, RA WEEKS, B BERNEMAN, Z KLOTMAN, P GALLO, RC AF LUNARDIISKANDAR, Y LAM, HH GILL, P BRYANT, J ZEMAN, RA WEEKS, B BERNEMAN, Z KLOTMAN, P GALLO, RC TI THE 1ST KAPOSIS-SARCOMA (KS)-DERIVED CELL LINE(KS Y-1) - RELATED TO AND DIFFERENCES FROM KS CELL STRAINS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,LTCB,BETHESDA,MD 20892. USC,SCH MED,LOS ANGELES,CA 90033. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 688 EP 688 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100099 ER PT J AU PAPAS, TS AF PAPAS, TS TI THE ETS FAMILY OF GENES - A PARADIGM FOR STUDYING TRANSCRIPTIONAL FACTOR - INTERACTIONS IN HUMAN RETROVIRAL INFECTED CELL SYSTEMS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 690 EP 690 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100107 ER PT J AU FAUCI, AS AF FAUCI, AS TI IMMUNOPATHOGENESIS OF HIV-INFECTION - AN UPDATE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 691 EP 691 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100114 ER PT J AU FRANZOSO, G BOURS, V PARK, S TOMITAYAMAGUCHI, M KELLY, K SIEBENLIST, U AF FRANZOSO, G BOURS, V PARK, S TOMITAYAMAGUCHI, M KELLY, K SIEBENLIST, U TI A NOVEL FUNCTION FOR THE CANDIDATE ONCOPROTEIN BCL-3 - AN ANTAGONIST OF P50/NF-KB-MEDIATED REPRESSION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NIAID,PATHOL LAB,BETHESDA,MD 20892. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 691 EP 691 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100112 ER PT J AU REID, R BRADY, JN AF REID, R BRADY, JN TI ANALYSIS OF THE P53 TUMOR-SUPPRESSOR IN HTLV-I TRANSFORMED-CELLS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 691 EP 691 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100111 ER PT J AU ASJO, B KORNEYEVA, M VOJKOVIC, A ALBERT, J ESPEJO, R FENYO, EM AF ASJO, B KORNEYEVA, M VOJKOVIC, A ALBERT, J ESPEJO, R FENYO, EM TI THE BLOCKING OF SLOW LOW TYPE HIV REPLICATION IN CD4+ CELL-LINES TAKES PLACE AFTER PROVIRUS FORMATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 KAROLINSKA INST, DEPT VIROL, S-10401 STOCKHOLM 60, SWEDEN. NCI, FCRDC, ABL BASIC RES PROGR, FREDERICK, MD 21701 USA. CTR ESTUDIOS CIENT, SANTIAGO, CHILE. NATL BACTERIOL LAB, DEPT VIROL, S-10521 STOCKHOLM, SWEDEN. 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. PD JUN PY 1993 VL 6 IS 6 BP 692 EP 692 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100117 ER PT J AU MANN, DL ODONNELL, M CARRINGTON, M GOEDERT, JJ AF MANN, DL ODONNELL, M CARRINGTON, M GOEDERT, JJ TI HLA ALLELES ASSOCIATED WITH RELATIVE RATES OF DISEASE PROGRESSION AND DIFFERENT AIDS DIAGNOSIS IN HIV-1-INFECTED INDIVIDUALS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. NCI FCRDC,PRI DYNCORP,BCDP,FREDERICK,MD. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 692 EP 692 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100116 ER PT J AU CLERICI, M YARCHOAN, R AMMANN, AJ BRODER, S SHEARER, GM AF CLERICI, M YARCHOAN, R AMMANN, AJ BRODER, S SHEARER, GM TI EFFECT OF RECOMBINANT CD4-IGG ON INVITRO HELPER T-CELL FUNCTION - DATA FROM A PHASE I/II STUDY OF PATIENTS WITH THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME (AIDS) SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NCI,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. GENENTECH INC,S SAN FRANCISCO,CA 94080. 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. PD JUN PY 1993 VL 6 IS 6 BP 693 EP 693 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100122 ER PT J AU CLERICI, M SHEARER, GM AF CLERICI, M SHEARER, GM TI THE ROLE OF TH1 AND TH2 CYTOKINES IN HIV-INDUCED T-HELPER CELL DYSREGULATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 693 EP 693 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100121 ER PT J AU BISWAS, P POLI, G ORENSTEIN, JM FAUCI, AS AF BISWAS, P POLI, G ORENSTEIN, JM FAUCI, AS TI CYTOKINE-INDUCED CELL-DEATH AND EXPRESSION OF HIV-1 - DO TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA) AND INTERFERON-GAMMA (IFN-GAMMA) SELECTIVELY KILL HIV-INFECTED CELLS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC 20052. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 694 EP 694 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100125 ER PT J AU BROWN, C POLI, G KOVACS, A FAUCI, AS AF BROWN, C POLI, G KOVACS, A FAUCI, AS TI ELEVATED LEVELS OF TNF-ALPHA AND IL-6 IN PLASMAS FROM NORTH-AMERICAN INFANTS - IMPLICATIONS FOR PERINATAL INFECTION WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 694 EP 694 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100124 ER PT J AU POLI, G KINTER, AL BISWAS, P BRESSLER, P CHIANG, L STANLEY, SK RABSON, AB FAUCI, AS AF POLI, G KINTER, AL BISWAS, P BRESSLER, P CHIANG, L STANLEY, SK RABSON, AB FAUCI, AS TI CYTOKINE-DEPENDENT AND INDEPENDENT CONTROL OF HIV TRANSCRIPTION IN PERSISTENTLY INFECTED CELL-LINES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. CABM,PISCATAWAY,NJ. UMDNJ,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. PD JUN PY 1993 VL 6 IS 6 BP 694 EP 694 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100123 ER PT J AU PANTALEO, G GRAZIOSI, C DEMAREST, J SHAW, G KOTLER, DP FAUCI, AS AF PANTALEO, G GRAZIOSI, C DEMAREST, J SHAW, G KOTLER, DP FAUCI, AS TI TEMPORAL ASPECTS OF HIV DNA AND RNA-SYNTHESIS AND TISSUE DISTRIBUTION DURING HIV-INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. UNIV ALABAMA,BIRMINGHAM,AL. ST LUKES ROOSEVELT HOSP,NEW YORK,NY 10025. RI Pantaleo, Giuseppe/K-6163-2016 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. PD JUN PY 1993 VL 6 IS 6 BP 695 EP 695 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100127 ER PT J AU KOMAROFF, AL ABLASHI, DV HENRY, B GALLO, RC AF KOMAROFF, AL ABLASHI, DV HENRY, B GALLO, RC TI THE ROLE OF HUMAN HERPESVIRUS-6 IN CHRONIC POSTINFECTIOUS FATIGUE SYNDROME SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV NEVADA,RENO,NV 89557. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 696 EP 696 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100133 ER PT J AU BERNEMAN, ZN ABLASHI, DV LI, G GALLO, RC AF BERNEMAN, ZN ABLASHI, DV LI, G GALLO, RC TI HUMAN HERPESVIRUS 7 (HHV-7) IS RELATED TO BUT SIGNIFICANTLY DIFFERENT FROM HUMAN HERPESVIRUS 6 (HHV-6) AND HUMAN CYTOMEGALOVIRUS (HCMV) SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. NCI,C GALLO LAB TUMOR CELL BIOL,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 697 EP 697 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100138 ER PT J AU FLAMAND, L GOSSELIN, J ABLASHI, DV GALLO, RC MENEZES, J AF FLAMAND, L GOSSELIN, J ABLASHI, DV GALLO, RC MENEZES, J TI DIFFERENTIAL-EFFECTS OF HUMAN HERPESVIRUS-6 INFECTION ON CYTOKINE SYNTHESIS BY T-LYMPHOCYTES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 UNIV MONTREAL,IMMUNOVIROL LAB,MONTREAL H3T 1C5,PQ,CANADA. ST JUSTINE HOSP,MONTREAL H3T 1C5,PQ,CANADA. NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 697 EP 697 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100136 ER PT J AU LEVINE, PH JAHAN, N MURARI, P MANAK, M JAFFE, E AF LEVINE, PH JAHAN, N MURARI, P MANAK, M JAFFE, E TI ROSAI-DORFMAN DISEASE - EVIDENCE FOR AN ETIOLOGIC ROLE FOR HUMAN HERPESVIRUS-6 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 697 EP 697 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100135 ER PT J AU LUSSO, P MALNATI, M GARZINODEMO, A CROWLEY, RW GALLO, RC AF LUSSO, P MALNATI, M GARZINODEMO, A CROWLEY, RW GALLO, RC TI CYTOPATHIC INFECTION OF NATURAL-KILLER (NK) CELLS BY HHV-6 - INDUCTION OF CD4 AND SUSCEPTIBILITY TO HIV-1 INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,LIG,NCI,LTCB,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 697 EP 697 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100137 ER PT J AU ALTER, HJ AF ALTER, HJ TI THE HEPATITIS-C VIRUS - FROM CLONE TO CLINIC SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIH,DEPT TRANSFUS MED,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 698 EP 698 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100141 ER PT J AU SCHILLER, J SEDMAN, S COHEN, B HUBBERT, N LOWY, D AF SCHILLER, J SEDMAN, S COHEN, B HUBBERT, N LOWY, D TI PAPILLOMAVIRUS ONCOPROTEINS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,CELLULAR ONCOL 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 698 EP 698 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100142 ER PT J AU THOMPSON, J KASHANCHI, F CHOUDHURY, S BERNEMAN, Z FRENKEL, N DONIGER, J ROSENTHAL, L AF THOMPSON, J KASHANCHI, F CHOUDHURY, S BERNEMAN, Z FRENKEL, N DONIGER, J ROSENTHAL, L TI A TRANSFORMING HHV-6 FRAGMENT FROM THE DIRECT REPEAT REGION THAT TRANSACTIVATES HIV-1 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,WASHINGTON,DC 20007. NCI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 698 EP 698 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100139 ER PT J AU DIPAOLO, JA CHEN, M POPESCU, N WOODWORTH, C BERNEMAN, A LUSSO, P ABLASHI, DV AF DIPAOLO, JA CHEN, M POPESCU, N WOODWORTH, C BERNEMAN, A LUSSO, P ABLASHI, DV TI COOPERATION OF HUMAN PAPILLOMAVIRUS (HPV), HUMAN HERPESVIRUS-6(HHV-6), AND HUMAN IMMUNODEFICIENCY VIRUS-1 (HIV-1) IN CERVICAL NEOPLASIA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 699 EP 699 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100143 ER PT J AU KATZ, R JONES, K KULKOSKY, J LAUE, T MACK, JPG MERKEL, G SKALKA, AM AF KATZ, R JONES, K KULKOSKY, J LAUE, T MACK, JPG MERKEL, G SKALKA, AM TI NEW INSIGHTS FROM STUDIES OF THE RETROVIRAL ENZYMES WITH SPECIAL EMPHASIS ON INTEGRASE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 FOX CHASE CANC CTR,INST CANC RES,PHILADELPHIA,PA 19111. UNIV NEW HAMPSHIRE,DURHAM,NH 03824. NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,FREDERICK,MD 21701. 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. PD JUN PY 1993 VL 6 IS 6 BP 699 EP 699 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100145 ER PT J AU PAVLAKIS, GN FELBER, BK SCHWARTZ, S DAGOSTINO, DM CAMPBELL, M SALTARELLI, M KORNEYEVA, M AF PAVLAKIS, GN FELBER, BK SCHWARTZ, S DAGOSTINO, DM CAMPBELL, M SALTARELLI, M KORNEYEVA, M TI POSITIVE AND NEGATIVE REGULATORY ELEMENTS IMPORTANT FOR HIV-1 EXPRESSION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS SECT,FREDERICK,MD 21702. NCI,FCRDC,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS PATHOGENESIS GRP,FREDERICK,MD 21702. 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. PD JUN PY 1993 VL 6 IS 6 BP 700 EP 700 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100148 ER PT J AU ARYA, SK GARZINODEMO, A CHATTERJEE, P AF ARYA, SK GARZINODEMO, A CHATTERJEE, P TI HIV-2 LTR AND TAT - REGULATORY ELEMENTS AND FUNCTIONAL DOMAINS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 701 EP 701 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100152 ER PT J AU DAYTON, ET POWELL, DM BENDE, SM KONINGS, DAM LIM, SY BUTINI, L PANTALEO, G DAYTON, AI AF DAYTON, ET POWELL, DM BENDE, SM KONINGS, DAM LIM, SY BUTINI, L PANTALEO, G DAYTON, AI TI INTERACTION OF THE HIV-1 REV PROTEIN AND CELLULAR FACTORS WITH THE RRE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NCI,DIV CANC BIOL & DIAG,MATH BIOL LAB,FREDERICK,MD 21701. GEORGE WASHINGTON UNIV,DEPT GENET,WASHINGTON,DC 20052. IST CLIN MED,ANCONA,ITALY. UNIV COLORADO,DEPT MOLEC CELLULAR & DEV BIOL,BOULDER,CO 80309. UNIV MICHIGAN,ANN ARBOR,MI 48109. RI Pantaleo, Giuseppe/K-6163-2016 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. PD JUN PY 1993 VL 6 IS 6 BP 701 EP 701 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100154 ER PT J AU FELBER, BK ZOLOTHUKIN, A HARRISON, J CUNNINGHAM, C PAVLAKIS, GN AF FELBER, BK ZOLOTHUKIN, A HARRISON, J CUNNINGHAM, C PAVLAKIS, GN TI REV OF HIV-1 AND REX OF HTLV-I RESCUE UNSTABLE CELLULAR MESSENGER-RNAS - A MODEL FOR A COMMON POSTTRANSCRIPTIONAL REGULATORY PATHWAY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS PATHOGENESIS GRP,FREDERICK,MD 21702. NCI,FCRDC,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS SECT,FREDERICK,MD 21702. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 702 EP 702 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100158 ER PT J AU FRANCHINI, G KORALNIK, I GOLDSTEIN, DJ ANDRESSON, T GALLO, RC SCHLEGEL, R AF FRANCHINI, G KORALNIK, I GOLDSTEIN, DJ ANDRESSON, T GALLO, RC SCHLEGEL, R TI THE P12' PROTEIN OF HTLV-I EXHIBITS STRUCTURAL SIMILARITY TO THE E5 ONCOPROTEIN OF BOVINE PAPILLOMA-VIRUS AND BINDS THE 16K COMPONENT OF VACUOLAR H+ATPASE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20057. 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. PD JUN PY 1993 VL 6 IS 6 BP 702 EP 702 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100157 ER PT J AU KORALNIK, IJ GESSAIN, A KLOTMAN, ME LOMONICO, A BERNEMAN, ZN FRANCHINI, G AF KORALNIK, IJ GESSAIN, A KLOTMAN, ME LOMONICO, A BERNEMAN, ZN FRANCHINI, G TI CELLULAR-LOCALIZATION OF NOVEL PROTEIN ISOFORMS ENCODED BY THE HTLV-I PX REGION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 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. PD JUN PY 1993 VL 6 IS 6 BP 702 EP 702 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100156 ER PT J AU LI, CCH RUSCETTI, F RICE, N CHEN, E MIKOVITS, J LONGO, DL AF LI, CCH RUSCETTI, F RICE, N CHEN, E MIKOVITS, J LONGO, DL TI C-REL FAMILY GENE-EXPRESSION IN HTLV-I INFECTED-CELLS AND C-REL ACTIVATION BY TAX PROTEIN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,BRI BASIC RES PROGRAM MOLEC IMMUNOREGULAT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,BRI BASIC RES PROGRAM,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD 21702. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 703 EP 703 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100161 ER PT J AU BLUMENTHAL, R GOLDING, H BRODER, CC BERGER, EA PURI, A DIMITROV, DS AF BLUMENTHAL, R GOLDING, H BRODER, CC BERGER, EA PURI, A DIMITROV, DS TI KINETICS OF HIV-1 ENV-MEDIATED CELL-FUSION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NIH,BETHESDA,MD 20892. CBER,BETHESDA,MD 20892. FDA,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 704 EP 704 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100166 ER PT J AU TANI, Y BOONE, E DONOHUE, E ZOLLAPAZNER, S LANE, HC COHEN, DI AF TANI, Y BOONE, E DONOHUE, E ZOLLAPAZNER, S LANE, HC COHEN, DI TI EXPRESSION OF AN ANTI-GP41 RECEPTOR ON THE SURFACE OF A B-CELL ASSOCIATED WITH ENHANCED REPLICATION OF HIV-1 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NYU MED CTR,NEW YORK,NY 10016. 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. PD JUN PY 1993 VL 6 IS 6 BP 704 EP 704 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100165 ER PT J AU BRODER, CC DIMITROV, DS BLUMENTHAL, R BERGER, EA AF BRODER, CC DIMITROV, DS BLUMENTHAL, R BERGER, EA TI HIV-1 ENVELOPE GLYCOPROTEIN MEDIATED CELL-FUSION - STRUCTURAL FEATURES OF CD4 AND INVOLVEMENT OF ACCESSORY COMPONENTS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,LVD,BETHESDA,MD 20892. NCI,LMMB,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 705 EP 705 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100170 ER PT J AU DIMITROV, DS BRODER, CC BERGER, EA BLUMENTHAL, R AF DIMITROV, DS BRODER, CC BERGER, EA BLUMENTHAL, R TI CALCIUM-IONS ARE REQUIRED FOR CELL-FUSION MEDIATED BY THE CD4-HIV-1-ENVELOPE GLYCOPROTEIN INTERACTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,LMMB,MEMBRANE STRUCT & FUNCT SECT,BETHESDA,MD 20892. NIAID,VIRAL DIS 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 705 EP 705 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100167 ER PT J AU RAUSCH, DM VANCOTT, TC EIDEN, LE PADGETT, MP KALYANARAMAN, VS LIFSON, JD AF RAUSCH, DM VANCOTT, TC EIDEN, LE PADGETT, MP KALYANARAMAN, VS LIFSON, JD TI DEFINING MULTISITE INTERACTIONS BETWEEN HIV-1 GP120 AND CD4 DURING VIRAL ENTRY AND FUSION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. ADV BIOSCI LAB INC,KENSINGTON,MD. WRAIR,DEPT RETROVIRAL RES,ROCKVILLE,MD. GENELABS INC,REDWOOD CITY,CA. 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. PD JUN PY 1993 VL 6 IS 6 BP 705 EP 705 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100168 ER PT J AU VANCOTT, TC RAUSCH, DM BETHKE, FR KALYANARAMAN, VS LIFSON, JD REDFIELD, RR EIDEN, LE AF VANCOTT, TC RAUSCH, DM BETHKE, FR KALYANARAMAN, VS LIFSON, JD REDFIELD, RR EIDEN, LE TI BINDING INTERACTIONS BETWEEN PEPTIDES CORRESPONDING TO THE CDR3 REGION OF CD4 AND HIV-1 GP120 AS STUDIED BY BIOSPECIFIC INTERACTION ANALYSIS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 WRAIR,DEPT RETROVIRAL RES,ROCKVILLE,MD. NIMH,BETHESDA,MD 20892. ADV BIOSCI LAB INC,KENSINGTON,MD. GENELABS INC,REDWOOD CITY,CA. 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. PD JUN PY 1993 VL 6 IS 6 BP 705 EP 705 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100169 ER PT J AU CHANG, HK LISZIEWICZ, J GALLO, RC ENSOLI, B AF CHANG, HK LISZIEWICZ, J GALLO, RC ENSOLI, B TI BLOCK OF HIV-1 GENE-EXPRESSION BY COMBINING ANTISENSE TAT RNA AND POLY-TAR DECOY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 706 EP 706 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100173 ER PT J AU CLAUDIA, B LUSSO, P GALLO, RC CROWLEY, RW FRANCHINI, G AF CLAUDIA, B LUSSO, P GALLO, RC CROWLEY, RW FRANCHINI, G TI PHOSPHOROTHIOATED ANTISENSE OLIGODEOXYNUCLEOTIDES DIRECTED AGAINST THE YPR GENE INHIBIT HIV-1 REPLICATION IN PRIMARY HUMAN MACROPHAGES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,LTCB,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 706 EP 706 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100172 ER PT J AU KINTER, AL POLI, G FAUCI, AS AF KINTER, AL POLI, G FAUCI, AS TI N-ACETYL-CYSTEINE (NAC) IS A POTENT SUPPRESSOR OF HIV TRANSCRIPTION IN PERSISTENTLY INFECTED MONOCYTIC CELLS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 707 EP 707 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100175 ER PT J AU BERGER, EA MOSS, B KENNEDY, PE AF BERGER, EA MOSS, B KENNEDY, PE TI CD4-PSEUDOMONAS EXOTOXIN POTENTLY INHIBITS PRIMARY HIV-1 ISOLATES REFRACTORY TO NEUTRALIZATION BY SOLUBLE CD4 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,VIRAL DIS 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 708 EP 708 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100179 ER PT J AU TOBIN, GJ GONDA, MA AF TOBIN, GJ GONDA, MA TI INHIBITION OF BOVINE IMMUNODEFICIENCY-LIKE VIRUS (BIV) IN CELL-CULTURE BY ANTI-HIV-1 COMPOUNDS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 PRI DYNCORP,NCI,FREDERICK CANC RES & DEV CTR,CELL & MOLEC STRUCT LAB,FREDERICK,MD 21702. 