FN Thomson Reuters Web of Science™ VR 1.0 PT J AU SHIMIZU, Y SHAW, S GRABER, N GOPAL, TV HORGAN, KJ VANSEVENTER, GA NEWMAN, W AF SHIMIZU, Y SHAW, S GRABER, N GOPAL, TV HORGAN, KJ VANSEVENTER, GA NEWMAN, W TI ACTIVATION-INDEPENDENT BINDING OF HUMAN-MEMORY T-CELLS TO ADHESION MOLECULE ELAM-1 SO NATURE LA English DT Article ID HELPER-INDUCER; ENDOTHELIAL-CELLS; LYMPHOCYTES; RECEPTOR; PROTEINS; LFA-1; ADHESIVENESS; ICAM-1 AB THE induction of an ensemble of adhesion molecules on endothelial cells by inflammatory cytokines is likely to be crucial to the differential migration of T-lymphocyte subsets into inflammatory sites. Two molecular pathways involving the VLA-4 and LFA-1 integrins are known to mediate T-cell adhesion to activated endothelium 1-4. Here we show that a third pathway involving the rapidly inducible endothelial cell-surface adhesion molecule ELAM-1 (refs 5, 6) contributes to the binding of resting CD4+ T cells to IL-1-induced human endothelial cells. All three pathways contribute to the greater adhesion to endothelium of memory T cells than naive T cells. There are two unique features of T-cell adhesion to purified ELAM-1: first, ELAM-1 exclusively mediates adhesion of memory T cells; second, memory T-cell binding to ELAM-1 is independent of acute activation events that regulate integrin-mediated adhesion 7,8. Thus, ELAM-1 may be of primary importance in the initial attachment of memory T cells to inflamed endothelium in vivo and to the preferential migration of memory T cells into tissue and inflammatory sites. C1 OTSUKA AMER PHARMACEUT INC,DEPT IMMUNOL,ROCKVILLE,MD 20850. OTSUKA AMER PHARMACEUT INC,DEPT MOLEC BIOL,ROCKVILLE,MD 20850. RP SHIMIZU, Y (reprint author), NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892, USA. OI Shimizu, Yoji/0000-0001-9760-0288 NR 34 TC 385 Z9 385 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 28 PY 1991 VL 349 IS 6312 BP 799 EP 802 DI 10.1038/349799a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EZ666 UT WOS:A1991EZ66600059 PM 1705667 ER PT J AU KLEBANOFF, MA SHIONO, PH RHOADS, GG AF KLEBANOFF, MA SHIONO, PH RHOADS, GG TI OUTCOMES OF PREGNANCY IN RESIDENT PHYSICIANS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID PRETERM LABOR C1 CTR FUTURE CHILDREN,LOS ALTOS,CA 94022. UNIV MED & DENT NEW JERSEY,PISCATAWAY,NJ 08854. RP KLEBANOFF, MA (reprint author), NICHHD,BETHESDA,MD 20892, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 28 PY 1991 VL 324 IS 9 BP 631 EP 631 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EY886 UT WOS:A1991EY88600016 ER PT J AU HORN, VJ SHEEHY, PA GOODMAN, MB AMBUDKAR, IS AF HORN, VJ SHEEHY, PA GOODMAN, MB AMBUDKAR, IS TI ACTIVATION OF THE INOSITOL TRISPHOSPHATE 2ND MESSENGER SYSTEM BY CAMP IN A MOUSE FIBROBLAST CELL-LINE SO MOLECULAR AND CELLULAR BIOCHEMISTRY LA English DT Article DE CAMP; INOSITOL TRISPHOSPHATE; CALCIUM MOBILIZATION; FIBROBLASTS; RECEPTOR CROSS-TALK ID CROSS-TALK; CYCLIC-AMP; CALCIUM; MOBILIZATION; STIMULATION; EXPRESSION; HYDROLYSIS; RECEPTORS AB Intracellular Ca2+ mobilization events were assessed in mouse L cells, which contain native prostaglandin E1 receptors and transfected human beta-2 adrenergic receptors. Both Fura2 (single cell measurements) and Quin 2, (cuvette assays) were used to determine [Ca2+]i levels. Our results demonstrate that in the transfected cells there is a dose-dependent increase in [Ca2+]i in response to isoproterenol (0.1 nM-100 nM), which is inhibited by the beta-adrenergic antagonist, propranolol, and is a result of intracellular Ca2+ release. [Ca2+]i in these cells was also increased by prostaglandin E1, 8 bromo cyclic AMP, and aluminum fluoride. Both 8 bromo cAMP and isoproterenol induced a rapid increase in the levels of IP1, IP2, and IP3. The data presented demonstrate that the elevation of intracellular cyclic AMP induces an increase in IP3 production which leads to an elevation in [Ca2+]i. We propose that this cyclic AMP dependent activation of the IP3 generating system occurs at a post-receptor site. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BLDG 10,ROOM 1A05,BETHESDA,MD 20892. NINCDS,NEUROPHYSIOL LAB,BETHESDA,MD 20892. NR 18 TC 4 Z9 4 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0300-8177 J9 MOL CELL BIOCHEM JI Mol. Cell. Biochem. PD FEB 27 PY 1991 VL 101 IS 1 BP 43 EP 49 PG 7 WC Cell Biology SC Cell Biology GA EY404 UT WOS:A1991EY40400005 PM 1849229 ER PT J AU HARRINGTON, MA SLEIGHT, AJ PITHA, J PEROUTKA, SJ AF HARRINGTON, MA SLEIGHT, AJ PITHA, J PEROUTKA, SJ TI STRUCTURAL DETERMINANTS OF 5-HT1A VERSUS 5-HT1D RECEPTOR-BINDING SITE SELECTIVITY SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE 5-HT1A RECEPTORS; 5-HT1D RECEPTORS; STRUCTURE-ACTIVITY; ADENYLATE CYCLASE ID STIMULATED ADENYLATE-CYCLASE; RECOGNITION SITES; BRAIN MEMBRANES; MEDIATED INHIBITION; RADIOLIGAND BINDING; SEROTONIN RECEPTORS; MOLECULAR PHARMACOLOGY; RAT HIPPOCAMPUS; BOVINE BRAIN; GUINEA-PIG AB A structure-activity analysis was used to identify selective 5-HT1A versus 5-HT1D receptor agents. An analysis of published data identified 13 drugs which display nanomolar affinity for the 5-HT1A receptor and that have been analyzed at 5-HT1D receptor binding sites. Four agents display greater-than-or-equal-to 100-fold selectivity for the 5-HT1A receptor. Two structural features were identified which hypothetically result in selectivity for 5-HT1A versus 5-HT1D binding sites. The linkage of an indole ring to a basic nitrogen atom via the 4 position on the indole ring or the absence of an indole ring are two features which lower the affinity for the 5-HT1D receptor, but do not necessarily lower the affinity for the 5-HT1A receptor. A series of 7 agents (5 indoles, 2 quinolines) was identified which met these hypothetical selectivity criteria. These compounds were then analyzed in radioligand binding studies. These 7 agents display affinities of 1.3 - 170 nM for the 5-HT1A receptor binding site, and 1 800 - 13 000 nM for the 5-HT1D receptor binding site. All 7 agents display greater-than-or-equal-to 47-fold selectivity for the 5-HT1A versus 5-HT1D site and 4 of the agents are > 100-fold selective. Compound No. 1 (N,N'-bis[3-(4-indolyloxy)-2-hydroxypropyl]-(Z)-1,8-diamino-p-menthane) and compound No. 2 (N8-[3-(4-indolyloxy)-2-hydroxypropyl]-N1-(propioloyl)-(Z)-1,8-diamino-p-menthane) are the most selective agents yet described for 5-HT1A versus 5-HT1D receptor binding sites. Moreover, compound No. 1 displays agonist activity in inhibiting forskolin-stimulated adenylate cyclase activity in rat hippocampus, while compound No. 2 antagonizes the effect of 8-OH-DPAT on 5-HT1A-mediated adenylate cyclase activity in the system. These data indicate that a comparative structure-activity analysis can be an effective technique for the identification of potent and selective receptor agents. C1 NIA,BALTIMORE,MD 21224. RP PEROUTKA, SJ (reprint author), STANFORD UNIV,MED CTR,SCH MED,DEPT NEUROL,STANFORD,CA 94305, USA. FU NIMH NIH HHS [MH 17047-06]; NINDS NIH HHS [NS 12151-15] NR 40 TC 13 Z9 13 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 FEB 26 PY 1991 VL 194 IS 1 BP 83 EP 90 DI 10.1016/0014-2999(91)90127-C PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FA847 UT WOS:A1991FA84700013 PM 2060596 ER PT J AU TELLA, SR SCHINDLER, CW GOLDBERG, SR AF TELLA, SR SCHINDLER, CW GOLDBERG, SR TI RAPID SENSITIZATION TO THE CARDIOVASCULAR EFFECTS OF COCAINE IN RATS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note DE COCAINE; BLOOD PRESSURE; HEART RATE; SENSITIZATION; CARDIOVASCULAR TOXICITY; (RAT) ID MICE AB Effects of repeated daily administrations of cocaine on blood pressure and heart rate were studied in conscious rats. Cocaine (0.03-3.0 mg/kg i.v.) increased blood pressure and heart rate the first time it was administered (day 1) However, the magnitude and duration of the increases in blood pressure caused by cocaine (0.1-3.0 mg/kg) dramatically increased on day 2 and remained (except 1.0 mg/kg dose) at these levels through day 5. Following two drug-free days (days 6 and 7), the increase in blood pressure caused by cocaine (0.1, 0.3 and 3.0 mg/kg) on day 8 was still elevated. Unlike blood pressure, no enhancement in heart rate response to cocaine was observed. C1 GEORGETOWN UNIV,SCH MED,DEPT PHARMACOL,WASHINGTON,DC 20007. UNIV MARYLAND,DEPT PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21201. RP TELLA, SR (reprint author), NIDA,ADDICT RES CTR,PRECLIN PHARMACOL BRANCH,BEHAV PHARMACOL & GENET LAB,POB 5180,BALTIMORE,MD 21224, USA. NR 10 TC 21 Z9 21 U1 0 U2 1 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 FEB 26 PY 1991 VL 194 IS 1 BP 119 EP 122 DI 10.1016/0014-2999(91)90133-B PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FA847 UT WOS:A1991FA84700019 PM 2060588 ER PT J AU MARINI, A NOVELLI, A AF MARINI, A NOVELLI, A TI DL-THREO-3-HYDROXYASPARTATE REDUCES NMDA RECEPTOR ACTIVATION BY GLUTAMATE IN CULTURED NEURONS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note ID ASPARTATE C1 NINCDS,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892. RI Novelli, Antonello/P-7476-2015 OI Novelli, Antonello/0000-0002-0129-8350 NR 5 TC 19 Z9 19 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 FEB 26 PY 1991 VL 194 IS 1 BP 131 EP 132 DI 10.1016/0014-2999(91)90136-E PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FA847 UT WOS:A1991FA84700022 PM 1676372 ER PT J AU BOJA, JW PATEL, A CARROLL, FI RAHMAN, MA PHILIP, A LEWIN, AH KOPAJTIC, TA KUHAR, MJ AF BOJA, JW PATEL, A CARROLL, FI RAHMAN, MA PHILIP, A LEWIN, AH KOPAJTIC, TA KUHAR, MJ TI [I-125] RTI-55 - A POTENT LIGAND FOR DOPAMINE TRANSPORTERS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,POB 5180,BALTIMORE,MD 21224. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. FU NIDA NIH HHS [DA05477] NR 4 TC 160 Z9 162 U1 0 U2 1 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 FEB 26 PY 1991 VL 194 IS 1 BP 133 EP 134 DI 10.1016/0014-2999(91)90137-F PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FA847 UT WOS:A1991FA84700023 PM 2060590 ER PT J AU MOODY, EJ LEWIN, AH DECOSTA, BR RICE, KC SKOLNICK, P AF MOODY, EJ LEWIN, AH DECOSTA, BR RICE, KC SKOLNICK, P TI SITE-SPECIFIC ACYLATION OF GABA-GATED CL- CHANNELS - EFFECTS ON CL-36- UPTAKE SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION LA English DT Article DE TERT-BUTYLBICYCLOPHOSPHOROTHIONATE (TBPS); ACYLATING AGENTS; TERT-BUTYLBICYCLOORTHOBENZOATE (TBOB); CL- UPTAKE; SYNAPTONEUROSOMES; MUSCIMOL ID GAMMA-AMINOBUTYRIC ACID; RAT-BRAIN SYNAPTONEUROSOMES; REGULATED CHLORIDE IONOPHORE; BENZODIAZEPINE RECEPTORS; BINDING; CONVULSANTS; BARBITURATE; MECHANISMS; MODULATION AB Radioligand binding studies indicate that p-isothiocyanato-t-butylbicycloorthobenzoate (p-NCS-TBOB) specifically acylates GABA-gated chloride channels. Preincubation of synaptoneurosomes with p-NCS-TBOB followed by washing resulted in a concentration dependent (63-500 nM) inhibition of both muscimol-stimulated chloride uptake and [355]t-butylbi-cyclophosphorothionate (TBPS) binding. The extent of acylation (assessed by inhibition of [S-35]TBPS binding) was highly correlated (r = 0.89; p < 0.001) with the inhibition of muscimol-stimulated Cl- uptake. Neither basal Cl- uptake nor [H-3]muscimol binding to GABA(A) receptors were affected by p-NCS-TBOB. Preincubation with the nonacylating 'cage' convulsant t-butylbicycloorthobenzoate (500 nM) followed by washing had no effect on either muscimol-stimulated Cl- uptake or [S-35]TBPS binding. These findings indicate that p-NCS-TBOB interferes with the efficacy of muscimol promoted channel openings, but does not affect the recognition qualities of GABA(A) receptors, p-NCS-TBOB should prove useful in electrophysiological and biochemical studies examining the properties of GABA-gated Cl- channels. C1 NIDDK,NEUROSCI LABS,BLDG 8,ROOM 111,BETHESDA,MD 20892. NIDDK,MED CHEM LABS,BETHESDA,MD 20892. NR 24 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0922-4106 J9 EUR J PHARM-MOLEC PH JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect. PD FEB 25 PY 1991 VL 206 IS 2 BP 113 EP 118 DI 10.1016/0922-4106(91)90019-E PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FG903 UT WOS:A1991FG90300005 PM 1712308 ER PT J AU MANJI, HK CHEN, G BITRAN, JA GUSOVSKY, F POTTER, WZ AF MANJI, HK CHEN, G BITRAN, JA GUSOVSKY, F POTTER, WZ TI CHRONIC EXPOSURE OF C6 GLIOMA-CELLS TO DESIPRAMINE DESENSITIZES BETA-ADRENOCEPTORS, BUT INCREASES KL KH RATIO SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION LA English DT Note DE DESPIRAMINE; BETA-ADRENOCEPTORS; CYCLIC AMP; KL KH; C6 GLIOMA ID COUPLED ADENYLATE-CYCLASE; RECEPTOR AB Incubation of rat glioma C6 cells with 10-mu-M desipramine for five days in vitro resulted in a 31% reduction of beta-adrenoceptors and a 38% reduction in isoproterenol-stimulated cyclic AMP accumulation. In contrast, forskolin or cholera toxin-stimulated cyclic AMP was unaffected by desipramine. Surprisingly, the beta-adrenoceptor desensitization was accompanied by an increase in the ratio of dissociation constants (K(L)/K(H)) for the low and high affinity states of the beta-adrenoceptor respectively and supports the concept of a complex interaction between the receptor and G(s) protein. C1 NIADDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. RP MANJI, HK (reprint author), NIMH,CLIN NEUROSCI BRANCH,CLIN PHARMACOL SECT,BLDG 10,ROOM 2D46,BETHESDA,MD 20892, USA. RI Chen, Guang/A-2570-2017 NR 11 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0922-4106 J9 EUR J PHARM-MOLEC PH JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect. PD FEB 25 PY 1991 VL 206 IS 2 BP 159 EP 162 DI 10.1016/0922-4106(91)90025-D PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FG903 UT WOS:A1991FG90300011 PM 1648502 ER PT J AU TOZSER, J GUSTCHINA, A WEBER, IT BLAHA, I WONDRAK, EM OROSZLAN, S AF TOZSER, J GUSTCHINA, A WEBER, IT BLAHA, I WONDRAK, EM OROSZLAN, S TI STUDIES ON THE ROLE OF THE S4 SUBSTRATE BINDING-SITE OF HIV PROTEINASES SO FEBS LETTERS LA English DT Article DE HIV PROTEINASE; TYPE-1 AND TYPE-2; OLIGOPEPTIDE SUBSTRATE; ENZYME KINETICS; VARIATE NORMAL DISTRIBUTIONS ID IMMUNODEFICIENCY VIRUS PROTEASE; CHEMICAL SYNTHESIS; EXPRESSION; GENE AB Kinetic analysis of the hydrolysis of the peptide H-Val-Ser-Gln-Asn-Tyr*Pro-Ile-Val-Gln-NH2 and its analogs obtained by varying the length and introducing substitutions at the P4 site was carried out with both HIV-1 and HIV-2 proteinases. Deletion of the terminal Val and Gln had only moderate effect on the substrate hydrolysis, while the deletion of the P4, Ser as well as P'3 Val greatly reduced the substrate hydrolysis. This is predicted to be due to the loss of interactions between main chains of the enzyme and the substrate. Substitution of the P4 Ser by amino acids having high frequency of occurrence in beta-turns resulted in good substrates, while large amino acids were unfavorable in this position. The two proteinases acted similarly, except for substrates having Thr, Val and Leu substitutions, which were better accommodated in the HIV-2 substrate binding pocket. C1 NCI, FREDERIC CANC RES & DEV CTR, MOLEC VIROL & CARCINOGENESIS LAB, POB B, FREDERICK, MD 21702 USA. NCI, FREDERIC CANC RES & DEV CTR, CRYSTALLOG LAB, FREDERICK, MD 21702 USA. RI Tozser, Jozsef/A-7840-2008; OI Tozser, Jozsef/0000-0003-0274-0056; Tozser, Jozsef/0000-0001-5076-8729 FU NCI NIH HHS [N01-CO-74101] NR 27 TC 58 Z9 58 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 EI 1873-3468 J9 FEBS LETT JI FEBS Lett. PD FEB 25 PY 1991 VL 279 IS 2 BP 356 EP 360 DI 10.1016/0014-5793(91)80186-7 PG 5 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FA591 UT WOS:A1991FA59100046 PM 2001747 ER PT J AU IWASAKI, M JUVONEN, R LINDBERG, R NEGISHI, M AF IWASAKI, M JUVONEN, R LINDBERG, R NEGISHI, M TI ALTERATION OF HIGH AND LOW-SPIN EQUILIBRIUM BY A SINGLE MUTATION OF AMINO ACID-209 IN MOUSE CYTOCHROMES-P450 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID AXIAL LIGAND TRANS; TESTOSTERONE 16-ALPHA-HYDROXYLASE; STEROID 15-ALPHA-HYDROXYLASE; SUBSTRATE-SPECIFICITY; II P-45015-ALPHA; LIVER; IDENTIFICATION; OXYGEN; GENE; CYTOCHROME-P-450 AB The identities of the amino acid at position 209 are most critical in determining specific coumarin 7- and steroid 15-alpha-hydroxylase activity in P450coh and P450(15-alpha), respectively. This system, therefore, provides us with an excellent model to study the structural basis for P450 specificity as a monooxygenase. We expressed in Saccharomyces cerevisiae a series of the mutated P450s in which residue 209 was substituted with the various amino acids and characterized the spectral property and hydroxylase activity of these mutated P450s. The positioning of a hydrophobic residue including Phe, Leu, and Val at position 209 resulted in shifting the P450 to the high-spin state, while a charged amino acid such as Lys or Asp produced the low-spin form. Moreover, a P450 with Asn or Gly in this position exhibited spectra indicating a mixture of the high- and low-spin forms. This spin alteration, depending upon the hydrophobicity and size of residue at position 209, indicates that this position is likely to reside close to the sixth axial ligand on the distal surface of the heme in these P450s. This proximity of residue 209 to the ligand may explain the critical role of this residue in determining the hydroxylase specificity and activity of these P450s. RP IWASAKI, M (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,PHARMACOGENET SECT,RES TRIANGLE PK,NC 27709, USA. NR 22 TC 56 Z9 56 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1991 VL 266 IS 6 BP 3380 EP 3382 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200007 PM 1995602 ER PT J AU STEINBERG, RA GORMAN, KB OGREID, D DOSKELAND, SO WEBER, IT AF STEINBERG, RA GORMAN, KB OGREID, D DOSKELAND, SO WEBER, IT TI MUTATIONS THAT ALTER THE CHARGE OF TYPE-I REGULATORY SUBUNIT AND MODIFY ACTIVATION PROPERTIES OF CYCLIC AMP-DEPENDENT PROTEIN-KINASE FROM S49 MOUSE LYMPHOMA-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CAMP-BINDING DOMAINS; PREDICTED STRUCTURES; NUCLEOTIDE-BINDING; CYTOSINE RESIDUES; ESCHERICHIA-COLI; GENE-EXPRESSION; MOLECULAR-BASIS; POINT MUTATION; SITE-A; AMPLIFICATION AB Mutations in regulatory (R) subunit of cAMP-dependent protein kinase were analyzed from cAMP-resistant mutants of S49 mouse lymphoma cells by direct sequencing of amplified regions of mutant R subunit cDNAs. Eight distinct single base-change lesions were identified in 24 independent mutants that were hemizygous for expression of mutant R subunits with altered protein charge. CG --> TA transitions predominated, but AT --> GC transitions and GC --> TA transversions were also observed. Four of five spontaneous mutants had identical C --> T transitions at CG causing substitution of Trp for Arg-334. Sites mutated in isolates obtained after mutagenesis with ethyl methane-sulfonate or N-methyl-N'-nitrosoguanidine were more varied. Six of the lesions (two in binding site A and four in site B) were at amino acid residues that are highly conserved among cAMP-binding sites of R subunits and the Escherichia coli catabolite activator protein. These mutations all either prevented or strongly hindered binding of cyclic nucleotides to the mutated site. One of the remaining lesions (at Arg-242) also prevented cyclic nucleotide binding to the mutated binding site; the other (at Gly-170) had only minimal effects on binding of cyclic nucleotides but, nevertheless, increased the apparent constant for cAMP-dependent kinase activation. These results are discussed with reference to a model for the cAMP-binding sites of R subunit based on the crystal structure of the E. coli catabolite activator protein. C1 UNIV BERGEN,INST ANAT,CELL BIOL RES GRP,N-5009 BERGEN,NORWAY. NCI,FREDERICK CANC RES FACIL,CRYSTALLOG LAB,ADV BIOSCI LABS,BASIC RES PROGRAM,FREDERICK,MD 21701. RP STEINBERG, RA (reprint author), UNIV OKLAHOMA,HLTH SCI CTR,DEPT BIOCHEM & MOLEC BIOL,POB 26901,OKLAHOMA CITY,OK 73190, USA. FU NIDDK NIH HHS [DK37583]; PHS HHS [N01-C01-74101] NR 39 TC 29 Z9 30 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1991 VL 266 IS 6 BP 3547 EP 3553 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200034 PM 1847378 ER PT J AU MOULD, AP KOMORIYA, A YAMADA, KM HUMPHRIES, MJ AF MOULD, AP KOMORIYA, A YAMADA, KM HUMPHRIES, MJ TI THE CS5 PEPTIDE IS A 2ND SITE IN THE IIICS REGION OF FIBRONECTIN RECOGNIZED BY THE INTEGRIN ALPHA-4-BETA-1 - INHIBITION OF ALPHA-4-BETA-1 FUNCTION BY RGD PEPTIDE HOMOLOGS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ARG-GLY-ASP; HUMAN-PLASMA FIBRONECTIN; CELL-BINDING DOMAIN; CONNECTING SEGMENT; ADHESION RECEPTOR; DIVALENT-CATIONS; MESSENGER-RNAS; BETA-SUBUNIT; GAMMA-CHAIN; IDENTIFICATION AB The alternatively spliced type III connecting segment (IIICS) region of fibronectin contains two distinct sites that support the adhesion of melanoma cells. These sites are contained within the synthetic peptides CS1 and CS5 (residues 1-25 and 90-109 of the IIICS, respectively). Recently, the cellular receptor for the CS1 site has been identified as the integrin heterodimer alpha-4-beta-1. In this report, we have investigated the role of the CS5 sequence in melanoma cell adhesion and the identity of its receptor. Adhesion to CS5, when presented to cells as an immobilized IgG conjugate, was blocked by antifunctional monoclonal antibodies directed against either the alpha-4 or beta-1-integrin subunits, but not by antibodies against other subunits, implying that alpha-4-beta-1 is also the receptor for CS5. In peptide inhibition experiments, CS5 was inhibitory for melanoma cell spreading on both CS5-IgG and CS1-IgG conjugates; conversely, CS1 inhibited spreading on both CS1-IgG and CS5-IgG. In both cases, peptide inhibition could be outcompeted by increasing the concentration of substrate-bound conjugate. These results suggest that CS1 and CS5 are recognized by the same or overlapping sites on alpha-4-beta-1. The minimal active sequence within CS5, the tetrapeptide Arg-Glu-Asp-Val (REDV), is somewhat related to the Arg-Gly-Asp-Ser (RGDS) sequence that represents a major active site in the central cell-binding domain (CCBD) of fibronectin. When RGDS peptide homologues were tested for their ability to inhibit spreading of melanoma cells on CS1- and CS5-IgG conjugates, GRGDS, GRGES, and REDV were found to be inhibitory, while GRDGS had no effect. In contrast, spreading on a fibronectin fragment containing the CCBD was inhibited by GRGDS only. GRGDS was also able to elute alpha-4-beta-1 specifically from a CS1 affinity column, confirming directly that alpha-4-beta-1-IIICS interactions are sensitive to peptides containing this recognition motif. Because the minimal active sequence within CS1 is the tripeptide Leu-Asp-Val (LDV; Komoriya et al., manuscript submitted for publication), these findings together define a new adhesive recognition sequence, X-Asp-Y, used by alpha-4-beta-1 for binding to fibronectin. The central aspartate residue in this tripeptide is almost always essential, but some flexibility in the amino acid residues at X (glycine, leucine, or glutamic acid) and Y (serine or valine) is tolerated. Potential models for the interaction of the IIICS region with alpha-4-beta-1 are discussed. C1 NCI,MOLEC BIOL LAB,MEMBRANE BIOCHEM SECT,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,CELL BIOL LAB,BETHESDA,MD 20892. RP MOULD, AP (reprint author), UNIV MANCHESTER,SCH MED,DEPT BIOCHEM & MOLEC BIOL,MANCHESTER M13 9PT,LANCS,ENGLAND. FU Wellcome Trust NR 56 TC 211 Z9 212 U1 1 U2 6 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 FEB 25 PY 1991 VL 266 IS 6 BP 3579 EP 3585 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200038 PM 1750929 ER PT J AU IKEDASAITO, M SHELLEY, DA LU, L BOOTH, KS CAUGHEY, WS KIMURA, S AF IKEDASAITO, M SHELLEY, DA LU, L BOOTH, KS CAUGHEY, WS KIMURA, S TI SALICYLHYDROXAMIC ACID INHIBITS MYELOPEROXIDASE ACTIVITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SPLEEN GREEN HEMEPROTEIN; INTESTINAL PEROXIDASE; LIGAND-BINDING; LACTOPEROXIDASE; SPECTROSCOPY; CHLORIDE; DIFFERENCE; COMPLEXES; SITE AB Salicylhydroxamic and benzohydroxamic acids were found to bind to the resting state of myeloperoxidase and inhibit ligand binding to the heme iron. An ionizable group on the enzyme with pK(a) = 4 affects salicylhydroxamic acid binding; binding occurs when this group is not protonated. The binding of the heme iron ligands (e.g. cyanide, nitrite, and chloride) is probably controlled by the same ionizable group. The equilibrium dissociation constant of the salicylhydroxamic acid-myeloperoxidase complex is about 2 x 10(-6) M, and the association rate constant is 7.4 x 10(6) M-1.S-1. Salicylhydroxamic acid serves as a donor to the higher oxidation state of myeloperoxidase and thereby inhibits guaiacol oxidation. Salicylhydroxamic acid was also found to bind to intestinal peroxidase and lactoperoxidase. Salicylhydroxamic acid binding to all three mammalian peroxidases was about 3 orders of magnitude stronger than benzohydroxamic acid binding. We conclude that the salicylhydroxamic and benzohydroxamic acids bind in the distal heme cavity of these peroxidases and interact with the heme ligand binding site. C1 COLORADO STATE UNIV,DEPT BIOCHEM,FT COLLINS,CO 80523. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP IKEDASAITO, M (reprint author), CASE WESTERN RESERVE UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,CLEVELAND,OH 44106, USA. RI Ikeda-Saito, Masao/A-5992-2008; Ikeda-Saito, Masao/K-2703-2015 FU NHLBI NIH HHS [HL15890]; NIGMS NIH HHS [GM 29492] NR 25 TC 53 Z9 53 U1 1 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 FEB 25 PY 1991 VL 266 IS 6 BP 3611 EP 3616 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200042 PM 1847381 ER PT J AU KAPLAN, O COHEN, JS AF KAPLAN, O COHEN, JS TI LYMPHOCYTE-ACTIVATION AND PHOSPHOLIPID PATHWAYS - P-31 MAGNETIC-RESONANCE STUDIES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TUMOR-INFILTRATING LYMPHOCYTES; HUMAN PERIPHERAL LYMPHOCYTES; PROTEIN KINASE-C; PHOSPHATIDYLCHOLINE BIOSYNTHESIS; FRIEND-ERYTHROLEUKEMIA; HELA-CELLS; INTERLEUKIN-2; STIMULATION; MEMBRANE; METABOLISM AB P-31 NMR spectra of perfused lymphocytes, embedded in alginate capsules and activated by interleukin-2, were remarkably different from those of control lymphocytes. The main differences were the appearance and gradual increase in phosphodiester signals, glycerophosphocholine and glycerophosphoethanolamine. These metabolic changes also occurred following perfusion with phorbol ester and after incubation with phytohemagglutinin (PHA) and were not dependent on a special growth medium. Nifedipine, a calcium channel blocking drug, inhibited the effects of phytohemagglutinin, but not of interleukin-2. There were no NMR spectral differences between peripheral lymphocytes, stimulated for 3 weeks, and tumor-infiltrating lymphocytes. Thus, sustained accelerated turnover of phosphatidylcholine and phosphatidylethanolamine is an inherent feature of the activation process. P-31 NMR spectra of lymphocytes are characterized by a low signal of phosphocholine. Perfusion studies with high concentrations of choline and the use of dapsone, an inhibitor of cytidylyltransferase, indicated that choline kinase plays a key role in regulating phosphatidylcholine synthesis in human lymphocytes. C1 NCI,DIV CANC TREATMENT,MED BRANCH,BETHESDA,MD 20892. NR 54 TC 22 Z9 22 U1 2 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 FEB 25 PY 1991 VL 266 IS 6 BP 3688 EP 3694 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200053 PM 1995623 ER PT J AU AMBRUS, JL CHESKY, L CHUSED, T YOUNG, KR MCFARLAND, P AUGUST, A BROWN, EJ AF AMBRUS, JL CHESKY, L CHUSED, T YOUNG, KR MCFARLAND, P AUGUST, A BROWN, EJ TI INTRACELLULAR SIGNALING EVENTS ASSOCIATED WITH THE INDUCTION OF PROLIFERATION OF NORMAL HUMAN LYMPHOCYTES-B BY 2 DIFFERENT ANTIGENICALLY RELATED HUMAN B-CELL GROWTH-FACTORS (HIGH-MOLECULAR-WEIGHT B-CELL GROWTH-FACTOR (HMW-BCGF) AND THE COMPLEMENT FACTOR-BB) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-KINASE-C; NECROSIS FACTOR-ALPHA; DIACYLGLYCEROL PRODUCTION; INTERLEUKIN-2 RECEPTORS; MONOCLONAL-ANTIBODY; ACTIVATION; HYDROLYSIS; CALCIUM; EXPRESSION; LINE AB High molecular weight B cell growth factor (HMW-BCGF) and the complement component, Factor B, are antigenically related. HMW-BCGF and the physiologic Factor B activation fragment Bb, are both mitogenic for B lymphocytes and compete for binding to the B cell plasma membrane (Peters, M., Ambrus, J. L., Jr., Fauci, A., and Brown, E. (1988) J. Exp. Med. 168, 1225-1235). To understand which second messengers that occur after ligand-receptor interaction are associated with mitogenesis, we have examined the early signaling events after stimulation of activated B cells with these related growth factors. HMW-BCGF but not Bb increased [cAMP]i with a maximum between 45 and 60 min after stimulation. The increase in [cAMP]i was inhibited by indomethacin, suggesting that prostaglandin synthesis is involved in this response. Increase in [cAMP]i induced by HMW-BCGF, cholera toxin, or dibutyryl cAMP was associated with increased expression of the HMW-BCGF receptor, but there was no increase in proliferation of activated B cells when they were stimulated with cAMP agonists other than HMW-BCGF. These data suggest that cAMP is associated with regulation of receptor expression but is neither necessary nor sufficient for induction of proliferation. Both HMW-BCGF and Bb increased cellular levels of diacylglycerol and a water-soluble molecule which could be labeled with both [H-3]myoinositol and [C-14] glucosamine. However, only HMW-BCGF induced increases in intracellular calcium. Thus, two antigenically related B cell growth factors, HMW-BCGF and Bb, produce overlapping but distinct sets of second messengers after incubation with Sac-activated B cells. Since both induced increases in diacylglycerol and water-soluble inositol, one or both of these molecules may be involved in the proliferative signal generated by the related growth factors. In contrast, the increase in [cAMP]i caused by HMW-BCGF but not Bb is involved in the signal to increase HMW-BCGF receptor expression, but is unrelated to proliferation. C1 MED UNIV S CAROLINA,CHARLESTON,SC 29425. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. UNIV ALABAMA,DIV PULM & CRIT CARE MED,BIRMINGHAM,AL 35294. WASHINGTON UNIV,ST LOUIS CHILDRENS HOSP,DIV NEWBORN MED,ST LOUIS,MO 63110. WASHINGTON UNIV,DEPT MED,DIV INFECT DIS,ST LOUIS,MO 63130. RP AMBRUS, JL (reprint author), WASHINGTON UNIV,JEWISH HOSP ST LOUIS,MED CTR,DEPT MED,DIV RHEUMATOL,660 S EUCLID,CAMPUS BOX 8045,ST LOUIS,MO 63110, USA. FU NIAID NIH HHS [AI-24674] NR 53 TC 22 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 FEB 25 PY 1991 VL 266 IS 6 BP 3702 EP 3708 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200055 PM 1847385 ER PT J AU THOMAS, DC ROBERTS, JD KUNKEL, TA AF THOMAS, DC ROBERTS, JD KUNKEL, TA TI HETERODUPLEX REPAIR IN EXTRACTS OF HUMAN HELA-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DNA MISMATCH-REPAIR; BASE-PAIR MISMATCHES; ESCHERICHIA-COLI; SACCHAROMYCES-CEREVISIAE; MUTATIONAL SPECIFICITY; DIFFERENT EFFICIENCIES; POLYMERASES-ALPHA; PROTEIN BINDS; GENE; REPLICATION AB A general repair process for DNA heteroduplexes has been detected in HeLa cell extracts. Using a variety of M13mp2 DNA substrates containing single-base mismatches and extra nucleotides, extensive repair is observed after incubation with HeLa cell cytoplasmic extracts and subsequent transfection of bacterial cells with the treated DNA. Most, but not all, mispairs as well as two frameshift heteroduplexes are repaired efficiently. Parallel measurements of repair in HeLa extracts and in Escherichia coli suggest that repair specificities are similar for the two systems. The presence of a nick in the molecule is required for efficient repair in HeLa cell extracts, and the strand containing the nick is the predominantly repaired strand. Mismatch-dependent DNA synthesis is observed when radiolabeled restriction fragments, produced by reaction of the extract with heteroduplex and homoduplex molecules, are compared. Specific labeling of fragments, representing a region of approximately 1,000 base pairs and containing the nick and the mismatch, is detected for the heteroduplex substrate but not the homoduplex. The repair reaction is complete after 20 min and requires added Mg2+, ATP, and an ATP-regenerating system, but not dNTPs, which are present at sufficient levels in the extract. An inhibitor of DNA polymerase-beta, dideoxythymidine 5'-triphosphate, does not inhibit mismatch-specific DNA synthesis. Aphidicolin, an inhibitor of DNA polymerases-alpha, delta, and epsilon, inhibits both semiconservative replication and repair synthesis in the extract. Butylphenyl-dGTP also inhibits both replicative and repair synthesis but at a concentration known to inhibit DNA polymerase-alpha preferentially rather than delta or epsilon. This suggests that DNA polymerase-alpha may function in mismatch repair. C1 NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709. NR 57 TC 285 Z9 289 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 FEB 25 PY 1991 VL 266 IS 6 BP 3744 EP 3751 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200062 PM 1995629 ER PT J AU SCHREIBER, G METZGER, S AIZENMAN, E ROZA, S CASHEL, M GLASER, G AF SCHREIBER, G METZGER, S AIZENMAN, E ROZA, S CASHEL, M GLASER, G TI OVEREXPRESSION OF THE RELA GENE IN ESCHERICHIA-COLI SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RIBOSOMAL-RNA PROMOTERS; RATE-DEPENDENT REGULATION; ELONGATION-FACTOR-TU; GUANOSINE TETRAPHOSPHATE; INDIVIDUAL PROTEINS; STRINGENT RESPONSE; PPGPP; STRAINS; INVIVO; STARVATION AB Intracellular levels of guanosine 3', 5'-bispyrophosphate (ppGpp) governed by the relA gene are normally regulated by aminoacyl-tRNA availability for protein synthesis. An experimental system is described in which cellular levels of ppGpp are controlled instead by induction of plasmid pKK223-3 derivatives with the relA structural gene, or portions thereof, under control of the P(tac) promoter. In amino acid-rich media, isopropyl-l-thio-beta-D-galactopyranoside induction of transcription of the wild type relA gene in pSM10 yields about a 100-fold overexpression of a metabolically stable, full length (743 amino acid) RelA protein to levels approximating the number of cellular ribosomes. This overexpression is accompanied by a roughly parallel and relC-dependent elevation of ppGpp levels. Induction of a relA gene deletion mutant in pSM11 containing 455 amino-terminal amino acids results in much lower levels of expression of a metabolically unstable 55-kDa protein and elevated ppGpp levels that are almost equivalent to induced pSM10 and are relC-independent. Induction of a larger deletion in pSM12 containing 331 amino-terminal amino acids does not provoke ppGpp accumulation. We are able to elicit high levels of ppGpp without changing nutritional abundance and without massive overexpression of the RelA protein by inducing the metabolically unstable, truncated RelA protein. We find the effects of elevated ppGpp levels to include a slowing of growth, an inhibition of stable RNA accumulation, an inhibition of cellular rrn P1 promoter activities as measured by primer extension, and changes in the pattern of gene expression viewed by two-dimensional electrophoresis of cellular proteins. C1 NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. RP SCHREIBER, G (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT CELLULAR BIOCHEM,IL-91010 JERUSALEM,ISRAEL. FU NIGMS NIH HHS [GM25282] NR 45 TC 134 Z9 134 U1 0 U2 5 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 FEB 25 PY 1991 VL 266 IS 6 BP 3760 EP 3767 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200064 PM 1899866 ER PT J AU BUBB, MR LEWIS, MS KORN, ED AF BUBB, MR LEWIS, MS KORN, ED TI THE INTERACTION OF MONOMERIC ACTIN WITH 2 BINDING-SITES ON ACANTHAMOEBA ACTOBINDIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID F-ACTIN; POLYMERIZATION; INHIBITION; PROFILIN AB Actobindin was previously shown to be an 88-residue polypeptide (M(r) 9761) with an internal tandem repeat of 33-34 amino acids. Sedimentation equilibrium experiments have confirmed this M(r) for native actobindin. Pyreneglyoxal-labeled actobindin had a similar M(r) by sedimentation equilibrium analysis and bound to actin in a manner qualitatively similar to unmodified actobindin as determined by gel electrophoretic analysis of covalently cross-linked products. The stoichiometry of the actin-actobindin interaction was determined from the change in apparent M(r) of pyreneglyoxal-labeled actobindin in the presence of actin, as determined by scanning the ultracentrifuge cell at a wavelength that detected only the labeled protein. These data were consistent with the formation of a complex containing two actin and one actobindin molecules. The overall K(D) describing the binding of the first actin to either of the two sites on actobindin was 3.3-mu-M. The binding constant for the second actin suggested either negative cooperativity or inequality of the two actin-binding sites. Similar binding constants were obtained by analysis of the fluorescence enhancement that occurred when actobindin bound to actin labeled with either pyrene iodoacetamide or 4-(N-iodoacetoxyethyl-N-methyl)-7-nitrobenz-2-oxa-1,3-diazole. Cross-linking experiments with 1-ethyl-3-(3-dimethylaminopropyl)-carbodiimide and N-hydroxysulfosuccinimide qualitatively agreed with predictions made from a two-binding site model. Additionally, both the fluorescence and cross-linking experiments suggested that the interaction of the two actin molecules may contribute to the stability of the heterotrimeric complex. C1 NIH, NATL CTR RES RESOURCES, BIOMED ENGN & INSTRUMENTAT PROGRAM, BETHESDA, MD 20892 USA. RP NHLBI, CELL BIOL LAB, BETHESDA, MD 20892 USA. RI Korn, Edward/F-9929-2012 NR 14 TC 40 Z9 40 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 FEB 25 PY 1991 VL 266 IS 6 BP 3820 EP 3826 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200071 PM 1995634 ER PT J AU MANROW, RE SBURLATI, AR HANOVER, JA BERGER, SL AF MANROW, RE SBURLATI, AR HANOVER, JA BERGER, SL TI NUCLEAR TARGETING OF PROTHYMOSIN-ALPHA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMINO-ACID SEQUENCE; MONOCLONAL-ANTIBODY; ESCHERICHIA-COLI; MULTIDRUG RESISTANCE; BINDING-PROTEINS; P-GLYCOPROTEIN; CYTOCHALASIN-B; ALPHA GENE; TRANSPORT; LOCATION AB Prothymosin-alpha is a highly acidic protein which lacks an amino-terminal signal peptide, yet was once thought to be a precursor for thymosin-alpha-1, a putative peptide hormone secreted by the thymus. Here, two lines of evidence are presented that strongly implicate prothymosin-alpha as a nuclear protein: 1) in COS cells transfected with the human prothymosin-alpha gene copious amounts of prothymosin-alpha were present in sealed nuclei obtained by treating these cells with cytochalasin B and enucleating them centrifugally. 