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. PD JUN PY 1993 VL 6 IS 6 BP 708 EP 708 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100181 ER PT J AU WEINSTEIN, JN MUENZ, LR KAGEYAMA, S MITSUYA, H BUNOW, B AF WEINSTEIN, JN MUENZ, LR KAGEYAMA, S MITSUYA, H BUNOW, B TI OPTIMIZING THE DESIGN OF EXPERIMENTS ON COMBINATION THERAPY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CIVILIZED SOFTWARE INC,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 708 EP 708 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100180 ER PT J AU VERONESE, FD REITZ, M ROBERTGUROFF, M BOYER, C LORI, F GALLO, RC LUSSO, P AF VERONESE, FD REITZ, M ROBERTGUROFF, M BOYER, C LORI, F GALLO, RC LUSSO, P TI LOSS OF A NEUTRALIZING EPITOPE BY A SPONTANEOUS POINT MUTATION IN THE V(3)-LOOP OF HIV-1(IIIB) ISOLATED FROM AN INFECTED LABORATORY WORKER SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 ADV BIOSCI LABS INC,KENSINGTON,MD. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 709 EP 709 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100185 ER PT J AU RIMSKYCLARKE, LT CLARK, LE ARTHUR, LO KOSLOFF, BR GREENWELL, TK WEINHOLD, K MATTHEWS, TJ AF RIMSKYCLARKE, LT CLARK, LE ARTHUR, LO KOSLOFF, BR GREENWELL, TK WEINHOLD, K MATTHEWS, TJ TI ESCAPE OF HIV-1 FROM IMMUNE PRESSURE - A CHIMPANZEE MODEL SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. NCI,FREDERICK CANC RES FACIL,FREDERICK,MD 21701. 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. PD JUN PY 1993 VL 6 IS 6 BP 712 EP 712 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100197 ER PT J AU BARILLARI, G BUONAGURO, L FIORELLI, V GALLO, RC ENSOLI, B AF BARILLARI, G BUONAGURO, L FIORELLI, V GALLO, RC ENSOLI, B TI IMMUNOACTIVATION RATHER THAN IMMUNODEFICIENCY MAY COOPERATE WITH HIV-1 INFECTION IN THE DEVELOPMENT OF AIDS-ASSOCIATED KAPOSIS-SARCOMA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 713 EP 713 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100202 ER PT J AU ENSOLI, B BUONAGURO, L FIORELLI, V GENDELMAN, R WINGFIELD, P GALLO, RC AF ENSOLI, B BUONAGURO, L FIORELLI, V GENDELMAN, R WINGFIELD, P GALLO, RC TI RELEASE, UPTAKE AND BIOLOGICAL EFFECTS (VASCULAR CELL-GROWTH AND VIRAL TRANSACTIVATION) OF EXTRACELLULAR HIV-1 TAT PROTEIN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIDDK,PROTEIN EXPRESS LAB,BETHESDA,MD. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 713 EP 713 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100201 ER PT J AU PLUDA, JM SHAY, LE FOLI, A COHEN, PJ ADAMO, D BRODER, S YARCHOAN, R AF PLUDA, JM SHAY, LE FOLI, A COHEN, PJ ADAMO, D BRODER, S YARCHOAN, R TI ADMINISTRATION OF PENTOSAN POLYSULFATE TO PATIENTS (PTS) WITH HIV-ASSOCIATED KAPOSIS-SARCOMA (KS) SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 713 EP 713 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100200 ER PT J AU FIORELLI, V GALLO, RC ENSOLI, B AF FIORELLI, V GALLO, RC ENSOLI, B TI STUDIES ON THE VASCULAR CELL-GROWTH EFFECT OF EXTRACELLULAR HIV-1 TAT PROTEIN DURING THE CELL-CYCLE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 714 EP 714 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100203 ER PT J AU CASOLI, C CIMARELLI, A ZELLA, D SALEMI, M LORI, F LUSSO, P ACHILLI, G CATTANEO, E BERTAZZONI, U AF CASOLI, C CIMARELLI, A ZELLA, D SALEMI, M LORI, F LUSSO, P ACHILLI, G CATTANEO, E BERTAZZONI, U TI HOST-RANGE OF HIV-1 IS ENLARGED TO T8 AND B-LYMPHOCYTES IN PATIENTS CO-INFECTED BY HIV-1 AND HTLV-II SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 UNIV PARMA,I-43100 PARMA,ITALY. CNR,GBE,PAVIA,ITALY. NCI,LTCB,BETHESDA,MD 20892. POLICLIN SAN MATTEO,RCCS,PAVIA,ITALY. 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. PD JUN PY 1993 VL 6 IS 6 BP 715 EP 715 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100207 ER PT J AU SCHULICK, RD CLERICI, M BLATT, S HENDRIX, C SHEARER, GM AF SCHULICK, RD CLERICI, M BLATT, S HENDRIX, C SHEARER, GM TI LIMITING DILUTION ANALYSIS OF INTERLEUKIN 2-PRODUCING T-CELLS RESPONSIVE TO RECALL AND ALLO ANTIGENS IN HUMAN-IMMUNODEFICIENCY-VIRUS (HIV)-INFECTED AND UNINFECTED INDIVIDUALS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. SGHMMM,HIV UNIT,LACKLAND AFB,TX 78236. 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. PD JUN PY 1993 VL 6 IS 6 BP 715 EP 715 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100210 ER PT J AU CORBELLINO, M GALLI, M PARRAVICINI, C MORONI, M GALLO, RC LUSSO, P AF CORBELLINO, M GALLI, M PARRAVICINI, C MORONI, M GALLO, RC LUSSO, P TI HUMAN HERPESVIRUS-6 IN TISSUE FROM PATIENTS WITH AIDS AND IN SERONEGATIVE INDIVIDUALS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 UNIV MILAN,INST PATHOL,I-20122 MILAN,ITALY. UNIV MILAN,INFECT DIS CLIN,I-20122 MILAN,ITALY. NCI,LTCB,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 716 EP 716 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100214 ER PT J AU GURGO, C LUSSO, P GROGG, D REITZ, MS AF GURGO, C LUSSO, P GROGG, D REITZ, MS TI ACTIVATION-INDUCED APOPTOSIS IN HIV-TRANSFECTED JURKAT CELLS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 716 EP 716 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100212 ER PT J AU OAVI, HB ABLASHI, DV GREEN, MT SEGALL, GK LUSSO, P KAHN, CR RHIM, J AF OAVI, HB ABLASHI, DV GREEN, MT SEGALL, GK LUSSO, P KAHN, CR RHIM, J TI AUGMENTATION OF HHV-6 DNA-SEQUENCES IN CORNEAL CELLS INFECTED WITH HIV-1 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030. NIH,GILLETTE MED EVALUAT LABS,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 717 EP 717 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100215 ER PT J AU BUONAGURO, L BARILLARI, G CHANG, HK KAO, V GALLO, RC ENSOLI, B AF BUONAGURO, L BARILLARI, G CHANG, HK KAO, V GALLO, RC ENSOLI, B TI CYTOKINE ACTIVATION DURING HIV-1 INFECTION - INDUCTION OF TUMOR-NECROSIS-FACTOR (TNF) GENE-EXPRESSION BY HIV-1 TAT SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 718 EP 718 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100221 ER PT J AU CARA, A ROBERTGUROFF, M GALLO, RC REITZ, MS LORI, F AF CARA, A ROBERTGUROFF, M GALLO, RC REITZ, MS LORI, F TI BIOLOGICAL AND MOLECULAR-PROPERTIES OF HIV-1 INTEGRASE DEFECTIVE-MUTANTS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,LTCB,BETHESDA,MD 20892. RI Cara, Andrea/M-4865-2015 OI Cara, Andrea/0000-0003-4967-1895 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. PD JUN PY 1993 VL 6 IS 6 BP 718 EP 718 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100220 ER PT J AU GITLIN, SD BRADY, JN AF GITLIN, SD BRADY, JN TI HTLV-1 TAX(1) AND ETS1 TRANSACTIVATION OF THE HTLV-I LTR SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 718 EP 718 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100222 ER PT J AU BERNEMAN, ZN GARTENHAUS, RB NELSON, PJ REITZ, MS GALLO, RC KLOTMAN, ME AF BERNEMAN, ZN GARTENHAUS, RB NELSON, PJ REITZ, MS GALLO, RC KLOTMAN, ME TI ALTERNATIVELY SPLICED MESSENGER-RNAS OF HUMAN T-LYMPHOTROPIC VIRUS TYPE-I (HTLV-I) - EVIDENCE FOR REGULATION AND INVIVO SEQUENCE DATA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 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. PD JUN PY 1993 VL 6 IS 6 BP 719 EP 719 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100225 ER PT J AU DITTMER, J GITLIN, SD BRADY, JN AF DITTMER, J GITLIN, SD BRADY, JN TI HTLV-1 TAX(1) INCREASES THE EXPRESSION OF THE PARATHYROID HORMONE-RELATED PROTEIN GENE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 719 EP 719 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100223 ER PT J AU KASHANCHI, F BOHAN, CA RADONOVICH, M ENSOLI, B BRADY, JN AF KASHANCHI, F BOHAN, CA RADONOVICH, M ENSOLI, B BRADY, JN TI TAT TRANSACTIVATES HUMAN-IMMUNODEFICIENCY-VIRUS TRANSCRIPTION INVITRO BY STIMULATING INITIATION AND ELONGATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 719 EP 719 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100226 ER PT J AU CONSTANTOULAKIS, P CAMPBELL, M AFONINA, E NASIOULAS, G FELBER, BK PAVLAKIS, GN AF CONSTANTOULAKIS, P CAMPBELL, M AFONINA, E NASIOULAS, G FELBER, BK PAVLAKIS, GN TI IDENTIFICATION OF AN INTERFERON-INDUCIBLE GENE INHIBITING HIV-1 EXPRESSION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,BASIC RES PROGRAM,FREDERICK,MD 21701. 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. PD JUN PY 1993 VL 6 IS 6 BP 720 EP 720 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100228 ER PT J AU BOERI, E GESSAIN, A GARIN, B DETHE, G KAZADI, K FRANCHINI, G AF BOERI, E GESSAIN, A GARIN, B DETHE, G KAZADI, K FRANCHINI, G TI LACK OF CORRELATION BETWEEN CHANGES IN THE HTLV-1 ENV GENE SEQUENCE AND DIFFERENT NEUROLOGICAL DISEASES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 CTR NATL NEUROPSYCHOPATHOL,KINSHASA,ZAIRE. INST RECH BIOMED,KINSHASA,ZAIRE. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. INST PASTEUR,F-75724 PARIS 15,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 721 EP 721 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100231 ER PT J AU GOLDING, H DIMITROV, D BLUMENTHAL, R GOLDING, B AF GOLDING, H DIMITROV, D BLUMENTHAL, R GOLDING, B TI FUSION OF HUMAN B-CELLS WITH HIV-1 ENVELOPE EXPRESSING T-CELLS IS ENHANCED BY ANTIGEN-SPECIFIC IMMUNOGLOBULIN (IG) RECEPTORS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 FDA,CBER,DIV VIROL,BETHESDA,MD. FDA,CBER,DIV HEMATOL,BETHESDA,MD. NCI,LMMB,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 722 EP 722 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100235 ER PT J AU MARSH, JW AF MARSH, JW TI NEF MODIFIES MURINE T-CELL FUNCTION - DOWN-MODULATION OF SURFACE EXPRESSION OF CD8-BETA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIMH,MOLEC BIOL LAB,BIOPHYS CHEM SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 722 EP 722 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100236 ER PT J AU BRUGGEMAN, LA ADLER, SH KOPP, JB RAPPAPORT, J NOTKINS, AL KLOTMAN, PE AF BRUGGEMAN, LA ADLER, SH KOPP, JB RAPPAPORT, J NOTKINS, AL KLOTMAN, PE TI EXPRESSION OF THE HIV-1 LTR IN TRANSGENIC MICE IS NF-KB DEPENDENT SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIH,HOWARD HUGHES MED INST,NIDR,LOM,RES SCHOLARS PROGRAM,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 723 EP 723 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100242 ER PT J AU COGGIANO, MA TRUCKENMILLER, ME ADAMS, AJ WYATT, RJ KULAGA, H AF COGGIANO, MA TRUCKENMILLER, ME ADAMS, AJ WYATT, RJ KULAGA, H TI NUCLEIC-ACID SEQUENCE OF RABBIT ADAPTED HIV-1 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIMH,NEUROSCI RES CTR,WASHINGTON,DC 20032. ST ELIZABETH HOSP,WASHINGTON,DC 20032. 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. PD JUN PY 1993 VL 6 IS 6 BP 723 EP 723 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100241 ER PT J AU HAGUE, BF SAWASDIKOSOL, S BROWN, TJ CHO, SG LEGUERN, A KINDT, TJ AF HAGUE, BF SAWASDIKOSOL, S BROWN, TJ CHO, SG LEGUERN, A KINDT, TJ TI ROLE OF RECEPTOR IN HIV-1 INFECTION OF TRANSFORMED RABBIT-CELL LINES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,TWINBROOK FACIL 2,IMMUNOGENET LAB,ROCKVILLE,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 723 EP 723 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100240 ER PT J AU KORALNIK, IJ LEMP, JF FRANCHINI, G AF KORALNIK, IJ LEMP, JF FRANCHINI, G TI INVITRO INFECTION OF HUMAN MACROPHAGES BY HUMAN T-CELL LEUKEMIA-VIRUS TYPE-I SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 ABI,COLOUMBIA,MD 21046. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 723 EP 723 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100239 ER PT J AU KOPP, JB ROONEY, JF WOHLENBERG, C DORFMAN, N MARINOS, NJ BRYANT, JL NOTKINS, AL KLOTMAN, PE AF KOPP, JB ROONEY, JF WOHLENBERG, C DORFMAN, N MARINOS, NJ BRYANT, JL NOTKINS, AL KLOTMAN, PE TI HYPERKERATOTIC SKIN DISORDERS IN HIV-TRANSGENIC MICE ARE ASSOCIATED WITH INCREASED TRANSGENE EXPRESSION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIDR,LDB,LOM,BETHESDA,MD 20892. NIDR,ACU,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 724 EP 724 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100243 ER PT J AU HENEINE, W WOODS, T GREEN, D GRACIA, F FUKUDA, K BLATTNER, W KAPLAN, JE AF HENEINE, W WOODS, T GREEN, D GRACIA, F FUKUDA, K BLATTNER, W KAPLAN, JE TI DETECTION OF HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-II (HTLV-II) IN THE BREAST-MILK OF HTLV-II INFECTED MOTHERS USING THE POLYMERASE CHAIN-REACTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 GORGAS MEM LAB,PANAMA CITY,PANAMA. CTR DIS CONTROL,ATLANTA,GA 30333. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 725 EP 725 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100247 ER PT J AU TAKAHASHI, H SCHNEEWIND, O IJICHI, S KAPLAN, MH GALLO, RC HALL, WW AF TAKAHASHI, H SCHNEEWIND, O IJICHI, S KAPLAN, MH GALLO, RC HALL, WW TI MOLECULAR CHARACTERIZATION OF HUMAN T-CELL LEUKEMIA-VIRUS, TYPE-II (HTLV-II) ISOLATES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 CORNELL UNIV,N SHORE UNIV HOSP,COLL MED,DEPT MED,MANHASSET,NY 11030. ROCKEFELLER UNIV,NEW YORK,NY 10021. NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 726 EP 726 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100251 ER PT J AU LEVINE, PH AF LEVINE, PH TI THE EPIDEMIOLOGY OF HTLV-II - AN OVERVIEW SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,DCE,EBP,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 727 EP 727 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100255 ER PT J AU SAXINGER, C AYUB, J LEVINE, P AF SAXINGER, C AYUB, J LEVINE, P TI IMPROVED CHARACTERIZATION USING PEPTIDE-BASED ASSAYS OF HTLV1-REACTIVE AND HTLV2-REACTIVE SEROLOGIES IN A NEW-WORLD REGION - THE DARIEN RAIN-FOREST OF PANAMA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,DCE,LTCB,BETHESDA,MD 20892. NCI,DCE,VEB,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 727 EP 727 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100256 ER PT J AU KANKI, P SAMUELS, K MBOUP, S MARLINK, R PAPAS, T ESSEX, M AF KANKI, P SAMUELS, K MBOUP, S MARLINK, R PAPAS, T ESSEX, M TI SERODIAGNOSIS OF HIV BY RECOMBINANT ENV AND VPX/VPU PEPTIDES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NCI,FREDERICK CANC RES FACIL,FREDERICK,MD 21701. UNIV DAKAR,DAKAR,SENEGAMBIA. 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. PD JUN PY 1993 VL 6 IS 6 BP 728 EP 728 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100260 ER PT J AU CORNAGLIAFERRARIS, P CARBONE, R CASARINO, L CARA, A VAMIER, OE DISTEFANO, F AF CORNAGLIAFERRARIS, P CARBONE, R CASARINO, L CARA, A VAMIER, OE DISTEFANO, F TI PERIPHERAL-BLOOD COLLECTED FROM A PYGMY POPULATION ON PAPER SPOT ALLOW TO ANALYZE CD4 POLYMORPHISM BY PCR AMPLIFICATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 UNIV GENOA,G GASLINI INST,PEDIAT ONCOL RES LAB,I-16126 GENOA,ITALY. UNIV GENOA,INST FORENS MED,I-16126 GENOA,ITALY. UNIV GENOA,INST MICROBIOL,I-16126 GENOA,ITALY. IST,IMMUNOGENET LAB,GENOA,ITALY. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Cara, Andrea/M-4865-2015 OI Cara, Andrea/0000-0003-4967-1895 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. PD JUN PY 1993 VL 6 IS 6 BP 730 EP 730 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100267 ER PT J AU LORI, F VERONESE, F DEVICO, A LUSSO, P BOYER, C CARA, A GAO, WY REITZ, MS GALLO, RC AF LORI, F VERONESE, F DEVICO, A LUSSO, P BOYER, C CARA, A GAO, WY REITZ, MS GALLO, RC TI INCOMPLETE HIV-1 VIRAL-DNA IN MATURE VIRIONS AND QUIESCENT LYMPHOCYTES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 ABL,KENSINGTON,MD. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,LMC,BETHESDA,MD 20892. RI Cara, Andrea/M-4865-2015 OI Cara, Andrea/0000-0003-4967-1895 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. PD JUN PY 1993 VL 6 IS 6 BP 731 EP 731 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100274 ER PT J AU LINDHOLM, PF TRINH, D BRADY, JN AF LINDHOLM, PF TRINH, D BRADY, JN TI EXTRACELLULAR TAX1 PROTEIN AND TAX1 PRODUCING CELL-LINES STIMULATE NF-KB IN UNINFECTED CELLS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 732 EP 732 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100276 ER PT J AU COLOMBINI, S POPESCU, N ZIMONJIC, D CHEN, M DIPAOLO, JA BIBERFELD, P GALLO, RC ABLASHI, D AF COLOMBINI, S POPESCU, N ZIMONJIC, D CHEN, M DIPAOLO, JA BIBERFELD, P GALLO, RC ABLASHI, D TI A NEW SIMIAN HERPESVIRUS CLOSELY RELATED TO EBV CONTRIBUTES SUBSTANTIALLY TO THE ESTABLISHMENT OF B-CELL LYMPHOMA IN IMMUNODEFICIENT CYNOMOLGUS MONKEYS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,CANC BIOL LAB,BETHESDA,MD 20892. KAROLINSKA INST,DEPT PATHOL,S-10401 STOCKHOLM 60,SWEDEN. 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. PD JUN PY 1993 VL 6 IS 6 BP 733 EP 733 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100282 ER PT J AU GERMAIN, RN AF GERMAIN, RN TI PEPTIDE BINDING, CONFORMATIONAL-CHANGES, AND INTRACELLULAR-TRANSPORT IN THE MHC CLASS-I AND CLASS-II PRESENTATION PATHWAYS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 734 EP 734 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100286 ER PT J AU FOLI, A YARCHOAN, R AF FOLI, A YARCHOAN, R TI MONOCYTE-MACROPHAGES (M/M) PRODUCE INTERLEUKIN-6 (IL-6) AND TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA) IN RESPONSE TO GRANULOCYTE MACROPHAGE-COLONY-STIMULATING FACTOR (GM-CSF), BUT NOT TO HIV-INFECTION ALONE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 736 EP 736 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100294 ER PT J AU STANLEY, SK SINGER, K HAYNES, B FAUCI, AS AF STANLEY, SK SINGER, K HAYNES, B FAUCI, AS TI INDUCTION OF HIV EXPRESSION FROM CHRONICALLY INFECTED PROMONOCYTIC AND T-CELLS BY IRRADIATED HUMAN KERATINOCYTES IS MEDIATED BY TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA) PRODUCTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 737 EP 737 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100295 ER PT J AU VACCHIO, MS HODES, RJ AF VACCHIO, MS HODES, RJ TI T-CELL RECEPTOR ALPHA-CHAIN AND BETA-CHAIN EXPRESSION IN REPERTOIRE SELECTION AND IN RESPONSES TO ENDOGENOUS SUPERANTIGENS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 737 EP 737 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100298 ER PT J AU GONDA, MA PALLANSCH, LA CENTANNI, JM GREENWOOD, JD AF GONDA, MA PALLANSCH, LA CENTANNI, JM GREENWOOD, JD TI DEVELOPMENT OF TRANSGENIC MICE USING INFECTIOUS PROVIRAL MOLECULAR CLONES OF THE BOVINE IMMUNODEFICIENCY-LIKE VIRUS (BIV) SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,PRI DYNCORP,FREDERICK CANC RES & DEV CTR,CELL & MOLEC STRUCT LAB,FREDERICK,MD 21702. 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. PD JUN PY 1993 VL 6 IS 6 BP 739 EP 739 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100304 ER PT J AU EIDEN, LE RAUSCH, DM DACUNHA, A LENDVAY, J REHM, S WARD, J SHARER, L WEIHE, E NOHR, D MURRAY, E AF EIDEN, LE RAUSCH, DM DACUNHA, A LENDVAY, J REHM, S WARD, J SHARER, L WEIHE, E NOHR, D MURRAY, E TI CEREBROCORTICAL GLIOSIS IN SIV-INFECTED RHESUS MACAQUES WITH MOTOR AND COGNITIVE IMPAIRMENTS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NCI,FCRDC,FREDERICK,MD 21701. UMD,NEW JERSEY MED SCH,NEWARK,NJ. UNIV MAINZ,DEPT ANAT,W-6500 MAINZ,GERMANY. 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 JUN PY 1993 VL 6 IS 6 BP 740 EP 740 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100310 ER PT J AU KLOTMAN, PE KOPP, JB KLOTMAN, ME RAY, PE SANTORO, TJ ADLER, SH BRYANT, JL WEEKS, BS BRUGGEMAN, LA RAPPAPORT, J NOTKINS, AL AF KLOTMAN, PE KOPP, JB KLOTMAN, ME RAY, PE SANTORO, TJ ADLER, SH BRYANT, JL WEEKS, BS BRUGGEMAN, LA RAPPAPORT, J NOTKINS, AL TI TRANSGENIC MICE AS MODELS FOR HIV PATHOGENESIS AND THERAPY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIDR,LDB,BETHESDA,MD 20892. NCI,LTCB,BETHESDA,MD 20892. NIDR,ACU,BETHESDA,MD 20892. NIDR,LOM,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 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. PD JUN PY 1993 VL 6 IS 6 BP 741 EP 741 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100312 ER PT J AU SIMPSON, RM SAWASDIKOSOL, S ZHAO, TM HAGUE, BF ROBINSON, MA BOWERS, F TELLER, R DAVIS, C KINDT, TJ AF SIMPSON, RM SAWASDIKOSOL, S ZHAO, TM HAGUE, BF ROBINSON, MA BOWERS, F TELLER, R DAVIS, C KINDT, TJ TI ACUTE FULMINANT STAGE ADULT T-CELL LEUKEMIA-LYMPHOMA IN RABBITS INOCULATED WITH AN HTLV-1 TRANSFORMED RABBIT-CELL LINE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD. 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. PD JUN PY 1993 VL 6 IS 6 BP 741 EP 741 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100314 ER PT J AU DACUNHA, A JACKSON, RW ANAND, R VITKOVIC, L AF DACUNHA, A JACKSON, RW ANAND, R VITKOVIC, L TI HIV-1 STIMULATES CYTOKINE EXPRESSION IN PRIMARY ASTROCYTES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 743 EP 743 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100320 ER PT J AU ENSOLI, F ENSOLI, B GALLO, RC PIZZO, PA THIELE, CJ AF ENSOLI, F ENSOLI, B GALLO, RC PIZZO, PA THIELE, CJ TI HIV-1 GENE-EXPRESSION IN NEURONAL AND GLIAL-DERIVED CELLS - EFFECTS OF NEURAL TROPHIC FACTORS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,LTCB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 JUN PY 1993 VL 6 IS 6 BP 743 EP 743 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100322 ER PT J AU GESSAIN, A BOERI, E YANAGIHARA, R GALLO, RC FRANCHINI, G AF GESSAIN, A BOERI, E YANAGIHARA, R GALLO, RC FRANCHINI, G TI COMPLETE NUCLEOTIDE-SEQUENCE OF A HIGHLY DIVERGENT HTLV-I ISOLATE FROM MELANESIA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 PASTEUR INST,PARIS,FRANCE. LAB TUMOR CELL BIOL,BETHESDA,MD. FCRDC,NINDS,CENT NERVOUS SYST STUDIES LAB,FREDERICK,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 744 EP 744 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100325 ER PT J AU KORALNIK, IJ LOMONICO, A FULLEN, J SAXINGER, C GESSAIN, A GALLO, RC MARKHAM, P KALYANARAMAN, V BOERI, E HIRSCH, V ALLAN, J MURTHY, K GUO, HG ALFORD, P FRANCHINI, G AF KORALNIK, IJ LOMONICO, A FULLEN, J SAXINGER, C GESSAIN, A GALLO, RC MARKHAM, P KALYANARAMAN, V BOERI, E HIRSCH, V ALLAN, J MURTHY, K GUO, HG ALFORD, P FRANCHINI, G TI A WIDE SPECTRUM OF SIMIAN T-LYMPHOTROPIC LEUKEMIA TYPE-I VIRUS VARIANTS IN NATURE - EVIDENCE FOR INTERSPECIES TRANSMISSION IN EQUATORIAL AFRICA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 SW FDN BIOMED RES,SAN ANTONIO,TX 78284. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. INST PASTEUR,F-75724 PARIS 15,FRANCE. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD. UNIV TEXAS,MD ANDERSON CANC CTR,BASTROP,TX. 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. PD JUN PY 1993 VL 6 IS 6 BP 745 EP 745 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100327 ER PT J AU LEGRENADE, L FLETCHER, V CARBERRY, C HANCHARD, B CRANSTON, B WILLIAMS, NP CHOW, M BLATTNER, W AF LEGRENADE, L FLETCHER, V CARBERRY, C HANCHARD, B CRANSTON, B WILLIAMS, NP CHOW, M BLATTNER, W TI FURTHER-STUDIES IN INFECTIVE DERMATITIS OF JAMAICAN CHILDREN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 UNIV W INDIES,DEPT MED,KINGSTON 7,JAMAICA. UNIV W INDIES,DEPT PATHOL,KINGSTON 7,JAMAICA. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 745 EP 745 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100329 ER PT J AU RABKIN, CS NASCA, P BAPTISTE, MS ABE, T BIGGAR, RJ AF RABKIN, CS NASCA, P BAPTISTE, MS ABE, T BIGGAR, RJ TI HIV-ASSOCIATED CANCERS IN WOMEN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. NEW YORK HLTH DEPT,ALBANY,NY. NEW JERSEY CANC REGISTRY,TRENTON,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. PD JUN PY 1993 VL 6 IS 6 BP 745 EP 745 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100330 ER PT J AU WIKTOR, SZ PATE, EJ BARNETT, M PALMER, P KIM, N BLATTNER, WA AF WIKTOR, SZ PATE, EJ BARNETT, M PALMER, P KIM, N BLATTNER, WA TI MATERNAL-INFANT TRANSMISSION OF HTLV-I - FREQUENCY AND TIME-COURSE OF SEROCONVERSION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. UNIV W INDIES,KINGSTON 7,JAMAICA. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. 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. PD JUN PY 1993 VL 6 IS 6 BP 745 EP 745 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100328 ER PT J AU VERMUND, SH LAWRENCE, DN FISCHER, RD FAST, P RIDA, WN SCHRAGER, LK BRADAC, J SHEON, AR CORDELL, JR DUNBAR, S BARKER, LF HOFF, R AF VERMUND, SH LAWRENCE, DN FISCHER, RD FAST, P RIDA, WN SCHRAGER, LK BRADAC, J SHEON, AR CORDELL, JR DUNBAR, S BARKER, LF HOFF, R TI PREPARATIONS FOR HIV VACCINE EFFICACY TRIALS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,DIV AIDS,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 746 EP 746 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100332 ER PT J AU ABIMIKU, AG ZWANDOR, A KYARI, S ALDRICH, K KIGBU, E GOMWALK, N WILLIAMS, E IDOKO, J ANTEYI, J ADENIYIJONES, S ROBERTGUROFF, M GALLO, RC AF ABIMIKU, AG ZWANDOR, A KYARI, S ALDRICH, K KIGBU, E GOMWALK, N WILLIAMS, E IDOKO, J ANTEYI, J ADENIYIJONES, S ROBERTGUROFF, M GALLO, RC TI HIV-1, NOT HIV-2, IS PREVALENT IN NIGERIA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. PLATEAU STATE HOSP,WORLD LAB AIDS RES,ICSC,JOS,NIGERIA. MINIST HLTH,JOS,NIGERIA. JOS UNIV,TEACHING HOSP,JOS,NIGERIA. UNICAL,TEACHING HOSP,CALABAR,NIGERIA. 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. PD JUN PY 1993 VL 6 IS 6 BP 747 EP 747 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100338 ER PT J AU GOEDERT, JJ DULIEGE, AM FELTON, S BIGGAR, RJ AF GOEDERT, JJ DULIEGE, AM FELTON, S BIGGAR, RJ TI UPDATE ON THE INTERNATIONAL REGISTRY OF HIV-EXPOSED TWINS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,VES,BETHESDA,MD 20892. GENENTECH INC,S SAN FRANCISCO,CA 94080. RTI,WASHINGTON,DC. 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. PD JUN PY 1993 VL 6 IS 6 BP 747 EP 747 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100336 ER PT J AU ROSENBERG, PS BIGGAR, RJ AF ROSENBERG, PS BIGGAR, RJ TI PORTRAIT OF THE HIV AIDS EPIDEMIC IN WASHINGTON DC SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,DCE,EPIDEMIOL & BIOSTAT,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1993 VL 6 IS 6 BP 747 EP 747 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LC751 UT WOS:A1993LC75100335 ER PT J AU SWANN, AC SECUNDA, SK KATZ, MM CROUGHAN, J BOWDEN, CL KOSLOW, SH BERMAN, N STOKES, PE AF SWANN, AC SECUNDA, SK KATZ, MM CROUGHAN, J BOWDEN, CL KOSLOW, SH BERMAN, N STOKES, PE TI SPECIFICITY OF MIXED AFFECTIVE STATES - CLINICAL COMPARISON OF DYSPHORIC MANIA AND AGITATED DEPRESSION SO JOURNAL OF AFFECTIVE DISORDERS LA English DT Article DE MANIA; AFFECTIVE DISORDER; DEPRESSION; MIXED STATES; ANXIETY ID DIAGNOSIS AB To investigate the clinical specificity of mixed affective states, we compared clinical characteristics of mixed (dysphoric) manics to those of agitated depressed patients. The subjects were inpatients studied in the NIMH Clinical Research Branch Collaborative Study on the Psychobiology of Depression, Biological Studies. Behavior and symptom ratings for depressive and manic symptoms were obtained during a 15-day placebo washout period. Patients with agitated depression were compared to those in acute manic episodes with and without prominent depressive symptoms. Mania ratings clearly distinguished agitated depressed from mixed manic patients. Concerning depression and general psychopathology, mixed manics had more severe agitation, hostility and cognitive impairment than did agitated depressed patients. Depressed mood and anxiety did not differ significantly between the two groups. Nurse ratings for depression and anxiety, based on ward behavior, were similar for mixed manics and agitated depressed patients, while physician-interview rated depression and anxiety were higher in agitated depressed patients. These data support the existence of superimposed depressive and manic syndromes in mixed manics. C1 NIMH,BETHESDA,MD 20892. YESHIVA UNIV ALBERT EINSTEIN COLL MED,MONTEFIORE MED CTR,BRONX,NY 10461. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. JEWISH HOSP ST LOUIS,ST LOUIS,MO 63110. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. UCLA,HARBOR MED CTR,INST RES & EDUC,TORRANCE,CA. CORNELL UNIV,MED CTR,COLL MED,DEPT PSYCHIAT,NEW YORK,NY 10021. RP SWANN, AC (reprint author), UNIV TEXAS,SCH MED,DEPT PSYCHIAT,POB 20708,HOUSTON,TX 77225, USA. FU NIMH NIH HHS [MH26975, MH26977, UO1 MH38084] NR 28 TC 77 Z9 80 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0327 J9 J AFFECT DISORDERS JI J. Affect. Disord. PD JUN PY 1993 VL 28 IS 2 BP 81 EP 89 DI 10.1016/0165-0327(93)90036-J PG 9 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LK233 UT WOS:A1993LK23300002 PM 8354772 ER PT J AU COHEN, GH AF COHEN, GH TI GEOM - A PROGRAM TO ASSESS THE RELIABILITY OF A PROTEIN MODEL SO JOURNAL OF APPLIED CRYSTALLOGRAPHY LA English DT Software Review DE PROTEIN STRUCTURE; REFINEMENT; STEREOCHEMISTRY ID MACROMOLECULAR STRUCTURES RP COHEN, GH (reprint author), NIDDK,LMB,BETHESDA,MD 20892, USA. NR 5 TC 4 Z9 4 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0021-8898 J9 J APPL CRYSTALLOGR JI J. Appl. Crystallogr. PD JUN 1 PY 1993 VL 26 BP 495 EP 496 DI 10.1107/S0021889892012548 PN 3 PG 2 WC Chemistry, Multidisciplinary; Crystallography SC Chemistry; Crystallography GA LL528 UT WOS:A1993LL52800033 ER PT J AU BOUJOUKOS, AJ MARTICH, GD SUPINSKI, E SUFFREDINI, AF AF BOUJOUKOS, AJ MARTICH, GD SUPINSKI, E SUFFREDINI, AF TI COMPARTMENTALIZATION OF THE ACUTE CYTOKINE RESPONSE IN HUMANS AFTER INTRAVENOUS ENDOTOXIN ADMINISTRATION SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE ALVEOLAR MACROPHAGES; TUMOR NECROSIS FACTOR; INTERLEUKIN-8 ID TUMOR-NECROSIS-FACTOR; INTERLEUKIN-8 GENE-EXPRESSION; BRONCHIAL EPITHELIAL-CELLS; ESCHERICHIA-COLI ENDOTOXIN; HUMAN ALVEOLAR MACROPHAGES; FACTOR-ALPHA; FACTOR CACHECTIN; LUNG; ACTIVATION; PERMEABILITY AB Lung cytokine production was examined after the intravenous administration of endotoxin to 23 normal human subjects. Bronchoalveolar lavage (BAL) was performed 7 days before and 1.5 or 5 h after endotoxin (4 ng/kg). Cytokine mRNA was evaluated in cell pellets (>98% macrophages) by use of reverse transcription and the polymerase chain reaction. Immunoreactivity was measured by enzyme-linked immunosorbent assay of 20- to 40-fold concentrated BAL. Interleukin- (IL) 8 was detected in BAL (4-130 pg/ml) but not in the serum at baseline. Few neutrophils were found in BAL (<1%) despite this IL-8 gradient. Peak serum IL-8 levels occurred 2 h after endotoxin (3,930 +/- 241 pg/ml), but BAL neutrophils and IL-8 did not increase. Peak serum tumor necrosis factor (TNF) levels occurred 1.5 h after endotoxin (1,844 +/- 210 pg/ml), but TNF was detected in only 1 of 20 BAL samples. TNF and IL-8 mRNA were detected by polymerase chain reaction in >70% of the BAL samples before endotoxin, whereas IL-1alpha, IL-1beta, and IL-6 were detected in <25% of the BAL samples. After endotoxin, no change was detected in cytokine mRNA expression. Actinomycin D treatment of the BAL did not alter the pattern of cytokine mRNA expression. These data suggest that mechanisms exist to insulate the alveolar space from the stimulatory effects of endotoxin and high circulating levels of cytokines. Additional factors appear to control the chemotactic effects of IL-8 on neutrophils in the air spaces during acute systemic inflammation. C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 35 TC 75 Z9 75 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JUN PY 1993 VL 74 IS 6 BP 3027 EP 3033 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA LL820 UT WOS:A1993LL82000058 PM 8366003 ER PT J AU KOLENBRANDER, PE LONDON, J AF KOLENBRANDER, PE LONDON, J TI ADHERE TODAY, HERE TOMORROW - ORAL BACTERIAL ADHERENCE SO JOURNAL OF BACTERIOLOGY LA English DT Review ID STREPTOCOCCUS-SANGUIS; ACTINOMYCES-VISCOSUS; BACTEROIDES-LOESCHEI; NUCLEOTIDE-SEQUENCE; APATITIC SURFACES; EUKARYOTIC CELLS; COAGGREGATION; ADHESIN; GINGIVALIS; COLONIZATION RP KOLENBRANDER, PE (reprint author), NIDR, MICROBIAL ECOL LAB, BETHESDA, MD 20892 USA. NR 49 TC 371 Z9 381 U1 1 U2 15 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0021-9193 EI 1098-5530 J9 J BACTERIOL JI J. Bacteriol. PD JUN PY 1993 VL 175 IS 11 BP 3247 EP 3252 PG 6 WC Microbiology SC Microbiology GA LE431 UT WOS:A1993LE43100001 PM 8501028 ER PT J AU HAYES, F DAVIS, MA AUSTIN, SJ AF HAYES, F DAVIS, MA AUSTIN, SJ TI FINE-STRUCTURE ANALYSIS OF THE P7 PLASMID PARTITION SITE SO JOURNAL OF BACTERIOLOGY LA English DT Article ID UNIT-COPY MINIPLASMIDS; INTEGRATION HOST FACTOR; CENTROMERE-LIKE SITE; P1 PLASMID; ESCHERICHIA-COLI; DAUGHTER CELLS; PROTEIN; BINDING; SYSTEM; MAINTENANCE AB The par region of bacteriophage P7 is responsible for active partition of the P7 plasmid prophage into daughter cells. The cis-acting partition site was defined precisely as a 75-bp sequence that was necessary and sufficient to promote correct segregation of an unstable vector plasmid when the two P7 partition proteins, ParA and ParB, were supplied in trans. Roughly the same region was necessary to exert partition-mediated incompatibility. The minimal site contains an integration host factor (IHF) protein binding site bracketed by regions containing heptamer repeat sequences that individually bind ParB. An additional sequence forms the left boundary of the site. Site-directed mutations in the latter sequence, as well as the IHF motif and the rightmost ParB box, blocked site function. Although the P7 site shares 55% sequence identity with its counterpart in bacteriophage P1, functional interactions between the partition sites and the Par proteins of the two plasmids were entirely species specific in vivo. The P1 sequence has similar IHF and ParB binding motifs, but the left boundary sequence differs radically and may define a point of species-specific contact with the Par proteins. No evidence was found for the existence of a functional P7 analog of the P1 parS core, a small subregion of the P1 site that, in isolation, acts as an enfeebled partition site with modified incompatibility properties. C1 NCI,FREDERICK CANC RES & DEV CTR,CHROMOSOME BIOL LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 38 TC 18 Z9 18 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JUN PY 1993 VL 175 IS 11 BP 3443 EP 3451 PG 9 WC Microbiology SC Microbiology GA LE431 UT WOS:A1993LE43100024 PM 8501048 ER PT J AU SOZHAMANNAN, S CHATTORAJ, DK AF SOZHAMANNAN, S CHATTORAJ, DK TI HEAT-SHOCK PROTEINS DNAJ, DNAK, AND GRPE STIMULATE-P1 PLASMID REPLICATION BY PROMOTING INITIATOR BINDING TO THE ORIGIN SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI; BACTERIOPHAGE-LAMBDA; NUCLEOPROTEIN STRUCTURES; CELLULAR DEFECTS; RNA-POLYMERASE; GENE; REPA; MUTATIONS; MUTANTS; SIGMA-32 AB Binding of the P1-encoded protein RepA to the origin of P1 plasmid replication is essential for initiation of DNA replication and for autoregulatory repression of the repA promoter. Previous studies have shown defects in both initiation and repression in hosts lacking heat shock proteins DnaJ, DnaK, and GrpE and have suggested that these proteins play a role in the RepA-DNA binding required for initiation and repression. In this study, using in vivo dimethyl sulfate footprinting, we have confirmed the roles of the three heat shock proteins in promoting RepA binding to the origin. The defects in both activities could be suppressed by increasing the concentration of wild-type RepA over the physiological level. We also isolated RepA mutants that were effective initiators and repressors without requiring the beat shock proteins. These data suggest that the heat shock proteins facilitate both repression and initiation by promoting only the DNA-binding activity of RepA. In a similar plasmid, F, initiator mutants that confer heat shock protein independence for replication were also found, but they were defective for repression. We propose that the initiator binding involved in repression and the initiator binding involved in initiation are similar in P1 but different in F. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 64 TC 43 Z9 43 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JUN PY 1993 VL 175 IS 11 BP 3546 EP 3555 PG 10 WC Microbiology SC Microbiology GA LE431 UT WOS:A1993LE43100036 PM 8501058 ER PT J AU MAKAROV, AA PROTASEVICH, II KUZNETSOVA, NV FEDOROV, BB KOROLEV, SV STRUMINSKAYA, NK BAZHULINA, NP LESHCHINSKAYA, IB HARTLEY, RW KIRPICHNIKOV, MP YAKOVLEV, GI ESIPOVA, NG AF MAKAROV, AA PROTASEVICH, II KUZNETSOVA, NV FEDOROV, BB KOROLEV, SV STRUMINSKAYA, NK BAZHULINA, NP LESHCHINSKAYA, IB HARTLEY, RW KIRPICHNIKOV, MP YAKOVLEV, GI ESIPOVA, NG TI COMPARATIVE-STUDY OF THERMOSTABILITY AND STRUCTURE OF CLOSE HOMOLOGS - BARNASE AND BINASE SO JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS LA English DT Article ID BACILLUS INTERMEDIUS; TRYPTOPHAN RESIDUES; RIBONUCLEASE; FLUORESCENCE; PROTEINS; BARSTAR AB Parameters of heat denaturation and intrinsic fluorescence of barnase and its close homologue, binase in the pH region 2-6 have been determined. The barnase heat denaturation (pH 2.8-5.5) proceeds according to the 'all-or-none' principle. Barnase denaturation temperature is lower than that of binase and this difference increases from 2.5-degrees-C at pH 5 to 7-degrees-C at pH 3. Enthalpy values of barnase and binase denaturation coincide only at pH 4.5-5.5, but as far as pH decreases the barnase denaturation enthalpy decreases significantly and in this respect it differs from binase. The fluorescence and CD techniques do not reveal any distinctions in the local environment of aromatic residues in the two proteins, and the obtained difference in the parameters of intrinsic fluorescence is due to fluorescence quenching of the barnase Trp94 by the His 18 residue, absent in binase. Secondary structures of both native and denaturated proteins also do not differ. Some differences in the barnase and binase electrostatic characteristics, revealed in the character of the dipole moments distribution, have been found. C1 KAZAN VI LENIN STATE UNIV,KAZAN,RUSSIA. NIDDKD,BETHESDA,MD 20892. RP MAKAROV, AA (reprint author), RUSSIAN ACAD SCI,ENGELHARDT INST MOLEC BIOL,MOSCOW 117984,RUSSIA. RI Makarov, Alexander/P-5279-2016 NR 22 TC 24 Z9 25 U1 0 U2 0 PU ADENINE PRESS INC PI GUILDERLAND PA PO BOX 355/340, GUILDERLAND, NY 12084 SN 0739-1102 J9 J BIOMOL STRUCT DYN JI J. Biomol. Struct. Dyn. PD JUN PY 1993 VL 10 IS 6 BP 1047 EP 1065 PG 19 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LG865 UT WOS:A1993LG86500008 PM 8357541 ER PT J AU RUNDHAUG, JE NETTESHEIM, P AF RUNDHAUG, JE NETTESHEIM, P TI GROWTH-REGULATION OF PRIMARY RAT TRACHEAL EPITHELIAL-CELL CULTURES BY ENDOGENOUS TRANSFORMING GROWTH FACTOR-BETA-S SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID SERUM-FREE MEDIUM; SQUAMOUS DIFFERENTIATION; EPIDERMAL-KERATINOCYTES; NEOPLASTIC PROGRESSION; CLONAL PROLIFERATION; CHOLERA-TOXIN; CYCLIC-AMP; EXPRESSION; FACTOR-BETA-1; QUANTITATION AB Primary rat tracheal epithelial (RTE) cell cultures have previously been shown to secrete transforming growth factor-beta (TGFbeta) and to be growth inhibited by exogenous TGFbeta. The purpose of the present studies was to determine whether the endogenous TGFbeta(s) were regulating the growth of RTE cell cultures and, if so, which isoforms were involved. Neutralizing antibodies specific to TGFbeta1 and TGFbeta2 were added to cultures, and their effects on several growth parameters were measured. Addition of antibodies to early cultures (day 1), resulted in 1.8- and 3-fold increases in colony formation and cell number, respectively, above control IgG-treated cultures. Antibody dose-response experiments revealed that TGFbeta2 was the predominant isoform inhibiting early RTE cell growth. The antibody treatments resulted in similar stimulation of early growth at low and high seeding densities, suggesting that the endogenous TGFbetas were acting locally. Anti-TGFbeta1 treatment of cultures at various stages of growth resulted in 1.2-1.7-fold increases in DNA synthesis above controls, whereas anti-TGFbeta2 treatment resulted in increased DNA synthesis only in early and late cultures (1.7- and 2.5-fold, respectively), but not during midlogarithmic growth. Continuous treatment with a combination of both antibodies resulted in increased growth and decreased exfoliation in early cultures, but had no effect on the slow down of growth in late cultures. Thus endogenous TGFbetas inhibited primarily early growth and contributed to, but did not appear to be responsible for, plateau of growth in late stage cultures. Antibody treatment of secondary cultures resulted in 4-70-fold increases in colony formation, depending on the age of the primary cultures when replated, indicating that endogenous production of both TGFbeta1 and TGFbeta2 greatly inhibits the subculturability of primary RTE cells. Other experiments suggested that cholera toxin enhances RTE cell growth in part by counteracting the inhibitory effects of endogenous TGFbetas. C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. NR 32 TC 4 Z9 4 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD JUN PY 1993 VL 155 IS 3 BP 483 EP 493 DI 10.1002/jcp.1041550307 PG 11 WC Cell Biology; Physiology SC Cell Biology; Physiology GA LC730 UT WOS:A1993LC73000006 PM 8491788 ER PT J AU SHEIKH, MS SHAO, ZM HUSSAIN, A CLEMMONS, DR CHEN, JC ROBERTS, CT LEROITH, D FONTANA, JA AF SHEIKH, MS SHAO, ZM HUSSAIN, A CLEMMONS, DR CHEN, JC ROBERTS, CT LEROITH, D FONTANA, JA TI REGULATION OF INSULIN-LIKE GROWTH FACTOR-BINDING-PROTEIN-1, FACTOR-BINDING-PROTEIN-2, FACTOR-BINDING-PROTEIN-3, FACTOR-BINDING-PROTEIN-4, FACTOR-BINDING-PROTEIN-5, AND FACTOR-BINDING-PROTEIN-6 - SYNTHESIS, SECRETION, AND GENE-EXPRESSION IN ESTROGEN RECEPTOR-NEGATIVE HUMAN BREAST-CARCINOMA CELLS SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID FACTOR-BINDING-PROTEINS; CANCER-CELLS; FACTOR-I; MOLECULAR-CLONING; IGF-I; RETINOID MODULATION; STIMULATED GROWTH; RIBONUCLEIC-ACID; FACTOR-BETA; RAT AB Insulin-like growth-factors I and II (IGF-I, II) are potent mitogens for breast carcinoma proliferation. In extracellular fluids, most of the IGF-I and II is associated with specific IGF-binding proteins (IGFBPs). The role of these IGFBPs in IGF action is still not clear, but it has been demonstrated that these proteins may either enhance or inhibit IGF-mediated cellular effects. Synthesis and secretion of IGFBPs have been demonstrated in breast carcinoma cells. In this study, we examined retinoic acid (RA) and IGF-I modulation of IGFBP mRNA and IGFBP levels in two ER-negative human breast carcinoma cell lines. Treatment of MDA-MB-231 and MDA-MB-468 cells with RA increased the levels in conditioned media of a Mr 42-46-kDa IGFBP, which was immunoprecipitated by an IGFBP-3 antibody. IGF-I also increased the accumulated levels of IGFBP-3 in the conditioned media of both cell lines. Both cell lines expressed high basal levels of IGFBP-3 mRNA; the addition of RA increased IGFBP-3 mRNA levels by 1.5-fold, whereas the addition of IGF-I had no effect on IGFBP-3 mRNA levels in either cell line. The difference in the magnitude of the RA enhancement of IGFBP-3 mRNA levels (1.5-fold) and RA stimulation of IGFBP-3 levels in conditioned media (3.54-fold) suggests that some of the effect of RA is at a posttranscriptional level. IGF-I increased the levels of IGFBP-2 and IGFBP-5 in conditioned media by greater than tenfold but had no effect on IGFBP-2 and IGFBP-5 mRNA levels, again suggesting the involvement of posttranscriptional controls. Pretreatment of MDA-MB-468 and MDA-MB-231 cells with IGF-I receptor antibody (alphaIR3) blocked the IGF-I effect on IGFBP-3 levels in the media in both cell lines and IGFBP-2 and IGFBP-5 secreted levels in MDA-MB-468 cell conditioned media. The addition of RA also blocked IGF-I stimulation of IGFBP-2 and IGFBP-5 levels. Cycloheximide treatment completely blocked the RA and/or IGF-I-mediated modulation of these binding proteins, suggesting that these agents enhance IGFBP-3, IGFBP-2, and IGFBP-5 synthesis and consequent secretion. MDA-MB-468 cells expressed IGFBP-5 mRNA, whereas both MDA-MB-231 and MDA-MB-468 expressed IGFBP-6 mRNA. RA enhanced IGFBP-6 gene expression by threefold in MDA-MB-231 cells, whereas IGF-1 had no effect on IGFBP-6 gene expression in either cell line. These results demonstrate that RA and IGF-I modulate IGFBP levels in a number of breast carcinoma cell lines. Such modulation of IGFBPs may in turn affect IGF mediated cellular responses and thus the biologic behavior of these malignant cells. C1 UNIV MARYLAND,DEPT MED,BALTIMORE,MD 21201. UNIV MARYLAND,CTR CANC,BALTIMORE,MD 21201. VET ADM MED CTR,BALTIMORE,MD 21201. NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. UNIV N CAROLINA,SCH MED,DEPT MED,CHAPEL HILL,NC 27514. NR 53 TC 76 Z9 77 U1 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 JUN PY 1993 VL 155 IS 3 BP 556 EP 567 DI 10.1002/jcp.1041550314 PG 12 WC Cell Biology; Physiology SC Cell Biology; Physiology GA LC730 UT WOS:A1993LC73000013 PM 7684042 ER PT J AU COLE, PM USHER, BA CARGO, AP AF COLE, PM USHER, BA CARGO, AP TI COGNITIVE RISK AND ITS ASSOCIATION WITH RISK FOR DISRUPTIVE BEHAVIOR DISORDER IN PRESCHOOLERS SO JOURNAL OF CLINICAL CHILD PSYCHOLOGY LA English DT Article ID ATTENTION-DEFICIT DISORDER; LEARNING-DISABILITIES; EXECUTIVE FUNCTION; SELF-REGULATION; RATING-SCALE; CHILDREN; PSYCHOPATHOLOGY; HYPERACTIVITY; ADOLESCENCE; PERFORMANCE AB Examined the relation between intellectual functioning and risk for disruptive behavior disorders in a sample of 82 preschoolers. Specific cognitive dimensions-verbal, visuospatial and executive functioning-were examined in relation to specific aspects of socioemotional functioning known to be problematic for behavior-problem children (i.e., labeling emotions and behavioral control). Difficulties in verbal and visuospatial dimension scores were associated with being above average in behavioral difficulty. Behavioral risk was associated with greater difficulty in behavioral regulation but not with difficulty in emotion accuracy. Verbal skills contributed to the prediction of emotion accuracy, and executive function skills were predictive of behavioral control. The findings are discussed in terms of the developmental aspects of relations between specific cognitive skills, specific difficulties in socioemotional functioning, and the risk for disruptive behavior disorders. RP COLE, PM (reprint author), NIMH,DEV PSYCHOL LAB,BLDG 15K,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 71 TC 45 Z9 45 U1 1 U2 4 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0047-228X J9 J CLIN CHILD PSYCHOL JI J. Clin. Child Psychol. PD JUN PY 1993 VL 22 IS 2 BP 154 EP 164 DI 10.1207/s15374424jccp2202_3 PG 11 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA LT894 UT WOS:A1993LT89400003 ER PT J AU MATSUO, K FRIEDMAN, E GEJMAN, PV FAGIN, JA AF MATSUO, K FRIEDMAN, E GEJMAN, PV FAGIN, JA TI THE THYROTROPIN RECEPTOR (TSH-R) IS NOT AN ONCOGENE FOR THYROID-TUMORS - STRUCTURAL STUDIES OF THE TSH-R AND THE ALPHA-SUBUNIT OF G(S) IN HUMAN THYROID NEOPLASMS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID STIMULATORY G-PROTEIN; SINGLE-BASE CHANGES; GEL-ELECTROPHORESIS; MOLECULAR-CLONING; POINT MUTATIONS; HUMAN DNA; SEQUENCE; TUMORIGENESIS; POLYMORPHISM; ACTIVATION AB The development and progression of thyroid tumors are associated with phenotype-specific mutations of genes involved in growth control. Thyroid cell growth is controlled in part by the interaction of TSH with its receptor, with subsequent activation of the GTP-binding protein and its effector, adenylyl cyclase. The resulting increase in intracellular cAMP stimulates growth in thyrocytes. The TSH receptor (TSH-R) is a seven-transmembrane domain receptor. Intracellular domains of the TSH-R important for signal transduction and which may serve as targets for mutational activation have been defined. In addition, mutations at specific loci of the a-subunit of G-protein in human thyroid tumors have been described. We examined 92 benign and malignant neoplastic thyroid tissues for possible mutations of the intracytoplasmic domains of the TSH-R known to be involved in signal transduction and for mutations within the hot spots of G(s)alpha. Screening was carried out by single strand conformation polymorphism (TSH-R) or denaturing gradient gel electrophoresis (G(s)alpha) of polymerase chain reaction-amplified tumor DNA. No mutations were observed in the cytoplasmic domains of the TSH-R, except for a neutral base substitution in codon 460 (GCG [Ala]-->CA [Ala]) in 3 tumors, which was also present in constitutional DNA from the affected individuals. A heterozygous mutation of codon 201 of G(s)alpha (GGT [Arg]-CAT [His]) was observed in a nodule from an adenomatous goiter. In addition, a codon 227 mutation (CAG [Glu]-CAT [His]) was identified in a follicular adenoma. We conclude that mutational activation of the intracytoplasmatic domains of the TSH-R is not a significant mechanism of thyroid tumorigenesis, whereas putative activating mutations within exons 8 and 9 of G(s)alpha occur infrequently in some benign follicular tumors. C1 UNIV CALIF LOS ANGELES, CEDARS SINAI MED CTR,SCH MED,DIV ENDOCRINOL, BECKER BLDG 131, LOS ANGELES, CA 90048 USA. NIDDKD, MOLEC PATHOPHYSIOL BRANCH, BETHESDA, MD 20892 USA. NIMH, CLIN NEUROGENET BRANCH, BETHESDA, MD 20892 USA. FU NCI NIH HHS [CA-50706]; NIDDK NIH HHS [DK-42792] NR 35 TC 71 Z9 73 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 JUN PY 1993 VL 76 IS 6 BP 1446 EP 1451 DI 10.1210/jc.76.6.1446 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LF088 UT WOS:A1993LF08800011 PM 8501149 ER PT J AU FLIER, JS MOLLER, DE MOSES, AC ORAHILLY, S CHAIKEN, RL GRIGORESCU, F ELAHI, D KAHN, BB WEINREB, JE EASTMAN, R AF FLIER, JS MOLLER, DE MOSES, AC ORAHILLY, S CHAIKEN, RL GRIGORESCU, F ELAHI, D KAHN, BB WEINREB, JE EASTMAN, R TI INSULIN-MEDIATED PSEUDOACROMEGALY - CLINICAL AND BIOCHEMICAL-CHARACTERIZATION OF A SYNDROME OF SELECTIVE INSULIN-RESISTANCE SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID POLYMERASE CHAIN-REACTION; GROWTH-FACTOR; TYROSINE KINASE; RECEPTOR GENE; ACANTHOSIS NIGRICANS; NIDDM; FIBROBLASTS; MUTATIONS; AUTOPHOSPHORYLATION; PHOSPHORYLATION AB We have performed clinical, physiological, in vitro biochemical and genetic studies of a patient with severe insulin resistance associated with the phenotype of ''pseudoacromegaly,'' defined as the presence of acromegaloid features in the absence of elevated levels of GH or insulin-like growth factor-I (IGF-I). Despite marked hyperinsulinemia, insulin and IGF-I binding to circulating blood cells and cultured skin fibroblasts was normal. Insulin and IGF-1-stimulated autophosphorylation of their respective receptors in cultured skin fibroblasts was also normal. However, neither insulin nor IGF-I were able to stimulate 2-deoxy D-glucose uptake by cultured skin fibroblasts. In contrast, the ability of insulin and IGF-I (or IGF-II) to stimulate amino acid uptake and thymidine incorporation into DNA was not impaired. This unique discordant signaling defect through both insulin and IGF-I receptors appeared not to be the consequence of altered expression or primary structure of the insulin receptor or the GLUT-4 glucose transporter, as assessed by several genetic and biochemical techniques. GLUT-4 expression in muscle was normal on Western blots, and SSCP screening of all 11 exons of the gene for nucleotide variation revealed no variations from normal. DNA sequencing and SSCP screening of exons 2-22 of the insulin receptor gene revealed only one variation predicted to alter the amino acid sequence (Val985-->Met). No functional differences between Met985 and wild-type human insulin receptors were evident in studies performed with Chinese hamster ovary cell transfectants that overexpress either receptor. This data combined with our previously published epidemiological data concerning the frequency of the Met985 allele, indicate that this variant insulin receptor is not responsible for the insulin resistant glucose uptake or the clinical syndrome of pseudoacromegaly. We conclude that: 1) The molecular lesion responsible for the selective biochemical defect in this individual appears to involve a signaling intermediate required for insulin and IGF-I regulation of glucose transport, and/or an effector mechanism operative in this process. 2) Cells derived from this patient may be a valuable tool in the search for such molecular mechanisms. 3) The Met985 allele is a relatively common variant which has no demonstrable adverse consequences for insulin receptor function. 