2) Constructs in which human prothymosin-alpha nucleic acid sequences were fused in-frame either near the amino terminus of the beta-galactosidase gene in pCH110 or at the carboxyl terminus, when expressed in COS cells, resulted in nuclear localization of the fusion protein; indirect immunofluorescence in situ was used as the assay. The basic cluster of amino acids at the carboxyl terminus of prothymosin-alpha, TKKQKT, has been identified as part of the nuclear targeting signal, whereas the basic cluster of amino acids situated within the thymosin-alpha-1 sequence at the amino terminus failed to effect nuclear transport. C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. RP MANROW, RE (reprint author), NCI,BIOCHEM LAB,GENES & GEN PROD SECT,BETHESDA,MD 20892, USA. NR 52 TC 114 Z9 114 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 FEB 25 PY 1991 VL 266 IS 6 BP 3916 EP 3924 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200085 PM 1899869 ER PT J AU ABBOTTS, J JAJU, M WILSON, SH AF ABBOTTS, J JAJU, M WILSON, SH TI THERMODYNAMICS OF A-G MISMATCH POLY(DG) SYNTHESIS BY HUMAN IMMUNODEFICIENCY VIRUS-1 REVERSE-TRANSCRIPTASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DNA-POLYMERASE-I; STEADY-STATE KINETICS; ESCHERICHIA-COLI; DEOXYRIBONUCLEIC-ACID; FIDELITY; MECHANISM; HIV-1; PROCESSIVITY; KLENOW; BETA AB Human immunodeficiency virus 1 (HIV-1) reverse transcriptase has been found to conduct error-prone synthesis on DNA and RNA templates. We find here that tolerance of an A:G mispair with poly(rA) as template is particularly strong, such that extensive poly(dG) synthesis is conducted. This type of extensive misincorporation is not observed with several reference DNA polymerases. Surprisingly, HIV reverse transcriptase processivity and k(cat) for dGMP misincorporation and normal dTMP incorporation are about the same. However, the K(m) value for dGTP in poly(dG) synthesis is approximately 1000-fold higher than the K(m) for dTTP in poly(dT) synthesis. Comparison of thermodynamic parameters for dGMP misincorporation and normal dNMP incorporation indicates a lower energy of activation for dGMP misincorporation than for normal dNMP incorporation. Entropy of activation (DELTA-S*) for normal dTMP incorporation is positive (approximately 10 cal/kmol), whereas DELTA-S* for dGMP misincorporation is negative (-36 cal/kmol). Since differences in DELTA-S* are usually considered to reflect differences in solvation for the transition state complex, these results are consistent with the interpretation that the active site of HIV reverse transcriptase is flexible enough to misincorporate dGMP without the usual dispersion of water molecules. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 42 TC 12 Z9 12 U1 1 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 FEB 25 PY 1991 VL 266 IS 6 BP 3937 EP 3943 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200087 PM 1704895 ER PT J AU KUMJIAN, DA BARNSTEIN, A RHEE, SG DANIEL, TO AF KUMJIAN, DA BARNSTEIN, A RHEE, SG DANIEL, TO TI PHOSPHOLIPASE-C-GAMMA COMPLEXES WITH LIGAND-ACTIVATED PLATELET-DERIVED GROWTH-FACTOR RECEPTORS - AN INTERMEDIATE IMPLICATED IN PHOSPHOLIPASE ACTIVATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INOSITOL TRISPHOSPHATE FORMATION; PROTEIN-TYROSINE KINASES; SWISS 3T3 CELLS; SIGNAL TRANSDUCTION; PDGF RECEPTOR; C-GAMMA; CALCIUM MOBILIZATION; PHOSPHORYLATION; PHOSPHOTYROSINE; SIMILARITY AB Several steps implicated in platelet-derived growth factor (PDGF) receptor-coupled signaling are activated by PDGF exposure at 0-4-degrees-C. These include receptor self-phosphorylation, physical association with and phosphorylation of phospholipase C-gamma (PLC-gamma). Reduced temperature blocks PDGF internalization, making it possible to dissociate bound PDGF after PLC-gamma tyrosine phosphorylation. We addressed the functional consequences of PDGF dissociation from intact cell PDGF receptors. PDGF exposure at 0-4-degrees-C for 15 min stimulated self-phosphorylation of a subpopulation of BALB/c 3T3 cell PDGF beta-type receptors (35%) and initiated subsequent inositol phosphate production. A small fraction of cellular PLC-gamma (1-3%) coprecipitated with ligand-activated PDGF receptors; 3-5% of cellular PLC-gamma acquired phosphotyrosine. The PLC-gamma coprecipitating with PDGF receptors did not contain detectable phosphotyrosine. Phosphotyrosine antibody recovered similar amounts of PLC-gamma from soluble and particulate fractions of PDGF-stimulated cells. Acid dissociation of bound PDGF from receptor caused rapid dephosphorylation of PDGF receptors and PLC-gamma, and interrupted PLC-gamma-PDGF receptor coprecipitation. Orthovanadate blocked tyrosine dephosphorylation of both PDGF receptors and PLC-gamma and stabilized coprecipitation. Orthovanadate reversed the acid wash effect to abrogate PDGF-stimulated inositol phosphate production. PDGF receptor remains competent to coprecipitate with PLC-gamma and stimulate PLC-mediated inositol phosphate production if PDGF-induced receptor phosphorylation is maintained. Formation of a coprecipitable PDGF receptor-PLC-gamma complex appears required for PDGF-stimulated inositol phosphate production. C1 VANDERBILT UNIV,DEPT MED,DIV NEPHROL,MCN S3223,NASHVILLE,TN 37232. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. VANDERBILT UNIV,DEPT CELL BIOL,NASHVILLE,TN 37232. FU NIDDK NIH HHS [DK38517] NR 41 TC 44 Z9 44 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 FEB 25 PY 1991 VL 266 IS 6 BP 3973 EP 3980 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200093 PM 1847394 ER PT J AU KHAN, E MACK, JPG KATZ, RA KULKOSKY, J SKALKA, AM AF KHAN, E MACK, JPG KATZ, RA KULKOSKY, J SKALKA, AM TI RETROVIRAL INTEGRASE DOMAINS - DNA-BINDING AND THE RECOGNITION OF LTR SEQUENCES SO NUCLEIC ACIDS RESEARCH LA English DT Article ID MURINE LEUKEMIA-VIRUS; DEPENDENT PROTEIN-KINASE; AVIAN-SARCOMA; ESCHERICHIA-COLI; POL GENE; SECONDARY-STRUCTURE; REVERSE-TRANSCRIPTASE; CATALYTIC SUBUNIT; LEUKOSIS VIRUSES; TERMINAL REPEATS AB Integration of retroviral DNA into the host chromosome requires a virus-encoded integrase (IN). IN recognizes, cuts and then joins specific viral DNA sequences (LTR ends) to essentially random sites in host DNA. We have used computer-assisted protein alignments and mutagenesis in an attempt to localize these functions within the avian retroviral IN protein. A comparison of the deduced amino acid sequences for 80 retroviral/retrotransposon IN proteins reveals strong conservation of an HHCC N-terminal 'Zn finger'-like domain, and a central D(35)E region which exhibits striking similarities with sequences deduced for bacterial IS elements. We demonstrate that the HHCC region is not required for DNA binding, but contributes to specific recognition of viral LTRs in the cutting and joining reactions. Deletions which extend into the D(35)E region destroy the ability of IN to bind DNA. Thus, we propose that the D(35)E region may specify a DNA-binding/cutting domain that is conserved throughout evolution in enzymes with similar functions. C1 FOX CHASE CANC INST,INST CANC RES,PHILADELPHIA,PA 19111. NCI,FREDERICK CANC RES & DEV CTR,CRYSTALLOG LAB,FREDERICK,MD 21702. FU NCI NIH HHS [CA-49042, CA-48703]; NCRR NIH HHS [RR-05539] NR 61 TC 241 Z9 243 U1 0 U2 3 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 FEB 25 PY 1991 VL 19 IS 4 BP 851 EP 860 DI 10.1093/nar/19.4.851 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900023 PM 1850126 ER PT J AU MIZROKHI, LJ MAZO, AM AF MIZROKHI, LJ MAZO, AM TI CLONING AND ANALYSIS OF THE MOBILE ELEMENT GYPSY FROM D-VIRILLIS SO NUCLEIC ACIDS RESEARCH LA English DT Article ID DROSOPHILA-MELANOGASTER; REVERSE TRANSCRIPTION; TRANSPOSABLE ELEMENT; GENE; SEQUENCE; DNA; CONSERVATION; MUTATIONS; ENCODES; PROTEIN AB The homologue of the Drosophila melanogaster mobile element gypsy was cloned from the distantly related species D. virilis. It has three ORFs highly homologous to those of the element from D. melanogaster. gypsy from D. virilis appears to be actively transcribed and is capable of transposition. Comparison of the untranslated regions of both elements revealed conserved sequences including those which had previously been demonstrated to be important in transcription regulation. Distribution of gypsy among the different strains of D. virilis and different species within the D. virilis group was analyzed. Possible involvement of horizontal transmission in the process of spreading and evolution of gypsy is discussed. C1 NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. RP MIZROKHI, LJ (reprint author), NCI,BIOCHEM LAB,BETHESDA,MD 20892, USA. NR 27 TC 46 Z9 48 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 FEB 25 PY 1991 VL 19 IS 4 BP 913 EP 916 DI 10.1093/nar/19.4.913 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900032 PM 1708127 ER PT J AU HATFIELD, D LEE, BJ HAMPTON, L DIAMOND, AM AF HATFIELD, D LEE, BJ HAMPTON, L DIAMOND, AM TI SELENIUM INDUCES CHANGES IN THE SELENOCYSTEINE TRANSFER RNA[SER]SEC POPULATION IN MAMMALIAN-CELLS SO NUCLEIC ACIDS RESEARCH LA English DT Article ID GLUTATHIONE-PEROXIDASE GENE; TRANSFER-RNA; BOVINE LIVER; CODON; EXPRESSION; UGA AB Two isoacceptors of selenocysteine tRNA[Ser]Sec are present in higher vertebrates which are responsible for donating selenocysteine to protein. One such selenocysteine containing protein, gluthione peroxidase, requires selenium for its translation and transcription. Since tRNA[Ser]Sec is a critical component of the glutathione peroxidase translational machinery, the levels and distributions of its isoacceptors were examined from both human and rat cells grown in chemically defined media with and without selenium. Not only did the level of the selenocysteine tRNA[Ser]Sec population increase approximately 20% in cells grown in the presence of selenium, but the distributions of the two isoacceptors also changed relative to each other. C1 UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60639. RP HATFIELD, D (reprint author), NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 19 TC 59 Z9 60 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 FEB 25 PY 1991 VL 19 IS 4 BP 939 EP 943 DI 10.1093/nar/19.4.939 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900037 PM 2017375 ER PT J AU LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB37-97'' SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 1 Z9 1 U1 0 U2 10 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 FEB 25 PY 1991 VL 19 IS 4 BP 961 EP 961 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900047 PM 2017379 ER PT J AU LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB38-85 SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 1 Z9 1 U1 1 U2 11 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 FEB 25 PY 1991 VL 19 IS 4 BP 961 EP 961 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900048 PM 2017379 ER PT J AU DELISIO, J LATIF, F GLENN, GM BRAUCH, H HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF DELISIO, J LATIF, F GLENN, GM BRAUCH, H HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB24-12' SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 0 Z9 0 U1 1 U2 6 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 FEB 25 PY 1991 VL 19 IS 4 BP 962 EP 962 DI 10.1093/nar/19.4.962-a PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900050 PM 2017380 ER PT J AU LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB31-38 SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 2 Z9 2 U1 1 U2 6 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 FEB 25 PY 1991 VL 19 IS 4 BP 962 EP 962 DI 10.1093/nar/19.4.962 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900049 PM 1708131 ER PT J AU LATIF, F GLENN, GM TORY, K BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM TORY, K BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB08-60''' SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 1 Z9 1 U1 1 U2 11 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 FEB 25 PY 1991 VL 19 IS 4 BP 963 EP 963 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900052 PM 1708132 ER PT J AU LATIF, F GLENN, GM TORY, K BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM TORY, K BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB43-55' SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 1 Z9 1 U1 0 U2 10 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 FEB 25 PY 1991 VL 19 IS 4 BP 963 EP 963 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900051 PM 1708132 ER PT J AU LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME 3P - LAMBDA-LIB33-29' SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 1 Z9 1 U1 1 U2 11 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 FEB 25 PY 1991 VL 19 IS 4 BP 964 EP 964 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900053 PM 2017382 ER PT J AU LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB03-23 SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 1 Z9 1 U1 0 U2 10 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 FEB 25 PY 1991 VL 19 IS 4 BP 964 EP 964 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900054 PM 2017382 ER PT J AU LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB15-44 SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 1 Z9 1 U1 0 U2 10 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 FEB 25 PY 1991 VL 19 IS 4 BP 965 EP 965 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900056 PM 2017384 ER PT J AU LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB05-24 SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 1 Z9 1 U1 1 U2 11 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 FEB 25 PY 1991 VL 19 IS 4 BP 965 EP 965 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900055 PM 2017384 ER PT J AU DELISIO, J LATIF, F GLENN, GM YAO, M BRAUCH, H HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF DELISIO, J LATIF, F GLENN, GM YAO, M BRAUCH, H HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB09-75' SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 6 Z9 6 U1 0 U2 10 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 FEB 25 PY 1991 VL 19 IS 4 BP 966 EP 966 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900057 PM 2017386 ER PT J AU DELISIO, J LATIF, F GLENN, GM YAO, M BRAUCH, H HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF DELISIO, J LATIF, F GLENN, GM YAO, M BRAUCH, H HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P - LAMBDA-LIB19-63' SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NR 3 TC 6 Z9 6 U1 1 U2 11 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 FEB 25 PY 1991 VL 19 IS 4 BP 966 EP 966 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900058 PM 2017386 ER PT J AU POLYMEROPOULOS, MH RATH, DS XIAO, H MERRIL, CR AF POLYMEROPOULOS, MH RATH, DS XIAO, H MERRIL, CR TI DINUCLEOTIDE REPEAT POLYMORPHISM AT THE HUMAN ANKYRIN GENE (ANK1) SO NUCLEIC ACIDS RESEARCH LA English DT Note RP POLYMEROPOULOS, MH (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,ROOM 131,2700 MARTIN LUTHER KING AVE,WASHINGTON,DC 20032, USA. NR 3 TC 29 Z9 29 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 FEB 25 PY 1991 VL 19 IS 4 BP 969 EP 969 DI 10.1093/nar/19.4.969 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900063 PM 1826765 ER PT J AU MAVALANKAR, DV AF MAVALANKAR, DV TI HEALTH IN INDIA SO BRITISH MEDICAL JOURNAL LA English DT Letter RP MAVALANKAR, DV (reprint author), NIH,PUBL HLTH SERV,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0959-8138 J9 BRIT MED J JI Br. Med. J. PD FEB 23 PY 1991 VL 302 IS 6774 BP 470 EP 470 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EZ033 UT WOS:A1991EZ03300037 ER PT J AU MARLEY, RJ WITKIN, JM GOLDBERG, SR AF MARLEY, RJ WITKIN, JM GOLDBERG, SR TI GENETIC-FACTORS INFLUENCE CHANGES IN SENSITIVITY TO THE CONVULSANT PROPERTIES OF COCAINE FOLLOWING CHRONIC TREATMENT SO BRAIN RESEARCH LA English DT Article DE COCAINE; KINDLING; GENETICS; TOLERANCE; INBRED MOUSE STRAIN; SEIZURE ID INBRED MOUSE STRAINS; INDUCED SEIZURES; MICE; GABA; PENTYLENETETRAZOL; PROCONVULSANT; CHANNELS; BINDING; DEATH; BRAIN AB Repeated administration of doses of cocaine below the threshold for seizure induction results in the development of an increased susceptibility to cocaine-induced seizures (cocaine-kindling). Genetic differences in susceptibility to cocaine-kindled seizures were evaluated in 4 inbred mouse strains and compared with susceptibility to seizures induced by acute administration of cocaine. The acute administration of cocaine produced convulsant activity in mice from all 4 genotypes, however, there were significant differences in the dose of cocaine required to induce seizures. C57 mice were highly susceptible and SJL mice highly resistant to convulsions induced by acute administration of cocaine, while BALB and DBA mice showed an intermediate degree of seizure susceptibility. The repeated administration of subconvulsant doses of cocaine resulted in rapid sensitization to cocaine-induced seizures. The 4 strains differed in the rate at which sensitization to cocaine-induced seizures developed, with the SJL strain being most sensitive and the C57 strain the least sensitive to the cocaine-kindling process. The susceptibility of the 4 strains to cocaine kindling was virtually opposite to their susceptibility to seizures induced by the acute administration of cocaine, suggesting that different mechanisms may be involved in the control of acute and kindled seizures. In 3 of the 4 genotypes sensitization to cocaine-induced seizures did not persist upon further exposure to cocaine. Following a period of increased sensitivity to cocaine-induced seizures, tolerance to the convulsant properties of cocaine developed among C57, BALB and DBA mice. Only among the SJL mice did the development of a kindled state persist upon repeated exposure to cocaine. These differences emphasize the potential importance of inheritance in determining the effects of cocaine and suggest novel approaches to understanding the mechanisms underlying the effects of cocaine. RP MARLEY, RJ (reprint author), NIDA,ADDICT RES CTR,BOX 5180,BALTIMORE,MD 21224, USA. NR 32 TC 38 Z9 38 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 FEB 22 PY 1991 VL 542 IS 1 BP 1 EP 7 DI 10.1016/0006-8993(91)90989-9 PG 7 WC Neurosciences SC Neurosciences & Neurology GA FB740 UT WOS:A1991FB74000001 PM 2054648 ER PT J AU SZEMEREDI, K KOMOLY, S KOPIN, IJ BAGDY, G KEISER, HR GOLDSTEIN, DS AF SZEMEREDI, K KOMOLY, S KOPIN, IJ BAGDY, G KEISER, HR GOLDSTEIN, DS TI SIMULTANEOUS MEASUREMENT OF PLASMA AND BRAIN EXTRACELLULAR FLUID CONCENTRATIONS OF CATECHOLS AFTER YOHIMBINE ADMINISTRATION IN RATS SO BRAIN RESEARCH LA English DT Article DE NORADRENALINE; CATECHOLAMINE; YOHIMBINE; MICRODIALYSIS; HYPOTHALAMUS; DIHYDROXYPHENYLGLYCOL; METHOXYHYDROXYPHENYLGLYCOL ID CONSCIOUS RATS; NOREPINEPHRINE; MICRODIALYSIS; METABOLISM; RESPONSES; CLONIDINE; SEROTONIN; URAPIDIL; PRAZOSIN; DOPAMINE AB The present study examined whether systemic injection of the alpha-2 adrenoceptor blocker, yohimbine, affects concentrations of norepinephrine (NE) and its metabolites in extracellular fluid in the brain and in blood. Microdialysis probes were inserted into the posterior hypothalamus, medulla, and caudate/putamen in rats. Microdialysate and arterial blood were sampled after intravenous administration of yohimbine. In the hypothalamus yohimbine produced significant increases in extracellular fluid concentrations of NE, its intraneuronal metabolite, dihydroxyphenylglycol (DHPG), and methoxyhydroxyphenylglycol (MHPG), a major neuronal and extraneuronal metabolite of NE. The increases in these levels were small or absent in the caudate/putamen, where dopamine is the primary catecholamine transmitter. During systemic infusion of tracer amounts of [H-3]NE, little if any radioactive NE or DHPG appeared in the microdialysate, whereas substantial levels of [H-3]MHPG were present and increased as plasma [H-3]MHPG levels rose. The results support the view that alpha-2 adrenoceptor blockade in the brain increases hypothalamic and medullary release, reuptake, and metabolism of NE. The findings cannot be explained by disruption of the blood-brain barrier for catecholamines by insertion of the microdialysis probes. Enhanced sympathetic outflow and peripheral release of NE when alpha-2 adrenoceptors are blocked appears to be attended by enhanced central NE release, presumably as a result of presynaptic alpha-2 adrenoceptor blockade at noradrenergic terminals in the brain. This is consistent with the hypothesis that central noradrenergic NE release is regulated by presynaptic alpha-2 adrenoceptors. C1 NINCDS,CLIN NEUROSCI BRANCH,BLDG 10,ROOM 5N214,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NHLBI,HYPERTENS ENDOCRINE BRANCH,BETHESDA,MD 20892. NINCDS,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20892. NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. OI Bagdy, Gyorgy/0000-0001-8141-3410 NR 30 TC 34 Z9 34 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 FEB 22 PY 1991 VL 542 IS 1 BP 8 EP 14 DI 10.1016/0006-8993(91)90990-D PG 7 WC Neurosciences SC Neurosciences & Neurology GA FB740 UT WOS:A1991FB74000002 PM 2054662 ER PT J AU PINTO, JEB FLUGGE, G VIGLIONE, PN TORDA, T NAZARALI, AJ SAAVEDRA, JM AF PINTO, JEB FLUGGE, G VIGLIONE, PN TORDA, T NAZARALI, AJ SAAVEDRA, JM TI INCREASED BETA-2-ADRENOCEPTORS IN THE SUPERIOR CERVICAL-GANGLIA OF GENETICALLY HYPERTENSIVE RATS SO BRAIN RESEARCH LA English DT Article DE BETA-ADRENOCEPTOR; SYMPATHETIC GANGLIA; HYPERTENSION; GENETIC; POSTGANGLIONIC FIBER; RENIN ANGIOTENSIN SYSTEM; AUTORADIOGRAPHY ID BETA-ADRENERGIC RECEPTORS; SYMPATHETIC-GANGLIA; NORADRENALINE RELEASE; AXONAL-TRANSPORT; ANGIOTENSIN-II; MODULATION; CATECHOLAMINES; DEPOLARIZATION; ADRENOCEPTORS; EPINEPHRINE AB [I-125]Iodocyanopindolol binding sites were characterized by autoradiography in the superior cervical ganglia of Wistar-Kyoto (WKY) rats. A high concentration of (-)-[I-125]iodocyanopindolol binding sites, characterized as beta-adrenoceptors by (-)-propranolol displacement, was distributed throughout the ganglia and in the postganglionic (internal carotid) nerve. ICI 118,551, a beta-2-selective antagonist, displaced more than 85% of the binding sites, whereas CGP 20712A, a beta-1-selective antagonist, displaced less than 10% of the binding sites, indicating that the beta-adrenoceptors were primarily of the beta-2-subtype. Emulsion autoradiography demonstrated that at least part of the binding sites were associated with principal ganglion cells. Unilateral deafferentation did not modify the number of binding sites in the superior cervical ganglia of WKY or spontaneously hypertensive rat (SHR). These results suggest that at least part of these receptors may correspond to prejunctional beta-2-adrenoceptors originated in principal ganglion cells. The concentration of beta-2-receptors was increased in the superior cervical ganglia of young and adult SHR when compared to age-matched WKY rats (49% and 39%, respectively). There were no differences in beta-2-adrenoceptor number in the stellate ganglia of young and adult WKY and SHR. These results suggest that beta-2-adrenoceptor stimulation may be selectively enhanced in some peripheral sympathetic ganglia in SHR and this could play a role in the development and maintenance of the increased sympathetic activity in this strain. C1 NIMH,CLIN SCI LAB,PHARMACOL SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2D-45,BETHESDA,MD 20892. NR 42 TC 7 Z9 7 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 FEB 22 PY 1991 VL 542 IS 1 BP 35 EP 42 DI 10.1016/0006-8993(91)90994-7 PG 8 WC Neurosciences SC Neurosciences & Neurology GA FB740 UT WOS:A1991FB74000006 PM 1675921 ER PT J AU HEROUX, JA GRIGORIADIS, DE DESOUZA, EB AF HEROUX, JA GRIGORIADIS, DE DESOUZA, EB TI AGE-RELATED DECREASES IN CORTICOTROPIN-RELEASING FACTOR (CRF) RECEPTORS IN RAT-BRAIN AND ANTERIOR-PITUITARY GLAND SO BRAIN RESEARCH LA English DT Note DE AGING; ADRENOCORTICOTROPIC HORMONE; CORTICOTROPIN-RELEASING FACTOR; CORTICOSTERONE; HYPOTHALAMIC-PITUITARY-ADRENOCORTICAL AXIS; HYPOTHALAMUS; PROOPIOMELANOCORTIN; RECEPTOR DOWN-REGULATION ID ADRENOCORTICAL STRESS-RESPONSE; FACTOR-LIKE IMMUNOREACTIVITY; ALZHEIMERS-DISEASE; CEREBRAL-CORTEX; ACTH; CORTICOSTERONE AB Corticotropin-releasing factor (CRF) receptors were measured in discrete areas of brain and in anterior pituitary of 4-, 12-, 18-, and 24-month-old male Fischer rats. No significant age-related alterations in [I-125]ovine CRF binding were observed in the olfactory bulb, cerebral cortex, hippocampus, brainstem, and cerebellum; there was a trend for CRF binding to decrease in the striatum as a consequence of aging. Significant age-related decreases were observed in I-125-ovine CRF binding in the anterior pituitary and hypothalamus with maximal reductions of 60 and 27%, respectively. Saturation analysis in the anterior pituitary indicated an age-related reduction in the density of CRF receptors (i.e. B(max)) without an alteration in the affinity (i.e. K(d)) of CRF for its binding site. Northern analysis of proopiomelanocortin (POMC) mRNA in the anterior pituitary indicated no significant differences in the levels of POMC mRNA between 4- and 24-month-old rats. These and other data suggest that the age-related decrease in anterior pituitary CRF receptors may be due to hypersecretion of hypothalamic CRF rather than a loss of corticotropes in the anterior pituitary. C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,NEUROBIOL LAB,BALTIMORE,MD 21224. NR 20 TC 39 Z9 40 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 FEB 22 PY 1991 VL 542 IS 1 BP 155 EP 158 DI 10.1016/0006-8993(91)91011-O PG 4 WC Neurosciences SC Neurosciences & Neurology GA FB740 UT WOS:A1991FB74000023 PM 1647252 ER PT J AU RIUS, RA BARG, J BEM, WT COSCIA, CJ LOH, YP AF RIUS, RA BARG, J BEM, WT COSCIA, CJ LOH, YP TI THE PRENATAL DEVELOPMENTAL PROFILE OF EXPRESSION OF OPIOID-PEPTIDES AND RECEPTORS IN THE MOUSE-BRAIN SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE ONTOGENY; OPIOID PEPTIDE; OPIOID RECEPTOR; PHENOTYPIC EXPRESSION; MOUSE; CENTRAL NERVOUS SYSTEM; EMBRYO ID DIFFERENTIAL POSTNATAL-DEVELOPMENT; DEVELOPING RAT-BRAIN; BINDING-SITES; OPIATE RECEPTOR; ONTOGENETIC DEVELOPMENT; BETA-ENDORPHIN; GUINEA-PIG; DELTA; KAPPA; MU AB Although the postnatal development of opioid systems of mammalian brain has been well studied, little is known about the ontogeny of and relationship between embryonic (E) opioid peptides and their receptors. Moreover, a simultaneous assessment of levels of the 3 classes of opioid peptides and their putative receptors during embryonal development has not been made. To this end, the ontogeny of opioid peptides and receptors in mouse brain were examined during the period E11.5 to postnatal day 1 (P1). Met-enkephalin, dynorphin and beta-endorphin immunoreactivity were detected before their putative opioid receptors. beta-Endorphin can be discerned as early as E11.5, whereas mu binding was first observed at E12.5. Although dynorphin and Met-enkephalin were measurable at the same time as beta-endorphin, kappa-receptors were not detected until E14.5 and delta sites were not found at all prenatally. Differences in immunoreactivity leveles of the 3 peptides occur with dynorphin being lower than Met-enkephalin and beta-endorphin, consistent with a low B(max) for kappa binding. Expression of the 3 opioid peptides as well as mu and kappa opioid receptors rapidly increase in parallel from E14.5 to E18.5. Interestingly, levels of beta-endorphin diminish by P1, the stage at which a sharp rise of mu receptors occurs. In a comparative study of the binding of beta-endorphin1-31, its truncated form (1-27) and their N-acetyl derivatives to E14.5 brain membranes, beta-endorphin1-31 exhibited the highest affinity. C1 NICHHD,DEV NEUROBIOL LAB,CELLULAR NEUROBIOL SECT,BLDG 36,ROOM 2A21,BETHESDA,MD 20892. ST LOUIS UNIV,SCH MED,DEPT BIOCHEM,ST LOUIS,MO 63104. NR 47 TC 37 Z9 38 U1 0 U2 1 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 FEB 22 PY 1991 VL 58 IS 2 BP 237 EP 241 DI 10.1016/0165-3806(91)90010-G PG 5 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA FA638 UT WOS:A1991FA63800010 ER PT J AU BENNETT, PH STERN, MP AF BENNETT, PH STERN, MP TI WORKSHOP-VII - PATIENT POPULATION AND GENETICS - ROLE IN DIABETES SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN EPIDEMIOL,SAN ANTONIO,TX 78284. RP BENNETT, PH (reprint author), NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,1550 E INDIAN SCH RD,PHOENIX,AZ 85015, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD FEB 21 PY 1991 VL 90 SU 2A BP S76 EP S79 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA EZ476 UT WOS:A1991EZ47600019 PM 1994724 ER PT J AU MERCER, JA SEPERACK, PK STROBEL, MC COPELAND, NG JENKINS, NA AF MERCER, JA SEPERACK, PK STROBEL, MC COPELAND, NG JENKINS, NA TI NOVEL MYOSIN HEAVY-CHAIN ENCODED BY MURINE DILUTE COAT COLOR LOCUS SO NATURE LA English DT Article ID INTESTINAL MICROVILLUS; MESSENGER-RNA; SEQUENCE; PROTEIN; GENE; COMPLEX; CLONING; ACTIN; DNA; PHENOTYPE AB HUNDREDS of murine dilute mutations have been identified and analysed, making dilute one of the best genetically characterized of all mammalian loci. The recessive dilute (d) coat colour mutation carried by many inbred strains of mice produces a lightening of coat colour, caused by an abnormal adendritic melanocyte morphology that results in an uneven release of pigment granules into the developing hair shaft 1,2. Most dilute alleles (dilute-lethal) also produce a neurological defect, characterized by convulsions and opisthotonus, apparent at 8-10 days of age and continuing until the death of the animal at 2-3 weeks of age 3. The discovery that the original dilute allele (now termed dilute-viral or d(V)) is the result of the integration of an ecotropic murine leukaemia provirus 4 has allowed the cloning of genomic DNA 5,6 and in this study complementary DNA, from the dilute locus. The predicted dilute amino-acid sequence indicates that dilute encodes a novel type of myosin heavy chain, with a tail, or C-terminal, region that has elements of both type II (alpha-helical coiled-coil) and type I (non-coiled-coil) myosin heavy chains. Dilute transcripts are differentially expressed in both embryonic and adult tissues and are very abundant in neurons of the central nervous system, cephalic ganglia, and spinal ganglia. These results suggest an important role for the dilute gene product in the elaboration, maintenance, or function of cellular processes of melanocytes and neurons. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. NR 32 TC 453 Z9 454 U1 0 U2 9 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 21 PY 1991 VL 349 IS 6311 BP 709 EP 713 DI 10.1038/349709a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EY627 UT WOS:A1991EY62700052 PM 1996138 ER PT J AU HENEINE, W KAPLAN, JE GRACIA, F LAL, R ROBERTS, B LEVINE, PH REEVES, WC AF HENEINE, W KAPLAN, JE GRACIA, F LAL, R ROBERTS, B LEVINE, PH REEVES, WC TI HTLV-II ENDEMICITY AMONG GUAYMI INDIANS IN PANAMA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID INFECTION C1 GORGAS MEM LAB,PANAMA CITY,PANAMA. CTR DIS CONTROL,ATLANTA,GA 30333. NCI,BETHESDA,MD 20892. RP HENEINE, W (reprint author), CTR DIS CONTROL,ATLANTA,GA 30333, USA. NR 9 TC 61 Z9 62 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 FEB 21 PY 1991 VL 324 IS 8 BP 565 EP 565 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EX918 UT WOS:A1991EX91800024 PM 1992314 ER PT J AU BRINTON, LA LI, JY RONG, SD HUANG, S SHENG, XB SHI, BG ZHU, ZJ SCHIFFMAN, MH DAWSEY, S AF BRINTON, LA LI, JY RONG, SD HUANG, S SHENG, XB SHI, BG ZHU, ZJ SCHIFFMAN, MH DAWSEY, S TI RISK-FACTORS FOR PENILE CANCER - RESULTS FROM A CASE-CONTROL STUDY IN CHINA SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID SMOKE CONSTITUENTS; CERVICAL-CANCER; UTERINE CERVIX; CARCINOMA; NEOPLASIA; BRAZIL; PARTNERS; WOMEN; WIVES AB An epidemiologic study of penile cancer involving 141 cases and 150 community controls was undertaken in a high-risk area in China. Personal interviews, as well as physical examinations among the prospectively ascertained subjects, enabled evaluation of a variety of potential risk factors. Strongly related to risk were conditions restricting the motility of the foreskin, including phimosis or paraphimosis, particularly when so severe that circumcision was used for treatment. Poor hygiene practices also appeared to increase risk, particularly as evidenced by detection of smegma on physical examination, although it was difficult to decipher whether this association was etiologic or merely a consequence of disease. A sexual relationship outside of marriage was associated with a RR of 1.7, and appeared to be a more important discriminator than number of lifetime sexual partners. Risk was increased among subjects reporting previous genital conditions, particularly sexually transmitted diseases, and physical examinations revealed the appearance of genital warts among 13 cases vs. 1 control. Interviews with wives of study subjects failed to provide evidence of a "female factor" in the etiology of penile cancer. This study supports the need for further evaluation of the role of hygiene and sexually transmitted agents in the etiology of penile cancer. C1 CHINESE ACAD MED SCI,BEIJING,PEOPLES R CHINA. WESTAT CORP,ROCKVILLE,MD. HUNAN PROVINCE TUMOR HOSP,CHANGSHA,PEOPLES R CHINA. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. RP BRINTON, LA (reprint author), NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 443,BETHESDA,MD 20892, USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 32 TC 61 Z9 61 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD FEB 20 PY 1991 VL 47 IS 4 BP 504 EP 509 DI 10.1002/ijc.2910470406 PG 6 WC Oncology SC Oncology GA EZ573 UT WOS:A1991EZ57300005 PM 1995481 ER PT J AU CENCIARELLI, C CURRIER, SJ WILLINGHAM, MC THIEBAUT, F GERMANN, UA RUTHERFORD, AV GOTTESMAN, MM BARCA, S TOMBESI, M MORRONE, S SANTONI, A MARIANI, M RAMONI, C DUPUIS, ML CIANFRIGLIA, M AF CENCIARELLI, C CURRIER, SJ WILLINGHAM, MC THIEBAUT, F GERMANN, UA RUTHERFORD, AV GOTTESMAN, MM BARCA, S TOMBESI, M MORRONE, S SANTONI, A MARIANI, M RAMONI, C DUPUIS, ML CIANFRIGLIA, M TI CHARACTERIZATION BY SOMATIC-CELL GENETICS OF A MONOCLONAL-ANTIBODY TO THE MDR1 GENE-PRODUCT (P-GLYCOPROTEIN) - DETERMINATION OF P-GLYCOPROTEIN EXPRESSION IN MULTI-DRUG-RESISTANT KB AND CEM CELL VARIANTS SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID TUMOR-CELLS; PLASMA-MEMBRANE; CARCINOMA-CELLS; PROTEINS; DNA; LOCALIZATION; SEQUENCES; TRANSPORTER; VINBLASTINE; COLCHICINE AB We isolated an IgG(2a) murine monoclonal antibody (MAb) termed MAb57, specifically reactive with multi-drug-resistant (MDR) human cells. Its specificity toward the MDRI gene product (P-glycoprotein) has been demonstrated by the concordant segregation of the MAb57 epitope with the MDRI gene in interspecific mouse x human cell hybrids, and the reactivity of several different MDRI gene-expressing cells with MAb57, particularly insect cells acutely infected with a baculovirus encoding the MDRI gene. MAb57 can be used to detect, by flow cytometry, variations in the relative drug-resistance levels of several MDR KB and CEM cell variants. This immunological probe has also proven useful in selectively destroying MDR target cells in an antibody-dependent cell-mediated (ADCC) assay system as well as in detecting P-glycoprotein expression in normal and malignant tissues and cells. C1 IST SUPER SANITA,IMMUNOL LAB,VIALE REGINA ELENA 299,I-00161 ROME,ITALY. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. UNIV ROME LA SAPIENZA,FAC MED,CATTEDRA 3A,IST PATOL GEN,I-00185 ROME,ITALY. SORIN BIOMED SPA,ONCOL BIOCHIM LAB,SALUGGIA,ITALY. RI DUPUIS, MARIA LUISA/D-7949-2016 NR 40 TC 51 Z9 51 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 FEB 20 PY 1991 VL 47 IS 4 BP 533 EP 543 DI 10.1002/ijc.2910470411 PG 11 WC Oncology SC Oncology GA EZ573 UT WOS:A1991EZ57300010 PM 1704872 ER PT J AU FRADKIN, JE SCHONBERGER, LB MILLS, JL GUNN, WJ PIPER, JM WYSOWSKI, DK THOMSON, R DURAKO, S BROWN, P AF FRADKIN, JE SCHONBERGER, LB MILLS, JL GUNN, WJ PIPER, JM WYSOWSKI, DK THOMSON, R DURAKO, S BROWN, P TI CREUTZFELDT-JAKOB DISEASE IN PITUITARY GROWTH-HORMONE RECIPIENTS IN THE UNITED-STATES SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID THERAPY; FRANCE AB To assess the magnitude of Creutzfeldt-Jakob disease (CJD) occurrence among recipients of pituitary-derived human growth hormone (HGH), we conducted an epidemiologic follow-up of 6284 recipients of HGH distributed through the National Hormone and Pituitary Program. Seven neuropathologically confirmed cases of CJD have occurred in this population to date: six patients with clinical CJD presented with ataxia and imbalance, rather than with altered mentation, which is the most common initial manifestation in sporadic CJD, and one patient died in the preclinical incubation state of the disease. All seven cases occurred among the nearly 700 HGH recipients who started therapy before 1970. Since only 10% of the cohort has been followed up for the 15-year average incubation interval from midpoint of HGH treatment to onset of symptoms, the great majority of potentially exposed patients have not yet attained the requisite incubation period for expression of CJD. The median duration of HGH therapy of 100 months in the CJD cases was significantly longer than 41 months for all patients starting treatment before 1970; thus, the duration of pituitary HGH therapy is a major risk factor for CJD. C1 CTR DIS CONTROL,ATLANTA,GA 30333. NICHHD,BETHESDA,MD 20892. US FDA,ROCKVILLE,MD 20857. WESTAT CORP,ROCKVILLE,MD. NINCDS,BETHESDA,MD 20892. RP FRADKIN, JE (reprint author), NIDDKD,ENDOCRINOL & METAB DIS PROGRAMS BRANCH,WESTWOOD BLDG,ROOM 603,BETHESDA,MD 20892, USA. NR 28 TC 121 Z9 123 U1 0 U2 5 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 20 PY 1991 VL 265 IS 7 BP 880 EP 884 DI 10.1001/jama.265.7.880 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA EX587 UT WOS:A1991EX58700039 PM 1992185 ER PT J AU SANTAMARINAFOJO, S BREWER, HB AF SANTAMARINAFOJO, S BREWER, HB TI THE FAMILIAL HYPERCHYLOMICRONEMIA SYNDROME - NEW INSIGHTS INTO UNDERLYING GENETIC-DEFECTS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID APOLIPOPROTEIN-C-II; LIPOPROTEIN-LIPASE DEFICIENCY; AMYLASE ACTIVITY; MUTATION; PATIENT; HYPERTRIGLYCERIDEMIA; ABETALIPOPROTEINEMIA; PANCREATITIS; HYPERLIPEMIA RP SANTAMARINAFOJO, S (reprint author), NHLBI,MOLEC DIS BRANCH,9000 ROCKVILLE PIKE,BLDG 10,ROOM 7N117,BETHESDA,MD 20892, USA. NR 34 TC 46 Z9 47 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 FEB 20 PY 1991 VL 265 IS 7 BP 904 EP 908 DI 10.1001/jama.265.7.904 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA EX587 UT WOS:A1991EX58700045 PM 1992190 ER PT J AU CLORE, GM GRONENBORN, AM AF CLORE, GM GRONENBORN, AM TI COMPARISON OF THE SOLUTION NUCLEAR-MAGNETIC-RESONANCE AND CRYSTAL-STRUCTURES OF INTERLEUKIN-8 - POSSIBLE IMPLICATIONS FOR THE MECHANISM OF RECEPTOR-BINDING SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article ID PANCREATIC TRYPSIN-INHIBITOR; DISTANCE GEOMETRY; RESOLUTION; PROTEIN; FORM RP CLORE, GM (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 2,ROOM 123,BETHESDA,MD 20892, USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 20 TC 56 Z9 57 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD FEB 20 PY 1991 VL 217 IS 4 BP 611 EP 620 DI 10.1016/0022-2836(91)90518-B PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA350 UT WOS:A1991FA35000004 PM 2005614 ER PT J AU BROCK, KE GRIDLEY, G MORRIS, JS WILLETT, WC AF BROCK, KE GRIDLEY, G MORRIS, JS WILLETT, WC TI SERUM SELENIUM LEVEL IN RELATION TO INSITU CERVICAL-CANCER IN AUSTRALIA SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Note ID SEROLOGIC PRECURSORS; SUBSEQUENT RISK; VITAMIN-A; NUTRIENTS; SMOKING; SYDNEY C1 NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 443,BETHESDA,MD 20892. UNIV MISSOURI,RES REACTOR FACIL,COLUMBIA,MO 65201. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. NR 23 TC 10 Z9 10 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 FEB 20 PY 1991 VL 83 IS 4 BP 292 EP 293 DI 10.1093/jnci/83.4.292 PG 2 WC Oncology SC Oncology GA EX522 UT WOS:A1991EX52200016 PM 1994059 ER PT J AU FREEDMAN, LS CLIFFORD, CK AF FREEDMAN, LS CLIFFORD, CK TI ENHANCEMENT OF MAMMARY CARCINOGENESIS BY HIGH-LEVELS OF DIETARY-FAT AND ITS ASSOCIATION WITH AD-LIBITUM FEEDING SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter C1 NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT RES PROGRAM,FREDERICK,MD 21701. RP FREEDMAN, LS (reprint author), NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,EXECUT PLAZA N,RM 344,FREDERICK,MD 21701, USA. NR 2 TC 2 Z9 2 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 FEB 20 PY 1991 VL 83 IS 4 BP 299 EP 300 DI 10.1093/jnci/83.4.299 PG 2 WC Oncology SC Oncology GA EX522 UT WOS:A1991EX52200017 PM 1994060 ER PT J AU GAGLIARDINO, JJ KRINKS, MH GAGLIARDINO, EE AF GAGLIARDINO, JJ KRINKS, MH GAGLIARDINO, EE TI IDENTIFICATION OF THE CALMODULIN-REGULATED PROTEIN PHOSPHATASE, CALCINEURIN, IN RAT PANCREATIC-ISLETS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE ISLET PHOSPHATASE; ISLET CALCINEURIN; CALMODULIN-REGULATED PHOSPHATASE; ISOLATED ISLET ID INDUCED INSULIN RELEASE; B-CELL; SECRETION; KINASE; LANGERHANS; PHOSPHORYLATION; PARTICIPATION; SYSTEM AB The aim of this work was the identification of the calmodulin-stimulated protein phosphatase, calcineurin, in rat pancreatic islets. For this purpose, a high-affinity calcineurin antibody and the Western blotting technique were used to detect the presence of calcineurin in freshly collagenase-isolated islets. The calcineurin content detected by this method was about 0.30 ng islet (approx. 0.07% of the total islet protein). The subunit composition and M(r) of islet calcineurin were similar to those of bovine brain calcineurin. Incubation of nitrocellulose membranes of the Western blotting, containing the islet protein fractions, with I-125-labeled calmodulin and (Ca2+)-Ca-45 demonstrated that the A subunit bound calmodulin, while the B subunit bound Ca2+. The presence of calcineurin in the islets of Langerhans would suggest its possible participation, as a counterpart of the kinases effect, in the regulatory mechanism of insulin secretion. C1 NCI,BETHESDA,MD 20892. RP GAGLIARDINO, JJ (reprint author), NATL UNIV LA PLATA,FAC CIENCIAS MED,CTR ENDOCRINOL EXPTL & APLICADA,RA-1900 LA PLATA,ARGENTINA. NR 28 TC 34 Z9 34 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 FEB 19 PY 1991 VL 1091 IS 3 BP 370 EP 373 DI 10.1016/0167-4889(91)90202-9 PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FC631 UT WOS:A1991FC63100016 PM 1848110 ER PT J AU MCELVANEY, NG HUBBARD, RC BIRRER, P CHERNICK, MS CAPLAN, DB FRANK, MM CRYSTAL, RG AF MCELVANEY, NG HUBBARD, RC BIRRER, P CHERNICK, MS CAPLAN, DB FRANK, MM CRYSTAL, RG TI AEROSOL ALPHA-1-ANTITRYPSIN TREATMENT FOR CYSTIC-FIBROSIS SO LANCET LA English DT Note ID HUMAN NEUTROPHIL ELASTASE AB In cystic fibrosis neutrophil-dominated inflammation on the respiratory epithelial surface results in a chronic epithelial burden of the destructive enzyme, neutrophil elastase. Alpha-1-antitrypsin (alpha-1AT), the main inhibitor of neutrophil elastase in lung, was given in aerosol form to 12 cystic fibrosis patients. It suppressed neutrophil elastase in the respiratory epithelial lining fluid (ELF) and restored the ELF anti-neutrophil elastase capacity when ELF alpha-1AT reached 8-mu-mol/l. This treatment also reversed the inhibitory effect of cystic fibrosis ELF on pseudomonas killing by neutrophils, which suggests that it may augment host defence in cystic fibrosis. C1 NHLBI,PULM BRANCH,BLDG 10,ROOM 6DO3,BETHESDA,MD 20892. NIDDKD,PEDIAT METAB BRANCH,BETHESDA,MD. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. EMORY UNIV,SCH MED,DEPT PEDIAT,DIV GASTROENTEROL & CYST FIBROSIS,ATLANTA,GA 30322. RI McElvaney, Noel/A-6809-2010 NR 7 TC 271 Z9 273 U1 0 U2 5 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD FEB 16 PY 1991 VL 337 IS 8738 BP 392 EP 394 DI 10.1016/0140-6736(91)91167-S PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA EX605 UT WOS:A1991EX60500005 PM 1671425 ER PT J AU PERRONEFILARDI, P BACHARACH, SL DILSIZIAN, V BONOW, RO AF PERRONEFILARDI, P BACHARACH, SL DILSIZIAN, V BONOW, RO TI IMPAIRED LEFT-VENTRICULAR FILLING AND REGIONAL DIASTOLIC ASYNCHRONY AT REST IN CORONARY-ARTERY DISEASE AND RELATION TO EXERCISE-INDUCED MYOCARDIAL-ISCHEMIA SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID BETA-ADRENERGIC TONE; WALL MOTION; RELAXATION; CONTRACTION; ANGIOPLASTY; PRESSURE; NONUNIFORMITY; OCCLUSION; HYPOXIA; HEART AB Impaired left ventricular (LV) diastolic filing at rest is frequently observed in patients with coronary artery disease (CAD) who have normal LV systolic function and no previous infarction. To test the hypothesis that abnormal diastolic function at rest might reflect the functional severity of CAD, as estimated by exercise-induced ischemia, the relation between regional and global LV diastolic function at rest and during exercise-induced ischemia was evaluated in 49 patients with radionuclide angiography. All patients had normal systolic function at rest. Group 1 (n = 26) patients manifested a normal ejection fraction response to exercise and group 2 (n = 23) patients an abnormal response. Data obtained from 22 age-comparable normal volunteers were used for comparison. Although regional and global diastolic function were not different between normal subjects and group 1 patients, peak filling rate was lower in group 2 patients than in normal subjects (2.5 +/- 0.8 vs 3.2 +/- 0.6 end-diastolic counts/s; p < 0.01). Moreover, regional diastolic asynchrony, as assessed from the radionuclide data by using a regional sector analysis of the LV region of interest, was greater in group 2 patients (46 +/- 44 ms) than in both normal subjects (25 +/- 16 ms; p < 0.05) and group 1 patients (23 +/- 16 ms; p < 0.05). Thus, among patients with CAD and with normal LV systolic function at rest, impaired LV filling and regional asynchrony predict a greater degree of exercise-induced ischemia, suggesting a greater extent of jeopardized myocardium. RP PERRONEFILARDI, P (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 30 TC 25 Z9 28 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD FEB 15 PY 1991 VL 67 IS 5 BP 356 EP 360 DI 10.1016/0002-9149(91)90041-I PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA EX487 UT WOS:A1991EX48700004 PM 1994658 ER PT J AU PANZA, JA MARON, BJ AF PANZA, JA MARON, BJ TI SIMULTANEOUS OCCURRENCE OF MITRAL-VALVE PROLAPSE AND SYSTOLIC ANTERIOR MOTION IN HYPERTROPHIC CARDIOMYOPATHY SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID TWO-DIMENSIONAL ECHOCARDIOGRAPHY; ASYMMETRIC SEPTAL HYPERTROPHY; LEFT-VENTRICULAR HYPERTROPHY; M-MODE ECHOCARDIOGRAPHY; CLINICAL MANIFESTATIONS; SUBAORTIC STENOSIS; PATHO-PHYSIOLOGY; WIDE-ANGLE; PATTERNS; INTERRELATIONS AB This report describes the simultaneous occurrence of mitral valve prolapse (MVP) and systolic anterior motion (SAM) in hypertrophic cardiomyopathy (HC). In 25 patients (aged 7 to 62 years, mean 29), 15 (60%) of whom were male, distal portions of the anterior or posterior mitral leaflets approached or made midsystolic contact with the ventricular septum, whereas the proximal portion of the mitral leaflets showed marked cephalad excursion into the left atrium, 5 to 15 mm beyond the mitral anular plane. Three mitral valves that were available for gross visual inspection were not morphologically typical of patients with primary MVP. Clinical features and natural history (1 to 14 years [mean 6] of follow-up), cardiac dimensions, and distribution of left ventricular hypertrophy defined in the study patients did not appear to differ distinctly from those in the overall referral population of patients with HC evaluated at our institution. Hence, patients with HC may show a striking pattern of mitral valvular motion involving SAM into the left ventricular outflow tract, as well as MVP; this prolapse motion is probably due to anatomic disproportion between the mitral valve and the small left ventricular cavity rather than to the coexistence of 2 separate disease entities. Such patients further define the great diversity evident within the broad clinical spectrum of HC. RP PANZA, JA (reprint author), NHLBI,ECHOCARDIOG LAB,BLDG 10,ROOM 7B15,BETHESDA,MD 20892, USA. NR 29 TC 8 Z9 8 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD FEB 15 PY 1991 VL 67 IS 5 BP 404 EP 410 DI 10.1016/0002-9149(91)90050-U PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA EX487 UT WOS:A1991EX48700013 PM 1994665 ER PT J AU HARLOW, SD LINET, MS AF HARLOW, SD LINET, MS TI AGREEMENT BETWEEN QUESTIONNAIRE DATA AND MEDICAL RECORDS - THE EVIDENCE FOR ACCURACY OF RECALL - REPLY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BIOSTAT BRANCH,BETHESDA,MD 20892. RP HARLOW, SD (reprint author), UNIV N CAROLINA,DEPT EPIDEMIOL,CHAPEL HILL,NC 27599, USA. NR 5 TC 0 Z9 0 U1 1 U2 1 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 15 PY 1991 VL 133 IS 4 BP 409 EP 410 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA EZ157 UT WOS:A1991EZ15700013 ER PT J AU TAKAHASHI, N BREITMAN, TR AF TAKAHASHI, N BREITMAN, TR TI RETINOYLATION OF PROTEINS IN LEUKEMIA, EMBRYONAL CARCINOMA, AND NORMAL KIDNEY-CELL LINES - DIFFERENCES ASSOCIATED WITH DIFFERENTIAL RESPONSES TO RETINOIC ACID SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID ACUTE PROMYELOCYTIC LEUKEMIA; RECEPTOR; HL-60; IDENTIFICATION; INDUCTION; ACYLATION; CULTURE; PATIENT; THERAPY; GROWTH C1 NCI,DIV CANC TREATMENT,BIOL CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NR 30 TC 37 Z9 37 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 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD FEB 15 PY 1991 VL 285 IS 1 BP 105 EP 110 DI 10.1016/0003-9861(91)90334-F PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EV516 UT WOS:A1991EV51600014 PM 1990968 ER PT J AU GARLAND, D RAO, PV DELCORSO, A MURA, U ZIGLER, JS AF GARLAND, D RAO, PV DELCORSO, A MURA, U ZIGLER, JS TI ZETA-CRYSTALLIN IS A MAJOR PROTEIN IN THE LENS OF CAMELUS-DROMEDARIUS SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID GUINEA-PIG; DEHYDROGENASES; EVOLUTION C1 UNIV PISA,DIPARTIMENTO FISIOL & BIOCHIM,I-56100 PISA,ITALY. RP GARLAND, D (reprint author), NEI,MECHANISMS OCULAR DIS LAB,BLDG 6,ROOM 235,BETHESDA,MD 20892, USA. NR 10 TC 54 Z9 54 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 FEB 15 PY 1991 VL 285 IS 1 BP 134 EP 136 DI 10.1016/0003-9861(91)90339-K PG 3 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EV516 UT WOS:A1991EV51600019 PM 1990971 ER PT J AU IWAHASHI, H ALBRO, PW MCGOWN, SR TOMER, KB MASON, RP AF IWAHASHI, H ALBRO, PW MCGOWN, SR TOMER, KB MASON, RP TI ISOLATION AND IDENTIFICATION OF ALPHA-(4-PYRIDYL-1-OXIDE)-N-TERT-BUTYLNITRONE RADICAL ADDUCTS FORMED BY THE DECOMPOSITION OF THE HYDROPEROXIDES OF LINOLEIC-ACID, LINOLENIC ACID, AND ARACHIDONIC-ACID BY SOYBEAN LIPOXYGENASE SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID ELECTRON-SPIN RESONANCE; PERFORMANCE LIQUID-CHROMATOGRAPHY; INDUCED LIPID-PEROXIDATION; INVIVO PENTANE PRODUCTION; DIETARY VITAMIN-E; ANAEROBIC REACTION; ETHANE EVOLUTION; FATTY-ACIDS; RAT; SEPARATION C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RI Tomer, Kenneth/E-8018-2013 NR 49 TC 66 Z9 67 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD FEB 15 PY 1991 VL 285 IS 1 BP 172 EP 180 DI 10.1016/0003-9861(91)90346-K PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EV516 UT WOS:A1991EV51600026 PM 1846731 ER PT J AU CHUNG, SI PARK, MH FOLK, JE LEWIS, MS AF CHUNG, SI PARK, MH FOLK, JE LEWIS, MS TI EUKARYOTIC INITIATION-FACTOR 5A - THE MOLECULAR-FORM OF THE HYPUSINE-CONTAINING PROTEIN FROM HUMAN ERYTHROCYTES SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Note DE EUKARYOTIC INITIATION FACTOR; HYPUSINE; PROTEIN SYNTHESIS INITIATION FACTOR ID FACTOR EIF-4D; AMINO-ACID; TRANSLATION; IDENTIFICATION; PURIFICATION; PRECURSOR AB Eukaryotic initiation factor 5A (eIF-5A, formerly known as eIF-4D [1]) purified from human erythrocytes has been found to have a monomeric molecular weight between 17 500 and 18 000. In this study, using exclusion chromatography and analytical ultracentrifugation, we demonstrate that eIF-5A normally exists as a dimer in solution and appears to be capable of undergoing reversible association to form higher polymers. C1 NATL CTR RES RESOURCE 27,BETHESDA,MD. RP CHUNG, SI (reprint author), NIDR,BETHESDA,MD 20892, USA. NR 16 TC 14 Z9 15 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD FEB 15 PY 1991 VL 1076 IS 3 BP 448 EP 451 PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FB257 UT WOS:A1991FB25700020 PM 1900436 ER PT J AU GERACIOTI, TD POST, RM AF GERACIOTI, TD POST, RM TI ONSET OF PANIC DISORDER ASSOCIATED WITH RARE USE OF COCAINE SO BIOLOGICAL PSYCHIATRY LA English DT Article ID ABUSE; COMPLICATIONS C1 NIMH,BETHESDA,MD 20892. RP GERACIOTI, TD (reprint author), VANDERBILT UNIV,MED CTR,SCH MED,DEPT PSYCHIAT,MED CTR N,ROOM A2215,NASHVILLE,TN 37232, USA. NR 26 TC 27 Z9 27 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD FEB 15 PY 1991 VL 29 IS 4 BP 403 EP 406 DI 10.1016/0006-3223(91)90227-D PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA EZ690 UT WOS:A1991EZ69000012 PM 2036481 ER PT J AU STEIS, RG SMITH, JW URBA, WJ VENZON, DJ LONGO, DL BARNEY, R EVANS, LM ITRI, LM EWEL, CH AF STEIS, RG SMITH, JW URBA, WJ VENZON, DJ LONGO, DL BARNEY, R EVANS, LM ITRI, LM EWEL, CH TI LOSS OF INTERFERON ANTIBODIES DURING PROLONGED CONTINUOUS INTERFERON-ALPHA-2A THERAPY IN HAIRY-CELL LEUKEMIA SO BLOOD LA English DT Article ID CHRONIC MYELOGENOUS LEUKEMIA; RECOMBINANT ALPHA-INTERFERON; INITIAL THERAPY; LEUKOCYTE; MULTICENTER C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. FREDERICK MEM HOSP,FREDERICK,MD. CLIN ONCOL PROGRAM,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD. HOFFMANN LA ROCHE INC,CLIN INVEST,NUTLEY,NJ 07110. RP STEIS, RG (reprint author), NCI,FREDERICK CANC RES & DEV CTR,CLIN RES BRANCH,501 W 7TH ST,SUITE 3,FREDERICK,MD 21701, USA. FU PHS HHS [N01-C0-74102] NR 26 TC 45 Z9 46 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1991 VL 77 IS 4 BP 792 EP 798 PG 7 WC Hematology SC Hematology GA EX922 UT WOS:A1991EX92200016 PM 1704264 ER PT J AU GINSBERG, AM RAFFELD, M COSSMAN, J AF GINSBERG, AM RAFFELD, M COSSMAN, J TI INACTIVATION OF THE RETINOBLASTOMA GENE IN HUMAN LYMPHOID NEOPLASMS SO BLOOD LA English DT Article ID SUSCEPTIBILITY GENE; CELL-CYCLE; LYMPHOCYTIC-LEUKEMIA; OSTEO-SARCOMA; BETA-TUBULIN; EXPRESSION; PRODUCT; PHOSPHORYLATION; MECHANISMS; MUTATION C1 GEORGETOWN UNIV,SCH MED,DEPT PATHOL,119 BASIC SCI BLDG,3900 RESERVOIR RD NW,WASHINGTON,DC 20007. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 36 TC 97 Z9 97 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1991 VL 77 IS 4 BP 833 EP 840 PG 8 WC Hematology SC Hematology GA EX922 UT WOS:A1991EX92200021 PM 1993222 ER PT J AU MANNS, A MURPHY, EL WILKS, R HAYNES, G FIGUEROA, JP HANCHARD, B BARNETT, M DRUMMOND, J WATERS, D CERNEY, M SEALS, JR ALEXANDER, SS LEE, H BLATTNER, WA AF MANNS, A MURPHY, EL WILKS, R HAYNES, G FIGUEROA, JP HANCHARD, B BARNETT, M DRUMMOND, J WATERS, D CERNEY, M SEALS, JR ALEXANDER, SS LEE, H BLATTNER, WA TI DETECTION OF EARLY HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I ANTIBODY PATTERNS DURING SEROCONVERSION AMONG TRANSFUSION RECIPIENTS SO BLOOD LA English DT Article ID HTLV-I; LEUKEMIA-VIRUS; BLOOD-TRANSFUSION; INFECTION; TRANSMISSION; MYELOPATHY C1 PROGRAM RESOURCES INST,FREDERICK,MD. BIOTECH LABS,ROCKVILLE,MD. ABBOTT LABS,CHICAGO,IL. MINIST HLTH,KINGSTON,JAMAICA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. UNIV W INDIES,KINGSTON 7,JAMAICA. CAMBRIDGE BIOSCI INC,WORCESTER,MA. RP MANNS, A (reprint author), NCI,6130 EXECUT BLVD,SUITE 434,ROCKVILLE,MD 20892, USA. FU NCI NIH HHS [N01-CP-31006] NR 22 TC 57 Z9 57 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1991 VL 77 IS 4 BP 896 EP 905 PG 10 WC Hematology SC Hematology GA EX922 UT WOS:A1991EX92200030 PM 1993227 ER PT J AU SHAPIRO, LE LEONARD, CM SESSIONS, CE DEWSBURY, DA INSEL, TR AF SHAPIRO, LE LEONARD, CM SESSIONS, CE DEWSBURY, DA INSEL, TR TI COMPARATIVE NEUROANATOMY OF THE SEXUALLY DIMORPHIC HYPOTHALAMUS IN MONOGAMOUS AND POLYGAMOUS VOLES SO BRAIN RESEARCH LA English DT Article DE SEXUAL DIMORPHISM; PRAIRIE VOLE; MONTANE VOLE; MEDIAL PREOPTIC AREA; MONOGAMY; MICROTUS ID MEDIAL PREOPTIC AREA; SOCIAL-ORGANIZATION; COPULATORY-BEHAVIOR; MICROTUS-MONTANUS; PRAIRIE VOLES; PROGESTERONE TREATMENT; SEX-DIFFERENCES; FEMALE BRAINS; GUINEA-PIG; RAT AB In the present work we evaluated the degree of sexual dimorphism in two cell groups of the medical preoptic-anterior hypothalamus (MPOA-AH) in monogamous and polygamous voles. Quantitative determinations were made of volume, cell number, and cell density for the anteroventral-periventricular nucleus (AVPV) and the sexually dimorphic nucleus of the preoptic area (SDN-POA). Polygamous montane voles (Microtus montanus) had a greater degree of sexual dimorphism in both cell groups than did monogamous prairie voles (M. ochrogaster). Most notable was the complete absence of the AVPV in male montane voles; male montane voles also had a significantly larger SDN-POA volume than did females. The only sexual dimorphism in prairie voles was a greater cell density in the female AVPV. In addition, prairie voles had larger relative brain size than did montane voles. Comparative behavioral studies have revealed a correlation between the degree of sexual dimorphism in external morphology and mating system, i.e., polygamous species display greater levels of dimorphism than do monogamous species. The present results indicate that the effects of sexual selection can also be seen in those brain regions, like the hypothalamus, that underlie social and reproductive behavior. Moreover, these results support the hypothesis that neuroanatomic dimorphisms in the MPOA-AH may be related to sex differences in behavior. C1 UNIV FLORIDA,COLL MED,DEPT NEUROSCI,GAINESVILLE,FL 32611. UNIV FLORIDA,DEPT PSYCHOL,GAINESVILLE,FL 32611. RP SHAPIRO, LE (reprint author), NIMH,CLIN SCI LAB,POB 289,POOLESVILLE,MD 20837, USA. FU NINDS NIH HHS [NS 13516] NR 59 TC 52 Z9 52 U1 1 U2 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD FEB 15 PY 1991 VL 541 IS 2 BP 232 EP 240 DI 10.1016/0006-8993(91)91023-T PG 9 WC Neurosciences SC Neurosciences & Neurology GA EY927 UT WOS:A1991EY92700007 PM 2054639 ER PT J AU MIRVISH, SS HUANG, Q JI, C WANG, SH PARK, SS GELBOIN, HV AF MIRVISH, SS HUANG, Q JI, C WANG, SH PARK, SS GELBOIN, HV TI POSITIONAL SPECIFICITY FOR METHYL-N-AMYLNITROSAMINE HYDROXYLATION BY CYTOCHROME-P-450 ISOZYMES DETERMINED WITH MONOCLONAL-ANTIBODIES SO CANCER RESEARCH LA English DT Article ID RAT-LIVER CYTOCHROME-P-450; MICROSOMAL CYTOCHROME-P-450; CONSTITUTIVE FORMS; METABOLISM; NITROSAMINES; ESOPHAGUS; TISSUES; NITROSODIMETHYLAMINE; CYTOCHROMES-P-450; DERIVATIVES AB Inhibitory monoclonal antibodies (MAbs) were used to determine the contribution of epitope-specific cytochrome P-450 isozymes in rat liver microsomes to hydroxylation of the esophageal carcinogen methyl-n-amylnitrosamine. These P-450-catalyzed reactions form 2-,3-,4-, and 5-hydroxymethyl-n-amylnitrosamine, formaldehyde (demethylation), and pentaldehyde (depentylation). With uninduced microsomes from male rats, MAb 1-68-11 inhibited 4-hydroxylation by 73% and demethylation by 46%. This indicated the major contribution of constitutive male-specific P-450 IIC11 to the metabolism. Inhibition studies with MAbs 2-66-3 and 1-91-3 indicated that P-450 IIB1 contributed 19% and IIE1 35% to demethylation. With uninduced microsomes from females, MAb 1-68-11 produced similar inhibitions to those in male rats, indicating that female-specific P-450 IIC12 (which is closely related to IIC11) also catalyzed 4-hydroxylation and demethylation. With microsomes from 3-methylcholanthrene-induced male rats, P-450 IA1 and/or IA2 were responsible for 60% of 3-hydroxylation and 40% of depentylation. With microsomes from phenobarbital-treated rats, P-450 IIB1 and IIB2 catalyzed all 6 reactions but especially 4-hydroxylation and depentylation, which were 50-75% inhibited by MAb 2-66-3. Microsomes from Aroclor-induced males behaved as if they were induced by both 3-methylcholanthrene and phenobarbital. After treatment with isoniazid (a P-450 IIE1 inducer), inhibition by MAb 1-91-3 indicated a 45% contribution of P-450 IIE1 to demethylation, and both P-450 IIE1 and IIB1 (or IIB2) appear to have been induced. A major finding with uninduced microsomes was the high specificity of MAb 1-68-11 for inhibiting 4-hydroxylation, indicating that P-450 IIC11 and IIC12 catalyzed most of this omega-1-hydroxylation. In microsomes from induced rats, the MAb inhibitions showed the role of the induced P-450 IA1 (or IA2), IIB1 (or IIB2), and IIE1 in methyl-n-amylnitrosamine hydroxylation at different positions, as well as the presence of P-450 IIC11. This study illustrates the usefulness of inhibitory MAbs for defining the contribution of individual P-450s to position-specific metabolism. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP MIRVISH, SS (reprint author), UNIV NEBRASKA,MED CTR,EPPLEY INST RES CANC,OMAHA,NE 68105, USA. FU NCI NIH HHS [R01-CA-35628, CA-36727] NR 26 TC 19 Z9 19 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1991 VL 51 IS 4 BP 1059 EP 1064 PG 6 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700001 PM 1997155 ER PT J AU ANGLARD, P TORY, K BRAUCH, H WEISS, GH LATIF, F MERINO, MJ LERMAN, MI ZBAR, B LINEHAN, WM AF ANGLARD, P TORY, K BRAUCH, H WEISS, GH LATIF, F MERINO, MJ LERMAN, MI ZBAR, B LINEHAN, WM TI MOLECULAR ANALYSIS OF GENETIC CHANGES IN THE ORIGIN AND DEVELOPMENT OF RENAL-CELL CARCINOMA SO CANCER RESEARCH LA English DT Article ID HUMAN ADRENOCORTICAL CARCINOMAS; VONHIPPEL-LINDAU DISEASE; WILMS TUMOR; SHORT ARM; DNA-SEQUENCE; REGIONAL LOCALIZATION; HUMAN CHROMOSOME-3; POLYMORPHIC LOCI; LUNG-CARCINOMA; LINKAGE MAP AB Renal cell carcinoma has been characterized by an abnormality on the short arm of chromosome 3 which suggests the presence of a tumor suppressor gene at this location. In order to more precisely define the location of the renal cell carcinoma gene and to differentiate molecular changes occurring in early stages of renal neoplasia versus those occurring later in malignant progression, DNA from normal and tumor tissue from 60 patients with various stages of renal cell carcinoma was analyzed for loss of alleles at different chromosomal loci. In tumor tissue from 51 of 58 evaluable patients (88%) there was loss of heterozygosity at one or more of 10 loci tested on chromosome 3 independently of tumor stage. Analysis of the genotypes identified the distal portion of 3p bounded by D3S2 and D3S22 (3p21-26) as the region of the disease gene. In tumor tissue from patients with advanced renal cell carcinoma, we found loss of heterozygosity on chromosome 11p in 5 of 21 (24%), on chromosome 13 in 3 of 9 (33%), and on chromosome 17 in 2 of 19 (11%). We found no loss of heterozygosity at the loci on chromosomes 11, 13, or 17 in tumor tissue from patients with localized renal cell carcinoma (N = 5). These data suggest the existence of a tumor suppressor gene on chromosome 3p which may be essential to the genesis of sporadic renal cell carcinoma and that other tumor suppressor genes are associated with progression of this malignancy. C1 NCI,DIV CANC TREATMENT,SURG BRANCH,UROL ONCOL SECT,BLDG 10,ROOM 2B47,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES FACIL,IMMUNOBIOL LAB,FREDERICK,MD 21701. NCI,DIV CANC BIOL & DIAG,BETHESDA,MD 20892. NR 72 TC 160 Z9 161 U1 0 U2 5 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1991 VL 51 IS 4 BP 1071 EP 1077 PG 7 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700003 PM 1671754 ER PT J AU CANDRIAN, U YOU, M GOODROW, T MARONPOT, RR REYNOLDS, SH ANDERSON, MW AF CANDRIAN, U YOU, M GOODROW, T MARONPOT, RR REYNOLDS, SH ANDERSON, MW TI ACTIVATION OF PROTOONCOGENES IN SPONTANEOUSLY OCCURRING NONLIVER TUMORS FROM C57BL/6 X C3H F1-MICE SO CANCER RESEARCH LA English DT Article ID K-RAS ONCOGENE; B6C3F1 MOUSE; HA-RAS; TRANSGENIC MICE; LUNG-TUMORS; GENE; MUTATIONS; ADENOCARCINOMA; MUTAGENESIS; LYMPHOMAS AB The C57BL/6 x C3H F1 (hereafter called B6C3F1) mouse is an important animal model for long-term carcinogenesis studies. Maintained under normal laboratory conditions, these mice develop various types of spontaneous tumors during their lifetime. Activated Ha-ras genes have been detected in 66% of spontaneous hepatocellular tumors in the B6C3F1 mouse [Reynolds et al., Science (Washington DC), 237: 1309, 1988]. In this study 49 spontaneous non-liver tumors were investigated for oncogene activation by DNA transfection techniques. Of the 49 tumor DNAs analyzed, only 5 yielded multiple foci in the NIH 3T3 focus assay: 2 of 10 pulmonary adenocarcinomas; 0 of 25 lymphomas; 2 of 2 Harderian gland adenomas; 0 of 1 adenocarcinoma of the small intestine; 1 of 6 malignant skin tumors; 0 of 4 hemangiosarcomas; and 0 of 1 lung metastasis of a hepatocellular carcinoma. DNA from six lymphomas which were negative in the NIH 3T3 focus assay were further analyzed for transforming genes by the nude mouse tumorigenicity assay. One of the five lymphomas tested positive with this assay. Southern blot analysis identified five activated ras genes: H-ras in two Harderian gland adenomas; K-ras in one pulmonary adenocarcinoma and in one s.c. adenocarcinoma; and N-ras in one s.c. adenocarcinoma; and N-ras in one lymphoma. The mutations involved were CG to AT and AT to TA in codon 61 of the H-ras genes, GC to AT or TA in codon 12 of the K-ras genes, and a GC to AT mutation in codon 12 of the N-ras gene. Transformant DNA from a pulmonary adenocarcinoma which yielded multiple foci in the transfection assay did not hybridize to DNA probes specific for the K-, H-, and N-ras, raf, neu, and met genes. Thirteen additional tumor DNAs yielded a single focus in the NIH 3T3 transfection assay. The transformant DNAs retransmitted in a second cycle transfection assay. Rearranged and/or amplified raf genes were detected in six of the transformant DNAs. At present we do not know whether these activated raf genes were present in the original tumor DNA. The other seven transformant DNAs did not hybridize with any of the above mentioned specific DNA probes utilized in Southern blot analysis. Unlike liver tumors, the activation of ras protooncogenes is not a frequent event in the development of spontaneous non-liver tumors of the B6C3F1 mouse. The results from this study should aid in understanding the neoplastic development associated with exposure to chemical carcinogens in the B6C3F1 mouse. C1 NIEHS,MOLEC TOXICOL LAB,RES TRIANGLE PK,NC 27709. NIEHS,CHEM PATHOL BRANCH,RES TRIANGLE PK,NC 27709. NR 36 TC 28 Z9 28 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1991 VL 51 IS 4 BP 1148 EP 1153 PG 6 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700015 PM 1997158 ER PT J AU BALE, AE NORTON, JA WONG, EL FRYBURG, JS MATON, PN OLDFIELD, EH STREETEN, E AURBACH, GD BRANDI, ML FRIEDMAN, E SPIEGEL, AM TAGGART, RT MARX, SJ AF BALE, AE NORTON, JA WONG, EL FRYBURG, JS MATON, PN OLDFIELD, EH STREETEN, E AURBACH, GD BRANDI, ML FRIEDMAN, E SPIEGEL, AM TAGGART, RT MARX, SJ TI ALLELIC LOSS ON CHROMOSOME-11 IN HEREDITARY AND SPORADIC TUMORS RELATED TO FAMILIAL MULTIPLE ENDOCRINE NEOPLASIA TYPE-1 SO CANCER RESEARCH LA English DT Article ID PARATHYROID TUMORS; RETINOBLASTOMA; GENES AB Familial multiple endocrine neoplasia type 1 (FMEN1) is an autosomal dominant disorder characterized by tumors of the parathyroid glands, pancreatic islets, and anterior pituitary. The gene for this disease maps to chromosome 11q12-11q13, and allelic loss in this region