4) Pseudoacromegaly can be viewed as the expected result of hyperinsulinemia driving the unopposed mitogenic and anabolic actions of insulin. C1 BETH ISRAEL HOSP, CHARLES A DANA RES INST, BOSTON, MA 02215 USA. BETH ISRAEL HOSP, DEPT MED, BOSTON, MA 02215 USA. BETH ISRAEL HOSP, HARVARD THORNDIKE LAB, BOSTON, MA 02215 USA. CNRS, INSERM, F-34033 MONTPELLIER, FRANCE. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. NIDDKD, DIABET BRANCH, BETHESDA, MD 20892 USA. FU NIA NIH HHS [AG-06599]; NIDDK NIH HHS [NIDDK 28082-10] NR 33 TC 66 Z9 68 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 JUN PY 1993 VL 76 IS 6 BP 1533 EP 1541 DI 10.1210/jc.76.6.1533 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LF088 UT WOS:A1993LF08800026 PM 8388881 ER PT J AU HOPEWELL, PC STANSELL, J TURNER, J OSMOND, D GLASSROTH, J MOSSAR, M HIRSCHTICK, R ROSEN, MJ MEISELMAN, L MANGHISI, KK CARDOZO, C KALB, TH REICHMAN, LB MANGURA, BT JENKINS, S HANSON, C DOWELL, F OTOOLE, M WALLACE, JM LEMAIRE, B RICHER, B AU, J COULSON, A CLEMENTE, V SHAPIRO, B KVALE, PA MARKOWITZ, N SARAVOLATZ, LD JOHNSON, C HUITSING, J KRYSTOFORSKI, A POOLE, WK RAO, AV CLAYTON, K HANSEN, N JORDAN, M THOMPSON, J MYERS, D LAVANGE, L KATZIN, J FULKERSON, W WILCOSKY, T LOU, Y GAME, S KALICA, A WITTES, J FOLLMANN, DA WISE, R CHERNIACK, R WARE, JH BARTLETT, JG CONNETT, JE DANIELE, RP FRENCH, JF GOEBEL, FD SNIDER, DE TURINO, GN AF HOPEWELL, PC STANSELL, J TURNER, J OSMOND, D GLASSROTH, J MOSSAR, M HIRSCHTICK, R ROSEN, MJ MEISELMAN, L MANGHISI, KK CARDOZO, C KALB, TH REICHMAN, LB MANGURA, BT JENKINS, S HANSON, C DOWELL, F OTOOLE, M WALLACE, JM LEMAIRE, B RICHER, B AU, J COULSON, A CLEMENTE, V SHAPIRO, B KVALE, PA MARKOWITZ, N SARAVOLATZ, LD JOHNSON, C HUITSING, J KRYSTOFORSKI, A POOLE, WK RAO, AV CLAYTON, K HANSEN, N JORDAN, M THOMPSON, J MYERS, D LAVANGE, L KATZIN, J FULKERSON, W WILCOSKY, T LOU, Y GAME, S KALICA, A WITTES, J FOLLMANN, DA WISE, R CHERNIACK, R WARE, JH BARTLETT, JG CONNETT, JE DANIELE, RP FRENCH, JF GOEBEL, FD SNIDER, DE TURINO, GN TI DESIGN OF A PROSPECTIVE-STUDY OF THE PULMONARY COMPLICATIONS OF HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE HIV; AIDS; PULMONARY DISEASE; EPIDEMIOLOGY; PROSPECTIVE STUDY; HOMOSEXUAL MEN; INJECTION DRUG USERS ID BLOOD-INSTITUTE WORKSHOP; NATIONAL-HEART; LUNG; AIDS AB Because no studies have systematically described the pulmonary complications associated with early stages of infection with the human immunodeficiency virus (HIV), the National Heart, Lung and Blood Institute and the National Institute of Allergy and Infectious Diseases jointly initiated a prospective cohort study in 1987 to describe the incidence and course of lung diseases at all stages of HIV infection. This paper describes the ongoing study and highlights some of its unusual features. Six clinical centers from different geographic areas in the U.S. began enrolling participants in 1988, and the resulting cohort comprises 1353 members. HIV seropositive participants were randomized to ''intensive'' (pulmonary disease screening and follow-up at 3-month intervals) or ''routine'' (6-month follow-up intervals with annual screening) follow-up to assess the impact of these strategies on patient outcomes. New information from this complex study will lead to a broader understanding of the pulmonary diseases associated with HIV infection and will have relevance to clinical as well as epidemiologic aspects of HIV disease. C1 RES TRIANGLE INST,CTR EPIDEMIOL & MED STUDIES,POB 12194,RES TRIANGLE PK,NC 27709. UNIV CALIF SAN FRANCISCO,CTR CLIN,COMM STEERING,SAN FRANCISCO,CA 94143. NORTHWESTERN UNIV,CTR CLIN,COMM STEERING,CHICAGO,IL 60611. MT SINAI MED CTR,CTR CLIN,NEW YORK,NY 10029. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,UNIV HOSP,CTR CLIN,NEWARK,NJ 07103. UNIV CALIF LOS ANGELES,CTR CLIN,LOS ANGELES,CA 90024. HENRY FORD HOSP,CTR CLIN,DETROIT,MI 48202. RES TRIANGLE INST,CTR COORDINATING,RES TRIANGLE PK,NC 27709. NHLBI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,NHLBI,BALTIMORE,MD 21218. NR 13 TC 15 Z9 15 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD JUN PY 1993 VL 46 IS 6 BP 497 EP 507 PG 11 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA LH250 UT WOS:A1993LH25000001 ER PT J AU ACHIM, CL HEYES, MP WILEY, CA AF ACHIM, CL HEYES, MP WILEY, CA TI QUANTITATION OF HUMAN-IMMUNODEFICIENCY-VIRUS, IMMUNE ACTIVATION FACTORS, AND QUINOLINIC ACID IN AIDS BRAINS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CYTOKINE; CENTRAL NERVOUS SYSTEM; ENZYME-LINKED IMMUNOSORBENT ASSAY; ENCEPHALITIS; MACROPHAGE ID DEMENTIA COMPLEX; HIV-INFECTION; MACROPHAGES; NEUROPATHOLOGY; EXPERIENCE; ENVELOPE; TISSUE; DAMAGE; BLOOD AB HIV encephalitis is unusual in that neurologic damage occurs in the absence of significant infection of neuronal or glial cells. Because the predominant infected cell in the brain is the macrophage, it has been proposed that release of viral or immune activation factors from macrophages may mediate neurologic damage. Numerous studies have examined the concentration of immune activation factors in the cerebrospinal fluid (CSF), however, there has been no correlation between these CSF measurements and severity of HIV encephalitis (Wiley, C. A., C. L. Achim, R. D. Schrier, M. P. Heyes, J. A. McCutchen, and 1. Grant. 1992. AIDS (Phila.). 6:1299-1307. Because CSF measurements may not represent tissue concentrations of these factors, we examined the concentrations of HIV p24, quinolinic acid (QUIN), IL-1, IL-3, IL-6, TNF-alpha, and GMCSF within the brains of 10 AIDS autopsies. Homogenization and extraction of cortical gray, cortical white and deep gray matter showed a good correlation between the amount of HIV gp41 immunostaining and extracted HIV gag protein p24. The concentrations of cytokines were low in the tissue extracts and showed no correlation with severity of HIV encephalitis. Brain extracts from mild cases of HIV encephalitis showed elevated levels of TNF-alpha in deep gray matter, while in more severe cases, elevated TNF-alpha levels were also found within cortical white and cortical gray matter. Brain tissue and CSF QUIN concentrations were substantially increased compared to control values. QUIN concentrations were not correlated with the severity of HIV encephalitis. We conclude that increased tissue levels of TNF-alpha and QUIN may have a role in the etiology of HIV-related neurologic dysfunction. C1 UNIV CALIF SAN DIEGO,DEPT PATHOL 0612,9500 GILMAN DR,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92093. NIMH,ANALYT BIOCHEM SECT,CLIN SCI LAB,BETHESDA,MD 20892. FU NINDS NIH HHS [NS-25178, NS-27810]; PHS HHS [R86SD001] NR 37 TC 175 Z9 179 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1993 VL 91 IS 6 BP 2769 EP 2775 DI 10.1172/JCI116518 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LH121 UT WOS:A1993LH12100055 PM 8514884 ER PT J AU CLERICI, M DEPALMA, L ROILIDES, E BAKER, R SHEARER, GM AF CLERICI, M DEPALMA, L ROILIDES, E BAKER, R SHEARER, GM TI ANALYSIS OF T-HELPER AND ANTIGEN-PRESENTING CELL FUNCTIONS IN CORD BLOOD AND PERIPHERAL-BLOOD LEUKOCYTES FROM HEALTHY-CHILDREN OF DIFFERENT AGES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE IMMUNITY; CELLULAR; INFANT; NEWBORN; INTERLEUKIN-2; MATERNAL FETAL EXCHANGE; HUMAN IMMUNODEFICIENCY VIRUS INFECTIONS ID IMMUNODEFICIENCY-VIRUS-INFECTION; IFN-GAMMA PRODUCTION; INTERFERON-GAMMA; LYMPHOCYTES; RESPONSES; ONTOGENY AB The development of antigen-specific functional T lymphocyte immunity in infants and children is an area of immunology that needs elucidation. Leukocytes from cord blood (CBL) and from PBL of children of different ages who were in the hospital for minor surgical procedures were compared with PBL from healthy adults for their ability to generate T helper cell (Th) responses assessed by in vitro proliferation and IL-2 production after stimulation with: influenza A virus (FLU); tetanus toxoid (TET); adult allogeneic PBL that were either undepleted (ALLO) or depleted of adherent antigen presenting cells (ALLONW); and PHA. CBL generated Th responses to ALLONW, ALLO, and PHA, but not to FLU or TET. PBL from infants between 6 and 13 mo of age responded to ALLO and PHA; none responded to FLU or ALLONW, and two of four responded weakly to TET. PBL from children between 13 and 26 mo of age responded to all stimuli except FLU, to which only one child responded marginally. PBL from children older than 36 mo responded to all stimuli at levels comparable to those of PBL from adults. The use of undepleted and adherent cell-depleted CBL and PBL from children of different ages as allogeneic stimulators of responses generated by PBL from adults indicated that the antigen presenting function of CBL and PBL from children 13 mo or older are sufficiently developed to present alloantigen, whereas PBL from children younger than 13 mo are not. Therefore, our results indicate that age-dependent differences exist in both T helper and antigen-presenting functions of CBL and PBL from children of different ages. Surprisingly, CBL appear to be more efficient in antigen-presenting function than PBL from children younger than 13 mo. These findings are important for establishing developmental parameters of T helper cell immunity relevant for pediatric infection and transplantation in infants and children. C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,GEORGE WASHINGTON SCH MED,DEPT PEDIAT & PATHOL,WASHINGTON,DC 20010. CHILDRENS NATL MED CTR,DEPT LAB MED,WASHINGTON,DC 20010. FAIRFAX HOSP,DEPT PEDIAT & NEONATOL,FALLS CHURCH,VA 22046. NR 19 TC 108 Z9 109 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1993 VL 91 IS 6 BP 2829 EP 2836 DI 10.1172/JCI116526 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LH121 UT WOS:A1993LH12100063 PM 8514891 ER PT J AU CUDA, G FANANAPAZIR, L ZHU, WS SELLERS, JR EPSTEIN, ND AF CUDA, G FANANAPAZIR, L ZHU, WS SELLERS, JR EPSTEIN, ND TI SKELETAL-MUSCLE EXPRESSION AND ABNORMAL FUNCTION OF BETA-MYOSIN IN HYPERTROPHIC CARDIOMYOPATHY SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Note DE CARDIAC HYPERTROPHY; BETA-MYOSIN HEAVY CHAIN; MOLECULAR GENETICS; MUTATION; MUSCLE ID HEAVY-CHAIN GENE; VENTRICULAR ALPHA-MYOSIN; COMPLETE SEQUENCE; MOLECULAR-BASIS; ASSAYS AB Hypertrophic cardiomyopathy is an important inherited disease. The phenotype has been linked, in some kindreds, to the beta-myosin heavy chain (beta-MHC) gene. Missense and silent mutations in the beta-MHC gene were used as markers to demonstrate the expression of mutant and normal cardiac beta-MHC gene message in skeletal muscle of hypertrophic cardiomyopathy patients. Mutant beta-myosin, also shown to be present in skeletal muscle by Western blot analysis, translocated actin filaments slower than normal controls in an in vitro motility assay. Thus, single amino acid changes in beta-myosin result in abnormal actomyosin interactions, confirming the primary role of missense mutations in beta-MHC gene in the etiology of hypertrophic cardiomyopathy. C1 NHLBI, CLIN HEMATOL BRANCH, BLDG 10, ROOM 7C-103, BETHESDA, MD 20892 USA. NHLBI, MOLEC CARDIOL LAB, BETHESDA, MD 20892 USA. NHLBI, CARDIOL BRANCH, BETHESDA, MD 20892 USA. RI Cuda, Giovanni/F-5359-2012 OI Cuda, Giovanni/0000-0001-6313-1866 NR 21 TC 195 Z9 200 U1 0 U2 6 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 EI 1558-8238 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1993 VL 91 IS 6 BP 2861 EP 2865 DI 10.1172/JCI116530 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LH121 UT WOS:A1993LH12100067 PM 8514894 ER PT J AU HINNEBUSCH, J SCHWAN, TG AF HINNEBUSCH, J SCHWAN, TG TI NEW METHOD FOR PLAGUE SURVEILLANCE USING POLYMERASE CHAIN-REACTION TO DETECT YERSINIA-PESTIS IN FLEAS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID DNA AB Yersinia pestis, the plague bacillus, infects a variety of mammals throughout the world and is transmitted by fleas. We developed a polymerase chain reaction (PCR) test using primers designed from the Y. pestis plasminogen activator gene to directly detect plague-infected fleas. As few as 10 Y. pestis cells were detected, even in the presence of flea tissue, by PCR and then agarose gel electrophoresis and ethidium bromide staining. The feasibility of the assay was demonstrated by using naturally infected Xenopsylla cheopis fleas. The detection of Y. pestis in fleas by PCR provides a rapid and sensitive way to monitor plague in wild animal populations, allowing public health officials to better assess the potential risk of transmission to humans. C1 NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,ARTHROPOD BORNE DIS SECT,HAMILTON,MT 59840. NR 21 TC 67 Z9 77 U1 0 U2 3 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 JUN PY 1993 VL 31 IS 6 BP 1511 EP 1514 PG 4 WC Microbiology SC Microbiology GA LC728 UT WOS:A1993LC72800019 PM 8314993 ER PT J AU PLUDA, JM VENZON, DJ TOSATO, G LIETZAU, J WYVILL, K NELSON, DL JAFFE, ES KARP, JE BRODER, S YARCHOAN, R AF PLUDA, JM VENZON, DJ TOSATO, G LIETZAU, J WYVILL, K NELSON, DL JAFFE, ES KARP, JE BRODER, S YARCHOAN, R TI PARAMETERS AFFECTING THE DEVELOPMENT OF NON-HODGKINS-LYMPHOMA IN PATIENTS WITH SEVERE HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION RECEIVING ANTIRETROVIRAL THERAPY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID AIDS-RELATED COMPLEX; IMMUNE-DEFICIENCY SYNDROME; HOMOSEXUAL MEN; HIV-INFECTION; MALIGNANT-LYMPHOMA; CANCER REGISTRY; B-CELLS; ZIDOVUDINE; INTERLEUKIN-6; 3'-AZIDO-3'-DEOXYTHYMIDINE C1 NCI,PATHOL LAB,MED BRANCH,CLIN ONCOL PROGRAM,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL PROD,BETHESDA,MD 20205. NCI,MED BRANCH,BETHESDA,MD 20892. NCI,OFF DIRECTOR,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 57 TC 139 Z9 139 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 JUN PY 1993 VL 11 IS 6 BP 1099 EP 1107 PG 9 WC Oncology SC Oncology GA LF310 UT WOS:A1993LF31000014 PM 8099121 ER PT J AU RAPOPORT, JL LEONARD, HL SWEDO, SE LENANE, MC AF RAPOPORT, JL LEONARD, HL SWEDO, SE LENANE, MC TI OBSESSIVE-COMPULSIVE DISORDER IN CHILDREN AND ADOLESCENTS - ISSUES IN MANAGEMENT SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT SATELLITE SYMP ON DIAGNOSIS AND TREATMENT OF OCD : A CLINICIANS PERSPECTIVE / 145TH ANNUAL MEETING OF THE AMERICAN PSYCHIATRIC ASSOC CY MAY 03, 1992 CL WASHINGTON, DC SP AMER PSYCHIAT ASSOC ID CLOMIPRAMINE TREATMENT; FOLLOW-UP; DESIPRAMINE AB Clinical experience with children and adolescents with obsessive compulsive disorder (OCD) suggests the need for long-term care. In addition to maintenance drug treatment. behavior therapy and family counseling are usually indicated. Family counseling can help prevent the avoidant behavior that is a serious complication of OCD. The outcome for OCD in children and adolescents has been improved by the use of these active long-term therapies. RP RAPOPORT, JL (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892, USA. NR 17 TC 20 Z9 20 U1 1 U2 1 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JUN PY 1993 VL 54 SU S BP 27 EP 29 PG 3 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA LP324 UT WOS:A1993LP32400005 PM 8331099 ER PT J AU RAPOPORT, JL BAER, L AF RAPOPORT, JL BAER, L TI OBSESSIVE-COMPULSIVE DISORDER IN CHILDREN AND ADOLESCENTS - ISSUES IN MANAGEMENT - DISCUSSION SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Discussion C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RAPOPORT, JL (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JUN PY 1993 VL 54 SU S BP 30 EP 30 PG 1 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA LP324 UT WOS:A1993LP32400006 ER PT J AU JACOBSEN, FM AF JACOBSEN, FM TI LOW-DOSE VALPROATE - A NEW TREATMENT FOR CYCLOTHYMIA, MILD RAPID-CYCLING DISORDERS, AND PREMENSTRUAL-SYNDROME SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID BIPOLAR DISORDER; SPECTRUM; EFFICACY AB Background: Valproate has proved useful in the treatment of manic-depressive and schizoaffective disorders, usually in daily doses above 500 mg with corresponding blood levels in the range established for treatment of epilepsy (50-100 mug/mL). Since milder bipolar disorders may be more prevalent than bipolar I disorder, a prospective study was undertaken to determine whether lower doses of valproate might be useful for stabilization of blood cycling in patients having primary diagnoses of cyclothymia or rapid cycling bipolar II disorder. Additionally, open trials of low-dose valproate were conducted in a small number of women complaining of premenstrual syndrome. Method: Over a 3-year period. outpatients with non-menstrually-related rapid cycling who had fulfilled DSM-111-R criteria for cyclothymia or bipolar II disorder were started on open trials of valproate at daily doses of 125 or 250 mg. Doses were adjusted upward on approximately a monthly basis depending upon clinical response, and valproate blood levels were obtained. Results: Twenty-six (79%) of 33 patients (15 cyclothymics, 11 bipolar II) reported sustained partial or complete stabilization of mood cycling with valproate doses ranging from 125 to 500 mg (mean = 351.0 mg) corresponding to serum valproate levels (mean = 32.5 mug/mL) substantially below the current recommended range. Cyclothymics required significantly lower doses and blood levels of valproate than patients with bipolar II disorder for stabilization of mood. Five patients (all bipolar II) failed to respond fully to low doses of valproate but improved with higher doses corresponding to blood levels in the 50 to 100 mug/mL range. Two patients had poor responses to valproate or intolerable side effects. In contrast to bipolar spectrum patients. only three (38%) of eight women with menstrually related cycling of mood reported good responses to low doses of valproate, while five reported no response to valproate. Conclusion: The findings suggest that (1) low-dose valproate may be useful in the treatment of cyclothymia and milder rapid cycling bipolar disorders and (2) there may be a correlation between the severity of bipolar disorder and the blood level of valproate required for stabilization such that milder forms of bipolar cycling require lower doses of valproate. C1 GEORGE WASHINGTON UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20052. GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20007. NIMH,CLIN SCI LAB,WASHINGTON,DC 20032. RP JACOBSEN, FM (reprint author), TRANSCULTURAL MENTAL HLTH INST,1301 20TH ST,NW SUITE 711,WASHINGTON,DC 20036, USA. NR 12 TC 97 Z9 99 U1 0 U2 2 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JUN PY 1993 VL 54 IS 6 BP 229 EP 234 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA LP323 UT WOS:A1993LP32300005 PM 8331092 ER PT J AU LINNOILA, M STAPLETON, JM GEORGE, DT LANE, E ECKARDT, MJ AF LINNOILA, M STAPLETON, JM GEORGE, DT LANE, E ECKARDT, MJ TI EFFECTS OF FLUVOXAMINE, ALONE AND IN COMBINATION WITH ETHANOL, ON PSYCHOMOTOR AND COGNITIVE PERFORMANCE AND ON AUTONOMIC NERVOUS-SYSTEM REACTIVITY IN HEALTHY-VOLUNTEERS SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID ANTI-DEPRESSANTS; LONG-TERM; SEROTONIN; ANTIDEPRESSANTS; DESIPRAMINE; INHIBITOR; DIAZEPAM; MEMORY; BRAIN AB The effects of fluvoxamine (50 or 100 mg), alone and in combination with ethanol (0.8 g/kg), on psychomotor and cognitive performance and on autonomic nervous system reactivity were studied in healthy male volunteers. Fluvoxamine produced neither serious psychomotor or cognitive impairment nor alterations in autonomic nervous system functioning at these doses. There was no evidence that fluvoxamine exacerbated, or improved, ethanol-induced impairments of memory or any other measures evaluated. Fluvoxamine tended to improve recognition, but not free recall, of words. C1 NIAAA,CLIN STUDIES LAB,BETHESDA,MD. NR 37 TC 24 Z9 24 U1 0 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD JUN PY 1993 VL 13 IS 3 BP 175 EP 180 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LD690 UT WOS:A1993LD69000004 PM 8354733 ER PT J AU MCCANN, UD RICAURTE, GA AF MCCANN, UD RICAURTE, GA TI REINFORCING SUBJECTIVE EFFECTS OF (+/-) 3,4-METHYLENEDIOXYMETHAMPHETAMINE (ECSTASY) MAY BE SEPARABLE FROM ITS NEUROTOXIC ACTIONS - CLINICAL-EVIDENCE SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID CENTRAL SEROTONERGIC NEURONS; RAT-BRAIN; MONOAMINERGIC SYSTEMS; MDMA ECSTASY; METHYLENEDIOXYMETHAMPHETAMINE; AMPHETAMINE; PSYCHOSIS; SYNAPTOSOMES; DERIVATIVES; TERMINALS AB (+/-)3,4-Methylenedioxymethamphetamine (MDMA), a synthetic amphetamine derivative used recreationally by humans, damages brain serotonin neurons in experimental animals. In preclinical studies, serotonin reuptake inhibitors block MDMA-induced serotonin release; they also block MDMA neurotoxicity. Whether serotonin reuptake inhibitors also block MDMA's psychoactive effects in humans has not been established. Reported herein are four individuals who describe their experiences after ingesting fluoxetine, a potent and selective serotonin reuptake inhibitor, before MDMA ingestion. Their reports indicate that fluoxetine does not block MDMA's reinforcing subjective effects and raise the possibility that MDMA's psychoactive effects may be separable from its neurotoxic actions. C1 JOHNS HOPKINS UNIV,SCH MED,FRANCIS SCOTT KEY MED CTR,DEPT NEUROL,BALTIMORE,MD 21205. RP MCCANN, UD (reprint author), NIMH,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS SECT,BLDG 10,BETHESDA,MD 20892, USA. FU NIDA NIH HHS [DA 05938] NR 25 TC 47 Z9 47 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD JUN PY 1993 VL 13 IS 3 BP 214 EP 217 PG 4 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LD690 UT WOS:A1993LD69000011 PM 8102623 ER PT J AU GEORGE, MS TRIMBLE, MR AF GEORGE, MS TRIMBLE, MR TI DYSTONIC REACTION ASSOCIATED WITH FLUVOXAMINE SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Letter ID FLUOXETINE; DOPAMINE C1 INST NEUROL,LONDON WC1N 3BG,ENGLAND. RP GEORGE, MS (reprint author), NIMH,BETHESDA,MD 20892, USA. NR 10 TC 29 Z9 29 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD JUN PY 1993 VL 13 IS 3 BP 220 EP 221 DI 10.1097/00004714-199306000-00014 PG 2 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LD690 UT WOS:A1993LD69000014 PM 8354740 ER PT J AU BERNSTEIN, EF SALOMON, GD HARISIADIS, L TALBOT, T HARRINGTON, F RUSSO, A UITTO, J AF BERNSTEIN, EF SALOMON, GD HARISIADIS, L TALBOT, T HARRINGTON, F RUSSO, A UITTO, J TI COLLAGEN GENE-EXPRESSION AND WOUND STRENGTH IN NORMAL AND RADIATION-IMPAIRED WOUNDS - A MODEL OF RADIATION-IMPAIRED WOUND-HEALING SO JOURNAL OF DERMATOLOGIC SURGERY AND ONCOLOGY LA English DT Article ID GROWTH-FACTOR-BETA; MOUSE SKIN; ADRIAMYCIN; REVERSAL; RATS; TISSUE; ASSAY AB BACKGROUND. Poorly healing wounds result in significant morbidity postoperatively. Numerous attempts have been made to study wound healing in vivo to understand better the normal healing process and factors that impair healing. Animal models of wound healing have been developed to evaluate wound healing in a systematic and controlled setting. Incisional wounds are created in animals to mimic the surgical patient. They may then be evaluated by a variety of methods for degree of healing. OBJECTIVE. To give insight into the mechanisms of wound healing impairment, we developed a model of impaired wound healing in guinea pigs using radiation applied to the skin surfaces only. METHODS. Wound bursting strength, a direct measure of the force required to burst apart healing linear incisions, was measured. Collagen content, measured indirectly as collagen gene expression, was measured. RESULTS. Significant reductions in wound bursting strength were noted after radiation administration. Collagen gene expression was decreased in wounds 7 days after radiation, but recovered to control levels 14 days after irradiation. Our model enables the inclusion of irradiated and unirradiated skin flaps within the same animal, thus eliminating intra-animal variation when comparing impaired and normal wounds. CONCLUSION. Wound bursting strength analysis, combined with techniques aimed at elucidating changes at the molecular level, provides a useful tool for the study of factors that impair healing and potential treatments for resulting healing deficits. C1 NIH,PHOTOTHERAPY SECT,BETHESDA,MD 20892. NIH,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,MED CTR,RADIAT THERAPY SECT,WASHINGTON,DC 20037. RP BERNSTEIN, EF (reprint author), THOMAS JEFFERSON UNIV,DEPT DERMATOL,233 S 10TH ST,SUITE 450,PHILADELPHIA,PA 19107, USA. NR 30 TC 32 Z9 32 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0148-0812 J9 J DERMATOL SURG ONC PD JUN PY 1993 VL 19 IS 6 BP 564 EP 570 PG 7 WC Oncology; Dermatology; Surgery SC Oncology; Dermatology; Surgery GA LJ073 UT WOS:A1993LJ07300007 PM 8509518 ER PT J AU BREEN, N AF BREEN, N TI BEYOND THE TYPEWRITER - GENDER, CLASS, AND THE ORIGINS OF MODERN AMERICAN OFFICE WORK, 1900-1930 - STROM,SH SO JOURNAL OF ECONOMIC HISTORY LA English DT Book Review RP BREEN, N (reprint author), NCI,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0022-0507 J9 J ECON HIST JI J. Econ. Hist. PD JUN PY 1993 VL 53 IS 2 BP 448 EP 449 PG 2 WC Economics; History; History Of Social Sciences SC Business & Economics; History; Social Sciences - Other Topics GA LH270 UT WOS:A1993LH27000042 ER PT J AU NADER, S CHARLES, MA SAAD, MF BERKOWITZ, AS BOGARDUS, C AF NADER, S CHARLES, MA SAAD, MF BERKOWITZ, AS BOGARDUS, C TI SERUM ANDROGENS IN HYPERINSULINEMIC PIMA INDIAN AND OBESE CAUCASIAN WOMEN AND THEIR RESPONSE TO SHORT-TERM INSULIN INFUSION SO JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION LA English DT Article DE ANDROGENS; HYPERINSULINEMIA; EUGLYCEMIC CLAMP STUDIES; OBESITY ID BODY-FAT DISTRIBUTION; POLYCYSTIC-OVARY-SYNDROME; HORMONE-BINDING GLOBULIN; GLUCOSE-TOLERANCE TEST; ACANTHOSIS NIGRICANS; HYPERANDROGENIC WOMEN; RESISTANCE; METABOLISM; SECRETION AB Insulin resistance and its attendant hyperinsulinemia has been linked with hyperandrogenism. Insulin resistance is characteristic of the Pima Indians of the Gila River Indian community in central Arizona. Serum androgens, testosterone and dehydroepiandrosterone sulfate (DHEA-S) were quantitated at baseline and in response to low- and high-dose insulin infusion in 11 obese, hyperinsulinemic Pima Indian and 10 obese, hyperinsulinemic Caucasian women and were compared with baseline androgens in 16 nonobese Caucasian women. While there was no significant testosterone or DHEA-S response to short-term insulin infusion in either Pimas or obese Caucasians, both these groups had higher baseline testosterone concentrations (67+/-6.5 ng/dl in the Pimas, 55+/-5.9 ng/dl in the obese Caucasians) as compared with the nonobese Caucasians (28+/-2 ng/dl; p<0.001). Baseline DHEA-S concentrations were not significantly different in the three groups. Given the hyperinsulinemic status of both the Pimas and the obese Caucasians, the finding of higher testosterone concentrations in these subjects as compared with nonobese Caucasians supports a role for insulin in ovarian androgen production and demonstrates that hormonal interactions that may be operating in obese hyperinsulinemic Caucasian subjects also operate in obese, hyperinsulinemic Pima Indians. C1 UNIV TEXAS,SCH MED,DEPT OBSTET GYNECOL & REPROD SCI,HOUSTON,TX 77025. NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,PHOENIX,AZ. NR 19 TC 3 Z9 3 U1 1 U2 1 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0391-4097 J9 J ENDOCRINOL INVEST JI J. Endocrinol. Invest. PD JUN PY 1993 VL 16 IS 6 BP 403 EP 406 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LL227 UT WOS:A1993LL22700001 PM 8370914 ER PT J AU LAPHAM, CK BACIK, I YEWDELL, JW KANE, KP BENNINK, JR AF LAPHAM, CK BACIK, I YEWDELL, JW KANE, KP BENNINK, JR TI CLASS-I MOLECULES RETAINED IN THE ENDOPLASMIC-RETICULUM BIND ANTIGENIC PEPTIDES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TOXIC LYMPHOCYTES-T; CELL-SURFACE EXPRESSION; INFLUENZA-VIRUS HEMAGGLUTININ; HLA-B ANTIGENS; BREFELDIN-A; INTRACELLULAR-TRANSPORT; GOLGI-APPARATUS; VIRAL PEPTIDES; INFECTED-CELLS; MEDIATED LYSIS AB We isolated major histocompatibility complex (MHC)-specific viral peptides from cells infected with influenza virus in the continuous presence of the drug brefeldin A, which blocks exocytosis of newly synthesized MHC class I molecules. MHC-specific peptides were also isolated from cells expressing mouse K(d) class I MHC molecules whose cytoplasmic domain was substituted by that of the adenovirus E3/19K glycoprotein. This molecule was retained in an intracellular pre-Golgi complex compartment as demonstrated by immunocytochemical and biochemical means. Since we show that intracellular association of antigenic peptides with such retained class I molecules is necessary for their isolation from cellular extracts, this provides direct evidence that naturally processed peptides associate with class I MHC molecules in an early intracellular exocytic compartment. C1 NIAID,VIRAL DIS LAB,BLDG 4,ROOM 213,BETHESDA,MD 20892. UNIV ALBERTA,DEPT IMMUNOL,EDMONTON T6G 2H7,ALBERTA,CANADA. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 50 TC 33 Z9 33 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JUN 1 PY 1993 VL 177 IS 6 BP 1633 EP 1641 DI 10.1084/jem.177.6.1633 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA LD660 UT WOS:A1993LD66000013 PM 8496682 ER PT J AU BIKOFF, EK HUANG, LY EPISKOPOU, V VANMEERWIJK, J GERMAIN, RN ROBERTSON, EJ AF BIKOFF, EK HUANG, LY EPISKOPOU, V VANMEERWIJK, J GERMAIN, RN ROBERTSON, EJ TI DEFECTIVE MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II ASSEMBLY, TRANSPORT, PEPTIDE ACQUISITION, AND CD4+ T-CELL SELECTION IN MICE LACKING INVARIANT CHAIN EXPRESSION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MHC CLASS-II; HLA-DR MOLECULES; SURFACE EXPRESSION; MONOCLONAL-ANTIBODIES; ANTIGEN PRESENTATION; ENDOPLASMIC-RETICULUM; IA ANTIGENS; STEM-CELLS; INTRACELLULAR-TRANSPORT; ALLELIC POLYMORPHISM AB We used gene targeting techniques to produce mice lacking the invariant chain associated with major histocompatibility complex (MHC) class II molecules. Cells from these mice show a dramatic reduction in surface class II, resulting from both defective association of class II alpha and beta chains and markedly decreased post-Golgi transport. The few class II alpha/beta heterodimers reaching the cell surface behave as if empty or occupied by an easily displaced peptide, and display a distinct structure. Mutant spleen cells are defective in their ability to present intact protein antigens, but stimulate enhanced responses in the presence of peptides. These mutant mice have greatly reduced numbers of thymic and peripheral CD4+ T cells. Overall, this striking phenotype establishes that the invariant chain plays a critical role in regulating MHC class II expression and function in the intact animal. C1 HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. ST MARYS HOSP,SCH MED,DEPT BIOCHEM & MOLEC GENET,LONDON W2 1PG,ENGLAND. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. RP BIKOFF, EK (reprint author), HARVARD UNIV,DEPT CELLULAR & DEV BIOL,BIOL LABS,16 DIVIN AVE,CAMBRIDGE,MA 02138, USA. RI Episkopou, Vasso/E-2952-2010; van Meerwijk, Joost/K-1345-2014 FU NIAID NIH HHS [AI-19047] NR 96 TC 267 Z9 270 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JUN 1 PY 1993 VL 177 IS 6 BP 1699 EP 1712 DI 10.1084/jem.177.6.1699 PG 14 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA LD660 UT WOS:A1993LD66000020 PM 8098731 ER PT J AU YEWDELL, JW ESQUIVEL, F ARNOLD, D SPIES, T EISENLOHR, LC BENNINK, JR AF YEWDELL, JW ESQUIVEL, F ARNOLD, D SPIES, T EISENLOHR, LC BENNINK, JR TI PRESENTATION OF NUMEROUS VIRAL PEPTIDES TO MOUSE MAJOR HISTOCOMPATIBILITY COMPLEX (MHC) CLASS-I RESTRICTED T-LYMPHOCYTES IS MEDIATED BY THE HUMAN MHC-ENCODED TRANSPORTER OR BY A HYBRID MOUSE-HUMAN TRANSPORTER SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID HLA-B ANTIGENS; INFLUENZA HEMAGGLUTININ; REGION; EXPRESSION; CELLS; RECOGNITION; PROTEINS AB The major histocompatibility complex-encoded transporter associated with antigen processing (TAP) is required for the efficient presentation of cytosolic antigens to class I-restricted T cells. TAP is thought to be formed by the interaction of two gene products, termed TAP1 and TAP2. We find that TAPs consisting either of human subunits, or mouse TAP1 and human TAP2, facilitate the presentation of numerous defined viral peptides to mouse class I-restricted T cells. As human and mouse TAP2 and TAP1 differ in 23 and 28% of their residues, respectively, this indicates that TAP1 and TAP2 can form a functional complex with partners considerably different from those they coevolved with. Moreover, these findings indicate that widely disparate TAPs facilitate delivery of the same peptides to class I molecules. These findings suggest that TAP polymorphism does not greatly influence the types of peptides presented to the immune system. C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RI yewdell, jyewdell@nih.gov/A-1702-2012 FU NIAID NIH HHS [AI-30581] NR 41 TC 30 Z9 30 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JUN 1 PY 1993 VL 177 IS 6 BP 1785 EP 1790 DI 10.1084/jem.177.6.1785 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA LD660 UT WOS:A1993LD66000029 PM 8496691 ER PT J AU TAUB, DD LLOYD, AR CONLON, K WANG, JM ORTALDO, JR HARADA, A MATSUSHIMA, K KELVIN, DJ OPPENHEIM, JJ AF TAUB, DD LLOYD, AR CONLON, K WANG, JM ORTALDO, JR HARADA, A MATSUSHIMA, K KELVIN, DJ OPPENHEIM, JJ TI RECOMBINANT HUMAN INTERFERON-INDUCIBLE PROTEIN-10 IS A CHEMOATTRACTANT FOR HUMAN MONOCYTES AND T-LYMPHOCYTES AND PROMOTES T-CELL ADHESION TO ENDOTHELIAL-CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID CYTOKINE FAMILY; IP-10; GENE; IDENTIFICATION; EXPRESSION; CHEMOTAXIS AB The human cytokine interferon-inducible protein 10 (IP-10) is a small glycoprotein secreted by activated T cells, monocytes, endothelial cells, and keratinocytes, and is structurally related to a family of chemotactic cytokines called chemokines. Although this protein is present in sites of delayed-type hypersensitivity reactions and lepromatous leprosy lesions, the biological activity of IP-10 remains unknown. We report here that recombinant human IP-10 stimulated significant in vitro chemotaxis of human peripheral blood monocytes but not neutrophils. Recombinant human IP-10 also stimulated chemotaxis of stimulated, but not unstimulated, human peripheral blood T lymphocytes. Phenotypic analysis of the stimulated T cell population responsive to IP-10 demonstrated that stimulated CD4+ and CD29+ T cells migrated in response to IP-10. This resembles the biological activity of the previously described T cell chemoattractant RANTES. Using an endothelial cell adhesion assay, we demonstrated that stimulated T cells pretreated with optimal doses of IP-10 exhibited a greatly enhanced ability to bind to an interleukin 1-treated endothelial cell monolayer. These results demonstrate that the IP-10 gene encodes for an inflammatory mediator that specifically stimulates the directional migration of T cells and monocytes as well as potentiates T cell adhesion to endothelium. C1 NCI,FREDERICK CANC RES & DEV CTR,EXPTL IMMUNOL LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. KANAZAWA UNIV,INST CANC RES,DEPT PHARMACOL,KANAZAWA,ISHIKAWA 920,JAPAN. RP TAUB, DD (reprint author), NCI,FREDERICK CANC RES & DEV CTR,MOLEC IMMUNOREGULAT LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702, USA. FU PHS HHS [N01 C0-74102] NR 20 TC 641 Z9 645 U1 1 U2 6 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JUN 1 PY 1993 VL 177 IS 6 BP 1809 EP 1814 DI 10.1084/jem.177.6.1809 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA LD660 UT WOS:A1993LD66000033 PM 8496693 ER PT J AU ANSEL, BM AF ANSEL, BM TI TREATMENT EFFICACY RESEARCH IN STUTTERING SO JOURNAL OF FLUENCY DISORDERS LA English DT Article RP ANSEL, BM (reprint author), NATL INST DEAFNESS & OTHER COMMUN DISORDERS,EXECUT PLAZA S,SUITE 400-B,BETHESDA,MD 20892, USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0094-730X J9 J FLUENCY DISORD JI J. Fluency Disord. PD JUN-SEP PY 1993 VL 18 IS 2-3 BP 121 EP 123 DI 10.1016/0094-730X(93)90001-K PG 3 WC Audiology & Speech-Language Pathology; Education, Special; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Education & Educational Research; Linguistics; Rehabilitation GA NN017 UT WOS:A1993NN01700001 ER PT J AU LUDLOW, CL BRAUN, A AF LUDLOW, CL BRAUN, A TI RESEARCH EVALUATING THE USE OF NEUROPHARMACOLOGICAL AGENTS FOR TREATING STUTTERING - POSSIBILITIES AND PROBLEMS SO JOURNAL OF FLUENCY DISORDERS LA English DT Article; Proceedings Paper CT Workshop on the Treatment Efficacy Research in Stuttering CY SEP 21-22, 1992 CL NIH, BETHESDA, MD SP NIDOCD HO NIH ID NEUROPSYCHOLOGICAL MODELS; SPEECH RP LUDLOW, CL (reprint author), NIDCD,VOICE & SPEECH SECT,BLDG 10,RM 5D38,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. OI Ludlow, Christy/0000-0002-2015-6171 NR 46 TC 13 Z9 13 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0094-730X J9 J FLUENCY DISORD JI J. Fluency Disord. PD JUN-SEP PY 1993 VL 18 IS 2-3 BP 169 EP 182 DI 10.1016/0094-730X(93)90005-O PG 14 WC Audiology & Speech-Language Pathology; Education, Special; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Education & Educational Research; Linguistics; Rehabilitation GA NN017 UT WOS:A1993NN01700005 ER PT J AU MOSCICKI, EK AF MOSCICKI, EK TI FUNDAMENTAL METHODOLOGICAL CONSIDERATIONS IN CONTROLLED CLINICAL-TRIALS SO JOURNAL OF FLUENCY DISORDERS LA English DT Article; Proceedings Paper CT Workshop on the Treatment Efficacy Research in Stuttering CY SEP 21-22, 1992 CL NIH, BETHESDA, MD SP NIDOCD HO NIH ID LONGITUDINAL DATA-ANALYSIS; BEHAVIOR; CHILDREN; MODELS AB This article raises some fundamental issues that need to be considered in experimental epidemiologic designs for tests of treatment efficacy. The basic design in such research is the randomized controlled clinical trial, in which subjects are randomly assigned to experimental and control groups, and conditions of masking, or blindness, are maintained. This general design has been used most often in pharmacotherapy trials; it is also applicable to trials of behavioral therapies. Tests of efficacy must have their conceptual underpinnings in empirically based, theoretical models that reflect the putative processes underlying the disorders being treated. Development of such tests must follow an organized, systematic research program, in which treatment research progresses in several phases, with each phase building on the preceding one. For specific studies, careful attention should be paid to the selection and representativeness of study participants. Sample size must be sufficiently large to demonstrate statistically significant differences between experimental and control groups. The outcome being studied must have a clear operational definition, with careful attention given to the instrumentation used in assessing and classifying outcomes. Reliability and validity of the chosen instruments must be addressed. The treatment being tested must be delivered under a standardized treatment protocol by clinicians who have received standardized training in the procedure. Treatment delivery should include procedures to monitor adherence to the treatment protocol by the intervening clinicians and by study participants. Because of the complexity inherent in well-designed controlled clinical trials, conducting one or more pilot studies is essential to resolving difficult design and other issues prior to initiation of the full-scale experimental study. Follow-up must be of sufficient duration to determine the differential effects of the treatment. Potential sources of bias need to be anticipated and accounted for in the study design and analytic models. Finally, data analysis procedures must be appropriate to the study design. RP MOSCICKI, EK (reprint author), NIMH,PREVENT RES BRANCH,ROOM 10-85,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 18 TC 21 Z9 21 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0094-730X J9 J FLUENCY DISORD JI J. Fluency Disord. PD JUN-SEP PY 1993 VL 18 IS 2-3 BP 183 EP 196 DI 10.1016/0094-730X(93)90006-P PG 14 WC Audiology & Speech-Language Pathology; Education, Special; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Education & Educational Research; Linguistics; Rehabilitation GA NN017 UT WOS:A1993NN01700006 ER PT J AU AGULNICK, AD THOMPSON, JR IYENGAR, S PEARSON, G ABLASHI, D RICCIARDI, RP AF AGULNICK, AD THOMPSON, JR IYENGAR, S PEARSON, G ABLASHI, D RICCIARDI, RP TI IDENTIFICATION OF A DNA-BINDING PROTEIN OF HUMAN HERPESVIRUS-6, A PUTATIVE DNA-POLYMERASE STIMULATORY FACTOR SO JOURNAL OF GENERAL VIROLOGY LA English DT Article ID HUMAN CYTOMEGALOVIRUS; SEQUENCE-ANALYSIS; INFECTED-CELLS; MESSENGER-RNAS; LYMPHOCYTES-T; VIRUS; HHV-6; HIV-1; GENE; TRANSLATION AB A 41K early nuclear antigen (p41), expressed in human herpesvirus type 6 (HHV-6)-infected T cells, was cloned by screening a cDNA expression library with the anti-p41 monoclonal antibody (MAb) C5. When expressed in mammalian cells, the cloned p41 protein comigrated with the authentic p41 protein from HHV-6-infected cells and localized to the nucleus. HHV-6 p41 shares 44% sequence identity with the human cytomegalovirus (HCMV) DNA-binding protein, ICP36 (UL44 gene product); p41 binds to ssDNA with the same apparent affinity as ICP36. Since ICP36 has recently been shown to be an HCMV DNA polymerase-associated stimulatory factor, a similar function is suggested for p41. C1 WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. GEORGETOWN UNIV,MED CTR,DEPT MICROBIOL,WASHINGTON,DC 20007. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA 09171]; NIAID NIH HHS [AI 07325, AI 29362] NR 33 TC 41 Z9 41 U1 0 U2 0 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1317 J9 J GEN VIROL JI J. Gen. Virol. PD JUN PY 1993 VL 74 BP 1003 EP 1009 DI 10.1099/0022-1317-74-6-1003 PN 6 PG 7 WC Biotechnology & Applied Microbiology; Virology SC Biotechnology & Applied Microbiology; Virology GA LG086 UT WOS:A1993LG08600007 PM 8389796 ER PT J AU GILBERT, CS PARMLEY, RT RICE, WG KINKADE, JM AF GILBERT, CS PARMLEY, RT RICE, WG KINKADE, JM TI HETEROGENEITY OF PEROXIDASE-POSITIVE GRANULES IN NORMAL HUMAN AND CHEDIAK-HIGASHI NEUTROPHILS SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article DE NEUTROPHILS (HUMAN); CYTOPLASMIC GRANULES; MORPHOMETRY; CHEDIAK-HIGASHI SYNDROME; MYELOPEROXIDASE; LYSOSOMES; ELECTRON MICROSCOPY ID HUMAN-BONE MARROW; HUMAN POLYMORPHONUCLEAR LEUKOCYTES; ULTRASTRUCTURAL-LOCALIZATION; INTRACELLULAR COMPARTMENT; SECRETORY PROPERTIES; DE-GRANULATION; AZUROPHIL; CELLS; MYELOPEROXIDASE; SUBPOPULATIONS AB Studies have demonstrated significant heterogeneity in neutrophil granule morphology and physical density. This study evaluated the heterogeneity morphometrically, morphologically, cytochemically, and biochemically. Intact human peripheral blood neutrophils collected from normal volunteers and a patient with Chediak-Higashi syndrome (CHS) and isolated normal neutrophil granules were processed for ultrastructural morphology and peroxidase staining. Intact cells, nuclei, and granule profiles were analyzed by computer-assisted planimetry. Peroxidase-positive granules (PPG) represented about 40% of normal neutrophil granules and covered the entire spectrum of granule size. PPG in the least-dense fractions of isolated granules were significantly smaller than in higher-density fractions. PPG in low- and intermediate-density fractions differed from high-density fractions by moderate to strong vicinal glycol staining with Thiery's periodate-thiocarbohydrazide-silver proteinate method. Differing ratios of % beta-glucuronidase/% myeloperoxidase (MPO) across granule fractions indicated PPG heterogeneity. Morphometric analysis of neutrophils treated with 1 muM calcium ionophore A23187 did not show significant differences in PPG size or number. Biochemically analyzed MPO in these cells was preserved, although the number of peroxidase-negative granules (PNG) and levels of vitamin B-12-binding protein were markedly decreased. In CHS, about 20% of granules were PPG. Analysis of CHS neutrophils revealed the persistence of microgranules similar to normals. PNG number and volume fractions of PPG and TG were not different from normals. Complex heterogeneity of normal PPG was quantitated using morphometry and appeared preserved in ionophore-treated cells but was uniquely modified in CHS. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PEDIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. NCI,FREDERICK CANC RES & DEV CTR,DYN CORP,PROGRAM RES INC,FREDERICK,MD 21701. EMORY UNIV,SCH MED,DEPT BIOCHEM,ATLANTA,GA 30322. FU NCI NIH HHS [NCI CA 22294] NR 46 TC 10 Z9 10 U1 0 U2 0 PU HISTOCHEMICAL SOC INC PI NEW YORK PA MT SINAI MEDICAL CENTER 19 EAST 98TH ST SUTIE 9G, NEW YORK, NY 10029 SN 0022-1554 J9 J HISTOCHEM CYTOCHEM JI J. Histochem. Cytochem. PD JUN PY 1993 VL 41 IS 6 BP 837 EP 849 PG 13 WC Cell Biology SC Cell Biology GA LC097 UT WOS:A1993LC09700006 PM 8315276 ER PT J AU ENGEL, P NOJIMA, Y ROTHSTEIN, D ZHOU, LJ WILSON, GL KEHRL, JH TEDDER, TF AF ENGEL, P NOJIMA, Y ROTHSTEIN, D ZHOU, LJ WILSON, GL KEHRL, JH TEDDER, TF TI THE SAME EPITOPE ON CD22 OF B-LYMPHOCYTES MEDIATES THE ADHESION OF ERYTHROCYTES, T-LYMPHOCYTES AND B-LYMPHOCYTES, NEUTROPHILS, AND MONOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL-SURFACE; CARCINOEMBRYONIC ANTIGEN; MONOCLONAL-ANTIBODY; BINDING-SITES; MOLECULE; IMMUNOGLOBULIN; EXPRESSION; PROTEIN; FAMILY; SIALYLTRANSFERASE AB CD22 is a B lineage-restricted member of the Ig superfamily that serves as an adhesion receptor expressed by mature B lymphocytes. In this study, the ability of different cell types to attach to COS cells transiently transfected with a full-length CD22 cDNA (COS-CD22) was examined to determine the cellular distribution of the ligand for CD22. T and B lymphocytes, monocytes, erythrocytes, and neutrophils formed specific rosettes with COS-CD22 cells at 4-degrees-C. A panel of 33 new mAb directed against CD22 were developed to examine the regions of CD22 that mediate adhesion. Four of these mAb, HB22-7, -22, -23, and -33 (at 1 to 5 mug/ml) specifically blocked adhesion (75 to 95%) of all cell types to COS-CD22 cells. Each of these mAb cross-blocked each other's binding, suggesting that ligand binding occurs through a single region of CD22. These mAb also identify a region of CD22 distinct from those defined by previously described CD22 mAb. CD22-mediated adhesion of cell lines to COS-CD22 cells was independent of CD45RO and CDw75 expression, and it was not inhibited by mAb against known integrins. Although alpha-2,6-linked sialic acid expressed on the surface of COS cells did not serve as a ligand for CD22, the CD22 ligand may contain a critical sialic acid determinant, as neuraminidase treatment of all target cells eliminated CD22-mediated adhesion. CD22-mediated adhesion was Ca2+/Mg2+ independent, again suggesting that integrins were not involved. An inhibitory substance for CD22-mediated adhesion was found to be present in FCS and some ascites fluid. Analysis of CD22 mRNA and protein revealed that although multiple mRNA splice variants of CD22 mRNA can be detected, only a single protein isoform was detected on the cell surface. Therefore, although the identity of the CD22 ligands remains incompletely characterized, it is possible that a single major ligand is expressed by RBC and leukocytes, which binds to a single region of CD22. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA-34183, CA-54464]; NIAID NIH HHS [AI-26872] NR 45 TC 153 Z9 156 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 1 PY 1993 VL 150 IS 11 BP 4719 EP 4732 PG 14 WC Immunology SC Immunology GA LD916 UT WOS:A1993LD91600002 PM 7684411 ER PT J AU WILSON, GL NAJFELD, V KOZLOW, E MENNIGER, J WARD, D KEHRL, JH AF WILSON, GL NAJFELD, V KOZLOW, E MENNIGER, J WARD, D KEHRL, JH TI GENOMIC STRUCTURE AND CHROMOSOMAL MAPPING OF THE HUMAN CD22 GENE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LYMPHOCYTES-PRE-B; CARCINOEMBRYONIC ANTIGEN; SURFACE EXPRESSION; ADHESION MOLECULE; CELL ANTIGEN; ALU SEQUENCE; II GENES; IMMUNOGLOBULIN; TRANSCRIPTION; ELEMENT AB The human CD22 gene is expressed specifically in B lymphocytes and likely has an important function in cell-cell interactions. A nearly full length human CD22 cDNA clone was used to isolate genomic clones that span the CD22 gene. The CD22 gene is spread over 22 kb of DNA and is composed of 15 exons. The first exon contains the major transcriptional start sites. The translation initiation codon is located in exon 3, which also encodes a portion of the signal peptide. Exons 4 to 10 encode the seven Ig domains of CD22, exon 11 encodes the transmembrane domain, exons 12 to 15 encode the intracytoplasmic domain of CD22, and exon 15 also contains the 3' untranslated region. A minor form of CD22 mRNA likely results from splicing of exon 5 to exon 8, skipping exons 6 and 7. A 4.6-kb Xbal fragment of the CD22 gene was used to map the chromosomal location of CD22 by fluorescence in situ hybridization. The hybridization locus was identified by combining fluorescent images of the probe with the chromosomal banding pattern generated by an Alu probe. The results demonstrate that CD22 is located within the band region q13.1 of chromosome 19. Two closely clustered major transcription start sites and several minor start sites were mapped by primer extension. Similarly to many other lymphoid-specific genes, the CD22 promoter lacks an obvious TATA box. Approximately 4 kb of DNA 5' of the transcription start sites were sequenced and found to contain multiple Alu elements. Potential binding sites for the transcriptional factors NF-kappaB, AP-1, and Oct-2 are located within 300 bp 5' of the major transcription start sites. A 400-bp fragment (bp -339 through +71) of the CD22 promoter region was subcloned into a pGEM-chloramphenicol acetyltransferase vector and after transfection into B and T cells was found to be active in both B and T cells. Further studies of the CD22 gene should lead to a greater understanding of the expression of CD22 during B cell development and differentiation. C1 NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B-13,BETHESDA,MD 20892. MT SINAI MED CTR,TUMOR CYTOGENET LAB,NEW YORK,NY 10029. YALE UNIV,SCH MED,DEPT HUMAN GENET,NEW HAVEN,CT 06510. OI Kehrl, John/0000-0002-6526-159X NR 44 TC 55 Z9 56 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 1 PY 1993 VL 150 IS 11 BP 5013 EP 5024 PG 12 WC Immunology SC Immunology GA LD916 UT WOS:A1993LD91600030 PM 8496602 ER PT J AU YOSHIMURA, T AF YOSHIMURA, T TI CDNA CLONING OF GUINEA-PIG MONOCYTE CHEMOATTRACTANT PROTEIN-1 AND EXPRESSION OF THE RECOMBINANT PROTEIN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID BLOOD MONONUCLEAR LEUKOCYTES; AMINO-ACID ANALYSIS; CHEMOTACTIC PROTEIN; SPLEEN-CELLS; JE GENE; MCP-1; IDENTIFICATION; PURIFICATION; PRODUCT; RABBIT AB Monocyte chemoattractant protein-1 (MCP-1) cDNA was cloned from guinea pig spleen cells stimulated with Con A. The cDNA comprised 647 bp with an open reading frame that encoded a 120 amino acid protein. The sequence similarity of the first 99 amino acids to human MCP-1 is 56%. Recombinant guinea pig MCP-1 was expressed in COS-7 cells, then purified by a three step procedure with orange A-agarose, carboxymethyl-HPLC, and reversed phase-HPLC. The purified protein was found around 25 kDa as a broad band on a polyacrylamide gel under reducing conditions. Guinea pig MCP-1 attracted about 34% of input human monocytes at 5 x 10(-9) M. Guinea pig peritoneal exudate macrophages migrated toward guinea pig MCP-1 dose dependently, but only 1% of input cells responded to guinea pig MCP-1 at its optimal concentration of 5 x 10(-9) M. Human MCP-1 attracted 1% of input guinea pig peritoneal exudate macrophages at its highest concentration of 2.5 x 10(-8) M. Neither human nor guinea pig MCP-1 attracted guinea pig peritoneal resident macrophages. These results suggest that monocytes lose responsiveness to MCP-1 after differentiating to macrophages. Finally, intradermal injection of the recombinant protein into guinea pigs caused marked macrophage infiltration. Cloned and expressed guinea pig MCP-1 will help in studying the role of MCP-1 in vivo. RP YOSHIMURA, T (reprint author), NCI,FREDERICK CANC RES & DEV CTR,IMMUNOPATHOL SECT,IMMUNOBIOL LAB,BLDG 560,ROOM 12-71,FREDERICK,MD 21702, USA. NR 34 TC 50 Z9 51 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 1 PY 1993 VL 150 IS 11 BP 5025 EP 5032 PG 8 WC Immunology SC Immunology GA LD916 UT WOS:A1993LD91600031 PM 8496603 ER PT J AU BLAYLOCK, BL KOUCHI, Y COMMENT, CE POLLOCK, PL LUSTER, MI AF BLAYLOCK, BL KOUCHI, Y COMMENT, CE POLLOCK, PL LUSTER, MI TI TOPICAL APPLICATION OF T-2 TOXIN INHIBITS THE CONTACT HYPERSENSITIVITY RESPONSE IN BALB/C MICE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EPIDERMAL LANGERHANS CELLS; DELAYED-TYPE HYPERSENSITIVITY; ANTIGEN-PRESENTING CELLS; LYMPH-NODES; IA-ANTIGEN; T-CELLS; EXPRESSION; INDUCTION; TRICHOTHECENES; DEPLETION AB T-2 toxin, a trichothecene mycotoxin, has previously been shown to alter immune functions and promote skin tumors. We demonstrate that topically applied T-2 toxin reduces the ear swelling response to oxazolone challenge in BALB/c mice. For this reduction in ear swelling to occur, toxin application must be at, or within, 1 h after challenge. Dose-response studies showed a 44% reduction in ear swelling with 30 ng of T-2 toxin as compared with a similar reduction with 300 ng of dexamethasone. T-2 toxin did not affect Ag transport from the challenge site to the draining lymph nodes as measured by FITC transport. However, T-2 toxin significantly reduced both MHC class II (Ia) expression and Ag presentation at the same concentrations. Because T-2 toxin, a known protein synthesis inhibitor, was found to inhibit protein synthesis in epidermal cell cultures as measured by [H-3]-leucine incorporation, cycloheximide was also examined. Cycloheximide reduced both oxazolone-induced ear swelling and Ag presentation in a similar manner to T-2 toxin. One mechanism of action for T-2 toxin in reducing the contact hypersensitivity response is via inhibition of protein synthesis and effective Ag presentation by epidermal Langerhans cells. This may involve alterations in la Ag expression, although a role for class II in the induction phase of the contact hypersensitivity response has not been established definitively. C1 NIEHS,ENVIRONM IMMUNOL SECT,RES TRIANGLE PK,NC 27709. TAIHO PHARMACEUT CO LTD,TOKUSHIMA,JAPAN. NR 51 TC 20 Z9 21 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 JUN 1 PY 1993 VL 150 IS 11 BP 5135 EP 5143 PG 9 WC Immunology SC Immunology GA LD916 UT WOS:A1993LD91600043 PM 8496607 ER PT J AU TSAREV, SA EMERSON, SU TSAREVA, TS YARBOUGH, PO LEWIS, M GOVINDARAJAN, S REYES, GR SHAPIRO, M PURCELL, RH AF TSAREV, SA EMERSON, SU TSAREVA, TS YARBOUGH, PO LEWIS, M GOVINDARAJAN, S REYES, GR SHAPIRO, M PURCELL, RH TI VARIATION IN COURSE OF HEPATITIS-E IN EXPERIMENTALLY INFECTED CYNOMOLOGUS MONKEYS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID NON-B HEPATITIS; TRANSMITTED NON-A; PUTATIVE CAUSATIVE VIRUS; MACACA-MULATTA; IDENTIFICATION; TRANSMISSION; MACAQUES; RELAPSE; GENOME; STOOLS AB Five cynomolgus monkeys (Macaca fascicularis) developed hepatitis after inoculation with a prototype strain of hepatitis E virus (HEV) from Pakistan. Although all 5 monkeys displayed liver enzyme elevations, viremia, virus secretion in feces, and seroconversion, two different patterns of these parameters were observed. For 4 monkeys, increased alanine aminotransferase (ALT) activity was first observed on days 21-26, viremia occurred before and during enzyme elevation, and the animals seroconverted coincidentally with the end of viremia or shortly thereafter. One of these monkeys had a more severe hepatitis, with peak ALT values more than twice the peak levels of the other monkeys. The fifth monkey developed biphasic hepatitis with peaks of ALT activity on days 26 and 54. In this case, viremia and seroconversion were correlated only with the second peak of enzyme elevation and liver histopathology only with the first peak. Viral shedding in this fifth animal lasted two times longer than in other animals. C1 BIOQUAL INC,ROCKVILLE,MD. GENELABS INC,DEPT MOLEC VIROL,REDWOOD CITY,CA. RANCHO LOS AMIGOS MED CTR,PATHOL & CLIN LABS,DOWNEY,CA 90242. RP TSAREV, SA (reprint author), NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BLDG 7,ROOM 200,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [AI-05069] NR 32 TC 58 Z9 58 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 JUN PY 1993 VL 167 IS 6 BP 1302 EP 1306 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LD694 UT WOS:A1993LD69400006 PM 8501318 ER PT J AU LIMAYE, AP OTTESEN, EA KUMARASWAMI, V ABRAMS, JS REGUNATHAN, J VIJAYASEKARAN, V JAYARAMAN, K NUTMAN, TB AF LIMAYE, AP OTTESEN, EA KUMARASWAMI, V ABRAMS, JS REGUNATHAN, J VIJAYASEKARAN, V JAYARAMAN, K NUTMAN, TB TI KINETICS OF SERUM AND CELLULAR INTERLEUKIN-5 IN POSTTREATMENT EOSINOPHILIA OF PATIENTS WITH LYMPHATIC FILARIASIS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID COLONY-STIMULATING FACTOR; DIFFERENTIATION; PROLIFERATION; CELLS; IL-5 AB Peripheral blood eosinophil counts and serum levels and in vitro production of eosinophilopoetic cytokines were assessed before and at frequent intervals after diethylcarbamazine treatment of Bancroftian filariasis. Eosinophil counts peaked at day 7 after the start of treatment (359% +/- 118% of pretreatment levels) and declined to pretreatment levels by day 17. Serum interleukin (IL)-5, undetectable in 14 of 15 patients before treatment, rose sharply but transiently, with peak levels (32 +/- 7 pg/mL) 2 days after diethylcarbamazine treatment. Granulocyte-macrophage colony-stimulating factor and IL-3 were not detectable in serum at any time. In vitro mitogen-induced IL-5 levels decreased significantly in 7 of 9 patients 3 days after treatment when serum IL-5 was at near-peak levels. By day 10 IL-5 values increased in 8 of 9 patients compared with treatment values (P < .02). These data define the temporal relation between serum IL-5 levels and the subsequent development of eosinophilia and suggest that lymphocytes are the source of IL-5. C1 NIAID,PARASIT DIS LAB,BLDG 4,RM 126,BETHESDA,MD 20892. DNAX RES INST MOLEC & CELLULAR BIOL INC,PALO ALTO,CA. UNIV MADRAS,TB RES CTR,MADRAS 600005,TAMIL NADU,INDIA. ANNA UNIV,MADRAS,INDIA. NR 21 TC 16 Z9 16 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 JUN PY 1993 VL 167 IS 6 BP 1396 EP 1400 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LD694 UT WOS:A1993LD69400020 PM 8501330 ER PT J AU CUTTS, FT MANDALA, K STLOUIS, M BROWN, C MAYALA, B ZELL, ER DEFOREST, A KAMENGA, M DAVACHI, F MARKOWITZ, LE AF CUTTS, FT MANDALA, K STLOUIS, M BROWN, C MAYALA, B ZELL, ER DEFOREST, A KAMENGA, M DAVACHI, F MARKOWITZ, LE TI IMMUNOGENICITY OF HIGH-TITER EDMONSTON-ZAGREB MEASLES-VACCINE IN HUMAN-IMMUNODEFICIENCY-VIRUS INFECTED CHILDREN IN KINSHASA, ZAIRE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID INFANTS AB The response to Edmonston-Zagreb vaccine (titer, 5.4 log10 pfu) was evaluated among children in a study of perinatal transmission of human immunodeficiency virus (HIV) in Kinshasa. Acute postvaccination adverse events were monitored for 49 HIV-infected and 376 non-HIV-infected infants, and measles antibody responses were assessed by ELISA for 34 HIV-infected and 255 non-HIV-infected infants. There was no increase in the incidence of common symptoms 7-10 days after vaccination. HIV-infected infants were more likely to have detectable prevaccination measles antibody, and seroconversion after vaccination was somewhat lower in HIV-infected (76.5%) than non-HIV-infected infants (85.5%). Seroconversion rates did not differ among children with or without rhinitis or fever at vaccination. High-titer Edmonston-Zagreb vaccine given at 6 months of age has the potential to provide earlier protection against measles; however, this vaccine is no longer recommended for routine use, and two doses of standard-titer vaccines remains the preferred option for measles vaccination of HIV-infected infants. C1 CTR DIS CONTROL & PREVENT,NATL CTR PREVENT SERV,DIV IMMUNIZAT,ATLANTA,GA. CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV HIV AIDS,ATLANTA,GA. NIAID,BETHESDA,MD 20892. ST CHRISTOPHERS HOSP CHILDREN,VIRUS LAB,PHILADELPHIA,PA 19133. MAMA YEMO HOSP,KINSHASA,ZAIRE. PROJECT SIDA,KINSHASA,ZAIRE. NR 14 TC 12 Z9 12 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 JUN PY 1993 VL 167 IS 6 BP 1418 EP 1421 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LD694 UT WOS:A1993LD69400025 PM 8501334 ER PT J AU MASUR, H POLIS, MA TUAZON, CU OGATAARAKAKI, D KOVACS, JA KATZ, D HILT, D SIMMONS, T FEUERSTEIN, I LUNDGREN, B LANE, HC CHABNER, BA ALLEGRA, CJ AF MASUR, H POLIS, MA TUAZON, CU OGATAARAKAKI, D KOVACS, JA KATZ, D HILT, D SIMMONS, T FEUERSTEIN, I LUNDGREN, B LANE, HC CHABNER, BA ALLEGRA, CJ TI SALVAGE TRIAL OF TRIMETREXATE-LEUCOVORIN FOR THE TREATMENT OF CEREBRAL TOXOPLASMOSIS IN PATIENTS WITH AIDS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; CHLOROQUINE RESISTANCE; PLASMODIUM-FALCIPARUM; ENCEPHALITIS; COMBINATION; THERAPY AB The clinical efficacy of trimetrexate, a dihydrofolate reductase inhibitor with potent in vitro antitoxoplasma activity, was assessed in 9 sulfonamide-intolerant patients with AIDS and biopsy-proven cerebral toxoplasmosis. The 9 patients were treated for 28-149 days with trimetrexate (30-280 mg/m2/day) plus leucovorin (20-90 mg/m2 every 6 h). Radiographic responses were documented in 8 patients, and clinical responses in 5 patients. Despite continued therapy, all patients deteriorated clinically and radiographically within 13-109 days of their initial improvement. Trimetrexate at very high doses for extended periods was not associated with serious toxicity. Trimetrexate alone had dramatic but transient activity in sulfonamide-intolerant patients and thus is not adequate as single-agent therapy for AIDS-associated toxoplasmosis. C1 GEORGETOWN UNIV,WASHINGTON,DC 20057. RP MASUR, H (reprint author), NIH,CCMD,BLDG 10,ROOM 7D43,BETHESDA,MD 20892, USA. OI Polis, Michael/0000-0002-9151-2268 NR 14 TC 33 Z9 34 U1 0 U2 2 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 JUN PY 1993 VL 167 IS 6 BP 1422 EP 1426 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LD694 UT WOS:A1993LD69400026 PM 8501335 ER PT J AU SANCHEZ, JL TROFA, AF TAYLOR, DN KUSCHNER, RA DEFRAITES, RF CRAIG, SC RAO, MR CLEMENS, JD SVENNERHOLM, AM SADOFF, JC HOLMGREN, J AF SANCHEZ, JL TROFA, AF TAYLOR, DN KUSCHNER, RA DEFRAITES, RF CRAIG, SC RAO, MR CLEMENS, JD SVENNERHOLM, AM SADOFF, JC HOLMGREN, J TI SAFETY AND IMMUNOGENICITY OF THE ORAL, WHOLE-CELL RECOMBINANT B-SUBUNIT CHOLERA VACCINE IN NORTH-AMERICAN VOLUNTEERS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID FIELD TRIAL; ESCHERICHIA-COLI; VIBRIO-CHOLERAE; FOLLOW-UP; BANGLADESH; TOXIN; RESPONSES; DIARRHEA AB A newly formulated, oral, inactivated whole cell plus recombinant B subunit (WC/rBS) cholera vaccine was evaluated in US military personnel. In the first study, 74 subjects were given two doses 14 days apart. In the second study, 186 subjects were randomized into four groups; two groups received vaccine with either full (4 g) or half (2 g) strength bicarbonate buffer, and two groups received either full or half strength buffer without vaccine. Mild gastrointestinal symptoms were associated with full buffer (P = .02) but not with the vaccine. In the first study, 36% of all subjects and 55% with low prevaccination titers (<1:40) had a greater-than-or-equal-to 2-fold rise in vibriocidal antibody level; >80% of subjects developed a 4-fold rise in anti-cholera toxin (CT) titers. Post-vaccination IgA and IgG anti-CT titers were approximately 1.5-fold higher among persons receiving full strength buffer (P = .05). The WC/rBS vaccine is safe and immunogenic in North Americans, although some mild gastrointestinal symptoms occur with the high concentration of buffer necessary to protect the B subunit from gastric acid denaturation. Prior immunity to cholera conferred by parenteral vaccine decreased vibriocidal antibody response. C1 WALTER REED ARMY INST RES,DEPT ADV PREVENT MED,DIV PREVENT MED,WASHINGTON,DC 20307. WALTER REED ARMY INST RES,DEPT ENTER INFECT,DIV COMMUNICABLE DIS & IMMUNOL,WASHINGTON,DC 20307. NICHHD,DIV PREVENT RES,BETHESDA,MD 20892. GOTHENBURG UNIV,DEPT MED MICROBIOL & IMMUNOL,S-41124 GOTHENBURG,SWEDEN. RP SANCHEZ, JL (reprint author), WALTER REED ARMY INST RES,DEPT FIELD STUDIES,DIV PREVENT MED,WASHINGTON,DC 20307, USA. NR 15 TC 45 Z9 46 U1 0 U2 2 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 JUN PY 1993 VL 167 IS 6 BP 1446 EP 1449 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LD694 UT WOS:A1993LD69400031 PM 8501336 ER PT J AU STEINERT, PM AF STEINERT, PM TI STRUCTURE, FUNCTION, AND DYNAMICS OF KERATIN INTERMEDIATE FILAMENTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Review ID EPIDERMOLYSIS-BULLOSA SIMPLEX; COILED-COIL MOLECULES; NUCLEAR LAMINA; MOUSE; PHOSPHORYLATION; INVITRO; PROTEINS; ORGANIZATION; SEQUENCES; NETWORKS RP STEINERT, PM (reprint author), NIAMSD,SKIN BIOL BRANCH,BETHESDA,MD 20892, USA. NR 63 TC 159 Z9 164 U1 2 U2 9 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JUN PY 1993 VL 100 IS 6 BP 729 EP 734 DI 10.1111/1523-1747.ep12475665 PG 6 WC Dermatology SC Dermatology GA LE329 UT WOS:A1993LE32900001 PM 7684423 ER PT J AU YAROSH, DB ALAS, L KIBITEL, J OCONNOR, A CARRIER, F FORNACE, AJ AF YAROSH, DB ALAS, L KIBITEL, J OCONNOR, A CARRIER, F FORNACE, AJ TI CYCLOBUTANE PYRIMIDINE DIMERS IN UV-DNA INDUCE RELEASE OF SOLUBLE MEDIATORS THAT ACTIVATE THE HUMAN-IMMUNODEFICIENCY-VIRUS PROMOTER SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID LONG TERMINAL REPEAT; INVIVO ACTIVATION; ULTRAVIOLET-B; HUMAN SKIN; TYPE-1; DAMAGE; REPAIR; ENHANCEMENT; RADIATION; CELLS AB Ultraviolet (UV) irradiation of human cells induced expression of a stably maintained fusion gene consisting of the human immunodeficiency virus long terminal repeat promoter controlling the bacterial chloramphenicol acetyltransferase gene. Two experiments demonstrated that DNA damage can initiate induction: UV induction was greater in DNA repair-deficient cells from a xeroderma pigmentosum patient than in repair-proficient cells, and transfection of UV-irradiated DNA into unirradiated cells activated gene expression. increased repair of cyclobutane pyrimidine dimers by T4 endonuclease V abrogated viral gene activation, suggesting that dimers in DNA are one signal leading to increased gene expression. This signal was spread from UV-irradiated cells to unirradiated cells by co-cultivation, implicating the release of soluble factors. Irradiation of cells from DNA repair-deficiency diseases resulted in greater release of soluble factors than irradiation of cells from unaffected individuals. These results suggest that UV-induced cyclobutane pyrimidine dimers can activate the human immunodeficiency virus promoter at least in part by a signal-transduction pathway that includes secretion of soluble mediators. C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. RP YAROSH, DB (reprint author), APPL GENET INC,205 BUFFALO AVE,FREEPORT,NY 11520, USA. RI Carrier, France/C-3063-2008; Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 22 TC 35 Z9 36 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JUN PY 1993 VL 100 IS 6 BP 790 EP 794 DI 10.1111/1523-1747.ep12476573 PG 5 WC Dermatology SC Dermatology GA LE329 UT WOS:A1993LE32900013 PM 8388427 ER PT J AU HE, XS LEE, KS WEINBERGER, D DECOSTA, BR AF HE, XS LEE, KS WEINBERGER, D DECOSTA, BR TI SYNTHESIS OF A NOVEL I-123 LABELED DERIVATIVE OF GBR12783, A POTENTIAL AGENT FOR SPECT IMAGING OF DOPAMINE-REUPTAKE SITES SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE [I-123]1-[2-(DIPHENYLMETHOXY)ETHYL]-4-[3-(M-IODOPHENYL)-2-PROPENYL]PIPER AZINE ([I-123]2), SPECT, DOPAMINE REUPTAKE, ORGANOTIN, 1-[2-(DIPHENYLMETHOXY)ETHYL]-4-[3-[(M-(TRIBUTYL STANNYL)PHENYL]-2-PROPENYL]PIPERAZINE (6) ID NUCLEUS ACCUMBENS; PHENCYCLIDINE; COCAINE; HYPERACTIVITY; LESIONS; BINDING; COMPLEX; SYSTEM AB [I-123]-[2-(Diphenylmethoxy)ethyl]-4-[3-(m-iodophenyl)-2-propenyl]piperazine ([I-123]2), a potential SPECT imaging agent for dopamine reuptake sites was efficiently synthesized in 4 steps from 1-[2-(diphenylmethoxy)ethyl]piperazine (3). A key step in the synthesis was the selective AlH3-mediated reduction of 1-[2-(diphenylmethoxy)ethyl]-4-[m-bromocinnamoyl] piperazine (4) to 1-[2-(diphenylmethoxy)ethyl]-4-[3-(m-bromophenyl)-2-propenyl]piperazine (5). The 1231 label of [I-123]2 was introduced in the final step in up to 90% radiochemical yield by treatment of the organotin precursor 1-[2-(diphenylmethoxy)ethyl]-4-[3-[(m-(tributyl stannyl)phenyl]-2-propenyl]piperazine (6) with Na I-123 in aqueous CH3CO3H. C1 NIMH,CLIN BRAIN DISORDERS,WASHINGTON,DC 20032. RP HE, XS (reprint author), NIDDKD,MED CHEM LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 19 TC 4 Z9 4 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0362-4803 J9 J LABELLED COMPD RAD JI J. Label. Compd. Radiopharm. PD JUN PY 1993 VL 33 IS 6 BP 493 EP 500 DI 10.1002/jlcr.2580330607 PG 8 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA LE139 UT WOS:A1993LE13900006 ER PT J AU CHANNING, MA SIMPSON, N AF CHANNING, MA SIMPSON, N TI RADIOSYNTHESIS OF 1-[C-11] POLYHOMOALLYLIC FATTY-ACIDS SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE 1-[C-11] LABELED FATTY ACID; 1-[C-11]ARACHIDONIC ACID; 1-[C-11]DOCOSA-HEXAENOIC ACID; RADICAL CHAIN DECARBOXYLATION BROMINATION; (ALL Z)-1-BROMONONADECA-4,7,10,13-TETRAENE; (ALL Z)-1-BROMOHENEICOSA-3,6,9,12,15,18-HEXAENE ID UNANESTHETIZED RATS; ARACHIDONIC-ACID; PALMITIC ACID; BRAIN AB A facile retro-synthesis involving the radical chain decarboxylation of the N-hydroxypyridine-2-thione esters of both arachidonic and docosahexaenoic acid was utilized to synthesize (all Z)-1-bromononadeca-4,7,10,13-tetraene, and (all Z)-1-bromoheneicosa-3,6,9,12,15,18-hexaene in 60% overall yield. The corresponding polyhomoallylic magnesium bromides were carbonated with [C-11]CO2 to afford the 1-[C-11]polyhomoallylic labeled fatty acids in good yield in less than 35 minutes. The final radiochemical purities were found to be in excess of 95% by radio-HPLC. RP CHANNING, MA (reprint author), NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT PET,RADIOCHEM SECT,BETHESDA,MD 20892, USA. NR 15 TC 31 Z9 31 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0362-4803 J9 J LABELLED COMPD RAD JI J. Label. Compd. Radiopharm. PD JUN PY 1993 VL 33 IS 6 BP 541 EP 546 DI 10.1002/jlcr.2580330611 PG 6 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA LE139 UT WOS:A1993LE13900010 ER EF