has been shown in both sporadic and FMEN1-related parathyroid tumors, FMEN1-related pancreatic islet tumors, and rarely in sporadic anterior pituitary tumors. We tested for allelic loss at 7 loci on chromosome 11 in 17 tumors outside the parathyroid. We found loss of heterozygosity in 2 of 2 FMEN1-related benign pancreatic islet tumors but in none of 8 informative sporadic islet tumors (P = 0.02) including 5 malignant gastrinomas. Of 3 islet tumors from patients who had some but not all features of FMEN1, one showed allelic loss for 5 of 5 informative restriction fragment length polymorphisms, and the other 2 retained heterozygosity for all informative markers. A bronchial carcinoid from an FMEN1 patient and 3 sporadic anterior pituitary tumors showed no allelic loss. These data provide new evidence that many sporadic pancreatic islet neoplasms, even when malignant, do not develop through homozygous inactivation of the MEN1 gene. C1 NCI,SURG BRANCH,BETHESDA,MD 20892. NIADDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. NIADDKD,METAB DIS BRANCH,BETHESDA,MD 20892. NIADDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892. WAYNE STATE UNIV,DEPT MOLEC BIOL & GENET,DETROIT,MI 48201. UNIV FLORENCE,DEPT PHYSIOPATHOL,I-50139 FLORENCE,ITALY. RP BALE, AE (reprint author), YALE UNIV,SCH MED,DEPT HUMAN GENET,BOX 3333,NEW HAVEN,CT 06510, USA. FU NCI NIH HHS [CA-50497] NR 20 TC 114 Z9 115 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 FEB 15 PY 1991 VL 51 IS 4 BP 1154 EP 1157 PG 4 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700016 PM 1671755 ER PT J AU DEBENEDETTI, F FALK, L RUSCETTI, FW COLBURN, NH FALTYNEK, CR OPPENHEIM, JJ AF DEBENEDETTI, F FALK, L RUSCETTI, FW COLBURN, NH FALTYNEK, CR OPPENHEIM, JJ TI SYNERGISTIC INHIBITION OF PHORBOL ESTER-INDUCED TRANSFORMATION OF JB6 CELLS BY TRANSFORMING GROWTH-FACTOR-BETA AND RETINOIC ACID SO CANCER RESEARCH LA English DT Article ID MOUSE EPIDERMAL-CELLS; FACTOR TYPE-BETA; CELLULAR RECEPTOR; ANALOGS RETINOIDS; MEMBRANE-RECEPTOR; VITAMIN-A; PROMOTER; DIFFERENTIATION; PROLIFERATION; STIMULATION AB Transforming growth factor-beta (TGF-beta) plays a complex role as a regulator of proliferation and differentiation of many cell types, including cells of epithelial origin. In this study, we examined whether TGF-beta, alone or in combination with retinoic acid, was able to inhibit the transformation of the murine epidermal cell line JB6. When treated with phorbol myristate acetate (PMA) and other tumor promoters, the nontumorigenic and anchorage-dependent JB6 cells acquired a tumor phenotype, as shown by the acquisition of tumorigenicity and anchorage independence. We found that TGB-beta inhibited the PMA-induced transformation of a subclone of JB6 cells. The effect of TGF-beta was due to an anti-transformation promoting activity, rather than to generalized growth inhibition, since TGF-beta neither inhibited the growth of monolayer cultures of JB6 cells, nor affected the colony-forming efficiency in agar of the JB6-derived permanently transformed RT101 cell line. TGF-beta was synergistic with retinoic acid, a known anti-tumor promoter, in inhibiting the PMA-induced transformation of JB6 cells. Examination of TGF-beta receptor expression on JB6 cells, by both binding and affinity labeling, showed that treatment with PMA significantly decreased TGF-beta receptor expression while retinoic acid counteracted this effect of PMA, thus suggesting that the synergy between retinoic acid and TGF-beta may be due, at least in part, to modulation of TGF-beta receptor expression. TGF-beta, therefore, appears to function as an incomplete antipromoter whose action can be permitted and/or complemented by retinoic acid. Our data demonstrating that TGF-beta has anti-transformation promoting activity suggest that TGF-beta plays a role in maintaining homeostasis of epithelial cells, not only by regulating cell proliferation and differentiation, but also by counteracting events that lead to malignant transformation. C1 NCI, FREDERICK CANC RES & DEV CTR MOLEC IMMUNOREGULAT L, FREDERICK, MD 21701 USA. NCI, FREDERICK CANC RES & DEV CTR, DYNCORP, PROGRAM RESOURCES INC, FREDERICK, MD 21701 USA. NCI, FREDERICK CANC RES & DEV CTR, VIRAL CARCINOGENESIS LAB, FREDERICK, MD 21701 USA. FU PHS HHS [N01-C0-74102] NR 43 TC 15 Z9 15 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 FEB 15 PY 1991 VL 51 IS 4 BP 1158 EP 1164 PG 7 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700017 PM 1847657 ER PT J AU ALLEY, MC PACULACOX, CM HURSEY, ML RUBINSTEIN, LR BOYD, MR AF ALLEY, MC PACULACOX, CM HURSEY, ML RUBINSTEIN, LR BOYD, MR TI MORPHOMETRIC AND COLORIMETRIC ANALYSES OF HUMAN TUMOR-CELL LINE GROWTH AND DRUG SENSITIVITY IN SOFT AGAR CULTURE SO CANCER RESEARCH LA English DT Article ID PROTAMINE SULFATE; STEM-CELLS; TETRAZOLIUM SALT; CYTO-TOXICITY; LUNG TUMOR; ASSAY; SURVIVAL; COLONIES; MOUSE; ESTABLISHMENT AB Previous studies have demonstrated the suitability of image analysis of tetrazolium-stained colonies to assess growth and drug sensitivity of human tumor cells cultivated in soft agar culture. In the present study, the potential utility of colorimetric analysis to expedite experimental drug evaluations using human tumor cell lines was investigated. The same culture dishes were assessed by image analysis and by formazan colorimetry for purposes of comparing multiple methods of measuring growth as well as growth inhibition. Replicate cultures treated with 2-(p-iodonitrophenyl)-3-p-nitrophenyl-5-phenyltetrazolium chloride or 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide exhibited nearly identical colony count and volume indices as well as excellent correlation in colorimetric end points. Colony-forming unit volume analysis versus colorimetric assessment of the same cultures following dimethyl sulfoxide extraction of protamine sulfate-rinsed, dried soft agar cultures exhibited excellent linear correlation for both growth (Pearson r ranging from 0.95 to 1.00) and drug sensitivity (Pearson r ranging from 0.90 to 0.99, and Spearman r ranging from 0.82 to 0.97) and similar drug sensitivity profiles. Results of the current investigation indicate that end points of soft agar culture remain stable for a period of at least 2 weeks following assay termination. In addition, a colorimetric detection range of 1.3-2.2 log units permits determinations of survival levels ranging from 100 to 5% of respective control levels. Colorimetric analysis is anticipated to expedite soft agar colony formation assay evaluations (a) by reducing the need to use the more rigorous and time-consuming image analysis procedures to measure activity in preliminary drug sensitivity assays and (b) by permitting the determination of effective concentration ranges of new experimental agents for subsequent, more detailed investigations. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOMETR RES BRANCH,FREDERICK,MD 21701. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,FREDERICK,MD 21701. RP ALLEY, MC (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DEV THERAPEUT PROGRAM,FREDERICK,MD 21701, USA. FU NCI NIH HHS [N01-CO-74102] NR 48 TC 41 Z9 42 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 FEB 15 PY 1991 VL 51 IS 4 BP 1247 EP 1256 PG 10 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700031 PM 1705170 ER PT J AU CRYSTAL, RG AF CRYSTAL, RG TI ALPHA-ANTITRYPSIN DEFICIENCY - PATHOGENESIS AND TREATMENT .6. SO HOSPITAL PRACTICE LA English DT Article AB Inherited defects of the gene coding for a serum protein that protects alveolar walls from proteolysis constitute one cause of emphysema, with or without liver disease. The deficiency can be reversed with intravenous administration of the antiprotease, keeping serum levels above the minimum needed for lung protection. RP CRYSTAL, RG (reprint author), NHLBI,PULM BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 14 Z9 14 U1 0 U2 1 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 8750-2836 J9 HOSP PRACT JI Hosp. Pract. PD FEB 15 PY 1991 VL 26 IS 2 BP 81 EP & PG 0 WC Medicine, General & Internal SC General & Internal Medicine GA EW970 UT WOS:A1991EW97000010 PM 1899256 ER PT J AU WALDMANN, TA AF WALDMANN, TA TI THE INTERLEUKIN-2 RECEPTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID CELL GROWTH-FACTOR; HUMAN T-CELLS; MONOCLONAL-ANTIBODY; TAC ANTIGEN; BETA-CHAIN; IL-2 RECEPTOR; MOLECULAR-CLONING; KINASE ACTIVATION; PHORBOL DIESTER; PROTEIN-KINASE RP WALDMANN, TA (reprint author), NCI,METAB BRANCH,BETHESDA,MD 20892, USA. NR 88 TC 293 Z9 301 U1 1 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 15 PY 1991 VL 266 IS 5 BP 2681 EP 2684 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000001 PM 1993646 ER PT J AU CRIPPA, MP NICKOL, JM BUSTIN, M AF CRIPPA, MP NICKOL, JM BUSTIN, M TI DEVELOPMENTAL-CHANGES IN THE EXPRESSION OF HIGH MOBILITY GROUP CHROMOSOMAL-PROTEINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID BINDING-SITES; CDNA; DNA; SEQUENCE; HMG-14; GENES; HMG1 AB The high mobility group (HMG) chromosomal proteins may modulate the structure of distinct regions in chromatin, thereby affecting processes such as development and differentiation. Here we report that the levels of the HMG chromosomal proteins and their mRNAs change significantly during erythropoiesis. Erythroid cells from 5-day chicken embryos contain 2.5-10 times more HMG mRNAs than cells from 14-day embryos, whereas circulating cells from adult animals are devoid of HMG and most other mRNAs. Nuclear run-off experiments and Northern analysis of RNA from various developmental stages and from Percoll-fractionated cells indicate that the genes are transcribed in early cells of either the primitive or definitive erythroid lineage. The rate of synthesis of the various HMGs changes during erythropoiesis; in erythroid cells from 7-day embryos the ratio of HMG-14b or HMG-17 to HMG-14a is, respectively, 8 and 10 times lower than in 9-day erythroids. HMG-14a, the major chicken HMG-14 species, is synthesized mainly in primitive cells, while HMG-14b is preferentially synthesized in definitive cells. Thus, the change from primitive to definitive erythroid lineage during embryogenesis is accompanied by a change in the expression of HMG chromosomal proteins. Conceivably, these changes may affect the structure of certain regions in chromatin; however, it is not presently clear whether the switch in HMG protein gene expression is a consequence or a prerequisite for proper differentiation. C1 NCI,MOLEC CARCINOGENESIS LAB,BLDG 37,RM 3D12,BETHESDA,MD 20892. NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. RI crippa, massimo/J-6514-2016; Bustin, Michael/G-6155-2015 OI crippa, massimo/0000-0003-3214-9670; NR 21 TC 19 Z9 19 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 FEB 15 PY 1991 VL 266 IS 5 BP 2712 EP 2714 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000009 PM 1993650 ER PT J AU TSUCHIYA, M PRICE, SR TSAI, SC MOSS, J VAUGHAN, M AF TSUCHIYA, M PRICE, SR TSAI, SC MOSS, J VAUGHAN, M TI MOLECULAR-IDENTIFICATION OF ADP-RIBOSYLATION FACTOR MESSENGER-RNAS AND THEIR EXPRESSION IN MAMMALIAN-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NUCLEOTIDE-BINDING-PROTEINS; RIBOSYLTRANSFERASE ACTIVITY; CHOLERA-TOXIN; ADENYLATE-CYCLASE; GTP; ALIGNMENTS; COFACTOR; SEQUENCE; BOVINE; ACID AB ADP-ribosylation factors (ARFs) are approximately 20-kDa guanine nucleotide-binding proteins that serve as GTP-dependent allosteric activators of cholera toxin ADP-ribosyltransferase activity. Four species of mammalian ARF, termed ARF 1-4, have been identified by cloning. Hybridization of a bovine ARF 2 cDNA under low stringency with mammalian poly(A)+ RNA resulted in multiple bands that were subsequently assigned to the known ARF genes using ARF-specific oligonucleotide probes. The relative signal intensities of some bands (e.g. the 3.8- and 1.3-kilobase (kb) mRNAs) that hybridized with the cDNA were not, however, consistent with the intensities observed with the individual ARF-specific oligonucleotide probes. These inconsistencies suggested that other ARF-like mRNAs were comigrating with known ARF mRNAs. To explore this possibility, a cyclic AMP-differentiated HL-60 Lambda ZAP library was screened using the bovine ARF 2 cDNA. Clones corresponding to known ARF genes (1, 3, and 4) were identified by hybridization of positive clones with oligonucleotide probes specific for each ARF species; ARF 2 cDNA-positive, oligonucleotide-negative clones were sequenced. Two new ARF-like genes, ARF 5 and 6, encoding proteins of 180 and 175 amino acids, respectively, were identified. Both proteins contain consensus sequences believed to be involved in guanine nucleotide binding and GTP hydrolysis. ARF 5 was most similar in deduced amino acid sequence to ARF 4, which also has 180 amino acids. ARF 6, whose deduced amino acid sequence is identical with that of a putative chicken pseudogene (CPS1) except for a serine/threonine substitution, was different from other ARF species in size and deduced amino acid sequence. With mammalian poly(A)+ RNA from a variety of tissues and cultured cells, ARF 5 preferentially hybridized with a 1.3-kb mRNA, whereas ARF 6 hybridized with 1.8- and 4.2- kb mRNAs. The fact that the sizes of these mRNAs are similar to those of other ARFs (ARF 1, 1.9 kb; ARF 2, 2.6 kb; ARF 3, approximately 3.8 and 1.3 kb; ARF 4, 1.8 kb) explain the previously observed inconsistencies between the cDNA and ARF-specific oligonucleotide hybridization patterns. All six ARF cDNAs are more similar to each other than to other approximately 20-kDa guanine nucleotide-binding proteins. RP TSUCHIYA, M (reprint author), NHLBI,CELLULAR METAB,BETHESDA,MD 20892, USA. NR 29 TC 177 Z9 182 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 FEB 15 PY 1991 VL 266 IS 5 BP 2772 EP 2777 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000019 PM 1993656 ER PT J AU HUNYADY, L MERELLI, F BAUKAL, AJ BALLA, T CATT, KJ AF HUNYADY, L MERELLI, F BAUKAL, AJ BALLA, T CATT, KJ TI AGONIST-INDUCED ENDOCYTOSIS AND SIGNAL GENERATION IN ADRENAL GLOMERULOSA CELLS - A POTENTIAL MECHANISM FOR RECEPTOR-OPERATED CALCIUM ENTRY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; SMOOTH-MUSCLE CELLS; ANGIOTENSIN-II; INTRACELLULAR POTASSIUM; MEDIATED ENDOCYTOSIS; DOWN-REGULATION; INTERNALIZATION; METABOLISM; SECRETION; DEPLETION AB The relationships between receptor-mediated endocytosis and the generation of intracellular signals were analyzed in angiotensin II (AII)-stimulated adrenal glomerulosa cells. In cells equilibrated with I-125-AII analogs at 4-degrees-C, specifically bound agonist but not antagonist AII derivatives were rapidly internalized at 37-degrees-C. AII-induced internalization was not influenced by the presence or absence of extracellular Ca2+ but was inhibited by treatment with phenylarsine oxide (PAO) or by arresting coated pit formation with hypotonic shock and potassium depletion. Inhibition of internalization by PAO was prevented by the bifunctional sulfhydryl reagent dithiothreitol but only partially reversed by mercaptoethanol, and readdition of K+ restored internalization in K+-depleted cells. Treatment with PAO did not impair the initial AII-induced elevations of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) and cytoplasmic calcium ([Ca2+]i) but reduced the sustained phase of the Ins(1,4,5)P3 response by 85% and abolished the second phase of the cytoplasmic Ca2+ response; these responses were restored by concomitant treatment with dithiothreitol. Inhibition of AII-receptor internalization by K+ depletion also caused selective loss of the sustained phase of the AII-induced Ca2+ response. Thus, blockade of AII-receptor internalization has similar effects as extracellular Ca2+ deficiency, which abolishes the sustained but not the early AII-induced increases in Ins(1,4,5)P3 production and and [Ca2+]i. The close correlations between AII-induced internalization and the generation of Ins(1,4,5)P3 and [Ca2+]i responses suggest that endocytosis of the agonist-receptor complex is necessary to maintain the production of these intracellular signals. It is also possible that receptor-operated vesicular uptake of extracellular Ca2+ makes a significant contribution to the sustained [Ca2+]i responses of certain agonist-stimulated target cells. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLDG 10,RM B1L-400,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. OI Balla, Tamas/0000-0002-9077-3335 NR 30 TC 81 Z9 81 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 FEB 15 PY 1991 VL 266 IS 5 BP 2783 EP 2788 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000021 PM 1993657 ER PT J AU SIEGMUND, HU KAUFMAN, S AF SIEGMUND, HU KAUFMAN, S TI HYDROXYLATION OF 4-METHYLPHENYLALANINE BY RAT-LIVER PHENYLALANINE-HYDROXYLASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID OXIDATION; CHROMATOGRAPHY; PURIFICATION; LYSOLECITHIN; SUBSTRATE; INVIVO AB Rat liver phenylalanine hydroxylase that has been activated with lysolecithin catalyzes the hydroxylation of 4-methylphenylalanine in the presence of a pterin cofactor. Two products, 4-hydroxymethylphenylalanine and 3-methyltyrosine, can be detected. The total amount of amino acids hydroxylated is equal to the amount of tetrahydropterin oxidized. Isotopic labeling studies with (O2)-O-18 and (H2O)-O-18 show that the hydroxyl groups of both products are derived from molecular oxygen and not from water. Results obtained with H-2-labeled substrates support the conclusion that these products are formed via different mechanistic pathways. Our previous investigations on substrate analogs, as well as the present results, indicate that a highly reactive oxygen-containing intermediate, such as an enzyme-bound iron-oxo compound, must be the hydroxylating species. Our present results could stimulate further discussion of the possibility that the reaction mechanism for the "NIH-shift" of the methyl group may not involve the spontaneous opening of an epoxide intermediate. C1 NIMH,NEUROCHEM LAB,BETHESDA,MD 20892. NR 29 TC 26 Z9 27 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 FEB 15 PY 1991 VL 266 IS 5 BP 2903 EP 2910 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000039 PM 1993664 ER PT J AU SAKAMOTO, K FORDIS, CM CORSICO, CD HOWARD, TH HOWARD, BH AF SAKAMOTO, K FORDIS, CM CORSICO, CD HOWARD, TH HOWARD, BH TI MODULATION OF HELA-CELL GROWTH BY TRANSFECTED 7SL RNA AND ALU GENE-SEQUENCES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID POLYMERASE-III TRANSCRIPTION; SIGNAL RECOGNITION PARTICLE; ADENOVIRUS VA RNA1; SURFACE ANTIGEN; DNA-SEQUENCES; NEURONAL DIFFERENTIATION; REPETITIVE SEQUENCES; NUCLEOTIDE-SEQUENCE; MAMMALIAN GENOMES; RODENT CELLS AB Alu and 7SL RNA gene sequences were tested for the potential to regulate mammalian cell growth by introducing these sequences into HeLa cells in a coupled DEAE-dextran transfection/affinity cell sorting system. Both Alu and 7SL RNA genes mediated inhibition of [H-3]thymidine and [S-35]methionine incorporation in recipient cells. In addition, short term growth curves were performed on calcium phosphate/DNA cotransfected, affinity-purified cells. This second assay revealed that transfected Alu and 7SL RNA can also cause suppression of HeLa cell proliferation. To investigate whether transcription or polymerase III (pol III) transcription factor binding was required for inhibitory activity, mutations were introduced into RNA pol III B block promoter elements in each of these genes. Suppression of [H-3]thymidine incorporation was dependent on the presence of this pol III element in both genes; likewise, 7SL RNA-mediated growth suppression required the presence of the pol III B block promoter element. The results of this study indicate that Alu and 7SL RNA gene sequences interact with cellular factors that are important for HeLa cell proliferation and suggest that these pol III-transcribed elements may be involved in the regulation of cellular growth. C1 NIH,HOWARD HUGHES MED INST,NIH,RES SCHOLARS PROGRAM,BETHESDA,MD 20892. NCI,DIV CANC BIOL & DIAG,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 81 TC 34 Z9 34 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 FEB 15 PY 1991 VL 266 IS 5 BP 3031 EP 3038 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000056 PM 1704372 ER PT J AU PETTEPHER, CC LEDOUX, SP BOHR, VA WILSON, GL AF PETTEPHER, CC LEDOUX, SP BOHR, VA WILSON, GL TI REPAIR OF ALKALI-LABILE SITES WITHIN THE MITOCHONDRIAL-DNA OF RINR-38 CELLS AFTER EXPOSURE TO THE NITROSOUREA STREPTOZOTOCIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID COVALENT BINDING; RAT-LIVER; ALKYLATION; MECHANISMS; NUCLEAR; DAMAGE; GENE; METABOLITES; CARCINOGENS; GLYCOSYLASE AB Studies were initiated to investigate whether mechanisms exist within mitochondria to repair damage incurred by mitochondrial DNA after exposure to alkylating toxins. A clonal isolate from a rat insulinoma cell line was utilized to measure the formation and repair of alkali-labile sites within the mitochondrial genome after exposure to the alkylating antibiotic streptozotocin. Alkali-labile sites were formed in mitochondrial DNA in a dose-dependent fashion. Eight hours after exposure to the toxin, 55% of the lesions were removed. The level of repair increased to 70% after 24 h. In comparison, only 46% of N7-methylguanines were removed across the entire cellular genome. These studies demonstrate that streptozotocin causes appreciable mitochondrial DNA damage in a dose-dependent manner and provide the first evidence that a repair mechanism for alkali-labile sites is present within the mitochondrion. C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. RP PETTEPHER, CC (reprint author), UNIV SO ALABAMA,DEPT STRUCT & CELLULAR BIOL,MOBILE,AL 36688, USA. FU NIEHS NIH HHS [ES00150, ES03456] NR 30 TC 117 Z9 128 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 FEB 15 PY 1991 VL 266 IS 5 BP 3113 EP 3117 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000067 PM 1825207 ER PT J AU POSSANI, LD MARTIN, BM FLETCHER, MD FLETCHER, PL AF POSSANI, LD MARTIN, BM FLETCHER, MD FLETCHER, PL TI DISCHARGE EFFECT ON PANCREATIC EXOCRINE SECRETION PRODUCED BY TOXINS PURIFIED FROM TITYUS-SERRULATUS SCORPION-VENOM SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMINO-ACID-SEQUENCE; 3-DIMENSIONAL STRUCTURE; CENTRUROIDES-NOXIUS; CHANNEL; PURIFICATION; HOFFMANN; CURRENTS; LIGHT; CELLS; MELLO AB Three toxic polypeptides were purified from the venom of the Brazilian scorpion Tityus serrulatus by means of gel filtration in Sephadex G-50 and ion-exchange chromatography in carboxymethylcellulose. The peptides are basic molecules with molecular weights in the range of 7000 for which the amino acid compositions and sequences were determined. The effect of the purified peptides on pancreatic exocrine secretion in the guinea pig was studied. Biochemical measurements show that the cells are stimulated by these peptides to discharge their zymogen granules. Light and electron microscopic images confirm the biochemical measurements. At the light microscope level, acinar cells show dramatically fewer zymogen granules than in control pancreas with the appearance of large vacuoles and some loss of morphological integrity. Electron micrographs display apical regions devoid of zymogen granules and condensing vacuoles whereas acinar lumina contain crystalline secretory material. The secretory effect observed in vitro is comparable to that of carbamylcholine and that of the peptidergic secretagogue cholecystokinin-pancreozymin. C1 E CAROLINA UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, GREENVILLE, NC 27858 USA. NIMH, ALCOHOL DRUG ABUSE & MENTAL HLTH ADM, CLIN NEUROSCI BRANCH, BETHESDA, MD 20892 USA. UNIV NACL AUTONOMA MEXICO, CTR INVEST INGN GENET & BIOTECNOL, DEPT BIOQUIM, CUERNAVACA 62270, MEXICO. RI Possani, Lourival/J-2397-2013 FU NIADDK NIH HHS [AM27114] NR 40 TC 58 Z9 61 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 FEB 15 PY 1991 VL 266 IS 5 BP 3178 EP 3185 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000077 PM 1993690 ER PT J AU OSAWA, Y HIGHET, RJ BAX, A POHL, LR AF OSAWA, Y HIGHET, RJ BAX, A POHL, LR TI CHARACTERIZATION BY NMR OF THE HEME-MYOGLOBIN ADDUCT FORMED DURING THE REDUCTIVE METABOLISM OF BRCCL3 - COVALENT BONDING OF THE PROXIMAL HISTIDINE TO THE RING-I VINYL GROUP SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RAT-LIVER CYTOCHROME-P-450; HEPATIC CYTOCHROME-P-450; PROSTHETIC HEME; PROTEIN ADDUCTS; SUICIDE INACTIVATION; MECHANISM; CHLORAMPHENICOL; HEMOPROTEINS; DEGRADATION; DESTRUCTION AB The reductive debromination of BrCCl3 by ferrous deoxymyoglobin leads to the covalent bonding of the prosthetic heme to the protein. We have previously shown, by the use of peptide mapping and mass spectrometry, that histidine residue 93 is covalently bound to the heme moiety. In the present study the structure of the heme adduct was more completely determined by H-1 and C-13 NMR techniques. We have found that the ring I vinyl group of the prosthetic heme was altered by the addition of a histidine imidazole nitrogen to the alpha-carbon and a CCl2 moiety to the beta-carbon. The electronic absorption spectra of the oxidized and reduced states of the altered heme-protein indicated that the heme-iron exists in a bis-histidine-ligated form. Analysis of the crystal structure of native myoglobin suggested that for the altered heme-protein, histidine residues 97 and 64 are ligated to the heme-iron and that residue 97 has replaced the native proximal histidine residue 93. These movements, in effect a "histidine shuffle" at the active site, may be responsible for the enhanced reducing activity of the altered protein. C1 NHLBI,CHEM LAB,BETHESDA,MD 20892. NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. RP OSAWA, Y (reprint author), NHLBI,CHEM PHARMACOL LAB,BLDG 10,RM 8N110,BETHESDA,MD 20892, USA. NR 39 TC 31 Z9 32 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 FEB 15 PY 1991 VL 266 IS 5 BP 3208 EP 3214 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000081 PM 1993694 ER PT J AU MAGENDZO, K SHIRVAN, A CULTRARO, C SRIVASTAVA, M POLLARD, HB BURNS, AL AF MAGENDZO, K SHIRVAN, A CULTRARO, C SRIVASTAVA, M POLLARD, HB BURNS, AL TI ALTERNATIVE SPLICING OF HUMAN SYNEXIN MESSENGER-RNA IN BRAIN, CARDIAC, AND SKELETAL-MUSCLE ALTERS THE UNIQUE N-TERMINAL DOMAIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHROMAFFIN GRANULES; MEMBRANE-FUSION; PHOSPHOLIPID-BINDING; SHAKER LOCUS; CALCIUM; PROTEIN; GENE; DIVERSITY; FAMILY; POLYADENYLATION AB Several synexin (annexin VII) mRNAs have been identified by screening a human fibroblast cDNA library. One type of message contained an alternatively spliced cassette exon, predicting two isoforms of synexin differing in the N-terminal domain. Polymerase chain reaction analysis of synexin mRNA from various fetal and adult tissues, from human and monkey, revealed that the alternative splicing event is tissue-regulated; synexin mRNA containing the cassette exon is prevalent in brain, heart, and skeletal muscle. This is supported by Western blot analysis showing that muscle synexin (annexin VIIb) is larger than synexin from lung (annexin VIIa). The muscle and lung isoforms have the same molecular mass as the recombinant synexins expressed in Escherichia coli using cDNAs containing or lacking the cassette exon, respectively. The difference in size is consistent with the molecular masses predicted from the proteins encoded by the alternatively spliced synexin mRNAs. Another type of synexin mRNA contained a longer 3'-noncoding region generated by the selection of an alternate poly(A) signal. Northern analysis of human fibroblast RNA showed the presence of two bands (2.0- and 2.4-kilobase) when hybridized to a cDNA fragment of the coding region of synexin, but only the 2.4-kilobase band hybridized to a probe made from the longer 3' end. C1 NIDDK,CELL BIOL & GENET LAB,BLDG 8,RM 403,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. US FDA,DIV CARDIORENAL,BETHESDA,MD 20014. NR 34 TC 45 Z9 47 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 FEB 15 PY 1991 VL 266 IS 5 BP 3228 EP 3232 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX600 UT WOS:A1991EX60000084 PM 1825209 ER PT J AU TAKAHAMA, Y KOSUGI, A SINGER, A AF TAKAHAMA, Y KOSUGI, A SINGER, A TI PHENOTYPE, ONTOGENY, AND REPERTOIRE OF CD4-CD8- T-CELL RECEPTOR ALPHA-BETA+ THYMOCYTES - VARIABLE INFLUENCE OF SELF-ANTIGENS ON T-CELL RECEPTOR V-BETA USAGE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; MONOCLONAL-ANTIBODY; MURINE THYMOCYTES; PRECURSOR CELLS; CLONAL DELETION; LYMPHOCYTES-T; B-CELLS; I-E; EXPRESSION; GENE AB We have characterized CD4-CD8- double negative (DN) thymocytes that express TCR-alpha-beta and represent a minor thymocyte subpopulation expressing a markedly skewed TCR repertoire. We found that DN TCR-alpha-beta-+ thymocytes resemble mature T cells in that they (a) are phenotypically CD2(hi)CD5(hi)Qa2+HSA-, (b) appear late in ontogeny, and (c) are susceptible to cyclosporin A-induced maturation arrest. In addition, we found that DNA sequences 5' to the CD8-alpha gene were demethylated relative to their germline state, suggesting that DN TCR-alpha-beta-+ thymocytes are derived from cells that had at one time expressed their CD8-alpha gene locus. Because DN TCR-alpha-beta-+ thymocytes are known to express an unusual TCR repertoire with significant overexpression of V-beta-8, we were interested in examining the possible role played by self-Ag in shaping their TCR repertoire. It has been suggested that DN TCR-alpha-beta-+ thymocytes are derived from potentially self-reactive thymocytes that have escaped clonal deletion by down-regulating their surface expression of CD4 and/or CD8 determinants. However, apparently inconsistent with such an hypothesis, we found that the frequency of DN thymocytes expressing various anti-self TCR (V-beta-6, V-beta-8.1, V-beta-11, V-beta-17a) were not increased in strains expressing their putative self-Ag, but instead were either unaffected or significantly reduced in those strains. With regard to V-beta-8 expression among DN TCR-alpha-beta-+ thymocytes, V-beta-8 overexpression in DN TCR-alpha-beta-+ thymocytes appeared to be independent of, and superimposed on, the developmental appearance of the basic DN thymocyte repertoire. Even though V-beta-8 overexpression appeared to be generated by a mechanism distinct from that generating the rest of the DN TCR-alpha-beta-+ thymocyte repertoire, we found that super-Ag against which V-beta-8 TCR react introduced into the neonatal differentiation environment also significantly reduced, rather than increased, the frequency of DN TCR-alpha-beta-+V-beta-8+ thymocytes. Thus, the present study is consistent with DN TCR-alpha-beta-+ thymocytes being mature cells derived from CD8+ precursors, and documents that their TCR repertoire can be influenced, at least negatively, by either self-Ag or Ag introduced into the neonatal differentiation environment. However, we found no evidence to support the hypothesis that DN TCR-alpha-beta-+ thymocytes are enriched in cells expressing TCR reactive against self-Ag. RP TAKAHAMA, Y (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM 4B-17,BETHESDA,MD 20892, USA. NR 41 TC 121 Z9 121 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 FEB 15 PY 1991 VL 146 IS 4 BP 1134 EP 1141 PG 8 WC Immunology SC Immunology GA EW681 UT WOS:A1991EW68100009 PM 1825105 ER PT J AU MUKAIDA, N ZACHARIAE, CCO GUSELLA, GL MATSUSHIMA, K AF MUKAIDA, N ZACHARIAE, CCO GUSELLA, GL MATSUSHIMA, K TI DEXAMETHASONE INHIBITS THE INDUCTION OF MONOCYTE CHEMOTACTIC-ACTIVATING FACTOR PRODUCTION BY IL-1 OR TUMOR-NECROSIS-FACTOR SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MESSENGER-RNA; GENOMIC STRUCTURE; GENE; GLUCOCORTICOIDS; INTERLEUKIN-1; TRANSCRIPTION; CELLS; LYMPHOCYTES; DEGRADATION; EXPRESSION AB Recently purified and molecularly cloned monocyte chemotactic and activating factor (MCAF) may play a major role in recruiting and activating monocytes in the inflammatory process. We examined the effects of a potent anti-inflammatory agent, dexamethasone (DXS), on the production of this factor. Over a wide range of concentrations (10(-5) to 10(-8) M), DXS inhibited the production of MCAF at the mRNA and protein level in a human fibrosarcoma cell line, which was stimulated with either IL-1 or TNF-alpha. We examined the turn-over of synthesized MCAF mRNA that showed DXS decreased the stability of MCAF mRNA. Furthermore, the addition of actinomycin D and cycloheximide abolished this effect of DXS, indicating that de novo mRNA and protein synthesis were required for this process. In addition, a nuclear run-off analysis revealed that DXS also inhibited the transcription of IL-1- or TNF-activated MCAF genes. Therefore, both the destabilization of MCAF mRNA and the inhibition of transcription of the gene contribute to the decrease in the MCAF mRNA steady state level by DXS. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,BLDG 560,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOCHEM PHYSIOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,DYNCORP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. RI Mukaida, Naofumi/D-7623-2011 OI Mukaida, Naofumi/0000-0002-4193-1851 FU NCI NIH HHS [N01-CO-74102] NR 33 TC 113 Z9 115 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 FEB 15 PY 1991 VL 146 IS 4 BP 1212 EP 1215 PG 4 WC Immunology SC Immunology GA EW681 UT WOS:A1991EW68100020 PM 1991962 ER PT J AU GRZYCH, JM PEARCE, E CHEEVER, A CAULADA, ZA CASPAR, P HEINY, S LEWIS, F SHER, A AF GRZYCH, JM PEARCE, E CHEEVER, A CAULADA, ZA CASPAR, P HEINY, S LEWIS, F SHER, A TI EGG DEPOSITION IS THE MAJOR STIMULUS FOR THE PRODUCTION OF TH2 CYTOKINES IN MURINE SCHISTOSOMIASIS-MANSONI SO JOURNAL OF IMMUNOLOGY LA English DT Article ID STIMULATORY FACTOR-I; GRANULOMA-FORMATION; MONOCLONAL-ANTIBODY; PROTECTIVE IMMUNITY; CELL LINES; ANTIGEN; RESPONSES; MICE; EOSINOPHILIA; INFECTION AB To characterize Th cell populations induced by helminth infection, spleen cells from mice infected with Schistosoma mansoni were stimulated with parasite (worm or egg Ag) or mitogen (Con A) and the supernatants assayed for the Th1-specific cytokines IFN-gamma and IL-2 and the Th2-specific cytokines IL-4 and IL-5. Th2 cytokine production was not detected in substantial quantity until the 6 to 8th wk of infection and after reaching peak levels at 8 to 12 wk declined slowly thereafter. The time courses of IL-4 and IL-5 production, whereas differing from each other, closely resembled corresponding published data on IgE and peripheral blood eosinophil levels during murine schistosome infection. In contrast, Th1 cytokine responses occurred only during the first 6 wk of infection and were virtually absent during the peak period of Th2 production. To assess the role of egg deposition in the observed pattern of Th response, cytokine production was assayed in mice carrying unisexual schistosome infections in which parasite eggs are absent. Splenocytes from these animals displayed only marginal Th2 cytokine synthesis but greater Th1 cytokine responses than the corresponding cells from mice with bisexual infections. Moreover, cultures of liver tissue or isolated granulomas from infected mice constitutively produced high levels of IL-4 and IL-5 but failed to synthesize significant amounts of IL-2 and IFN-gamma even when stimulated with egg Ag or mitogen. Taken together the data indicate that egg deposition is the major stimulus of Th2 cytokine response in S. mansoni-infected mice and suggest that T cells belonging to this subset must play a major role in egg granuloma formation. C1 NIAID,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,BLDG 4,ROOM 126,BETHESDA,MD 20892. BIOMED RES INST,ROCKVILLE,MD 20852. NIAID,PARASIT DIS LAB,HOST PARASITE RELAT SECT,BETHESDA,MD 20892. FU PHS HHS [IA-16006] NR 28 TC 455 Z9 463 U1 0 U2 11 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1991 VL 146 IS 4 BP 1322 EP 1327 PG 6 WC Immunology SC Immunology GA EW681 UT WOS:A1991EW68100037 PM 1825109 ER PT J AU SMYTH, MJ ORTALDO, JR AF SMYTH, MJ ORTALDO, JR TI COMPARISON OF THE EFFECT OF IL-2 AND IL-6 ON THE LYTIC ACTIVITY OF PURIFIED HUMAN PERIPHERAL-BLOOD LARGE ANTIGRANULOCYTES LYMPHOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NATURAL-KILLER CELLS; P75 INTERLEUKIN-2 RECEPTOR; MONOCLONAL-ANTIBODY; GAMMA PRODUCTION; HUMAN THYMOCYTES; T-CELLS; PROGENITORS; DEFINITION; EXPRESSION; ACTIVATION AB The effects of IL-6 and IL-2 on highly purified, human peripheral blood large granular lymphocytes (LGL) were investigated and compared. IL-6 enhanced LGL NK activity in a dose-dependent manner against K562, however IL-2 was a more potent stimulus of LGL NK function. Neither IL-2 nor IL-6 increased LGL cytotoxic potential in a parallel estimation of heteroconjugated antibody (anti-CD16 x anti-nitrophenyl mAb)-dependent cytotoxicity against nitrophenyl-modified YAC. Unlike IL-2, IL-6 did not significantly induce LGL lymphokine-activated killer activity, LGL proliferation, or LGL lymphokine production. In particular, IL-6 did not stimulate detectable LGL IL-2 production or IL-2R modulation, and mAb to the p75 IL-2R had no effect on IL-6 induction of LGL NK activity. Therefore, in the absence of T cells, IL-6 provided an IL-2-independent signal to LGL that resulted in augmentation of their NK activity without stimulating their proliferation or other LGL functions. RP SMYTH, MJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,EXPTL IMMUNOL LAB,CMIS,FREDERICK,MD 21702, USA. RI Smyth, Mark/H-8709-2014 OI Smyth, Mark/0000-0001-7098-7240 NR 41 TC 51 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 FEB 15 PY 1991 VL 146 IS 4 BP 1380 EP 1384 PG 5 WC Immunology SC Immunology GA EW681 UT WOS:A1991EW68100046 PM 1991975 ER PT J AU DAVIS, DG AF DAVIS, DG TI IMPROVED MULTIPLET EDITING OF PROTON-DETECTED, HETERONUCLEAR SHIFT-CORRELATION SPECTRA SO JOURNAL OF MAGNETIC RESONANCE LA English DT Note ID NMR RP DAVIS, DG (reprint author), NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 18 TC 41 Z9 41 U1 1 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-2364 J9 J MAGN RESON PD FEB 15 PY 1991 VL 91 IS 3 BP 665 EP 672 DI 10.1016/0022-2364(91)90398-D PG 8 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA EY507 UT WOS:A1991EY50700026 ER PT J AU SCHOONOVER, R BENAVRAHAM, D HAVLIN, S KOPELMAN, R WEISS, GH AF SCHOONOVER, R BENAVRAHAM, D HAVLIN, S KOPELMAN, R WEISS, GH TI NEAREST-NEIGHBOR DISTANCES IN DIFFUSION-CONTROLLED REACTIONS MODELED BY A SINGLE MOBILE TRAP SO PHYSICA A LA English DT Article ID STATE CHEMICAL-KINETICS; SEGREGATION; REACTANTS; DENSITY; MEDIA AB We consider a system consisting of an infinite number of identical particles on a lattice initially uniformly distributed, which diffuse in the presence of a single mobile trap and ask for the time-dependent behavior of the distance of the trap from the nearest particle. This quantity is a measure of the tendency of the system to self-segregate. We show, by a simulation incorporating the exact enumeration method, that in one dimension the expected distance [L(t)] scales as [L(t)] approximately t-alpha as t --> infinity, where the exponent alpha depends only on the ratio of the diffusion constants. A heuristic expression for alpha is suggested, analogous to a rigorous exponent found by ben-Avraham for a similar but not identical problem. The flux into the trap is found to vary as t-1/2 independent of the diffusion constants. C1 CLARKSON UNIV,POTSDAM,NY 13676. NIH,BETHESDA,MD 20892. BAR ILAN UNIV,DEPT PHYS,IL-52100 RAMAT GAN,ISRAEL. RP SCHOONOVER, R (reprint author), UNIV MICHIGAN,ANN ARBOR,MI 48109, USA. NR 19 TC 42 Z9 42 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4371 J9 PHYSICA A JI Physica A PD FEB 15 PY 1991 VL 171 IS 2 BP 232 EP 238 DI 10.1016/0378-4371(91)90275-H PG 7 WC Physics, Multidisciplinary SC Physics GA FC531 UT WOS:A1991FC53100002 ER PT J AU KLEIN, CB CONWAY, K WANG, XW BHAMRA, RK LIN, XH COHEN, MD ANNAB, L BARRETT, JC COSTA, M AF KLEIN, CB CONWAY, K WANG, XW BHAMRA, RK LIN, XH COHEN, MD ANNAB, L BARRETT, JC COSTA, M TI SENESCENCE OF NICKEL-TRANSFORMED CELLS BY AN X-CHROMOSOME - POSSIBLE EPIGENETIC CONTROL SO SCIENCE LA English DT Article ID TUMOR-SUPPRESSOR GENES; CHINESE-HAMSTER; RETINOBLASTOMA; LOCALIZATION; CANCER; REGION; MOUSE; DNA AB Transfer of a normal Chinese hamster X chromosome (carried in a mouse A9 donor cell line) to a nickel-transformed Chinese hamster cell line with an Xq chromosome deletion resulted in senescence of these previously immortal cells. At early passages of the A9/CX donor cells, the hamster X chromosome was highly active, inducing senescence in 100% of the colonies obtained after its transfer into the nickel-transformed cells. However, senescence was reduced to 50% when Chinese hamster X chromosomes were transferred from later passage A9 cells. Full senescing activity of the intact hamster X chromosome was restored by treatment of the donor mouse cells with 5-azacytidine, which induced demethylation of DNA. These results suggest that a senescence gene or genes, which may be located on the Chinese hamster X chromosome, can be regulated by DNA methylation, and that escape from senescence and possibly loss of tumor suppressor gene activity can occur by epigenetic mechanisms. C1 NYU MED CTR,INST ENVIRONM MED,NEW YORK,NY 10016. UNIV N CAROLINA,SCH MED,LINEBERGER CANC RES CTR,CHAPEL HILL,NC 27599. NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. RI Wang, Xin/B-6162-2009; costa, max/H-1754-2012 FU NIEHS NIH HHS [ES 04715, ES 04895, ES 05512] NR 35 TC 153 Z9 154 U1 1 U2 4 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 15 PY 1991 VL 251 IS 4995 BP 796 EP 799 DI 10.1126/science.1990442 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EX575 UT WOS:A1991EX57500045 PM 1990442 ER PT J AU BOTTARO, DP RUBIN, JS FALETTO, DL CHAN, AML KMIECIK, TE VANDEWOUDE, GF AARONSON, SA AF BOTTARO, DP RUBIN, JS FALETTO, DL CHAN, AML KMIECIK, TE VANDEWOUDE, GF AARONSON, SA TI IDENTIFICATION OF THE HEPATOCYTE GROWTH-FACTOR RECEPTOR AS THE C-MET PROTOONCOGENE PRODUCT SO SCIENCE LA English DT Article ID MOLECULAR-CLONING; TYROSINE KINASE; CELL-LINE; PURIFICATION; GENE; PHOSPHORYLATION; ACTIVATION; SEQUENCE; SUBUNIT; CDNA AB Hepatocyte growth factor (HGF) is a plasminogen-like protein thought to be a humoral mediator of liver regeneration. A 145-kilodalton tyrosyl phosphoprotein observed in rapid response to HGF treatment of intact target cells was identified by immunoblot analysis as the beta-subunit of the c-met proto-oncogene product, a membrane-spanning tyrosine kinase. Covalent cross-linking of I-125-labeled ligand to cellular proteins of appropriate size that were recognized by antibodies to c-met directly established the c-met product as the cell-surface receptor for HGF. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,FREDERICK,MD 21702. RP BOTTARO, DP (reprint author), NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892, USA. RI Bottaro, Donald/F-8550-2010 OI Bottaro, Donald/0000-0002-5057-5334 NR 35 TC 1853 Z9 1904 U1 7 U2 48 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 15 PY 1991 VL 251 IS 4995 BP 802 EP 804 DI 10.1126/science.1846706 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EX575 UT WOS:A1991EX57500047 PM 1846706 ER PT J AU GIBSON, CW GOLUB, E DING, WD SHIMOKAWA, H YOUNG, M TERMINE, J ROSENBLOOM, J AF GIBSON, CW GOLUB, E DING, WD SHIMOKAWA, H YOUNG, M TERMINE, J ROSENBLOOM, J TI IDENTIFICATION OF THE LEUCINE-RICH AMELOGENIN PEPTIDE (LRAP) AS THE TRANSLATION PRODUCT OF AN ALTERNATIVELY SPLICED TRANSCRIPT SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID MESSENGER-RNA; ENAMEL; PROTEINS; COMPONENTS; SEQUENCE C1 UNIV PENN,SCH DENT MED,DEPT ANAT & HISTOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH DENT MED,ORAL BIOL RES CTR,PHILADELPHIA,PA 19104. NIDR,BONE RES BRANCH,BETHESDA,MD 20892. FU NIDCR NIH HHS [DE08239, DE09164] NR 20 TC 88 Z9 91 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD FEB 14 PY 1991 VL 174 IS 3 BP 1306 EP 1312 DI 10.1016/0006-291X(91)91564-S PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EY145 UT WOS:A1991EY14500038 PM 1996994 ER PT J AU CHOCK, SP RHEE, SG TANG, LC SCHMAUDERCHOCK, EA AF CHOCK, SP RHEE, SG TANG, LC SCHMAUDERCHOCK, EA TI LINKING PHOSPHOLIPASE-A2 TO PHOSPHOLIPID TURNOVER AND PROSTAGLANDIN SYNTHESIS IN MAST-CELL GRANULES SO EUROPEAN JOURNAL OF BIOCHEMISTRY LA English DT Article ID SECRETORY GRANULE; ARACHIDONIC-ACID; BOVINE BRAIN; FATTY-ACIDS; RAT-BRAIN; PHOSPHATIDYLINOSITOL; ACTIVATION; PURIFICATION; INOSITOL; MEMBRANE AB Rapid incorporation of exogenous arachidonic acid into phospholipid has been detected in conjunction with eicosanoid synthesis by purified mast cell granules [Chock, S. P. & Schmauder-Chock, E. A. (1988) Biochem. Biophys. Res. Commun. 156, 1308-1315]. The species of phospholipid formed has now been identified primarily as phosphatidylinositol. A calcium-dependent phospholipase A2 has also been detected in the secretory granule. This enzyme, like the cyclooxygenase [Schmauder-Chock, E. A. & Chock, S. P. (1989) J. Histochem. Cytochem. 37, 1319-1328], appears to bind tightly to the granule matrix components. It is heat resistant and requires millimolar concentrations of calcium for optimal activity. It prefers phosphatidylinositol over phosphatidylcholine as substrate. Since the granule contains a large amount of phospholipid, the action of this phospholipase A2 can provide the required substrate for the arachidonic acid cascade. These findings provide the basis for linking phospholipase A2 to the production of eicosanoids during granule exocytosis. Since the granule also contains both an active acylating system that can rapidly reacylate lysophosphatidylinositol to form phosphatidylinositol, and an active phospholipase A2 which hydrolyzes phosphatidylinositol, a rapid turnover involving the fatty acid at the sn-2 position of phosphatidylinositol may occur. These findings are consistent with our postulation that the secretory granule is the source and/or the cause of many of the early biochemical events associated with the process of stimulus-secretion coupling. C1 WALTER REED ARMY MED CTR,DIV EXPTL THERAPEUT,WASHINGTON,DC 20307. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. ARMED FORCES RADIOBIOL RES INST,DEPT EXPTL HEMATOL,BETHESDA,MD 20814. NR 59 TC 15 Z9 15 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-2956 J9 EUR J BIOCHEM JI Eur. J. Biochem. PD FEB 14 PY 1991 VL 195 IS 3 BP 707 EP 713 DI 10.1111/j.1432-1033.1991.tb15757.x PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY552 UT WOS:A1991EY55200016 PM 1900237 ER PT J AU DALTON, JP HUDSON, D ADAMS, JH MILLER, LH AF DALTON, JP HUDSON, D ADAMS, JH MILLER, LH TI BLOCKING OF THE RECEPTOR-MEDIATED INVASION OF ERYTHROCYTES BY PLASMODIUM-KNOWLESI MALARIA WITH SULFATED POLYSACCHARIDES AND GLYCOSAMINOGLYCANS SO EUROPEAN JOURNAL OF BIOCHEMISTRY LA English DT Article ID BINDS; MEROZOITES; PROTEIN; ANTIGEN; SPECIFICITY; GLYCOLIPIDS; PARASITES; ANTIBODY; VIVAX AB Invasion of human erythrocytes by Plasmodium knowlesi requires the Duffy blood group antigen. P. knowlesi merozoites synthesize a 135-kDa polypeptide which binds to the Duffy antigen with receptor-like specificity. In this study, we show that the sulfated polysaccharide fucoidan and the glycosaminoglycan dextran sulfate inhibit the binding of the 135-kDa polypeptide to human Duffy-positive and rhesus erythrocytes while the chondroitin sulfates do not. Fucoidan and dextran sulphate also blocked the in vitro invasion of human Duffy b and rhesus erythrocytes cells by P. knowlesi merozoites. These inhibitors were more effective at blocking the binding of the 135-kDa polypeptide to human Duffy b erythrocytes than to rhesus erythrocytes, which correlated with them having a greater inhibitory effect on invasion of merozoites into human than into rhesus erythrocytes. The blocking by these sulfated sugars is not related to charge density on the polysaccharides; fucoidan with a relatively low charge density blocks binding of the 135-kDa polypeptide at 4-mu-g/ml, while the highly negatively charged chondroitin sulfates do not block binding even at the concentration of 1 mg/ml. Furthermore, fucoidan-Sepharose bound and removed the 135-kDa polypeptide from parasite culture supernatants with a selectivity equal to that of the Duffy blood group antigen. The negatively charged sulfate groups on fucoidan and dextran sulfate and the conformation in which they are held possibly mimic similarly charged groups on the Duffy antigen which bind the 135-kDa P. knowlesi polypeptide. C1 NIAID,PARASIT DIS LAB,MALARIA SECT,BETHESDA,MD 20892. RP DALTON, JP (reprint author), DUBLIN CITY UNIV,SCH BIOL SCI,GLASNEVIN,DUBLIN 9,IRELAND. RI Dalton, John/K-4457-2014; Adams, John/G-1800-2015 OI Adams, John/0000-0003-3707-7979 NR 18 TC 32 Z9 32 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-2956 J9 EUR J BIOCHEM JI Eur. J. Biochem. PD FEB 14 PY 1991 VL 195 IS 3 BP 789 EP 794 DI 10.1111/j.1432-1033.1991.tb15767.x PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY552 UT WOS:A1991EY55200026 PM 1999196 ER PT J AU PHILLIPS, MJ BLENDIS, LM POUCELL, S PATTERSON, J PETRIC, M ROBERTS, E LEVY, GA SUPERINA, RA GREIG, PD CAMERON, R LANGER, B PURCELL, RH AF PHILLIPS, MJ BLENDIS, LM POUCELL, S PATTERSON, J PETRIC, M ROBERTS, E LEVY, GA SUPERINA, RA GREIG, PD CAMERON, R LANGER, B PURCELL, RH TI SYNCYTIAL GIANT-CELL HEPATITIS - SPORADIC HEPATITIS WITH DISTINCTIVE PATHOLOGICAL FEATURES, A SEVERE CLINICAL COURSE, AND PARAMYXOVIRAL FEATURES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CHRONIC ACTIVE HEPATITIS; SUBACUTE SCLEROSING PANENCEPHALITIS; FATAL MEASLES INFECTION; CANINE-DISTEMPER VIRUS; ANTIBODY TITERS; MULTIPLE-SCLEROSIS; RUBELLA-VIRUS; YOUNG-ADULTS; MORBILLIVIRUSES; PHOSPHOPROTEIN AB Background and Methods. We describe a new form of hepatitis, occurring in 10 patients over a period of six years, characterized clinically by manifestations of severe hepatitis, histologically by large syncytial giant hepatocytes, and ultrastructurally by intracytoplasmic structures consistent with paramyxoviral nucleocapsids. Results. The patients ranged in age from 5 months to 41 years. The tentative clinical diagnosis before biopsy was non-A, non-B hepatitis in five patients and autoimmune chronic active hepatitis in the others. Five patients underwent liver transplantation; the others died. The diagnosis of syncytial giant-cell hepatitis was established pathologically. The liver cords were replaced in all 10 patients by syncytial giant cells with up to 30 nuclei. In 8 of the 10 the cytoplasm contained pleomorphic particles of 150 to 250 mu-m, filamentous strands, and particles of 14 t o 17 nm with peripherally disposed spikes resembling paramyxoviral nucleocapsids. Structures resembling degenerated forms were found in the other two patients. One of two chimpanzees injected with a liver homogenate from the index patient had an increase in the titer of paramyxoviral antibodies, probably an anamnestic reaction to previous paramyxoviral infection, suggesting that a paramyxoviral antigen but not viable virus was present in the liver homogenate. Conclusions. Although further virologic studies will be required for precise classification, we believe that paramyxoviruses should be considered in patients with severe sporadic hepatitis. C1 HOSP SICK CHILDREN, DEPT MICROBIOL, TORONTO M5G 1X8, ONTARIO, CANADA. HOSP SICK CHILDREN, DEPT PEDIAT, TORONTO M5G 1X8, ONTARIO, CANADA. HOSP SICK CHILDREN, DEPT SURG, TORONTO M5G 1X8, ONTARIO, CANADA. UNIV TORONTO, TORONTO M5S 1A1, ONTARIO, CANADA. TORONTO GEN HOSP, DEPT MED, TORONTO M5G 1L7, ONTARIO, CANADA. TORONTO GEN HOSP, DEPT PATHOL, TORONTO M5G 1L7, ONTARIO, CANADA. TORONTO GEN HOSP, DEPT SURG, TORONTO M5G 1L7, ONTARIO, CANADA. NIAID, INFECT DIS LAB, BETHESDA, MD 20892 USA. RP PHILLIPS, MJ (reprint author), HOSP SICK CHILDREN, DEPT PATHOL, 555 UNIV AVE, TORONTO M5G 1X8, ONTARIO, CANADA. NR 44 TC 133 Z9 134 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 14 PY 1991 VL 324 IS 7 BP 455 EP 460 DI 10.1056/NEJM199102143240705 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA EX363 UT WOS:A1991EX36300005 PM 1988831 ER PT J AU KORALNIK, IJ MAYER, E HIRSCHEL, B AF KORALNIK, IJ MAYER, E HIRSCHEL, B TI EARLY NEUROLOGIC ABNORMALITIES IN HIV-INFECTION - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID AIDS C1 HOP CANTONAL GENEVA,CH-1211 GENEVA 4,SWITZERLAND. RP KORALNIK, IJ (reprint author), NCI,BETHESDA,MD 20892, USA. NR 21 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 14 PY 1991 VL 324 IS 7 BP 493 EP 493 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EX363 UT WOS:A1991EX36300018 ER PT J AU HOWLEY, PM LEVINE, AJ LI, FP LIVINGSTON, DM RABSON, AS AF HOWLEY, PM LEVINE, AJ LI, FP LIVINGSTON, DM RABSON, AS TI LACK OF SV40 DNA IN TUMORS FROM SCIENTISTS WORKING WITH SV40 VIRUS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 PRINCETON UNIV,PRINCETON,NJ 08544. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HOWLEY, PM (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 TC 2 Z9 2 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 FEB 14 PY 1991 VL 324 IS 7 BP 494 EP 494 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EX363 UT WOS:A1991EX36300020 PM 1846436 ER PT J AU RAUB, W AF RAUB, W TI NEW CONJUGATE VACCINE PROTECTS YOUNGER CHILDREN AGAINST MENINGITIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP RAUB, W (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 2 Z9 2 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 FEB 13 PY 1991 VL 265 IS 6 BP 706 EP 706 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EW479 UT WOS:A1991EW47900007 PM 1990184 ER PT J AU RAUB, W AF RAUB, W TI RISK OF OCCUPATIONAL TRANSMISSION OF HUMAN-IMMUNODEFICIENCY-VIRUS EVALUATED SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP RAUB, W (reprint author), NIH,BETHESDA,MD 20892, USA. NR 1 TC 2 Z9 2 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 FEB 13 PY 1991 VL 265 IS 6 BP 706 EP 706 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EW479 UT WOS:A1991EW47900009 PM 1990184 ER PT J AU RAUB, W AF RAUB, W TI SALIVARY-GLAND FUNCTION NOT AFFECTED BY MENOPAUSE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP RAUB, W (reprint author), NIH,BETHESDA,MD 20892, USA. NR 1 TC 2 Z9 2 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 FEB 13 PY 1991 VL 265 IS 6 BP 706 EP 706 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EW479 UT WOS:A1991EW47900008 PM 1990184 ER PT J AU JAMISON, KR WYATT, RJ AF JAMISON, KR WYATT, RJ TI VANGOGH - MENIERES-DISEASE - EPILEPSY - PSYCHOSIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter C1 NIMH,WASHINGTON,DC 20032. RP JAMISON, KR (reprint author), JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205, USA. NR 3 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 FEB 13 PY 1991 VL 265 IS 6 BP 723 EP 724 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA EW479 UT WOS:A1991EW47900016 ER PT J AU JASKOLSKI, M TOMASSELLI, AG SAWYER, TK STAPLES, DG HEINRIKSON, RL SCHNEIDER, J KENT, SBH WLODAWER, A AF JASKOLSKI, M TOMASSELLI, AG SAWYER, TK STAPLES, DG HEINRIKSON, RL SCHNEIDER, J KENT, SBH WLODAWER, A TI STRUCTURE AT 2.5-A RESOLUTION OF CHEMICALLY SYNTHESIZED HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PROTEASE COMPLEXED WITH A HYDROXYETHYLENE-BASED INHIBITOR SO BIOCHEMISTRY LA English DT Article ID SYNTHETIC HIV-1 PROTEASE; ASPARTIC PROTEINASES; CRYSTAL-STRUCTURE; RATIONAL DESIGN; X-RAY; REFINEMENT; MECHANISM AB The crystal structure of a complex between chemically synthesized human immunodeficiency virus type 1 (HIV-1) protease and an octapeptide inhibitor has been refined to an R factor of 0.138 at 2.5-angstrom resolution. The substrate-based inhibitor, H-Val-Ser-Gln-Asn-Leu-PSI[CH(OH)CH2]Val-Ile-Val-OH (U-85548e) contains a hydroxyethylene isostere replacement at the scissile bond that is believed to mimic the tetrahedral transition state of the proteolytic reaction. This potent inhibitor has K(i) < 1 nM and was developed as an active-site titrant of the HIV-1 protease. The inhibitor binds in an extended conformation and is involved in beta-sheet interactions with the active-site floor and flaps of the enzyme, which form the substrate/inhibitor cavity. The inhibitor diastereomer has the S configuration at the chiral carbon atom of the hydroxyethylene insert, and the hydroxyl group is within H-bonding distance of the two active-site carboxyl groups in the enzyme dimer. The two subunits of the enzyme are related by a pseudodyad, which superposes them at a 178-degrees rotation. The main difference between the subunits is in the beta turns of the flaps, which have different conformations in the two monomers. The inhibitor has a clear preferred orientation in the active site and the alternative conformation, if any, is a minor one (occupancy of less than 30%). A new model of the enzymatic mechanism is proposed in which the proteolytic reaction is viewed as a one-step process during which the nucleophile (water molecule) and electrophile (an acidic proton) attack the scissile bond in a concerted manner. C1 NCI,FREDERICK CANC RES FACIL,MACROMOLEC STRUCT LAB,FREDERICK,MD 21701. BASIC RES PROGRAM,ANAT BIOL LAB,CTR DEV,FREDERICK,MD 21702. BOND UNIV,GRAD SCH SCI & TECHNOL,GOLD COAST,QLD 4229,AUSTRALIA. UPJOHN CO,BIOPOLYMER CHEM UNIT,KALAMAZOO,MI 49001. CALTECH,DIV BIOL,PASADENA,CA 91125. FU NCI NIH HHS [N01-CO-74101] NR 45 TC 219 Z9 220 U1 2 U2 9 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 12 PY 1991 VL 30 IS 6 BP 1600 EP 1609 DI 10.1021/bi00220a023 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX189 UT WOS:A1991EX18900023 PM 1993177 ER PT J AU PETRIC, A BHAT, B LEONARD, NJ GUMPORT, RI AF PETRIC, A BHAT, B LEONARD, NJ GUMPORT, RI TI LIGATION WITH T4 RNA LIGASE OF AN OLIGODEOXYRIBONUCLEOTIDE TO COVALENTLY-LINKED CROSS-SECTIONAL BASE-PAIR ANALOGS OF SHORT, NORMAL, AND LONG DIMENSIONS SO NUCLEIC ACIDS RESEARCH LA English DT Article ID DNA-LIGASE; BLUNT-END; DUPLEXES; OLIGORIBONUCLEOTIDES; 3',5'-BISPHOSPHATES; FRAGMENTS AB Compounds that are covalent analogues of nucleic acid base pairs of normal, long, and short C1' to C1' dimensions [B. Devadas and N.J. Leonard (1990) J. Am. Chem. Soc., 112, 3125 - 3135.] have been added to the oligodeoxyribonucleotide d(A)6 with bacteriophage T4 RNA ligase as a prelude to placing them at defined loci within nuclei acid duplexes. Analogue cross sections that represent a normal Watson-Crick base pair as well as a pyrimidine-pyrimidine and a purine-purine apposition were ligated in modest yields (approximately 20%) to the oligonucleotide. Ligation conditions were optimized for each analogue, and the cross section was joined to only a single oligonucleotide in each case. The structures of the ligated products were proved by HPLC, enzymatic degradation, and spectroscopic analyses. C1 UNIV ILLINOIS,COLL MED,DEPT BIOCHEM,URBANA,IL 61801. UNIV ILLINOIS,SCH CHEM SCI,ROGER ADAMS LAB,URBANA,IL 61801. EDVARD KARDELJ UNIV,DEPT CHEM & CHEM TECHNOL,YU-61000 LJUBLJANA,YUGOSLAVIA. NIH,BETHESDA,MD 20892. FU NIGMS NIH HHS [GM 25621] NR 27 TC 5 Z9 5 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 FEB 11 PY 1991 VL 19 IS 3 BP 585 EP 590 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY712 UT WOS:A1991EY71200024 PM 2011530 ER PT J AU RUDD, KE MILLER, W WERNER, C OSTELL, J TOLSTOSHEV, C SATTERFIELD, SG AF RUDD, KE MILLER, W WERNER, C OSTELL, J TOLSTOSHEV, C SATTERFIELD, SG TI MAPPING SEQUENCED ESCHERICHIA-COLI GENES BY COMPUTER - SOFTWARE, STRATEGIES AND EXAMPLES SO NUCLEIC ACIDS RESEARCH LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; DICITRATE TRANSPORT-SYSTEM; ESCHERICHIA-COLI; NITRATE REDUCTASE; LINKAGE MAP; NAR OPERON; PROTEIN; K-12; CLONING; IDENTIFICATION AB Methods are presented for organizing and integrating DNA sequence data, restriction maps, and genetic maps for the same organism but from a variety of sources (databases, publications, personal communications). Proper software tools are essential for successful organization of such diverse data into an ordered, cohesive body of information, and a suite of novel software to support this endeavor is described. Though these tools automate much of the task, a variety of strategies is needed to cope with recalcitrant cases. We describe such strategies and illustrate their application with numerous examples. These strategies have allowed us to order, analyze, and display over one megabase of E. coli DNA sequence information. The integration task often exposes inconsistencies in the available data, perhaps caused by strain polymorphisms or human oversight, necessitating the application of sound biological judgment. The examples illustrate both the level of expertise required of the database curator and the knowledge gained as apparent inconsistencies are resolved. The software and mapping methods are applicable to the study of any genome for which a high resolution restriction map is available. They were developed to support a weakly coordinated sequencing effort involving many laboratories, but would also be useful for highly orchestrated sequencing projects. C1 NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20892. PENN STATE UNIV,DEPT COMP SCI,UNIVERSITY PK,PA 16802. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. RP RUDD, KE (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV BACTERIAL PROD,BACTERIAL TOXINS LAB,BETHESDA,MD 20892, USA. FU NLM NIH HHS [R01 LM5110] NR 64 TC 73 Z9 74 U1 1 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD FEB 11 PY 1991 VL 19 IS 3 BP 637 EP 647 DI 10.1093/nar/19.3.637 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY712 UT WOS:A1991EY71200032 PM 2011534 ER PT J AU LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI AF LATIF, F GLENN, GM BRAUCH, H DELISIO, J HAMPSCH, K ORCUTT, ML ZBAR, B LERMAN, MI TI A NEW POLYMORPHIC PROBE ON CHROMOSOME-3P-LAMBDA-LIB13-49' (D3S723) SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,BLDG 560,ROOM 12-71,FREDERICK,MD 21701. PROGRAM RESOURCES INC,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. NR 2 TC 0 Z9 0 U1 0 U2 5 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 FEB 11 PY 1991 VL 19 IS 3 BP 681 EP 681 DI 10.1093/nar/19.3.681-a PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY712 UT WOS:A1991EY71200044 PM 1707167 ER PT J AU POLYMEROPOULOS, MH RATH, DS XIAO, H MERRIL, CR AF POLYMEROPOULOS, MH RATH, DS XIAO, H MERRIL, CR TI DINUCLEOTIDE REPEAT POLYMORPHISM AT THE HUMAN PREPROGLUCAGON GENE SO NUCLEIC ACIDS RESEARCH LA English DT Note RP POLYMEROPOULOS, MH (reprint author), ST ELIZABETH HOSP, NIMH, CTR NEUROSCI, ROOM 131, 2700 MARTIN LUTHER KING AVE, WASHINGTON, DC 20032 USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 EI 1362-4962 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD FEB 11 PY 1991 VL 19 IS 3 BP 688 EP 688 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY712 UT WOS:A1991EY71200057 ER PT J AU POLYMEROPOULOS, MH XIAO, H RATH, DS MERRIL, CR AF POLYMEROPOULOS, MH XIAO, H RATH, DS MERRIL, CR TI DINUCLEOTIDE REPEAT POLYMORPHISM AT THE HUMAN INTERLEUKIN-9 GENE SO NUCLEIC ACIDS RESEARCH LA English DT Note RP POLYMEROPOULOS, MH (reprint author), ST ELIZABETH HOSP, NIMH, CTR NEUROSCI, ROOM 131, 2700 MARTIN LUTHER KING AVE, WASHINGTON, DC 20032 USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 EI 1362-4962 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD FEB 11 PY 1991 VL 19 IS 3 BP 688 EP 688 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY712 UT WOS:A1991EY71200058 ER PT J AU POLYMEROPOULOS, MH RATH, DS XIAO, H MERRIL, CR AF POLYMEROPOULOS, MH RATH, DS XIAO, H MERRIL, CR TI A SIMPLE SEQUENCE REPEAT POLYMORPHISM AT THE HUMAN GROWTH-HORMONE LOCUS SO NUCLEIC ACIDS RESEARCH LA English DT Note RP POLYMEROPOULOS, MH (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,ROOM 131,2700 MARTIN LUTHER KING AVE,WASHINGTON,DC 20032, USA. NR 3 TC 67 Z9 68 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 FEB 11 PY 1991 VL 19 IS 3 BP 689 EP 689 DI 10.1093/nar/19.3.689 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY712 UT WOS:A1991EY71200059 PM 2011542 ER PT J AU WIKTOR, SZ JACOBSON, S WEISS, SH SHAW, GM REUBEN, JS SHORTY, VJ MCFARLIN, DE BLATTNER, WA AF WIKTOR, SZ JACOBSON, S WEISS, SH SHAW, GM REUBEN, JS SHORTY, VJ MCFARLIN, DE BLATTNER, WA TI SPONTANEOUS LYMPHOCYTE-PROLIFERATION IN HTLV-II INFECTION SO LANCET LA English DT Note AB We measured lymphocyte proliferation in the absence of antigenic stimulation in 45 HTLV-II infected, 9 HTLV-I infected, and 19 HTLV-I seronegative intravenous drug users (IVDU). Lymphocyte proliferation was higher in IVDUs infected with HTLV-II than in seronegative IVDUs but lower than among those infected with HTLV-I. Higher rates of proliferation were also associated with needle sharing, CD4+ and IL2R+ lymphocyte counts, and HTLV-I antibody titres. C1 NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. DESIRE NARCOT REHABIL CTR,NEW ORLEANS,LA. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT PREVENT MED & COMMUNITY HLTH,NEWARK,NJ 07103. UNIV ALABAMA,SCH MED,DEPT MED,BIRMINGHAM,AL 35233. RP WIKTOR, SZ (reprint author), NCI,VIRAL EPIDEMIOL SECT,6130 EXECUT BLVD,EPN 434,ROCKVILLE,MD 20852, USA. NR 6 TC 18 Z9 18 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 FEB 9 PY 1991 VL 337 IS 8737 BP 327 EP 328 DI 10.1016/0140-6736(91)90947-N PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA EX362 UT WOS:A1991EX36200006 PM 1671234 ER PT J AU MURPHY, SB COHN, SL CRAFT, AW WOODS, WG SAWADA, T CASTLEBERRY, RP LEVY, HL PROROK, PC HAMMOND, GD AF MURPHY, SB COHN, SL CRAFT, AW WOODS, WG SAWADA, T CASTLEBERRY, RP LEVY, HL PROROK, PC HAMMOND, GD TI DO CHILDREN BENEFIT FROM MASS-SCREENING FOR NEUROBLASTOMA - CONSENSUS STATEMENT FROM THE AMERICAN-CANCER-SOCIETY WORKSHOP ON NEUROBLASTOMA SCREENING SO LANCET LA English DT Editorial Material ID NEURO-BLASTOMA; PROGNOSIS C1 UNIV MINNESOTA,MINNEAPOLIS,MN 55455. KYOTO PREFECTURAL UNIV MED,KYOTO 602,JAPAN. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. UNIV NEWCASTLE UPON TYNE,NEWCASTLE TYNE NE1 7RU,TYNE & WEAR,ENGLAND. UNIV ALABAMA,UNIVERSITY,AL 35486. NCI,BETHESDA,MD 20892. UNIV SO CALIF,LOS ANGELES,CA 90089. OI Cohn, Susan/0000-0001-5749-7650 NR 17 TC 70 Z9 70 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 FEB 9 PY 1991 VL 337 IS 8737 BP 344 EP 346 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA EX362 UT WOS:A1991EX36200015 PM 1671243 ER PT J AU MAVALANKAR, DV AF MAVALANKAR, DV TI INDOOR AIR-POLLUTION IN DEVELOPING-COUNTRIES SO LANCET LA English DT Letter ID BIOMASS FUEL; SMOKING; INFANT RP MAVALANKAR, DV (reprint author), NICHHD,DIV PREVENT RES,BETHESDA,MD 20892, USA. NR 8 TC 0 Z9 0 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 FEB 9 PY 1991 VL 337 IS 8737 BP 358 EP 359 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA EX362 UT WOS:A1991EX36200030 ER PT J AU FREO, U SONCRANT, TT HOLLOWAY, HW RAPOPORT, SI AF FREO, U SONCRANT, TT HOLLOWAY, HW RAPOPORT, SI TI DOSE-DEPENDENT AND TIME-DEPENDENT EFFECTS OF 1-(2,5-DIMETHOXY-4-IODOPHENYL)-2-AMINOPROPANE (DOI), A SEROTONERGIC 5-HT2 RECEPTOR AGONIST, ON LOCAL CEREBRAL GLUCOSE-METABOLISM IN AWAKE RATS SO BRAIN RESEARCH LA English DT Article DE 1-(2,5-DIMETHOXY-4-IODOPHENYL)-2-AMINOPROPANE; DEOXYGLUCOSE; CEREBRAL METABOLISM; SEROTONIN; HIPPOCAMPUS ID BINDING CHARACTERISTICS; BRAIN; ANTAGONISTS; RADIOLIGAND; HALLUCINOGENS; SECRETION; SUBTYPES; NEURONS; ANALOGS; SYSTEM AB The time course and the relation to dose of regional cerebral metabolic rates for glucose (rCMRglc) were measured in awake male Fischer-344 rats after administration of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), a selective serotonergic 5-HT2 agonist. rCMRglc was determined, using the quantitative autoradiographic [C-14]2-deoxyglucose technique, in 75 brain regions at 5, 15, 30, 60 and 90 min after administration of DOI 10 mg/kg i.p., and at 15 min after DOI 2.5, 25 or 50 mg/kg i.p. In non-hippocampal regions, peak effects were observed at 15-30 min, when rCMRglc in 12% of the regions was significantly different from control. In hippocampal regions rCMRglc effects peaked at 30 min (average rCMRglc reduction 21%) and were sustained for at least 60 min. Higher doses of DOI reduced rCMRglc in most prosencephalic regions (25 mg/kg, 35% of all regions studied; 50 mg/kg, 32%), where 5-HT2 receptors are present in high density. These data suggest that selective 5-HT2 receptor stimulation leads to rCMRglc reduction in areas with high densities of 5-HT2 receptors. C1 NIA,NEUROSCI LAB,10-6C103,BETHESDA,MD 20892. NR 46 TC 20 Z9 20 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 FEB 8 PY 1991 VL 541 IS 1 BP 63 EP 69 DI 10.1016/0006-8993(91)91074-B PG 7 WC Neurosciences SC Neurosciences & Neurology GA EX845 UT WOS:A1991EX84500009 PM 2029625 ER PT J AU BANKIEWICZ, KS OLDFIELD, EH PLUNKETT, RJ SCHUETTE, WH COGAN, DG HOGAN, N ZUDDAS, A KOPIN, IJ AF BANKIEWICZ, KS OLDFIELD, EH PLUNKETT, RJ SCHUETTE, WH COGAN, DG HOGAN, N ZUDDAS, A KOPIN, IJ TI APPARENT UNILATERAL VISUAL NEGLECT IN MPTP-HEMIPARKINSONIAN MONKEYS IS DUE TO DELAYED INITIATION OF MOTION SO BRAIN RESEARCH LA English DT Article DE MPTP; MONKEY; NEGLECT; PARKINSONS DISEASE; HYPOKINESIA ID CHRONIC PARKINSONISM; DISEASE; DEFICITS; NEURONS; TIME AB Monkeys made hemiparkinsonian by infusion of a solution of MPTP into one carotid artery appeared to ignore food presented from the contralateral side. Initial observations suggested neglect of visual stimuli presented as fruit treats by automated delivery system in the half-field contralateral to MPTP treatment. Further studies in which fruit treats were left in the 'neglected' visual field indicated that this apparent neglect, unlike neglect attending cortical lesions, was rather a marked delay in initiating movements (unilateral hypokinesia). These observations may explain apparent subcortical neglect and are consistent with the known role of nigrostriatal dopaminergic neurones in movement regulation. This is a useful animal model in which difficulties in initiation of movement (hypokinesia), a cardinal symptom of Parkinson's disease, can be studied separately from other deficits in motor performance. C1 NEI,BETHESDA,MD 20892. RP BANKIEWICZ, KS (reprint author), NINCDS,SURG NEUROL BRANCH,BLDG 10-5D37,BETHESDA,MD 20892, USA. NR 26 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 FEB 8 PY 1991 VL 541 IS 1 BP 98 EP 102 DI 10.1016/0006-8993(91)91080-K PG 5 WC Neurosciences SC Neurosciences & Neurology GA EX845 UT WOS:A1991EX84500015 PM 2029630 ER PT J AU KAELIN, WG PALLAS, DC DECAPRIO, JA KAYE, FJ LIVINGSTON, DM AF KAELIN, WG PALLAS, DC DECAPRIO, JA KAYE, FJ LIVINGSTON, DM TI IDENTIFICATION OF CELLULAR PROTEINS THAT CAN INTERACT SPECIFICALLY WITH THE T/E1A-BINDING REGION OF THE RETINOBLASTOMA GENE-PRODUCT SO CELL LA English DT Article ID SV40 LARGE-T; SUSCEPTIBILITY GENE; DNA-BINDING; ADENOVIRUS E1A; RB GENE; SV40-TRANSFORMED CELLS; ENCODED PROTEIN; OSTEO-SARCOMA; 1A PROTEINS; EXPRESSION AB The SV40 T antigen (T)/adenovirus E1A-binding domain of the retinoblastoma gene product (pRB) has been fused to S. japonicum glutathione S-transferase, and the chimera, bound to insoluble glutathione, was used to search for cellular proteins that can interact specifically with pRB. At least seven such proteins were detected in extracts of multiple human tumor cell lines. These proteins failed to bind to a family of pRB fusion proteins that harbor inactivating mutations in the T/E1A-binding domain and to the wild-type fusion protein in the presence of a peptide replica of the pRB-binding domain of T. Therefore, the binding of one or more of these proteins may contribute to the growth-suppressing function of pRB. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. NCI,USN,MED ONCOL BRANCH,BETHESDA,MD 20814. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. RP KAELIN, WG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. RI Wang, Nianshuang/C-1463-2010; kaye, frederic/E-2437-2011 FU NCI NIH HHS [R01 CA057327] NR 66 TC 535 Z9 537 U1 1 U2 13 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD FEB 8 PY 1991 VL 64 IS 3 BP 521 EP 532 DI 10.1016/0092-8674(91)90236-R PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EX361 UT WOS:A1991EX36100008 PM 1825028 ER PT J AU JACOBOWITZ, DM WINSKY, L AF JACOBOWITZ, DM WINSKY, L TI IMMUNOCYTOCHEMICAL LOCALIZATION OF CALRETININ IN THE FOREBRAIN OF THE RAT SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE CALCIUM BINDING PROTEINS; BRAIN MAPPING; IMMUNOCYTOCHEMISTRY; CEREBRAL CORTEX; THALAMUS; SUBSTANTIA NIGRA ID CALCIUM-BINDING PROTEIN; VASOACTIVE INTESTINAL POLYPEPTIDE; ACETYLCHOLINESTERASE-CONTAINING NEURONS; SOMATOSTATIN-LIKE IMMUNOREACTIVITY; CENTRAL NERVOUS-SYSTEM; OLFACTORY-BULB; CEREBRAL-CORTEX; IMMUNOHISTOCHEMICAL LOCALIZATION; INTERPEDUNCULAR NUCLEUS; HIPPOCAMPAL-NEURONS AB The distribution of the calcium binding protein calretinin (protein 10) was examined in the rat forebrain by immunohistochemistry. The main and accessory olfactory bulbs had immunoreactive label in granule, periglomerular, and mitral cells. Positive fibers were noted in the external plexiform and granule cell layers, glomeruli, and in the molecular layer of the anterior olfactory nucleus. The cerebral cortex contained calretinin label in nonpyramidal bipolar cells. Cells in the substantia nigra compacta and ventral tegmental area were also calretinin positive as were nigrostriatal and mesolimbic projections (caudate-putamen, nucleus accumbens). In the hippocampus, interneurons were stained in all the subfields of the CA1-CA4 regions. In the thalamus, many positive cells were observed in the periventricular, reticular, lateral habenula, and reunions nuclei. Calretinin immunoreactive cells were particularly abundant in the lateral mamillary and septofimbrial nuclei. Several fiber tracts were also revealed, i. e., the lateral olfactory tract, mamillothalamic tract, fasciculus retroflexus, optic tract, and stria medullaris. These results demonstrate a distinct distribution of calretinin within cell bodies and fibers. RP JACOBOWITZ, DM (reprint author), NIMH,CLIN SCI LAB,BLDG 10,RM 3D-48,BETHESDA,MD 20892, USA. NR 55 TC 325 Z9 325 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD FEB 8 PY 1991 VL 304 IS 2 BP 198 EP 218 DI 10.1002/cne.903040205 PG 21 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA EW294 UT WOS:A1991EW29400004 PM 2016417 ER PT J AU ZHOU, RP OSKARSSON, M PAULES, RS SCHULZ, N CLEVELAND, D VANDEWOUDE, GF AF ZHOU, RP OSKARSSON, M PAULES, RS SCHULZ, N CLEVELAND, D VANDEWOUDE, GF TI ABILITY OF THE C-MOS PRODUCT TO ASSOCIATE WITH AND PHOSPHORYLATE TUBULIN SO SCIENCE LA English DT Article ID PROTO-ONCOGENE PRODUCT; CELL-CYCLE; MEIOTIC MATURATION; XENOPUS OOCYTES; GERM-CELLS; EXPRESSION; EGGS; OOGENESIS; CLEAVAGE; PROTEINS AB The mos proto-oncogene product, pp39mos, is a protein kinase and has been equated with cytostatic factor (CSF), an activity in unfertilized eggs that is thought to be responsible for the arrest of meiosis at metaphase II. The biochemical properties and potential substrates of pp39mos were examined in unfertilized eggs and in transformed cells in order to study how the protein functions both as CSF and in transformation. The pp39mos protein associated with polymers under conditions that favor tubulin oligomerization and was present in an approximately 500-kilodalton "core" complex under conditions that favor depolymerization. beta-Tubulin was preferentially coprecipitated in pp39mos immunoprecipitates and was the major phosphorylated product in a pp39mos-dependent immune complex kinase assay. Immunofluorescence analysis of NIH 3T3 cells transformed with Xenopus c-mos showed that pp39mos colocalizes with tubulin in the spindle during metaphase and in the midbody and asters during telophase. Disruption of microtubules with nocodazole affected tubulin and pp39mos organization in the same way. It therefore appears that pp39mos is a tubulin-associated protein kinase and may thus participate in the modification of microtubules and contribute to the formation of the spindle. This activity expressed during interphase in somatic cells may be responsible for the transforming activity of pp39mos. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21205. RP ZHOU, RP (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 40 TC 135 Z9 136 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 8 PY 1991 VL 251 IS 4994 BP 671 EP 675 DI 10.1126/science.1825142 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EW399 UT WOS:A1991EW39900045 PM 1825142 ER PT J AU WEISS, SRB POST, RM AF WEISS, SRB POST, RM TI CONTINGENT TOLERANCE TO CARBAMAZEPINE - A PERIPHERAL-TYPE BENZODIAZEPINE MECHANISM SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE CONTINGENT TOLERANCE; BENZODIAZEPINE RECEPTORS (PERIPHERAL-TYPE); CARBAMAZEPINE; KINDLING ID AMYGDALA-KINDLED SEIZURES; BINDING-SITES; ANTICONVULSANT DRUGS; RAT-BRAIN; 2 LIGANDS; RECEPTORS; PK-11195; RO5-4864; DIAZEPAM; SYSTEM AB Rats were tested for anticonvulsant responsivity to agents active at central and peripheral-type benzodiazepine receptors before and after they were made tolerant to the anticonvulsant effects of carbamazepine on amygdala-kindled seizures. Tolerance to carbamazepine in this paradigm is a contingent process; it occurs when the drug is administered prior to, but not following the kindled seizure. In animals tolerant to carbamazepine, cross-tolerance was observed to the anticonvulsant effects of PK11195, which is active at peripheral-type benzodiazepine receptors, but not to diazepam, which affects central-type benzodiazepine receptors. In animals treated with carbamazepine after the kindled seizure (not tolerant), no alteration in the anticonvulsant effect of PK11195 was observed. These data extend previous biochemical and pharmacological findings suggesting the importance of peripheral-type benzodiazepine receptor mechanisms in the anticonvulsant effects of carbamazepine and suggest a role for this site in the process of contingent tolerance development. C1 NIMH,BIOL PSYCHIAT BRANCH,BLDG 10,ROOM 3N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 33 TC 30 Z9 30 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 FEB 7 PY 1991 VL 193 IS 2 BP 159 EP 163 DI 10.1016/0014-2999(91)90031-K PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ905 UT WOS:A1991EZ90500004 PM 1646732 ER PT J AU WOZNIAK, KM DURCAN, MJ LINNOILA, M AF WOZNIAK, KM DURCAN, MJ LINNOILA, M TI IS NAN-190 AN EFFECTIVE ANTAGONIST OF THE HYPOTHERMIA AND HYPERGLYCEMIA INDUCED BY THE 5-HT1A RECEPTOR AGONIST, 8-OH-DPAT SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note DE NAN-190; 8-OH-DPAT (8-HYDROXY-2-(DI-N-PROPYLAMINO)TETRALIN); BODY TEMPERATURE; BLOOD GLUCOSE; 5-HT1A RECEPTORS; (MOUSE) ID 8-HYDROXY-2-(DI-N-PROPYLAMINO)TETRALIN; RAT AB The putative 5-HT1A receptor antagonist properties of 1-(2-methoxyphenyl)-4-[4-(2-phtalimmido)butyl] piperazine (NAN-190) were studied in mice. The responses studied were hypothermia- and hyperglycemia-induced by the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). NAN-190 (0.3-3 mg/kg) did not antagonize either response, but rather appeared to be additive with the effect produced by 8-OH-DPAT (0.25 mg/kg) alone, at least with respect to temperature. NAN-190, given alone in similar doses, caused hypothermia and hyperglycemia. These results suggest that NAN-190 has similar properties to 8-OH-DPAT with regard to temperature and glucose effects. Therefore, it does not appear to be a effective antagonist for all 5-HT1A-mediated responses. RP WOZNIAK, KM (reprint author), NIAAA,DICBR,CLIN STUDIES LAB,BLDG 10-3B19,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 10 TC 24 Z9 24 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 FEB 7 PY 1991 VL 193 IS 2 BP 253 EP 256 DI 10.1016/0014-2999(91)90044-Q PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ905 UT WOS:A1991EZ90500017 PM 1828770 ER PT J AU BENNAIM, A AF BENNAIM, A TI THE ROLE OF HYDROGEN-BONDS IN PROTEIN FOLDING AND PROTEIN ASSOCIATION SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID HYDROPHOBIC INTERACTION; STRUCTURAL-CHANGES; SOLVENT; SOLVATION AB The contribution of a pair of functional groups that can form either intermolecular or intramolecular hydrogen bonds to the total standard free energy of the process of protein folding or protein association is examined. It is found that this contribution can be quite large, either positive or negative, depending on the particular process and on the solvent density. This is in contrast to the common belief that the hydrogen-bond energies tend to be compensated in these processes. For the binding process, in which the two functional groups are completely removed from the aqueous environment, the contribution of such a pair of functional groups to DELTA-G-degrees can be as high as +6.4 kcal/mol. This is the main reason why hydrophobic rather than hydrophilic surfaces tend to attach to each other. In contrast, when the two functional groups are only partially removed from the aqueous environment, as in the case of the formation of alpha-helix, their contribution to DELTA-G-degrees can be negative and of the order of about 1 kcal/mol. C1 NCI,MATH BIOL LAB,BETHESDA,MD 20892. NR 24 TC 70 Z9 71 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3654 J9 J PHYS CHEM-US JI J. Phys. Chem. PD FEB 7 PY 1991 VL 95 IS 3 BP 1437 EP 1444 DI 10.1021/j100156a074 PG 8 WC Chemistry, Physical SC Chemistry GA EW478 UT WOS:A1991EW47800074 ER PT J AU LUSSO, P DEMARIA, A MALNATI, M LORI, F DEROCCO, SE BASELER, M GALLO, RC AF LUSSO, P DEMARIA, A MALNATI, M LORI, F DEROCCO, SE BASELER, M GALLO, RC TI INDUCTION OF CD4 AND SUSCEPTIBILITY TO HIV-1 INFECTION IN HUMAN CD8+ LYMPHOCYTES-T BY HUMAN HERPESVIRUS-6 SO NATURE LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; CELLS; VIRUS; EXPRESSION; ANTIGEN; GENE; DIFFERENTIATION; CYTOMEGALOVIRUS; INDIVIDUALS; RETROVIRUS AB DURING intrathymic T-cell ontogenesis, functionally competent CD3+CD4+CD8- and CD3+CD4-CD8+ T lymphocytes develop from immature CD4-CD8- thymocytes after transiently acquiring a double-positive CD4+CD8+ phenotype 1-3. The partition between CD4+CD8- and CD4-CD8+ T cells is generally considered to be irreversible, although a small percentage of circulating CD3+ T lymphocytes coexpressing CD4 and CD8 molecules has been identified 4. It has been suggested that in CD8+ T cells the CD4 genes may be methylated and thus highly repressed 5, whereas in CD4+ T cells the CD8 genes are unmethylated 6 and their transcription can be induced by physiological stimuli such as interleukin-4 (ref. 7). Here, we demonstrate that infection with human herpesvirus 6 (HHV-6) (ref. 8), a virus proposed as a potential cofactor in AIDS (ref. 9), dramatically upregulates the expression of CD4-the receptor for human immunodeficiency virus type-1 (HIV-1) (refs 10-12)-in a human neoplastic T-cell line. More importantly, HHV-6 induces de novo expression of CD4 messenger RNA and protein in normal mature CDE8+ T lymphocytes, rendering them susceptible to infection with HIV-1. These findings demonstrate that human CD3+CD4-CD8+ T lymphocytes can reacquire CD4 in the post-thymic life and elucidate a novel mechanism-receptor regulation-through which HHV-6 may positively interact with HIV-1 in coinfected patients. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NIAID,IMMUNOGENET LAB,BETHESDA,MD 20892. ADV BIOSCI LABS,DEPT CELL BIOL,KENSINGTON,MD 20895. RP LUSSO, P (reprint author), NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892, USA. RI de maria, andrea/F-7116-2016 OI de maria, andrea/0000-0001-5782-333X NR 30 TC 231 Z9 232 U1 0 U2 2 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 7 PY 1991 VL 349 IS 6309 BP 533 EP 535 DI 10.1038/349533a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EW571 UT WOS:A1991EW57100070 PM 1846951 ER PT J AU JANERICH, DT THOMPSON, WD GREENWALD, P CHOROST, S TUCCI, C ZAMAN, MB MELAMED, MR KIELY, M MCKNEALLY, MF AF JANERICH, DT THOMPSON, WD GREENWALD, P CHOROST, S TUCCI, C ZAMAN, MB MELAMED, MR KIELY, M MCKNEALLY, MF TI LUNG-CANCER AND EXPOSURE TO TOBACCO-SMOKE IN THE HOUSEHOLD - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 UNIV SO MAINE, PORTLAND, ME 04103 USA. NCI, BETHESDA, MD 20892 USA. NEW YORK STATE DEPT HLTH, ALBANY, NY 12237 USA. MEM SLOAN KETTERING CANC CTR, NEW YORK, NY 10021 USA. UNION UNIV, ALBANY, NY 12208 USA. TORONTO GEN HOSP, TORONTO M56 2C4, ONTARIO, CANADA. RP JANERICH, DT (reprint author), YALE UNIV, SCH MED, NEW HAVEN, CT 06510 USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 7 PY 1991 VL 324 IS 6 BP 414 EP 415 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA EW296 UT WOS:A1991EW29600015 ER PT J AU SILLS, MR MAHAFFEY, KR SILBERGELD, EK AF SILLS, MR MAHAFFEY, KR SILBERGELD, EK TI THE LONG-TERM EFFECTS OF EXPOSURE TO LOW-DOSES OF LEAD IN CHILDHOOD SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 NIEHS,RES TRIANGLE PK,NC 27709. ENVIRONM DEF FUND,WASHINGTON,DC 20036. RP SILLS, MR (reprint author), JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205, USA. OI Sills, Marion/0000-0003-1322-0822 NR 7 TC 1 Z9 1 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 FEB 7 PY 1991 VL 324 IS 6 BP 416 EP 417 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA EW296 UT WOS:A1991EW29600018 ER PT J AU FANTL, JA WYMAN, JF MCCLISH, DK HARKINS, SW ELSWICK, RK TAYLOR, JR HADLEY, EC AF FANTL, JA WYMAN, JF MCCLISH, DK HARKINS, SW ELSWICK, RK TAYLOR, JR HADLEY, EC TI EFFICACY OF BLADDER TRAINING IN OLDER WOMEN WITH URINARY-INCONTINENCE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID TEST-RETEST ANALYSIS; DETRUSOR INSTABILITY; TRIAL AB The efficacy of bladder training was evaluated in a randomized clinical trial involving 123 noninstitutionalized women 55 years and older with urinary incontinence. Subjects were urodynamically categorized as those with urethral sphincteric incompetence (N = 88) and those with detrusor instability with or without concomitant sphincteric incompetence (N = 35). Bladder training reduced the number of incontinent episodes by 57%; the effect was similar for both urodynamic diagnostic groups. The quantity of fluid loss was reduced by 54%. This was greater for patients with detrusor instability than for those without it. Diurnal and nocturnal voluntary micturitions were also reduced. The effect on nocturnal micturition, however, was not observed in subjects with unstable detrusor function. It is recommended that bladder training be considered as an initial step in treatment of women with urinary incontinence. Provided prior comprehensive clinical evaluation is done, it can be prescribed without the need for urodynamic characterization. C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT COMMUNITY & PSYCHIAT NURSING,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT BIOSTAT,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT GERONTOL,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT NEUROL,RICHMOND,VA 23298. NIA,GERIATR PROGRAM,BETHESDA,MD 20892. RP FANTL, JA (reprint author), VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT OBSTET & GYNECOL,CONTINENCE PROGRAM WOMEN,RICHMOND,VA 23298, USA. FU NIA NIH HHS [AG05170] NR 28 TC 209 Z9 212 U1 0 U2 6 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 FEB 6 PY 1991 VL 265 IS 5 BP 609 EP 613 DI 10.1001/jama.265.5.609 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA EV718 UT WOS:A1991EV71800017 PM 1987410 ER PT J AU STADTMAN, ER OLIVER, CN AF STADTMAN, ER OLIVER, CN TI METAL-CATALYZED OXIDATION OF PROTEINS - PHYSIOLOGICAL CONSEQUENCES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID LOW-DENSITY LIPOPROTEIN; COLI GLUTAMINE-SYNTHETASE; INDUCED BIOLOGICAL DAMAGE; ACTIVE TRANSITION-METALS; MIXED-FUNCTION OXIDATION; SITE-SPECIFIC MECHANISM; RED BLOOD-CELLS; ESCHERICHIA-COLI; DENATURED PROTEINS; OXYGEN RADICALS RP STADTMAN, ER (reprint author), NHLBI,BIOCHEM LAB,9000 ROCKVILLE PIKE,BLDG 3,RM 222,BETHESDA,MD 20892, USA. NR 53 TC 763 Z9 784 U1 4 U2 25 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 FEB 5 PY 1991 VL 266 IS 4 BP 2005 EP 2008 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EV515 UT WOS:A1991EV51500001 PM 1989966 ER PT J AU ELWOOD, PC DEUTSCH, JC KOLHOUSE, JF AF ELWOOD, PC DEUTSCH, JC KOLHOUSE, JF TI THE CONVERSION OF THE HUMAN MEMBRANE-ASSOCIATED FOLATE BINDING-PROTEIN (FOLATE RECEPTOR) TO THE SOLUBLE FOLATE BINDING-PROTEIN BY A MEMBRANE-ASSOCIATED METALLOPROTEASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN KB-CELLS; AMINO-ACID-SEQUENCE; MYELOGENOUS LEUKEMIA-CELLS; GLYCOSYL-PHOSPHATIDYLINOSITOL; HUMAN-PLACENTA; FOLIC-ACID; COWS MILK; PURIFICATION; TRANSPORT; IDENTIFICATION AB The membrane-associated (M-FBP) and soluble (S-FBP) forms of human folate binding proteins (FBP) have been well characterized. Although related in a precursor-product manner, the mechanism of conversion and the basis for differences between M-FBP and S-FBP are not known. The conversion of M-FBP to S-FBP in crude human nasopharyngeal carcinoma (KB) cell preparations is demonstrated based on characteristic gel filtration elution profiles of M-FBP and S-FBP (V(e)/V(o) = 1.3 and 1.7, respectively) in Triton X-100. M-FBP is stoichiometrically converted to S-FBP in a time- and temperature-dependent reaction by a metalloprotease which is: heat-labile; particulate; contained in human KB cell and placental membranes, and rat kidney homogenates; inhibited by EDTA, 1,10-phenanthroline, and parahydroxymercuribenzoate; requires divalent cations; is maximally active at neutral pH; and is active in the presence or absence of detergent. The purified soluble FBP product appears to be identical to S-FBP. Conversion of purified endogenously [H-3]leucine-labeled M-FBP yields a soluble FBP characterized by a 45% decrease in specific activity (moles of H-3/mol folate bound) relative to M-FBP and a non-folate binding fragment which contains 45% of the [H-3]eucine from M-FBP, requires detergent and/or urea to remain soluble, and migrates aberrantly on gel filtration in 1% (v/v) Triton X-100 and 8 M urea. Based on changes in the specific activity and the gel filtration elution profiles of purified labeled M-FBP associated with conversion to S-FBP, the endoproteolytic cleavage site is predicted between residues 226 and 229 of the cDNA predicted human FBP amino acid sequence. These results suggest that the cDNA predicted hydrophobic carboxyl terminus (residues 227-257) remains intact on the fully processed, membrane-anchored M-FBP, contains the Triton binding domain, and is involved in the formation of the membrane anchor of M-FBP. C1 UNIV COLORADO,HLTH SCI CTR,DEPT MED,DIV HEMATOL,DENVER,CO 80262. RP ELWOOD, PC (reprint author), NCI,DIV CANC TREATMENT,MED BRANCH,BLDG 10,RM 12N226,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU NIADDK NIH HHS [AM07709-01]; NIGMS NIH HHS [GM122610-01]; PHS HHS [26486] NR 49 TC 64 Z9 64 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 FEB 5 PY 1991 VL 266 IS 4 BP 2346 EP 2353 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EV515 UT WOS:A1991EV51500052 PM 1846624 ER PT J AU JOSEPHSON, RA SILVERMAN, HS LAKATTA, EG STERN, MD ZWEIER, JL AF JOSEPHSON, RA SILVERMAN, HS LAKATTA, EG STERN, MD ZWEIER, JL TI STUDY OF THE MECHANISMS OF HYDROGEN-PEROXIDE AND HYDROXYL FREE RADICAL-INDUCED CELLULAR INJURY AND CALCIUM OVERLOAD IN CARDIAC MYOCYTES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RAT HEART-CELLS; REPERFUSION INJURY; SUPEROXIDE-DISMUTASE; ISCHEMIA REPERFUSION; MYOCARDIAL ISCHEMIA; XANTHINE-OXIDASE; PERFUSED HEART; OXYGEN; REDUCTION; CATALASE AB There is evidence that myocardial injury, as would occur on post-ischemic reperfusion, may be caused by the generation of oxygen radicals, as well as by the induction of intracellular calcium overload; however, the relationship between these two mechanisms of injury is not known. To test the hypothesis that oxidants and oxygen radicals can cause cardiac myocyte injury and intracellular calcium overload, isolated adult rat ventricular myocytes were exposed to H2O2 (1-10 mM) and Fe3+-nitrilotriacetate. EPR measurements confirmed the production of the highly reactive .OH radical by this system. The oxygen radical generating system initially caused a transient augmentation of twitch amplitude in single field stimulated myocytes. This was followed by contractile oscillations occurring during the twitch prior to full cell relaxation, and spontaneous mechanical oscillations occurring between electrically stimulated contractions. Eventually, cells became inexcitable and abruptly underwent contracture. In the presence of lower bathing calcium concentrations, these oxidant-induced alterations were prevented or delayed. However, cells exposed to the radical generating system in the absence of extracellular calcium still eventually underwent contracture but stimulated contractions or mechanical oscillations were not seen. Measurements in single myocytes loaded with the fluorescent probe of intracellular calcium, Indo-1, demonstrated a rise in both systolic and diastolic fluorescence ratio, as well as oscillation and widening of the fluorescence transient, suggestive of cellular calcium loading, following exposure to the radical generating system. Injured myocytes did not take up trypan blue dye. Contractile dysfunction and calcium overload were prevented by the calcium channel blocker, nitrendipine. NMR measurements of cellular [ATP] demonstrated that these alterations in cellular calcium preceded the depletion of ATP. Subsequent depletion of ATP was accompanied by the appearance of increased concentrations of sugar phosphates indicative of a block in glycolysis and ATP depletion correlated with cellular rigor. Thus, oxygen free radicals can cause cardiac myocyte injury with contractile abnormalities which occur due to myocyte calcium loading. The mechanism of oxidant-induced calcium loading is not due to nonspecific membrane damage, or energy depletion, but rather due to increased calcium influx through voltage gated calcium channels. This early calcium overload state as well as oxidant induced block of glycolysis result in cellular energy depletion and cell death with the induction of contracture. C1 JOHNS HOPKINS MED INST,DEPT MED,DIV CARDIOL,ELECTRON PARAMAGNET RESONANCE LABS,BALTIMORE,MD 21224. NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. FU NHLBI NIH HHS [HL-07227, HL-17655-13, HL-38324] NR 36 TC 237 Z9 242 U1 1 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 5 PY 1991 VL 266 IS 4 BP 2354 EP 2361 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EV515 UT WOS:A1991EV51500053 PM 1846625 ER PT J AU ETINGIN, OR HAJJAR, DP HAJJAR, KA HARPEL, PC NACHMAN, RL AF ETINGIN, OR HAJJAR, DP HAJJAR, KA HARPEL, PC NACHMAN, RL TI LIPOPROTEIN (A) REGULATES PLASMINOGEN-ACTIVATOR INHIBITOR-1 EXPRESSION IN ENDOTHELIAL-CELLS - A POTENTIAL MECHANISM IN THROMBOGENESIS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TUMOR NECROSIS FACTOR; 3' UNTRANSLATED REGION; MESSENGER-RNA LEVELS; GROWTH-FACTOR; FIBRINOLYTIC SYSTEM; HUMAN-FIBROBLASTS; GENE-EXPRESSION; TISSUE-TYPE; PROTEIN-C; SEQUENCE AB Lipoprotein (a) (Lp(a)) is a low density lipoprotein-like particle which contains the plasminogen-like apolipoprotein a. Lp(a) levels are elevated in patients with atherosclerotic coronary artery disease. Recent studies suggest that Lp(a) competitively inhibits plasminogen binding to the endothelial cell and interferes with surface-associated plasmin generation. In this study, we present evidence for the presence of Lp(a) in the microvasculature of inflamed tissue. In addition, we demonstrate that Lp(a) regulates endothelial cell synthesis of a major fibrinolytic protein, plasminogen activator inhibitor-1 (PAI-1). In cultured human endothelial cells, Lp(a) enhanced PAI-1 antigen, activity, and steady-state mRNA levels without altering tissue plasminogen activator activity or mRNA transcript levels. This effect was cell-specific. Although other lipoproteins did not coordinately raise PAI-1 mRNA levels in endothelial cells, low density lipoprotein treatment selectively raised the level of the 3.4-kilobase mRNA species of PAI-1 without a concomitant increase in PAI-1 activity or antigen. Endothelial cell exposure to Lp(a) did not cause generalized endothelial cell activation since the functional activity and mRNA levels for tissue factor, platelet-derived growth factor and interleukin-6 were no elevated following Lp(a) exposure. These data suggest a molecular mechanism whereby (Lp(a) may support a specific prothrombotic endothelial cell phenotype, namely by increasing PAI-1 expression. C1 CORNELL UNIV,MED CTR,COLL MED,DEPT BIOCHEM,NEW YORK,NY 10021. CORNELL UNIV,MED CTR,COLL MED,DEPT PATHOL,NEW YORK,NY 10021. CORNELL UNIV,MED CTR,COLL MED,DEPT PEDIAT,NEW YORK,NY 10021. CORNELL UNIV,MED CTR,COLL MED,NIH,SPECIALIZED CTR THROMBOSIS RES,NEW YORK,NY 10021. RP ETINGIN, OR (reprint author), CORNELL UNIV,MED CTR,COLL MED,DEPT MED,NEW YORK,NY 10021, USA. FU NHLBI NIH HHS [HL-18828, HL-01687, HL-39701] NR 57 TC 223 Z9 226 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 FEB 5 PY 1991 VL 266 IS 4 BP 2459 EP 2465 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EV515 UT WOS:A1991EV51500068 PM 1824942 ER PT J AU KAHN, RA KERN, FG CLARK, J GELMANN, EP RULKA, C AF KAHN, RA KERN, FG CLARK, J GELMANN, EP RULKA, C TI HUMAN ADP-RIBOSYLATION FACTORS - A FUNCTIONALLY CONSERVED FAMILY OF GTP-BINDING PROTEINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHOLERA-TOXIN; ADENYLATE-CYCLASE; MAMMALIAN-CELLS; REGULATORY COMPONENT; NUCLEOTIDE-BINDING; STABLE REPLICATION; RNA-POLYMERASE; EXPRESSION; SEQUENCES; COFACTOR AB A new member, hARF4, of the ADP-ribosylation factor (ARF) family, a subset of the superfamily of regulatory GTP-binding proteins, has been cloned from a cDNA expression library. Two other human ARF cDNA sequences, designated human ARF1 and ARF3, have been reported previously and are 96% identical in amino acid sequence. A human ARF1 cDNA significantly longer than previously described clones, was obtained, by cross-species hybridization using a bovine ARF1 cDNA probe. Bovine ARF1p and human ARF1p are 100% identical while each is only 80% identical to hARF4p. Thus, hARF4p is the most divergent of the mammalian ARF proteins identified. Northern blot analysis revealed the expression of at least three different ARF messages in human placenta and adrenal carcinoma cells. Both hARF1 and hARF4 encode GTP-binding proteins with predicted molecular masses of 20,000- 21,000 Da. Biochemical analysis of the purified recombinant proteins revealed a high degree of conservation of nucleotide binding properties and in vitro ARF activities. ARF is an essential gene in the yeast, Saccharomyces cerevisiae, and is encoded by two genes. Expression of either hARF1p or hARF4p in yeast was found to rescue the lethal double mutant, arf1- arf2-, thus demonstrating the functional conservation of ARF functions between yeast and man. The combination of in vivo and in vitro assays for ARF function provides a specific and unambiguous means of determining bona fide ARF proteins from divergent species from among the rapidly increasing number of structurally related, small molecular weight GTP-binding proteins. C1 GEORGETOWN UNIV, MED CTR, VINCENT T LOMBARDI CANC RES CTR, DIV MED ONCOL, WASHINGTON, DC 20007 USA. GEORGETOWN UNIV, MED CTR, VINCENT T LOMBARDI CANC RES CTR, DEPT BIOCHEM & MOLEC BIOL, WASHINGTON, DC 20007 USA. RP NCI, DIV CANC TREATMENT, BIOL CHEM LAB, BETHESDA, MD 20892 USA. FU NCI NIH HHS [CA-50376] NR 36 TC 176 Z9 180 U1 0 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 FEB 5 PY 1991 VL 266 IS 4 BP 2606 EP 2614 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EV515 UT WOS:A1991EV51500090 PM 1899243 ER PT J AU BLANK, U RA, C KINET, JP AF BLANK, U RA, C KINET, JP TI CHARACTERIZATION OF TRUNCATED ALPHA-CHAIN PRODUCTS FROM HUMAN, RAT, AND MOUSE HIGH-AFFINITY RECEPTOR FOR IMMUNOGLOBULIN-E SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSFECTED CELLS; IGE RECEPTOR; MAST-CELLS; SUBUNIT; EXPRESSION; BINDING; DNA AB The high affinity receptor for immunoglobulin E (IgE) is a tetrameric structure (alpha-beta-gamma-2) consisting of noncovalently associated subunits: one IgE-binding alpha-chain, one 4-fold membrane spanning beta-chain, and two disulfide-linked gamma-chains. Here, we have engineered alpha-cDNA constructs (alpha-trunc) encoding exclusively the leader peptide and the extracellular domain of the alpha-subunit. Transfection of human alpha-trunc into COS-7 cells resulted in the secretion of soluble IgE-binding polypeptides. By contrast, the polypeptides generated from rat and mouse alpha-trunc transfections were sequestered in the endoplasmic reticulum and degraded even though they appeared to fold properly as judged by their capacity to bind IgE. Stable transfectants with human alpha-trunc were obtained from a dihydrofolate reductase-deficient Chinese hamster ovary cell line. Several clones secreted substantial amounts (0.1-mu-g/ml/10(6) cells) of IgE-binding polypeptides. The dissociation rate of bound IgE from this soluble truncated-alpha (k-1 = 4.9 x 10(-6) s-1 at 25-degrees-C) was characteristic of receptors on intact cells. After treatment with tunicamycin, the transfectants secreted unglycosylated 18-kDa polypeptides which could also bind IgE. These unglycosylated products had a tendency to form dimers and higher oligomers which were resistant to treatment by sodium dodecyl sulfate and reducing agents. These data demonstrate unequivocally that the extracellular domain of the alpha-subunit is sufficient to mediate high affinity binding of IgE. Furthermore, posttranslational addition of carbohydrates is not required for proper folding and function of the receptor binding site. The truncated human-alpha should be a suitable reagent for crystallographic analysis and for detailed analysis of the receptor binding site. C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,TWINBROOK II BLDG,12441 PARKLAWN DR,ROCKVILLE,MD 20852. NR 34 TC 108 Z9 110 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 FEB 5 PY 1991 VL 266 IS 4 BP 2639 EP 2646 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EV515 UT WOS:A1991EV51500094 PM 1824944 ER PT J AU BOHACEK, RS STRAUSS, UP JERNIGAN, RL AF BOHACEK, RS STRAUSS, UP JERNIGAN, RL TI CONFIGURATIONAL STATISTICS OF METHYL VINYL ETHER MALEIC-ANHYDRIDE COPOLYMER - SELECTION OF IMPORTANT ATOMIC INTERACTIONS AND CONFORMATIONS SO MACROMOLECULES LA English DT Article AB The conformations of methyl vinyl ether-maleic anhydride copolymer (MVEMA) are investigated by determining and analyzing the most important conformers of an appropriate subunit of the copolymer. Average dimensions of the unperturbed MVEMA copolymer chain are calculated by using the rotational isomeric state model. The relative energy of each rotational isomer has been approximated three ways: (1) by analogy to known atomic interactions as reported for small molecules and derived from polymer properties, (2) by computation of atomic interaction energies with the MM2 molecular mechanics program, and (3) by calculation of the relative energy of each conformation of the entire subunit using MM2. Each of these three methods leads to statistical weights for the individual conformers. When these weights are used, the characteristic ratio, (r2)0/nl2, at the limit of large n, is calculated separately for each of the four most important stereoisomers and compared to the experimental characteristic ratio. The characteristic ratios computed by using the three different sets of weighting factors for the first isomer were 9.0, 9.2, and 8.9. These values are in virtual agreement with the experimental characteristic ratio of 9.01 +/- 0.90. The characteristic ratios of the other three stereoisomers are significantly larger with average values of 25.0, 18.6, and 20.9. The large differences in the characteristic ratio between the first stereoisomer and the other three directly imply that the polymer consists principally of the first stereoisomer, with any of the other stereoisomers present only in insignificant amounts. C1 NCI,DCBDC,MATH BIOL LAB,BLDG 10,ROOM 4B-56,BETHESDA,MD 20892. RUTGERS STATE UNIV,DEPT CHEM,NEW BRUNSWICK,NJ 08903. RI Jernigan, Robert/A-5421-2012 NR 17 TC 2 Z9 2 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0024-9297 J9 MACROMOLECULES JI Macromolecules PD FEB 4 PY 1991 VL 24 IS 3 BP 731 EP 739 DI 10.1021/ma00003a016 PG 9 WC Polymer Science SC Polymer Science GA EV801 UT WOS:A1991EV80100016 ER PT J AU ROSS, HL HOWARD, JM GANIKOS, ML TAYLOR, ED AF ROSS, HL HOWARD, JM GANIKOS, ML TAYLOR, ED TI DRUNK DRIVING AMONG AMERICAN BLACKS AND HISPANICS SO ACCIDENT ANALYSIS AND PREVENTION LA English DT Article C1 NIAAA,PREVENTION RES BRANCH,ROCKVILLE,MD 20857. RP ROSS, HL (reprint author), UNIV NEW MEXICO,DEPT SOCIOL,ALBUQUERQUE,NM 87131, USA. NR 32 TC 53 Z9 53 U1 2 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0001-4575 J9 ACCIDENT ANAL PREV JI Accid. Anal. Prev. PD FEB PY 1991 VL 23 IS 1 BP 1 EP 11 DI 10.1016/0001-4575(91)90029-5 PG 11 WC Ergonomics; Public, Environmental & Occupational Health; Social Sciences, Interdisciplinary; Transportation SC Engineering; Public, Environmental & Occupational Health; Social Sciences - Other Topics; Transportation GA EY987 UT WOS:A1991EY98700001 PM 2021398 ER PT J AU RACKE, K SCHWORER, H AGOSTON, DV KILBINGER, H AF RACKE, K SCHWORER, H AGOSTON, DV KILBINGER, H TI EVIDENCE THAT NEURONALLY RELEASED VASOACTIVE INTESTINAL POLYPEPTIDE INHIBITS THE RELEASE OF SEROTONIN FROM ENTEROCHROMAFFIN CELLS OF THE GUINEA-PIG SMALL-INTESTINE SO ACTA ENDOCRINOLOGICA LA English DT Article ID PERFUSED SMALL-INTESTINE; GASTROINTESTINAL-TRACT; PEPTIDE; ILEUM; 5-HYDROXYTRYPTAMINE; IMMUNOREACTIVITY; MODULATION; SYSTEM; RAT AB Isolated small intestinal segments of the guinea pig were arterially perfused and the release of serotonin (5-hydroxytryptamine) and 5-hydroxyindoleacetic acid into the portal venous effluent was determined by HPLC with electrochemical detection. Test substances were intra-arterially applied. The muscarine receptor agonist oxotremorine (1-mu-mol/l) inhibited the release of 5-hydroxytryptamine by about 50%. In the presence of the neurotoxin tetrodotoxin, oxotremorine enhanced the release of 5-hydroxytryptamine by 145%, indicating that the inhibitory effect of oxotremorine was mediated by the release of a neurotransmitter. Exogenous vasoactive intestinal polypeptide (1-100 pmol/l) inhibited the release of 5-hydroxytryptamine by about 50%, an effect antagonized by a specific antibody to vasoactive intestinal polypeptide. This antibody to vasoactive intestinal polypeptide, on its own, had no effect on the release of 5-hydroxytryptamine. However, it prevented the inhibitory effect of oxotremorine. In the presence of the antibody to vasoactive intestinal polypeptide, unlike in the presence of tetrodotoxin, oxotremorine did not stimulate the release of 5-hydroxytryptamine. In conclusion, activation of neuronal muscarine receptors in the guinea pig small intestine enhances the release of several neurotransmitters which can inhibit the release of 5-hydroxytryptamine. The present experiments provide good evidence that vasoactive intestinal polypeptide is one of them. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP RACKE, K (reprint author), UNIV MAINZ,DEPT PHARMACOL,OBERE ZAHLBACHER STR 67,W-6500 MAINZ,GERMANY. NR 18 TC 12 Z9 13 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-5598 J9 ACTA ENDOCRINOL-COP JI Acta Endocrinol. PD FEB PY 1991 VL 124 IS 2 BP 203 EP 207 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FA754 UT WOS:A1991FA75400012 PM 1706126 ER PT J AU GUARDABASSO, V GENAZZANI, AD VELDHUIS, JD RODBARD, D AF GUARDABASSO, V GENAZZANI, AD VELDHUIS, JD RODBARD, D TI OBJECTIVE ASSESSMENT OF CONCORDANCE OF SECRETORY EVENTS IN 2 ENDOCRINE TIME-SERIES SO ACTA ENDOCRINOLOGICA LA English DT Article ID NORMAL MENSTRUAL-CYCLE; LUTEINIZING-HORMONE; DETECTION ALGORITHMS; PULSATILE RELEASE; PULSE-DETECTION; PROLACTIN; MEN; TESTOSTERONE AB A new objective method is presented for investigating the presence of a temporal relationship between episodic release of two hormones. The two time series of hormone concentrations are first analysed by an objective method for peak detection. Both data series are then transformed into "quantized" or discretized series by recording the occurrence of a hormone pulse as an "event", characterized by the onset, the maximum, or another unique feature. The two quantized series are then matched, and the number of concordant events and discordant events are counted. Each point in series A is compared with a "time-window" of a selected number of points in series B, to accommodate small degree of mismatch between events in the two series. An index of concordance is computed, compensating for any spurious random coincidence: the "Specific Concordance", to evaluate the frequency of concordant events in excess of those expected on the basis of chance alone. This calculation is systematically repeated, interposing a range of time-lags between the two series. A graph of Specific Concordance versus time-lag indicates the time-lag corresponding to a maximal concordance. Simulations of random series of events are performed, and their degree of concordance is evaluated in a similar fashion, thus generating frequency distributions of Specific Concordance values under the null hypothesis of no temporal relationship. This permits the selection of criteria for statistical significance at any desired p-level, for one or many lag times, and for one or multiple subjects. Various degrees of concordance can also be simulated to evaluate the performance (sensitivity, statistical power) of this approach. These methods have been implemented as a collection of short microcomputer programmes, and applied to the study of the temporal relationship between beta-endorphin and cortisol in normal subjects sampled every 10 min for 24 h. This analysis demonstrated concordance between events in the two series, with synchronous occurrence of beta-endorphin and cortisol release events significantly more frequently than expected on the basis of random association (p < 0.01). C1 NICHHD,THEORET & PHYS BIOL LAB,BLDG 12 A,3033,BETHESDA,MD 20892. MARIO NEGRI INST PHARMACOL RES,I-20157 MILAN,ITALY. UNIV MODENA,DEPT OBSTET & GYNECOL,I-41100 MODENA,ITALY. UNIV VIRGINIA,MED CTR,SCH MED,INTERDISCIPLINARY GRAD BIOPHYS PROGRAM,CHARLOTTESVILLE,VA 22901. CONSORZIO MARIO NEGRI SUD,SANTA MARIA IMBAR,ITALY. UNIV VIRGINIA,MED CTR,SCH MED,DEPT INTERNAL MED,DIV ENDOCRINOL & METAB,CHARLOTTESVILLE,VA 22901. RI Guardabasso, Vincenzo/A-8731-2011 OI Guardabasso, Vincenzo/0000-0002-4566-9491 FU NICHD NIH HHS [1K04 HD00634] NR 26 TC 28 Z9 28 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-5598 J9 ACTA ENDOCRINOL-COP JI Acta Endocrinol. PD FEB PY 1991 VL 124 IS 2 BP 208 EP 218 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FA754 UT WOS:A1991FA75400013 PM 2003377 ER PT J AU ENGEL, BT TALAN, MI AF ENGEL, BT TALAN, MI TI DIURNAL-VARIATIONS IN CENTRAL VENOUS-PRESSURE SO ACTA PHYSIOLOGICA SCANDINAVICA LA English DT Article DE BLOOD VOLUME; HEMODYNAMICS; NOCTURNAL ID PATTERNS AB We analysed the haemodynamic patterns of seven monkeys (Macaca mulatta) during a one-month period during which we monitored beat-to-beat levels of heart rate, stroke volume, intra-arterial pressure and central venous pressure 7 days/week, 18 h/day. We replicated an earlier finding that cardiac output falls and total peripheral resistance rises throughout the night: the fall in cardiac output was mediated by a fall in heart rate since stroke volume did not change; and the rise in peripheral resistance reflected a homeostatic adjustment to the fall in cardiac output since blood pressure was stable throughout the night although it fell early in the evening. In addition, we have shown for the first time that central venous pressure also falls throughout the night; this occurs even in the presence of alpha-and beta-adrenergic sympathetic blockade. Since stroke volume does not change overnight this indicates that the nocturnal fall in cardiac output is not due to a shift of blood volume into the venous compartment. These findings support our hypothesis that there is a nocturnal decline in plasma volume. RP ENGEL, BT (reprint author), NIA,GERONTOL RES CTR,BEHAV SCI LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 9 TC 14 Z9 14 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0001-6772 J9 ACTA PHYSIOL SCAND JI Acta Physiol. Scand. PD FEB PY 1991 VL 141 IS 2 BP 273 EP 278 DI 10.1111/j.1748-1716.1991.tb09077.x PG 6 WC Physiology SC Physiology GA EV638 UT WOS:A1991EV63800015 PM 2048411 ER PT J AU CHAISSON, RE FUCHS, E STANTON, DL QUINN, TC HENDRICKSEN, C BARTLETT, JG FARZADEGAN, H AF CHAISSON, RE FUCHS, E STANTON, DL QUINN, TC HENDRICKSEN, C BARTLETT, JG FARZADEGAN, H TI RACIAL HETEROGENEITY OF HIV ANTIGENEMIA IN PEOPLE WITH HIV-INFECTION SO AIDS LA English DT Article DE HIV ANTIGEN; P24 ANTIGEN; P24 ANTIBODY; RACE; SEROLOGY ID HUMAN IMMUNODEFICIENCY VIRUS; AIDS; SERUM; P24 AB We compared the prevalence of HIV p24 antigenemia in black and white US patients with HIV infection. The prevalence of HIV antigenemia increased with severity of HIV disease (P < 0.001). In all clinical categories, whites were more likely to be HIV-antigenemic than blacks (overall prevalence 38 versus 18%; P < 0.01). Anti-p24 antibodies were detected in a higher proportion of blacks (84%) than whites (65%; P = 0.02). Blacks had significantly higher total serum immunoglobulin levels than whites (median 3.8 versus 3.2 mg/dl; P < 0.00001). Racial differences in HIV antigen expression may result from differences in humoral response to HIV infection. These differences should be considered when HIV antigen is used as a surrogate marker in clinical trials. C1 JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,BALTIMORE,MD 21205. NIAID,IMMUNOREGULAT LAB,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD 21218. FU PHS HHS [5U01 A127668] NR 19 TC 24 Z9 24 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD FEB PY 1991 VL 5 IS 2 BP 177 EP 180 DI 10.1097/00002030-199102000-00007 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA FF379 UT WOS:A1991FF37900007 PM 1903261 ER PT J AU FUCHS, D SHEARER, GM BOSWELL, RN LUCEY, DR CLERICI, M REIBNEGGER, G WERNER, ER ZAJAC, RA WACHTER, H AF FUCHS, D SHEARER, GM BOSWELL, RN LUCEY, DR CLERICI, M REIBNEGGER, G WERNER, ER ZAJAC, RA WACHTER, H TI NEGATIVE CORRELATION BETWEEN BLOOD-CELL COUNTS AND SERUM NEOPTERIN CONCENTRATION IN PATIENTS WITH HIV-1 INFECTION SO AIDS LA English DT Note DE ANEMIA; CYTOKINE; HEMATOPOIESIS; HIV; IMMUNE STIMULATION; NEOPTERIN ID TUMOR NECROSIS FACTOR; IMMUNODEFICIENCY VIRUS TYPE-1; INTERFERON-GAMMA; PROGENITOR CELLS; BONE-MARROW; MARKER; LINES AB Hematopoietic disturbances are common in patients with HIV-1 infection. Recent studies on immune activation markers such as neopterin demonstrate that HIV-1 infection is associated with chronic immune activation. We investigated a possible association between serum neopterin concentrations and blood cell counts (CD4+ T cells, white blood cells, platelets, red blood cells) and hemoglobin and hematocrit in 94 HIV-1-seropositive individuals [52 Walter Reed (WR) stage 1, 31 WR2, one WR5, and 10 WR6]. There were significant negative correlations between neopterin concentrations and CD4+ T cells, hemoglobin, hematocrit and platelets. These correlations were also significant if either only WR1 and WR2 patients or the entire set of data were considered for calculations. Thus, hematological abnormalities are associated with chronic immune activation in patients with HIV-1 infection. Large amounts of neopterin are released by human macrophages on stimulation with interferon-gamma (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) further enhances the effect of IFN-gamma. Therefore, our data suggest that activated immune cells and specific cytokines such as IFN-gamma and TNF-alpha are involved inhibiting hematopoiesis. C1 UNIV INNSBRUCK, INST MED CHEM & BIOCHEM, FRITZ PREGL STR 3, A-6020 INNSBRUCK, AUSTRIA. UNIV INNSBRUCK, LUDWIG BOLTZMANN INST AIDS RES, A-6020 INNSBRUCK, AUSTRIA. NCI, EXPTL IMMUNOL BRANCH, BETHESDA, MD 20892 USA. USAF, SGHMMI, HIV UNIT, LACKLAND AFB, TX 78236 USA. RI Reibnegger, Gilbert/H-5742-2012 OI Reibnegger, Gilbert/0000-0001-7202-2426 NR 28 TC 27 Z9 27 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0269-9370 EI 1473-5571 J9 AIDS JI Aids PD FEB PY 1991 VL 5 IS 2 BP 209 EP 212 DI 10.1097/00002030-199102000-00012 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA FF379 UT WOS:A1991FF37900012 PM 1674419 ER PT J AU BRODER, S AF BRODER, S TI ANTIRETROVIRAL THERAPY - PAST, PRESENT AND FUTURE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 123 EP 123 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000003 ER PT J AU AGRAWAL, S SARIN, P ZAMECNIK, P AF AGRAWAL, S SARIN, P ZAMECNIK, P TI PROGRESS IN THE USE OF ANTISENSE OLIGONUCLEOTIDES FOR INHIBITION OF HIV IN TISSUE-CULTURE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 WORCESTER FDN EXPTL BIOL INC,SHREWSBURY,MA 01545. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 124 EP 124 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000004 ER PT J AU ROBERTS, MM OROSZLAN, S AF ROBERTS, MM OROSZLAN, S TI CLEAVAGE OF RETROVIRAL NUCLEOCAPSID PROTEIN BY THE VIRAL PROTEINASE DURING REVERSE TRANSCRIPTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 124 EP 125 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000006 ER PT J AU WALDMANN, TA TENDLER, CL GREENBERG, SJ GOLDMAN, CK JUNGHANS, RP AF WALDMANN, TA TENDLER, CL GREENBERG, SJ GOLDMAN, CK JUNGHANS, RP TI IL-2 RECEPTOR DIRECTED THERAPY OF PATIENTS WITH ATL OR WITH TSP HAM SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,METAB BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 124 EP 124 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000005 ER PT J AU ASHORN, P MOSS, B BERGER, EA AF ASHORN, P MOSS, B BERGER, EA TI ANTI-HIV ACTIVITIES OF CD4-PSEUDOMONAS EXOTOXIN HYBRID PROTEIN - HIGHLY SYNERGISTIC EFFECTS WITH RT INHIBITORS IN HUMAN T-CELLS, AND ACTIVITIES AGAINST OTHER INFECTED CELL-TYPES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 126 EP 127 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000009 ER PT J AU EIDEN, LE RAUSCH, DM KALYANARAMAN, VS NARA, PL BUCK, D HWANG, KM LIFSON, JD AF EIDEN, LE RAUSCH, DM KALYANARAMAN, VS NARA, PL BUCK, D HWANG, KM LIFSON, JD TI SYNTHETIC CD4-DERIVED PEPTIDES AND ANTI-CD4 ANTIBODIES MAP VIRAL ISOLATE-SPECIFIC GP120 INTERACTION SITES ON CD4 IMPORTANT FOR HIV-1 INFECTION AND PATHOGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI INC,ROCKVILLE,MD. NCI,TUMOR CELL BIOL LAB,FREDERICK,MD 21701. BECTON DICKENSON MONOCLONAL ANTIBODY CTR,MT VIEW,CA. GENELABS INC,REDWOOD CITY,CA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 126 EP 126 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000008 ER PT J AU SARVER, N CHANG, PS ZAIA, J CANTIN, E ROSSI, J AF SARVER, N CHANG, PS ZAIA, J CANTIN, E ROSSI, J TI EXPLOITING RIBOZYMES FOR HIV THERAPY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,DAIDS,DEV THERAPEUT BRANCH,BETHESDA,MD 20892. CITY HOPE NATL MED CTR,DUARTE,CA 91010. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 127 EP 127 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000010 ER PT J AU NIENHUIS, AW BODINE, D MCDONAGH, K AF NIENHUIS, AW BODINE, D MCDONAGH, K TI RETROVIRAL MEDIATED GENE-TRANSFER INTO HEMATOPOIETIC STEM-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 128 EP 129 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000012 ER PT J AU SHIRASAKA, T YARCHOAN, R AOKI, S FORD, H DEVICO, A SARNGADHARAN, MG RICHMAN, DD BRODER, S MITSUYA, H AF SHIRASAKA, T YARCHOAN, R AOKI, S FORD, H DEVICO, A SARNGADHARAN, MG RICHMAN, DD BRODER, S MITSUYA, H TI INVITRO STUDY OF DRUG-SENSITIVITY OF HIV STRAINS ISOLATED FROM PATIENTS WITH AIDS OR ARC BEFORE AND AFTER THERAPY WITH AZT AND OR 2',3'-DIDEOXYCYTIDINE (DDC) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD. UNIV CALIF SAN DIEGO,VET ADM MED CTR,SAN DIEGO,CA 92103. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 130 EP 131 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000015 ER PT J AU YARCHOAN, R PLUDA, JM THOMAS, RV MITSUYA, H WYVILL, KS BROUWERS, P BRODER, S AF YARCHOAN, R PLUDA, JM THOMAS, RV MITSUYA, H WYVILL, KS BROUWERS, P BRODER, S TI LONG-TERM ADMINISTRATION OF 2',3'-DIDEOXYINOSINE (DDI) TO PERSONS WITH AIDS OR AIDS-RELATED COMPLEX SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 130 EP 130 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000014 ER PT J AU ROILIDES, E CLERICI, M SHEARER, G BUTLER, K PIZZO, PA AF ROILIDES, E CLERICI, M SHEARER, G BUTLER, K PIZZO, PA TI T-HELPER LYMPHOCYTE FUNCTION IN HIV-INFECTED CHILDREN - EFFECTS OF ANTIRETROVIRAL THERAPY WITH DIDEOXYINOSINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 132 EP 132 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000017 ER PT J AU SHIRASAKA, T MURAKAMI, K FORD, H KELLEY, J YOSHIOKA, H KOJIMA, E AOKI, S DRISCOLL, JS BRODER, S MITSUYA, H AF SHIRASAKA, T MURAKAMI, K FORD, H KELLEY, J YOSHIOKA, H KOJIMA, E AOKI, S DRISCOLL, JS BRODER, S MITSUYA, H TI 6-HALOGENATED CONGENERS OF 2',3'-DIDEOXYPURINE NUCLEOSIDES ACTIVE AGAINST HIV INVITRO - A NEW CLASS OF LIPOPHILIC PRODRUG SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. SANYO KOKUSAKU PULP CO,IWAKUNI,YAMAGUCHI,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 132 EP 133 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000018 ER PT J AU PAL, R MUMBAUER, S HOKE, G SARNGADHARAN, MG STEIN, CA AF PAL, R MUMBAUER, S HOKE, G SARNGADHARAN, MG STEIN, CA TI COMPARATIVE EFFECTS OF POLYANIONIC COMPOUNDS ON SYNCYTIA FORMATION AND INFECTIVITY OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-I AND TYPE-II INVITRO SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ADV BIOSCI LABS INC,KENSINGTON,MD. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 133 EP 133 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000019 ER PT J AU PICARD, O IMBERT, JC SALAUN, JJ LURHAMA, Z MOSS, B GALLO, RC ZAGURY, D AF PICARD, O IMBERT, JC SALAUN, JJ LURHAMA, Z MOSS, B GALLO, RC ZAGURY, D TI IMMUNE THERAPY CLINICAL-TRIAL (PHASE-I) IN AIDS ARCS PATIENTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV PARIS 06,F-75230 PARIS 05,FRANCE. INST JEAN GODINOT,PARIS,FRANCE. HOP ST ANTOINE,F-75571 PARIS 12,FRANCE. INRB,KINSHASA,ZAIRE. CLIN UNIV KINSHASA,KINSHASA,ZAIRE. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 134 EP 135 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000021 ER PT J AU PSALLIDOPOULOS, M DEWAR, R VASUDEVACHARI, MB THOMPSON, LM LANE, HC SALZMAN, NP AF PSALLIDOPOULOS, M DEWAR, R VASUDEVACHARI, MB THOMPSON, LM LANE, HC SALZMAN, NP TI SURROGATE MARKERS IN EVALUATING THE EFFECTIVENESS OF THERAPEUTIC PROTOCOLS IN PATIENTS WITH AIDS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 GEORGETOWN UNIV,WASHINGTON,DC 20057. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 134 EP 134 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000020 ER PT J AU OBRIEN, MC MITSUYA, H AF OBRIEN, MC MITSUYA, H TI THE EFFECT OF DEMETHYLATION OF DNA ON HIV EXPRESSION INVITRO SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 136 EP 137 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000025 ER PT J AU GIRALDO, G BETHGIRALDO, E TAMBURINI, M SERVADDA, D KYALWAZI, SK GALLO, RC LUKA, J DEBIASI, R AF GIRALDO, G BETHGIRALDO, E TAMBURINI, M SERVADDA, D KYALWAZI, SK GALLO, RC LUKA, J DEBIASI, R TI SYNERGISTIC EFFECTS OF MULTIPLE VIRUS-INFECTIONS ON HIV DISEASE PROGRESSION - CROSS-SECTIONAL AND LONGITUDINAL IMMUNOVIROLOGIC ANALYSES ON HOSPITAL POPULATIONS AND HEALTHY-SUBJECTS, MAINLY FROM UGANDA AND ITALY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NATL CANC INST FOND PASCALE,NAPLES,ITALY. MED SOC,CTR HEMOPHILIA,NAPLES,ITALY. WHO,GPA,ENTEBBE,UGANDA. NEW MULAGO HOSP,KAMPALA,UGANDA. NCI,BETHESDA,MD 20892. UNIV NEBRASKA,MED CTR,OMAHA,NE 68105. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 137 EP 138 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000027 ER PT J AU LAN, XY HE, SH CHEN, J DETHE, G KOMURIAN, F GALLO, RC ZENG, Y AF LAN, XY HE, SH CHEN, J DETHE, G KOMURIAN, F GALLO, RC ZENG, Y TI DETECTION OF HTLV-1 ANTIGEN AND ANTIBODY FROM THE CHINESE PATIENTS WITH LEUKEMIA OR NEUROLOGICAL DISEASES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CHINESE ACAD PREVENT MED,INST VIROL,BEIJING,PEOPLES R CHINA. JIAN SI MED INST,NAN CHANG,PEOPLES R CHINA. NCI,BETHESDA,MD 20892. CNRS,F-69373 LYONS,FRANCE. INST MERIEUR,LYONS,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 139 EP 139 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000029 ER PT J AU BERZOFSKY, JA TAKAHASHI, H HOSMALIN, A CLERICI, M MOREIN, B TAKESHITA, T DEGROOT, AS HOUGHTEN, R PENDLETON, CD PUTNEY, SD MOSS, B GERMAIN, RN SHEARER, GM AF BERZOFSKY, JA TAKAHASHI, H HOSMALIN, A CLERICI, M MOREIN, B TAKESHITA, T DEGROOT, AS HOUGHTEN, R PENDLETON, CD PUTNEY, SD MOSS, B GERMAIN, RN SHEARER, GM TI INDUCTION OF CYTOTOXIC T-CELLS TO HIV PROTEINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,METAB BRANCH,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. TORREY PINES INST MOLEC STUDIES,SAN DIEGO,CA 92121. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. BIOMED CTR,NATL VET INST DEPT VIROL,S-75123 UPPSALA,SWEDEN. REPLIGEN CORP,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 144 EP 144 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000038 ER PT J AU ROBERTGUROFF, M REITZ, MS GUO, HG REED, R ALDRICH, K STERN, TS WATERS, D ZAGURY, D GALLO, RC AF ROBERTGUROFF, M REITZ, MS GUO, HG REED, R ALDRICH, K STERN, TS WATERS, D ZAGURY, D GALLO, RC TI ANALYSIS OF V3 LOOP REACTIVITIES AND CROSS NEUTRALIZATION PATTERNS OF ZAIRIAN SERA AND MATCHED VIRAL ISOLATES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. PROGRAM RESOURCES INC,FREDERICK,MD. UNIV PARIS 06,DEPT CELLULAR PHYSIOL,F-75230 PARIS 05,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 144 EP 145 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000039 ER PT J AU NARA, P BACK, N DUNLOP, N SMIT, L GOUDSMIT, J AF NARA, P BACK, N DUNLOP, N SMIT, L GOUDSMIT, J TI NEUTRALIZATION OF HIV-1 - A HUMORAL PARADOX DUE TO A LINEAR, CONFORMATIONALLY-INTERDEPENDENT STRAIN-SPECIFIC GP120 EPITOPE (V3) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. UNIV AMSTERDAM,ACAD MED CTR,1105 AZ AMSTERDAM,NETHERLANDS. RI Back, Nicole/K-3884-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 145 EP 146 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000041 ER PT J AU SAXINGER, C AYUB, J FREDERICK, W AF SAXINGER, C AYUB, J FREDERICK, W TI SEROPREVALENCE OF HUMAN-ANTIBODIES REACTING WITH HIV SIV VARIANT V3 LOOP STRUCTURES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. HOWARD UNIV HOSP,WASHINGTON,DC 20060. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 146 EP 146 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000042 ER PT J AU KLASSE, PJ HAN, KH PIPKORN, R BLOMBERG, J FERRETTI, JA AF KLASSE, PJ HAN, KH PIPKORN, R BLOMBERG, J FERRETTI, JA TI 3-DIMENSIONAL STRUCTURE AND ANTIGENICITY OF GP41 PEPTIDES - THE EFFECTS OF A NEUTRALIZATION-ESCAPE SUBSTITUTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV LUND,DEPT MED MICROBIOL,VIROL SECT,S-22101 LUND,SWEDEN. NOVA BIOCHEM,SANDHAUSEN,GERMANY. NIH,BIOPHYS CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 150 EP 150 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000049 ER PT J AU NIGIDA, SM BESS, JW PYLE, SW MOREIN, B PUTNEY, SD ARTHUR, LO AF NIGIDA, SM BESS, JW PYLE, SW MOREIN, B PUTNEY, SD ARTHUR, LO TI IMMUNIZATION OF CHIMPANZEES WITH BACULOVIRUS-EXPRESSED HIV-1(IIIB) GP160 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,AIDS VACCINE PROGRAM,FREDERICK,MD 21701. NATL VET INST,UPPSALA,SWEDEN. REPLIGEN CORP,CAMBRIDGE,MA. RI Bess, Jr., Julian/B-5343-2012 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 150 EP 151 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000050 ER PT J AU FUERST, TR HAUN, SS BANSAL, GP BENSON, LA STOVER, CK YOUNG, JF BERZOFSKY, JA MOSS, B DELACRUZ, VF AF FUERST, TR HAUN, SS BANSAL, GP BENSON, LA STOVER, CK YOUNG, JF BERZOFSKY, JA MOSS, B DELACRUZ, VF TI CONSTRUCTION OF AND IMMUNE-RESPONSES TO HIV-1 WHOLE PROTEIN AND SYNTHETIC POLYVALENT IMMUNOGENS USING RECOMBINANT VACCINIA VIRUS AND BCG EXPRESSION SYSTEMS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 MOLEC VACCINES INC,GAITHERSBURG,MD. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 151 EP 151 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000051 ER PT J AU STOVER, CK DELACRUZ, VF HATFULL, GF BURLEIN, JE BENNETT, LT BENSON, LA LEE, MH FRANCHINI, G YOUNG, JF JACOBS, WR BLOOM, BR FUERST, TR AF STOVER, CK DELACRUZ, VF HATFULL, GF BURLEIN, JE BENNETT, LT BENSON, LA LEE, MH FRANCHINI, G YOUNG, JF JACOBS, WR BLOOM, BR FUERST, TR TI DEVELOPMENT AND USE OF LIVE RECOMBINANT BCG VACCINE VECTORS FOR EXPRESSION OF HIV-1 AND HIV-2 PROTEINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV PITTSBURGH,PITTSBURGH,PA 15260. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 152 EP 152 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000052 ER PT J AU CLERICI, M TACKET, CO VIA, CS BERZOFSKY, JA SHEARER, GM AF CLERICI, M TACKET, CO VIA, CS BERZOFSKY, JA SHEARER, GM TI IMMUNIZATION OF HEALTHY-HUMAN VOLUNTEERS WITH HIV RECOMBINANT GP160 ELICITS STRONG HIV SPECIFIC LYMPHOCYTE-T FUNCTIONS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV MARYLAND,BALTIMORE,MD 21201. NR 0 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 154 EP 155 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000056 ER PT J AU GOLDSTEIN, AL NAYLOR, PH SARIN, PS KIRKLEY, JE STAMBUK, D RIOS, A ZAGURY, D ACHOUR, A GAZZARD, B YOULE, M AF GOLDSTEIN, AL NAYLOR, PH SARIN, PS KIRKLEY, JE STAMBUK, D RIOS, A ZAGURY, D ACHOUR, A GAZZARD, B YOULE, M TI PROGRESS IN THE DEVELOPMENT OF A P17 BASED HIV VACCINE - IMMUNOGENICITY OF HGP-30 IN HUMANS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NIH,BETHESDA,MD 20892. SW MEM HOSP,HOUSTON,TX. ST STEPHENS HOSP,LONDON SW10 9TH,ENGLAND. UNIV PARIS 06,INST PASTEUR,F-75230 PARIS 05,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 154 EP 154 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000055 ER PT J AU ACHOUR, A PICARD, O MBIKA, B TAKAHASHI, H BERZOFSKY, JA GALLO, RC ZAGURY, D AF ACHOUR, A PICARD, O MBIKA, B TAKAHASHI, H BERZOFSKY, JA GALLO, RC ZAGURY, D TI ENVELOPE PROTEIN AND P18IIIB PEPTIDE RECOGNIZED BY CYTOTOXIC LYMPHOCYTES-T FROM AIDS VIRAL ENVELOPE-IMMUNIZED HUMANS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV PARIS 06,PHYSIOL CELLULAIRE LAB,F-75230 PARIS 05,FRANCE. HOP ST ANTOINE,F-75571 PARIS 12,FRANCE. NCI,METAB BRANCH,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 155 EP 156 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000058 ER PT J AU MOSIER, DE GULIZIA, RJ MACISAAC, P SPECTOR, SA SPECTOR, DH BAIRD, SM SHEARER, GM TACKET, C MATHIESON, B KOUP, R SULLIVAN, J COREY, L GREENBERG, P AF MOSIER, DE GULIZIA, RJ MACISAAC, P SPECTOR, SA SPECTOR, DH BAIRD, SM SHEARER, GM TACKET, C MATHIESON, B KOUP, R SULLIVAN, J COREY, L GREENBERG, P TI EVALUATION OF CANDIDATE VACCINES IN THE HU-PBL-SCID MOUSE MODEL SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 MED BIOL INST,LA JOLLA,CA 92037. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. VET ADM MED CTR,LA JOLLA,CA 92161. NCI,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DEPT MED,BALTIMORE,MD 21201. NIAID,DAIDS,BETHESDA,MD 20892. UNIV MASSACHUSETTS,MED CTR,DEPT PEDIAT,WORCESTER,MA 01605. UNIV WASHINGTON,SCH MED,DEPT LAB MED & MED,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 155 EP 155 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000057 ER PT J AU BENVENISTE, R HEIDECKER, G HENDERSON, L POWELL, P LEWIS, M HU, SL MORTON, W EDDY, G BURKE, D SHAFFERMAN, A AF BENVENISTE, R HEIDECKER, G HENDERSON, L POWELL, P LEWIS, M HU, SL MORTON, W EDDY, G BURKE, D SHAFFERMAN, A TI PATHOGENESIS AND VACCINE STUDIES IN SIV AND TYPE D RETROVIRUS-INFECTED MACAQUES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. PROGRAM RESOURCES INC,FREDERICK,MD. USA,MED RES INST INFECT DIS,FREDERICK,MD 21701. ONCOGEN,SEATTLE,WA. WASHINGTON PRIMATE RES CTR,SEATTLE,WA. JACKSON FDN,RES LAB,ROCKVILLE,MD. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. ISRAEL INST BIOL RES,IL-70450 NESS ZIONA,ISRAEL. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 159 EP 160 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000066 ER PT J AU FRANCHINI, G MARKHAM, P GARD, L FARGNOLI, K HATTORI, N MARCON, L GALLO, RC AF FRANCHINI, G MARKHAM, P GARD, L FARGNOLI, K HATTORI, N MARCON, L GALLO, RC TI HIV-2 IN MACAQUES AS A MODEL FOR STUDYING THE ROLE OF ACCESSORY GENES IN VIRAL INFECTIVITY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 162 EP 162 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000071 ER PT J AU GONDA, MA OBERSTE, MS GARVEY, KJ PIFAT, DY BATTLES, JK WARD, JM PALLANSCH, LA NAGASHIMA, K AF GONDA, MA OBERSTE, MS GARVEY, KJ PIFAT, DY BATTLES, JK WARD, JM PALLANSCH, LA NAGASHIMA, K TI BOVINE IMMUNODEFICIENCY-LIKE VIRUS - MOLECULAR-GENETICS AND DEVELOPMENT OF ANIMAL-MODELS OF RELEVANCE TO HIV SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 PROGRAM RESOURCES INC,FREDERICK,MD 21072. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 163 EP 164 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000074 ER PT J AU HAGUE, BF SAWASDIKOSOL, S RECKER, DP KINDT, TJ AF HAGUE, BF SAWASDIKOSOL, S RECKER, DP KINDT, TJ TI HIV-1 AND HTLV-1 INFECTION OF A RABBIT T-CELL LINE TRANSFECTED WITH HUMAN CD4 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 164 EP 165 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000076 ER PT J AU PRIEL, E SHOWALTER, SD ROBERTS, M OROSZLAN, S SEGAL, S ABOUD, M BLAIR, DG AF PRIEL, E SHOWALTER, SD ROBERTS, M OROSZLAN, S SEGAL, S ABOUD, M BLAIR, DG TI TOPOISOMERASE-I ACTIVITY IN HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) AND EQUINE INFECTIOUS-ANEMIA VIRUS (EIAV) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 BEN GURION UNIV NEGEV,IL-84105 BEER SHEVA,ISRAEL. NCI,FREDERICK,MD 21701. PROGRAM RESOURCES INC,FREDERICK,MD. BRI,FREDERICK,MD. FREDERICK CANC RES FACIL,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 164 EP 164 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000075 ER PT J AU KULAGA, H RECKER, D KUTA, E HAGUE, BF TRUCKENMILLER, ME COGGIANO, M SHEN, Y LOCK, A KINDT, TJ AF KULAGA, H RECKER, D KUTA, E HAGUE, BF TRUCKENMILLER, ME COGGIANO, M SHEN, Y LOCK, A KINDT, TJ TI THE BRAIN IS A TARGET FOR HIV-1 INFECTION IN THE RABBIT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIMH,NEUROPSYCHIAT BRANCH,BETHESDA,MD 20892. NIAID,IMMUNOGENET LAB,BETHESDA,MD 20892. NIAID,VET PATHOL BRANCH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 165 EP 165 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000077 ER PT J AU REITZ, MS ROBERTGUROFF, M CHAWLA, A WILSON, C GALLO, RC AF REITZ, MS ROBERTGUROFF, M CHAWLA, A WILSON, C GALLO, RC TI INVITRO IMMUNOSELECTION OF NEUTRALIZATION RESISTANT VARIANTS OF HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 168 EP 169 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000083 ER PT J AU PINCUS, SH AF PINCUS, SH TI VARIANTS SELECTED BY TREATMENT OF HIV INFECTED-CELLS WITH AN IMMUNOTOXIN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 169 EP 169 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000084 ER PT J AU PAVLAKIS, GN SCHWARTZ, S BENKO, DM SOLOMIN, L CIMINALE, V FELBER, BK AF PAVLAKIS, GN SCHWARTZ, S BENKO, DM SOLOMIN, L CIMINALE, V FELBER, BK TI STRUCTURAL ORGANIZATION AND REGULATION OF EXPRESSION OF HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 171 EP 172 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000089 ER PT J AU FELBER, BK BENKO, DM SCHWARTZ, S PAVLAKIS, GN AF FELBER, BK BENKO, DM SCHWARTZ, S PAVLAKIS, GN TI NOVEL PROTEINS OF HIV-1 AS ALTERNATIVE REGULATORY FACTORS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 172 EP 172 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000090 ER PT J AU THEVENIN, C KIM, SJ RIECKMANN, P FUJIKI, H NORCROSS, MA SPORN, MB FAUCI, AS KEHRL, JH AF THEVENIN, C KIM, SJ RIECKMANN, P FUJIKI, H NORCROSS, MA SPORN, MB FAUCI, AS KEHRL, JH TI INDUCTION OF NUCLEAR FACTOR-KAPPA-B AND THE HUMAN-IMMUNODEFICIENCY-VIRUS LONG TERMINAL REPEAT BY OKADAIC ACID SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 174 EP 175 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000094 ER PT J AU KLOTMAN, ME KIM, SY WONGSTAAL, F AF KLOTMAN, ME KIM, SY WONGSTAAL, F TI KINETICS OF SPLICING OF HIV MESSENGER-RNA IN ACUTELY INFECTED LYMPHOCYTES AND MACROPHAGE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA. UNIV SAN DIEGO,DEPT MED,SAN DIEGO,CA 92110. NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 176 EP 176 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000097 ER PT J AU GARTENHAUS, RB MICHAELS, F HALL, L REITZ, M AF GARTENHAUS, RB MICHAELS, F HALL, L REITZ, M TI TAT AND LTR ACTIVITY IN PRIMARY MONOCYTES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 177 EP 177 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000099 ER PT J AU HATTORI, N MICHAELS, F FARGNOLI, K MARCON, L GARTENHAUS, R GALLO, RC FRANCHINI, G AF HATTORI, N MICHAELS, F FARGNOLI, K MARCON, L GARTENHAUS, R GALLO, RC FRANCHINI, G TI THE VPR GENE OF HIV-2 IS A TRANSACTIVATOR NECESSARY FOR VIRAL EXPRESSION IN PRIMARY MACROPHAGES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 177 EP 177 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000098 ER PT J AU ARYA, SK AF ARYA, SK TI HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-2 GENE-EXPRESSION - 2 ENHANCERS AND THEIR ACTIVATION BY T-CELL ACTIVATORS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 178 EP 178 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000101 ER PT J AU LISZIEWICZ, J RAPPAPORT, J DHAR, R AF LISZIEWICZ, J RAPPAPORT, J DHAR, R TI MULTIMERIZED TAR ELEMENTS DOWN-REGULATE TAT MEDIATED TRANSACTIVATION OF HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 178 EP 178 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000100 ER PT J AU DAYTON, AI POWELL, DM NISHIKURA, K KONINGS, D SHAPIRO, B DAYTON, ET AF DAYTON, AI POWELL, DM NISHIKURA, K KONINGS, D SHAPIRO, B DAYTON, ET TI STUDIES ON CAR/RRE, THE TARGET SEQUENCE FOR THE REV PROTEIN OF HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. WISTAR INST,PHILADELPHIA,PA 19104. NCI,FREDERICK CANC RES FACIL,DEPT MATH BIOL,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 179 EP 179 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000103 ER PT J AU RAPPAPORT, J LISZIEWICZ, J BITTERLICH, G COLOMBINI, S ARYA, S WONGSTAAL, F AF RAPPAPORT, J LISZIEWICZ, J BITTERLICH, G COLOMBINI, S ARYA, S WONGSTAAL, F TI MAPPING OF A SPECIFICITY DOMAIN IN HIV-1 AND SIV/HIV-2 TAT PROTEINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 179 EP 179 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000102 ER PT J AU ZWEIG, M SAMUEL, KP SHOWALTER, SD BLADEN, SV DUBOIS, GC LAUTENBERGER, JA HODGE, D PAPAS, TS AF ZWEIG, M SAMUEL, KP SHOWALTER, SD BLADEN, SV DUBOIS, GC LAUTENBERGER, JA HODGE, D PAPAS, TS TI HTLV-IIIB ISOLATE VARIANTS PRODUCING DIFFERENT FORMS OF THE NEF PROTEIN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,NAPS LAB,FREDERICK,MD 21701. NCI,FREDERICK CANC RES FACIL,MOLEC ONCOL LAB,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 180 EP 181 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000105 ER PT J AU MARCON, L MICHAELS, F HATTORI, N FARGNOLI, K ZICHT, R GALLO, RC FRANCHINI, G AF MARCON, L MICHAELS, F HATTORI, N FARGNOLI, K ZICHT, R GALLO, RC FRANCHINI, G TI FUNCTIONAL-STUDIES ON THE HIV-2 VPX GENE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 182 EP 182 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000108 ER PT J AU YOUNG, NS AF YOUNG, NS TI BIOLOGY OF PARVOVIRUS INFECTION IN HUMANS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 184 EP 185 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000112 ER PT J AU AGGARWAL, A GALLO, RC NASH, TE DIAMOND, LS FRANCHINI, G AF AGGARWAL, A GALLO, RC NASH, TE DIAMOND, LS FRANCHINI, G TI INVITRO ASSOCIATION OF GIARDIA-LAMBLIA AND ENTAMOEBA-HISTOLYTICA WITH HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,PROGRAMME RESOURCES INC,AVP,FREDERICK,MD 21701. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 188 EP 188 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000118 ER PT J AU DEBENEDETTI, F FALTYNEK, CR RUSCETTI, FW COLBURN, NH OPPENHEIM, JJ AF DEBENEDETTI, F FALTYNEK, CR RUSCETTI, FW COLBURN, NH OPPENHEIM, JJ TI TGF BETA INHIBITS WHEREAS TNF IMITATES PMA INDUCED TRANSFORMATION OF JB6 CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,BIOCHEM PHYSIOL LAB,FREDERICK,MD 21701. NCI,FREDERICK CANC RES FACIL,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21701. NCI,FREDERICK CANC RES FACIL,BCDP PROGRAM RESOURCES INC,FREDERICK,MD 21701. NCI,FREDERICK CANC RES FACIL,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 189 EP 190 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000120 ER PT J AU PAPAS, TS AF PAPAS, TS TI ONCOGENES AS PROBES FOR CELLULAR SIGNAL PROCESSES - THE FAMILY OF ETS GENES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 189 EP 189 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000119 ER PT J AU RIECKMANN, P POLI, G KEHRL, JH FAUCI, AS AF RIECKMANN, P POLI, G KEHRL, JH FAUCI, AS TI SPONTANEOUS TNF-ALPHA AND IL-6 SECRETION BY LYMPHOCYTES-B FROM HIV INFECTED INDIVIDUALS CONTRIBUTE TO VIRUS EXPRESSION IN INFECTED T-CELLS AND MONOCYTES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 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 FEB PY 1991 VL 7 IS 2 BP 191 EP 192 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000124 ER PT J AU TSCHACHLER, E BOHNLEIN, E FELTZMANN, S GALLO, RC REITZ, MS AF TSCHACHLER, E BOHNLEIN, E FELTZMANN, S GALLO, RC REITZ, MS TI HTLV-I TAX IS ABLE TO TRANSACTIVATE THE HUMAN LYMPOTOXIN GENE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV VIENNA,SCH MED,DEPT DERMATOL,DIV CUT IMMUNOBIOL,A-1010 VIENNA,AUSTRIA. SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 191 EP 191 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000123 ER PT J AU PADLAN, EA AF PADLAN, EA TI IMMUNOGLOBULINS - STRUCTURE AND APPLICATIONS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDDK,MOLEC BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 192 EP 193 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000125 ER PT J AU GORELICK, RJ NIGIDA, SM BESS, JW ARTHUR, LO HENDERSON, LE REIN, A AF GORELICK, RJ NIGIDA, SM BESS, JW ARTHUR, LO HENDERSON, LE REIN, A TI MUTATIONS IN THE ZINC FINGER-LIKE REGION OF HIV-1 NUCLEOCAPSID YIELD NONINFECTIOUS PARTICLES DEFICIENT IN GENOMIC RNA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,AIDS VACCINE PROGRAM,FREDERICK,MD 21701. NCI,FREDERICK CANC RES FACIL,ABL BASIC RES PROGRAM,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD 21701. RI Bess, Jr., Julian/B-5343-2012 NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 194 EP 194 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000128 ER PT J AU HENDERSON, LE SUMMERS, MF POWELL, PJ SOUTH, TL BLAKE, PR ARTHUR, LO AF HENDERSON, LE SUMMERS, MF POWELL, PJ SOUTH, TL BLAKE, PR ARTHUR, LO TI CYS-ARRAYS IN HIV-1 GAG PRECURSOR AND NUCLEO CAPSID PROTEIN MAY FUNCTION AS ZINC LIGAND IN THE NATIVE-STATE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,FREDERICK,MD 21701. UNIV MARYLAND,DEPT CHEM & BIOCHEM,BALTIMORE,MD 21201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 195 EP 195 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000129 ER PT J AU VENKATESAN, S MAITRA, RK HOLLAND, SM DICKIE, P AHMAD, N WINGFIELD, P AF VENKATESAN, S MAITRA, RK HOLLAND, SM DICKIE, P AHMAD, N WINGFIELD, P TI FUNCTIONAL-STUDIES OF HIV-1 REV AND NEF PROTEINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NIH,OFF DIRECTOR,PROT EXPRESS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 195 EP 196 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000130 ER PT J AU DOMS, RW EARL, PL MOSS, B AF DOMS, RW EARL, PL MOSS, B TI FOLDING, OLIGOMERIZATION, AND PROCESSING OF THE HIV-1 ENVELOPE PROTEIN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 196 EP 197 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000132 ER PT J AU SAXINGER, C LEE, S GALLO, R WONGSTAAL, F AF SAXINGER, C LEE, S GALLO, R WONGSTAAL, F TI CHARACTERIZATION OF A CELL-SURFACE INTERACTION WITH HIV-1 TAT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 196 EP 197 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000131 ER PT J AU KALYANARAMAN, VS RODRIGUEZ, V GALLO, RC SARNGADHARAN, MG AF KALYANARAMAN, VS RODRIGUEZ, V GALLO, RC SARNGADHARAN, MG TI SYNTHESIS AND PROCESSING OF HIV-1 GP160 IN CELLS WITH DEFECTIVE HIV-1 GENOMES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ADV SCI LABS,DEPT CELL BIOL,KENSINGTON,MD. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 197 EP 197 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000133 ER PT J AU BERGER, EA BRODER, CC AF BERGER, EA BRODER, CC TI STRUCTURAL-CHANGES IN THE HIV-1 ENVELOPE GLYCOPROTEIN INDUCED BY CD4 BINDING SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 199 EP 199 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000137 ER PT J AU AOKI, S BRODER, S MITSUYA, H AF AOKI, S BRODER, S MITSUYA, H TI EFFECT OF RECOMBINANT SOLUBLE CD4 (RCD4) AND RCD4-IGG ON COGNITIVE VIRAL TRANSMISSION FROM HIV-1-INFECTED MONOCYTES-MACROPHAGES TO T-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 200 EP 201 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000139 ER PT J AU FAUCI, AS AF FAUCI, AS TI IMMUNOPATHOGENESIS OF HIV-INFECTION - AN UPDATE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 202 EP 202 DI 10.1089/aid.1991.7.202 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000141 ER PT J AU SHEARER, GM CLERICI, M VIA, CS ROILIDES, E PIZZO, PA AF SHEARER, GM CLERICI, M VIA, CS ROILIDES, E PIZZO, PA TI ACTIVE DOWN-REGULATION OF T HELPER-CELL FUNCTION IN ASYMPTOMATIC, HIV-SEROPOSITIVE PATIENTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DEPT MED,DIV RHEUMATOL & CLIN IMMUNOL,BALTIMORE,MD 21201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 203 EP 203 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000143 ER PT J AU PANTALEO, G DEMARIA, A KOENIG, S BUTINI, L MOSS, B LANE, HC FAUCI, AS AF PANTALEO, G DEMARIA, A KOENIG, S BUTINI, L MOSS, B LANE, HC FAUCI, AS TI CD8+ LYMPHOCYTES-T OF PATIENTS WITH AIDS MAINTAIN NORMAL BROAD CYTOLYTIC FUNCTION DESPITE THE LOSS OF HIV-SPECIFIC CYTOTOXICITY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREG LAB,BETHESDA,MD 20892. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 205 EP 205 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000147 ER PT J AU MANN, DL HAMLIN, G BLATTNER, WA GOEDERT, JJ AF MANN, DL HAMLIN, G BLATTNER, WA GOEDERT, JJ TI ANALYSIS OF IMMUNOGLOBULIN CLASS AND SUBCLASS RESPONSE TO HIV-1 PROTEINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,VIRAL CARCINOGENESIS LAB,IMMUNOGENET SECT,BETHESDA,MD 20892. NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NCI,EEB,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 206 EP 206 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000148 ER PT J AU LORI, F HALL, L FRANCHINI, G MARKHAM, P GALLO, RC REITZ, MS AF LORI, F HALL, L FRANCHINI, G MARKHAM, P GALLO, RC REITZ, MS TI ISOLATION AND CHARACTERIZATION OF BIOLOGICALLY-ACTIVE MOLECULAR CLONES OF HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ABL,DEPT CELL BIOL,KENSINGTON,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 207 EP 208 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000151 ER PT J AU TANI, Y VENKATESAN, S LANE, HC COHEN, DI AF TANI, Y VENKATESAN, S LANE, HC COHEN, DI TI EXPRESSION OF HIV-1 ENVELOPE PROTEIN IN A CD4+ T-CELL LINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 209 EP 209 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000154 ER PT J AU LAYNE, SP MERGES, MJ DEMBO, M SPOUGE, JL GELDERBLOM, HR NARA, PL AF LAYNE, SP MERGES, MJ DEMBO, M SPOUGE, JL GELDERBLOM, HR NARA, PL TI DETERMINING BASIC MOLECULAR REQUIREMENTS FOR BLOCKING THERAPIES AND HIV VACCINES INVITRO SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV CALIF LOS ALAMOS SCI LAB,LOS ALAMOS,NM 87545. NCI,FREDERICK,MD 21701. NATL LIB MED,BETHESDA,MD 20892. ROBERT KOCH INST,W-1000 BERLIN 65,GERMANY. RI Dembo, Micah/C-2755-2013 NR 0 TC 0 Z9 0 U1 0 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 210 EP 211 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000156 ER PT J AU BALOTTA, C VERONESE, FD VARESIO, L CORBELLINO, M LORI, F GALLO, RC LUSSO, P AF BALOTTA, C VERONESE, FD VARESIO, L CORBELLINO, M LORI, F GALLO, RC LUSSO, P TI SUSCEPTIBILITY OF CIRCULATING HUMAN MONOCYTES TO HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. FREDERICK CANC RES FACIL,MOLEC IMMUNOL LAB,FREDERICK,MD 21701. ADV BIOSCI LABS INC,DEPT CELL BIOL,KENSINGTON,MD. RI varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 211 EP 211 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000157 ER PT J AU MICHAELS, FH ESPINOSA, L GALLO, RC AF MICHAELS, FH ESPINOSA, L GALLO, RC TI HIV-1 ASSOCIATED ARTHRITIS AND THE TYPE-A SYNOVIAL LINING CELL SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV S FLORIDA,COLL MED,DEPT INTERNAL MED,TAMPA,FL 33612. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 211 EP 212 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000158 ER PT J AU WEEKS, BS KLOTMAN, ME RAPPAPORT, J KLEINMAN, HK YAMADA, KM KLOTMAN, PE AF WEEKS, BS KLOTMAN, ME RAPPAPORT, J KLEINMAN, HK YAMADA, KM KLOTMAN, PE TI HIV-1 INDUCES INTEGRIN EXPRESSION ON HUMAN CD4+ LYMPHOCYTES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 1 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 212 EP 212 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000159 ER PT J AU CORBELLINO, M BALOTTA, C VERONESE, FD LORI, F GALLO, RC LUSSO, P AF CORBELLINO, M BALOTTA, C VERONESE, FD LORI, F GALLO, RC LUSSO, P TI AN INHIBITOR OF HIV-1 REVERSE-TRANSCRIPTASE IN THE CULTURE SUPERNATANT OF A HUMAN B-LYMPHOBLASTOID LINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,DEPT CELL BIOL,KENSINGTON,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 213 EP 214 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000161 ER PT J AU BOERI, E REINA, S LORI, F GIRI, A VARNIER, EO AF BOERI, E REINA, S LORI, F GIRI, A VARNIER, EO TI EVIDENCE FOR A POSSIBLE NUCLEASE INHIBITING THE DETECTION OF RT INVITRO ACTIVITY SUPERNATANTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 INST MICROBIOL,HUMAN RETROVIROL LAB,GENOA,ITALY. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 214 EP 215 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000163 ER PT J AU DEMARIA, AF PANTALEO, G SCHNITTMAN, SM FAUCI, AS AF DEMARIA, AF PANTALEO, G SCHNITTMAN, SM FAUCI, AS TI INVITRO GENERATION OF CHRONICALLY HIV-1 INFECTED CD3+CD8+CD4- T-CELLS FROM PERIPHERAL-BLOOD LYMPHOCYTES OF HEALTHY DONORS - VIRUS-REPLICATION IS ASSOCIATED WITH CELL ACTIVATION AND CD8+ CELL-DEATH SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 214 EP 214 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000162 ER PT J AU NAKAMURA, S SAKURADA, S GILL, P LUNARDIISKANDAR, Y GALLO, RC SALAHUDDIN, SZ AF NAKAMURA, S SAKURADA, S GILL, P LUNARDIISKANDAR, Y GALLO, RC SALAHUDDIN, SZ TI GLUCOCORTICOID ENHANCED INVITRO GROWTH OF AIDS-KS ASSOCIATED KAPOSIS SARCOMA-DERIVED SPINDLE CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV SO CALIF,LOS ANGELES,CA 90089. NR 0 TC 6 Z9 6 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 216 EP 217 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000166 ER PT J AU ENSOLI, B BUONAGURO, L BARILLARI, G LUSSO, P GALLO, RC AF ENSOLI, B BUONAGURO, L BARILLARI, G LUSSO, P GALLO, RC TI ROLE OF HIV-1 TAT GENE-PRODUCT AND OF CYTOKINES RELEASED BY ACTIVATED IMMUNE CELLS IN THE PATHOGENESIS OF AIDS-ASSOCIATED KAPOSIS-SARCOMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 217 EP 218 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000168 ER PT J AU SAKURADA, S NAKAMURA, S GALLO, RC SALAHUDDIN, SZ AF SAKURADA, S NAKAMURA, S GALLO, RC SALAHUDDIN, SZ TI CULTURED KAPOSIS-SARCOMA CELLS EXPRESS ACTIVITY INDUCING VASCULAR-PERMEABILITY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 217 EP 217 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000167 ER PT J AU BARILLARI, G HOFFMAN, J BUONAGURO, L MICHAEL, F GALLO, RC ENSOLI, B AF BARILLARI, G HOFFMAN, J BUONAGURO, L MICHAEL, F GALLO, RC ENSOLI, B TI CYTOKINES RELEASED BY ACTIVATED PRIMARY T-CELLS STIMULATE GROWTH OF AIDS-KS DERIVED CELLS AND OTHER CELLS OF MESENCHYMAL DERIVATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 218 EP 218 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000169 ER PT J AU LUNARDIISKANDAR, Y NAKAMURA, S GILL, P SAKURADA, S GALLO, RC SALAHUDDIN, SZ AF LUNARDIISKANDAR, Y NAKAMURA, S GILL, P SAKURADA, S GALLO, RC SALAHUDDIN, SZ TI CYTOKINE AND CYTOKINE RECEPTOR EXPRESSION IN AIDS-KAPOSI SARCOMA DERIVED CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV SO CALIF,LOS ANGELES,CA 90089. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 219 EP 219 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000170 ER PT J AU DEVICO, A NAIR, BC NAKAMURA, S SALAHUDDIN, SZ GALLO, RC SARNGADHARAN, MG AF DEVICO, A NAIR, BC NAKAMURA, S SALAHUDDIN, SZ GALLO, RC SARNGADHARAN, MG TI PURIFICATION OF A FACTOR THAT SUPPORTS THE GROWTH OF KAPOSIS SARCOMA-DERIVED CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ADV BIOSCI LABS INC,KENSINGTON,MD. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 220 EP 220 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000172 ER PT J AU GILL, PS NAIDU, Y NAKAMURA, S SALAHUDDIN, Z GALLO, RC AF GILL, PS NAIDU, Y NAKAMURA, S SALAHUDDIN, Z GALLO, RC TI IL-6 REGULATION BY STEROID-HORMONES AND AUTOCRINE ACTIVITY IN KAPOSIS-SARCOMA (KS) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90033. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 220 EP 220 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000173 ER PT J AU PARRAVICINI, C KAAYA, E GENDELMAN, R BERTI, E ENSOLI, B GALLO, RC BIBERFELD, P AF PARRAVICINI, C KAAYA, E GENDELMAN, R BERTI, E ENSOLI, B GALLO, RC BIBERFELD, P TI SPINDLE CELL SUBPOPULATIONS AND HIV-1 EXPRESSION IN AIDS KAPOSIS-SARCOMA (KS) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 KAROLINSKA INST,IMMUNOPATHOL LAB,S-10401 STOCKHOLM 60,SWEDEN. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. STATE UNIV MILANO,DERMATOL CLIN,MILAN,ITALY. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 221 EP 221 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000174 ER PT J AU PLUDA, JM YARCHOAN, R STEINBERG, SM WYVILL, KS BRODER, S AF PLUDA, JM YARCHOAN, R STEINBERG, SM WYVILL, KS BRODER, S TI OPPORTUNISTIC NON-HODGKINS-LYMPHOMA (ONHL) IN PATIENTS WITH SEVERE HIV-INFECTION ON LONG-TERM ANTIRETROVIRAL THERAPY WITH AZT-CONTAINING REGIMENS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 222 EP 223 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000177 ER PT J AU RABKIN, CS GOEDERT, JJ BIGGAR, RJ PEARSON, G GROSSMAN, RJ DIGIOIA, RA SANCHEZ, WC BLATTNER, WA AF RABKIN, CS GOEDERT, JJ BIGGAR, RJ PEARSON, G GROSSMAN, RJ DIGIOIA, RA SANCHEZ, WC BLATTNER, WA TI VIRAL ANTIBODY-TITERS BEFORE AIDS-RELATED MALIGNANCY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 223 EP 223 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000178 ER PT J AU BROWNING, PJ TREPEL, J FLETCHER, M SECHLER, J SALAHUDDIN, SZ GALLO, RC AF BROWNING, PJ TREPEL, J FLETCHER, M SECHLER, J SALAHUDDIN, SZ GALLO, RC TI ESTABLISHMENT OF CONTINUOUSLY GROWING MYELOMONOCYTIC CELLS FROM A PATIENT WITH MYCOSIS-FUNGOIDES WITH REVERSE-TRANSCRIPTASE ACTIVITY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 224 EP 224 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000180 ER PT J AU GESSAIN, A LOUIE, A GOUT, O SAAL, F DETHE, G FRANCHINI, G GALLO, RC AF GESSAIN, A LOUIE, A GOUT, O SAAL, F DETHE, G FRANCHINI, G GALLO, RC TI A DOCUMENTED CASE OF HTLV-1 TRANSMISSION AND HAM TSP INDUCTION - ANALYSIS OF DONOR-RECIPIENT PROVIRAL DNAS AND STUDIES ON VIRAL TRANSCRIPTS IN FRESH PBMCS FROM HAM TSP CASES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. SALPETRIERE HOSP,DEPT NEUROL & NEUROPSYCHOL,PARIS,FRANCE. HOP ST LOUIS,CNRS LAB,UPR0049,F-75475 PARIS 10,FRANCE. FAC MED ALEXIS CARREL,F-69372 LYONS 2,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 226 EP 226 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000183 ER PT J AU MUKHOPADHYAYA, R SARIN, PS RODGERSJOHNSON, P GIBBS, CJ GALLO, RC SADAIE, MR AF MUKHOPADHYAYA, R SARIN, PS RODGERSJOHNSON, P GIBBS, CJ GALLO, RC SADAIE, MR TI COMPARISON OF TSP-DERIVED HTLV-I ISOLATES WITH KNOWN ATL STRAINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NINCDS,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 226 EP 227 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000184 ER PT J AU BERNEMAN, ZN REITZ, MS GARTENHAUS, RB KLOTMAN, ME AF BERNEMAN, ZN REITZ, MS GARTENHAUS, RB KLOTMAN, ME TI ALTERNATIVE SPLICING OF HTLV-I PX MESSENGER-RNA INVIVO AND INVITRO SO AIDS RESEARCH AND HUMAN RETROVIRUSES 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 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 FEB PY 1991 VL 7 IS 2 BP 227 EP 227 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000185 ER PT J AU GREEN, JE AF GREEN, JE TI ACTIVATION OF NERVE GROWTH-FACTOR IN HTLV-1-TAX TRANSGENIC MICE - POTENTIAL AUTOCRINE MECHANISM FOR TRANSFORMATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 227 EP 228 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000186 ER PT J AU LINDHOLM, PF MARRIOTT, SJ BRADY, JN AF LINDHOLM, PF MARRIOTT, SJ BRADY, JN TI PURIFIED HTLV-I TAX1 PROTEIN INDUCES NUCLEAR NFKB BINDING-ACTIVITY IN 70Z/3 PRE-B CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 228 EP 228 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000187 ER PT J AU MARRIOTT, SJ LINDHOLM, PF BRADY, JN AF MARRIOTT, SJ LINDHOLM, PF BRADY, JN TI STIMULATION OF HUMAN PBL PROLIFERATION BY EXOGENOUS HTLV-I TAX1 PROTEIN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 228 EP 229 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000188 ER PT J AU GARTENHAUS, R KLOTMAN, ME AF GARTENHAUS, R KLOTMAN, ME TI SOLUBLE TAX IS TAKEN UP BY CNS CELLS AND PRIMARY LYMPHOCYTES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 229 EP 229 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000189 ER PT J AU MURPHY, E WILKS, R MORGAN, OS HANCHARD, B CRANSTON, B FIGUEROA, JP BRATHWAITE, A ALEXANDER, SS BLATTNER, WA AF MURPHY, E WILKS, R MORGAN, OS HANCHARD, B CRANSTON, B FIGUEROA, JP BRATHWAITE, A ALEXANDER, SS BLATTNER, WA TI ARE HTLV-I CARRIERS REALLY HEALTHY - HEMATOLOGIC AND NEUROLOGIC ABNORMALITIES IN ASYMPTOMATIC JAMAICAN SEROPOSITIVES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. UNIV W INDIES,KINGSTON 7,JAMAICA. MINIST HLTH,KINGSTON,JAMAICA. BIOTECH LABS,ROCKVILLE,MD. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 230 EP 230 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000191 ER PT J AU BLATTNER, WA AF BLATTNER, WA TI HTLV UPDATE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 232 EP 233 DI 10.1089/aid.1991.7.232 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000195 ER PT J AU LUSSO, P LORI, F MALNATI, M DEMARIA, A DEROCCO, SE GALLO, RC AF LUSSO, P LORI, F MALNATI, M DEMARIA, A DEROCCO, SE GALLO, RC TI HHV-6 AND HTLV-I - POSSIBLE MECHANISMS OF COFACTORIAL ROLE IN AIDS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIAID,LIG,BETHESDA,MD 20892. NIAID,LIR,BETHESDA,MD 20892. ABL,KENSINGTON,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 235 EP 236 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000200 ER PT J AU BERNEMAN, ZN ABLASHI, DV SALAHUDDIN, SZ AF BERNEMAN, ZN ABLASHI, DV SALAHUDDIN, SZ TI ISOLATION OF A POTENTIALLY NEW HERPESVIRUS FROM A PATIENT WITH CHRONIC FATIGUE SYNDROME SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 236 EP 236 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000201 ER PT J AU LEVINE, PH WIKTOR, S JACOBSON, S COLCLOUGH, G KAPLAN, J LAIRMORE, M BLATTNER, WA AF LEVINE, PH WIKTOR, S JACOBSON, S COLCLOUGH, G KAPLAN, J LAIRMORE, M BLATTNER, WA TI HTLV-I/II INFECTION IN WESTERN-HEMISPHERE NATIVE-AMERICANS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RES TRIANGLE INST,WASHINGTON,DC. CTR DIS CONTROL,ATLANTA,GA 30333. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 237 EP 238 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000204 ER PT J AU WEISS, SH PALUMBO, P KLEIN, C JAUREGUI, E DENNY, T BLATTNER, W FRENCH, J ALTMAN, R AF WEISS, SH PALUMBO, P KLEIN, C JAUREGUI, E DENNY, T BLATTNER, W FRENCH, J ALTMAN, R TI THE NEW-JERSEY PROSPECTIVE COHORT STUDY OF INTRAVENOUS DRUG-ABUSERS - HIGH PREVALENCE OF HTLV-II AND AIDS EPIDEMIOLOGIC UPDATE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,NEWARK,NJ 07103. NCI,BETHESDA,MD 20892. NEW JERSEY DEPT HLTH,TRENTON,NJ. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 239 EP 239 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000207 ER PT J AU WIKTOR, S JACOBSON, S SHAW, GM WEISS, SH SHORTY, VJ MCFARLIN, DE BLATTNER, WA AF WIKTOR, S JACOBSON, S SHAW, GM WEISS, SH SHORTY, VJ MCFARLIN, DE BLATTNER, WA TI SPONTANEOUS LYMPHOCYTE-PROLIFERATION (SLP) IN HTLV-II-INFECTED DRUG-ABUSERS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NNI,BETHESDA,MD. UNIV ALABAMA,BIRMINGHAM,AL 35294. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,NEWARK,NJ 07103. DESIRE CLIN,NEW ORLEANS,LA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 242 EP 243 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000213 ER PT J AU CAUSSY, D GOEDERT, JJ PALEFSKY, J GONZALES, J DIGIOIA, R SANCHEZ, W GROSSMAN, R COLCLOUGH, G WIKTOR, S RABKIN, C BLATTNER, W AF CAUSSY, D GOEDERT, JJ PALEFSKY, J GONZALES, J DIGIOIA, R SANCHEZ, W GROSSMAN, R COLCLOUGH, G WIKTOR, S RABKIN, C BLATTNER, W TI INTERACTION OF HUMAN IMMUNODEFICIENCY AND PAPILLOMA VIRUSES - ASSOCIATION WITH ANAL EPITHELIAL ABNORMALITY IN A COHORT OF HOMOSEXUAL MEN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. RES TRIANGLE INST,WASHINGTON,DC 20036. NR 0 TC 0 Z9 0 U1 1 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 248 EP 248 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000223 ER PT J AU ABLASHI, DV BALACHANDRAN, N JOSEPHS, SF HUNG, CL KRAMARSKY, B KRUEGER, GRF SALAHUDDIN, SZ PEARSON, GR GALLO, RC AF ABLASHI, DV BALACHANDRAN, N JOSEPHS, SF HUNG, CL KRAMARSKY, B KRUEGER, GRF SALAHUDDIN, SZ PEARSON, GR GALLO, RC TI BIOLOGIC, IMMUNOLOGICAL AND MOLECULAR ANALYSIS OF HHV-6 ISOLATES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV KANSAS,MED CTR,SCH MED,KANSAS CITY,KS 66103. ELECTRO NUCLEON INC,SILVER SPRING,MD. UNIV COLOGNE,INST PATHOL,W-5000 COLOGNE 41,GERMANY. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20057. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 249 EP 249 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000225 ER PT J AU NAYLOR, PH CHU, FN GOLDSTEIN, AL SARIN, P KALE, A KIRKLEY, J ERDOS, M WANG, SS BEKESI, G AF NAYLOR, PH CHU, FN GOLDSTEIN, AL SARIN, P KALE, A KIRKLEY, J ERDOS, M WANG, SS BEKESI, G TI DIAGNOSTIC ANTIBODY-ASSAYS FOR HIV-INFECTION AND CLINICAL PROGRESSION USING SYNTHETIC P17 PEPTIDE EPITOPES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. MT SINAI MED CTR,NEW YORK,NY 10029. NIH,WASHINGTON,DC. VIRAL TECHNOL INC,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 250 EP 251 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000227 ER PT J AU SAXINGER, C FREDERICK, W BIANCO, C AF SAXINGER, C FREDERICK, W BIANCO, C TI REPRESENTATION OF HTLV1 AND HTLV2 SEROPOSITIVITY IN NORMAL BLOOD-DONORS AND DRUG-ABUSERS BASED ON SYNTHETIC PEPTIDE ASSAYS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. HOWARD UNIV HOSP,WASHINGTON,DC 20060. NEW YORK BLOOD CTR,NEW YORK,NY 10021. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 250 EP 250 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000226 ER PT J AU NERURKAR, LS AF NERURKAR, LS TI CONCLUDING REMARKS - 1990 ANNUAL-MEETING SPONSORED BY THE LABORATORY OF TUMOR-CELL BIOLOGY - FRONTIERS IN HUMAN RETROVIROLOGY AND RELATED TOPICS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material RP NERURKAR, LS (reprint author), NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP R9 EP R9 DI 10.1089/aid.1991.7.ix PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000002 ER PT J AU POMMERENKE, FA WEED, DL AF POMMERENKE, FA WEED, DL TI PHYSICIAN COMPLIANCE - IMPROVING SKILLS IN PREVENTIVE MEDICINE PRACTICES SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Physicians may not comply with all of the preventive medicine recommendations issued by recognized medical consensus groups. Compliance with recommendations for mammography, Papanicolaou tests and smoking cessation counseling is particularly important because of the potential to save lives. Compliance failure rates are often underestimated, in part because of misconceptions about the nature of physician compliance. An understanding of the difficulty in accurately estimating compliance and an awareness of the factors that affect compliance are fundamental to improving the delivery of preventive services. RP POMMERENKE, FA (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 TC 52 Z9 52 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD FEB PY 1991 VL 43 IS 2 BP 560 EP 568 PG 9 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA EV963 UT WOS:A1991EV96300018 PM 1990739 ER PT J AU ROBERTS, WC DOLLAR, AL AF ROBERTS, WC DOLLAR, AL TI EXTREME OBSTRUCTION TO LEFT-VENTRICULAR OUTFLOW BY A BIOPROSTHESIS IN THE MITRAL-VALVE POSITION SO AMERICAN HEART JOURNAL LA English DT Note ID PROSTHESIS; REPLACEMENT RP ROBERTS, WC (reprint author), NHLBI,PATHOL BRANCH,BETHESDA,MD 20892, USA. NR 13 TC 4 Z9 4 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD FEB PY 1991 VL 121 IS 2 BP 607 EP 608 DI 10.1016/0002-8703(91)90738-4 PN 1 PG 2 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA EW634 UT WOS:A1991EW63400033 PM 1990773 ER PT J AU FANANAPAZIR, L EPSTEIN, SE AF FANANAPAZIR, L EPSTEIN, SE TI HEMODYNAMIC AND ELECTROPHYSIOLOGIC EVALUATION OF PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY SURVIVING CARDIAC-ARREST SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID SUDDEN-DEATH; ARRHYTHMIA AB Hemodynamic and electrophysiologic studies were performed in 30 survivors of sudden cardiac arrest with hypertrophic cardiomyopathy (HC) to determine responsible factors. Electrophysiologic abnormalities alone were present in 27 patients (90%): sinus node dysfunction in 14 (47%), delayed atrioventricular nodal conduction in 1 (3%), abnormal His-Purkinje conduction in 7 (23%), an inducible atrial tachycardia in 7 (23%), and inducible sustained ventricular arrhythmia in 21 (70%). Sustained ventricular arrhythmia was polymorphic ventricular tachycardia (VT) in 18 patients (86%), monomorphic VT in 2 patients (7%) and ventricular fibrillation in 1 patient (3%). In 1 patient the arrhythmia recorded during an episode of cardiac arrest and induced at electrophysiologic study was polymorphic VT. VT was induced with less-than-or-equal-to 2 extra-stimuli in only 1 patient (3%) but with less-than-or-equal-to 3 extra-stimuli in 20 patients (97%). Potential causes of sudden cardiac arrest were found in all patients and were multiple in 13 patients (43%). These were (1) ventricular electrical instability in 21 patients (70%), (2) severe left ventricular outflow tract obstruction in 8 patients (27%), (3) bradycardia in 5 patients (17%), (4) myocardial ischemia associated with hypotension in 5 patients (17%), and (5) atrial tachycardia resulting in hypotension in 4 patients (13%). Of the 21 patients with inducible sustained ventricular arrhythmia, 17 received an implantable defibrillator device and 4 were treated with antiarrhythmic drugs. Seven patients underwent left ventricular septal myectomy. Three patients with atrial tachycardia received antiarrhythmic medication. One patient had catheter ablation of a concealed posteroseptal accessory pathway. Three patients with myocardial ischemia as the only abnormality were treated with verapamil and propranolol (2 also received implantable defibrillators). During a mean follow-up period of 18 +/- 19 months (maximum 75), 4 patients died suddenly and 4 patients received a total of 13 defibrillator shocks (1-year survival rate of 93% and a 1-year event-free rate of 80%). Thus, electrophysiologic studies identify potential mechanisms for cardiac arrest in most patients with HC. Although most cardiac arrest survivors with HC have an inducible sustained VT and may benefit from an implantable defibrillator, hemodynamic plus hemodynamic studies in many patients identify other potential etiologic or aggravating factors that may also require treatment. RP FANANAPAZIR, L (reprint author), NHLBI,CARDIOL BRANCH,CARDIOVASC DIAGNOSIS SECT,BLDG 10,ROOM 7B-14,BETHESDA,MD 20892, USA. NR 14 TC 47 Z9 51 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD FEB 1 PY 1991 VL 67 IS 4 BP 280 EP 287 DI 10.1016/0002-9149(91)90560-8 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA EV352 UT WOS:A1991EV35200011 PM 1990792 ER PT J AU LOPRINZI, CL INGLE, JN SCHAID, DJ BUCKNER, JC EDMONSON, JH ALLEGRA, CJ AF LOPRINZI, CL INGLE, JN SCHAID, DJ BUCKNER, JC EDMONSON, JH ALLEGRA, CJ TI 5-FLUOROURACIL PLUS LEUCOVORIN IN WOMEN WITH METASTATIC BREAST-CANCER - A PHASE-II STUDY SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS LA English DT Article DE LEUCOVORIN; FLUOROURACIL; METASTATIC BREAST CANCER ID TRIAL AB Because leucovorin increases the antitumor activity of 5-fluorouracil (5-FU) in multiple tumor model systems, we performed a clinical trial to evaluate this combination in women who had received one or no prior chemotherapy regimens for metastatic breast cancer. Thirty-six women with measurable metastatic disease were treated with five consecutive days of i.v. leucovorin, 500 mg/m2/day infused over 30 min, followed 1 h later by i.v. bolus 5-FU, 375 mg/m2/day. Repeat cycles were planned at 4-week intervals. Tumor regression occurred in 10 of 36 patients (28%; 95% confidence interval, 14-45%) with a median time to disease progression (TTP) of 8.7 months (range 3.2-16.8 months) in the responding patients. The median TTP and survival for all patients were 3.0 and 12.4 months, respectively. Among 30 patients who had received prior 5-FU, tumor regressions were seen in seven (23%; 95% confidence interval 10-42%). The major dose-limiting toxicity in this study was mucositis, affecting 89% of the patients. Other toxicities were tolerable in the majority of patients. Although the role of leucovorin in breast cancer clinical practice remains undefined, the data from this trial support the hypothesis that leucovorin enhances the cytotoxic activity of 5-FU against human breast cancer. C1 MAYO CLIN & MAYO FDN,DIV CANC CTR STAT,ROCHESTER,MN 55905. NCI,MED BRANCH,BETHESDA,MD 20892. RP LOPRINZI, CL (reprint author), MAYO CLIN & MAYO FDN,DIV MED ONCOL,ROCHESTER,MN 55905, USA. FU NCI NIH HHS [CM57733B] NR 8 TC 21 Z9 21 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3732 J9 AM J CLIN ONCOL-CANC JI Am. J. Clin. Oncol.-Cancer Clin. Trials PD FEB PY 1991 VL 14 IS 1 BP 30 EP 32 DI 10.1097/00000421-199102000-00006 PG 3 WC Oncology SC Oncology GA EV479 UT WOS:A1991EV47900006 PM 1987734 ER PT J AU BLAIR, SN DOWDA, M PATE, RR KRONENFELD, J HOWE, HG PARKER, G BLAIR, A FRIDINGER, F AF BLAIR, SN DOWDA, M PATE, RR KRONENFELD, J HOWE, HG PARKER, G BLAIR, A FRIDINGER, F TI RELIABILITY OF LONG-TERM RECALL OF PARTICIPATION IN PHYSICAL-ACTIVITY BY MIDDLE-AGED MEN AND WOMEN SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE BIOMETRY; EXERTION, HEALTH SURVEYS; QUESTIONNAIRES ID QUESTIONNAIRE; CANCER; RISK AB The reliability of long-term recall of physical activity participation was examined in 322 women and 129 men in a worksite health study conducted at the Liberty Corporation, Greenville, South Carolina during 1976-1987. Leisure time physical activity was assessed at baseline; and energy expenditure in total, light, moderate, and vigorous activities was calculated. The long-term recall of baseline activities was determined 1-10 years after the examination. The relation between actual baseline and recalled activity was positive and in most cases the coefficients were statistically significant at p < 0.05. The correlations were modest, most in the range of 0.20 to 0.50. Percent agreement between baseline and recalled activity generally ranged from 60 to 75%. Multiple regression analyses suggested that recalled activity was a significant predictor of baseline activity, but recall interval and age were not important contributors to the regression model. R2 values for the model were 0.10 for light activity and 0.26 for vigorous activity. Questionnaire assessment of long-term physical activity recall appeared to be reliable, length of recall interval up to 10 years was not an important factor, and recall of vigorous activity was more accurate than for less intensive activities. C1 UNIV S CAROLINA,SCH PUBL HLTH,COLUMBIA,SC 29208. ARKANSAS STATE UNIV,STATE UNIV,AR 72467. LIBERTY CORP,GREENVILLE,SC. NCI,ROCKVILLE,MD. UNIV N TEXAS,DENTON,TX. RP BLAIR, SN (reprint author), INST AEROBICS RES,12330 PRESTON RD,DALLAS,TX 75230, USA. FU NIA NIH HHS [AG06945] NR 16 TC 113 Z9 113 U1 5 U2 6 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 1 PY 1991 VL 133 IS 3 BP 266 EP 275 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA EY297 UT WOS:A1991EY29700007 PM 2000844 ER PT J AU ROSENBERG, PS BIGGAR, RJ GOEDERT, JJ GAIL, MH AF ROSENBERG, PS BIGGAR, RJ GOEDERT, JJ GAIL, MH TI BACKCALCULATION OF THE NUMBER WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION IN THE UNITED-STATES SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ACQUIRED IMMUNODEFICIENCY SYNDROME; EPIDEMIOLOGIC METHODS; HIV-1; INFECTION; PREVALENCE ID IMMUNE-DEFICIENCY SYNDROME; SHORT-TERM PROJECTIONS; AIDS EPIDEMIC; HIV INFECTION; HEMOPHILIA; PREVALENCE; SIZE AB The method of backcalculation was applied to national surveillance data on the acquired immunodeficiency syndrome (AIDS) in order to estimate the cumulative number of adults with human immunodeficiency virus type 1 (HIV-1) infection as of January 1, 1985 and July 1, 1987. A "plausible range" of estimates was constructed which reflected both uncertainty about the AIDS incubation distribution and random variation from selection and fitting of flexible models of the HIV-1 infection curve. The authors estimated that, as of 1985, 411,000 to 756,000 persons were infected. The infected population included 266,000 to 492,000 homosexual men, 69,000 to 136,000 intravenous drug users, 24,000 to 49,000 homosexual intravenous drug users, and 11,000 to 26,000 persons infected through heterosexual contact. The estimated prevalence of infection among persons aged 15-55 years was 0.31% in whites, 0.78% in Hispanics, and 0.81% in blacks. An estimated 32,000 to 66,000 women were infected. Compared with white women aged 15-55 years, the prevalence of infection was 5.3-fold higher in Hispanic women and 10.2-fold higher in black women. Plausible estimates for the total number infected by July 1987 ranged from 707,000 to 1,376,000, with the most likely estimate equal to 992,000. Backcalculation provides an assessment of the magnitude of the HIV-1 epidemic that is independent of estimates based on prevalence surveys in special populations. The estimates obtained from both methods are consistent and emphasize the need for vigorous programs to prevent the spread of HIV-1, especially in minority communities. RP ROSENBERG, PS (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,EPIDEMIOL METHODS SECT,6130 EXECUT BLVD,EXECUT PLAZA N,ROOM 403,ROCKVILLE,MD 20892, USA. NR 39 TC 33 Z9 33 U1 1 U2 1 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 1 PY 1991 VL 133 IS 3 BP 276 EP 285 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA EY297 UT WOS:A1991EY29700008 PM 2000845 ER PT J AU NOGUCHI, CT MOHANDAS, N BLANCHETTEMACKIE, J MACKIE, S RAIK, E CHARACHE, S AF NOGUCHI, CT MOHANDAS, N BLANCHETTEMACKIE, J MACKIE, S RAIK, E CHARACHE, S TI HEMOGLOBIN AGGREGATION AND PSEUDOSICKLING INVITRO OF HEMOGLOBIN SETIF-CONTAINING ERYTHROCYTES SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE ERYTHROCYTE DEFORMABILITY; ABNORMAL ERYTHROCYTES; HEMOGLOBIN ID SICKLE HEMOGLOBIN; ASP-> TYR; HB SETIF; POLYMERIZATION; GELATION; FAMILY AB Erythrocytes from individuals heterozygous for hemoglobin Setif (alpha-94 Asp --> Tyr) sickle in vitro without deoxygenation when incubated in chloride buffer due to hemoglobin aggregation. We now report quantitative studies of hemoglobin polymerization and deformability in these cells. Hemoglobin polymer gradually increased in intact cells during a 24 h incubation period at 24-degrees-C. After 24 hr, about 80% of the cells in 290 mOsm sodium chloride buffer contained polymer which appeared as short rods compared to > 99% containing polymer at 450 mOsm. Similar proportions of cells were morphologically sickled. Deformability of erythrocytes with 40% hemoglobin Setif incubated in 290 mOsm buffer at 37-degrees-C decreased to 80% of normal by 210 min but in 450 mOsm decreased to 50% after only 30 min as measured by the ektacytometer. However, at 4-degrees-C deformability remained normal even in 450 mOsm buffer. The solubility of gelled hemolysate containing 40% hemoglobin Setif was 24 g/dl and 21 g/dl at 290 and 459 mOsm buffer respectively. The gel persisted at 4-degrees-C with a solubility of 26 g/dl, but melted when dialyzed into sodium phosphate or potassium phosphate buffer. These data suggest that hemoglobin polymerization, reduced deformability, and sickling of hemoglobin Setif-containing erythrocytes are related to reduced hemoglobin solubility. The rate and extent of intracellular polymerization in vitro are considerably reduced (as in the case of sickle trait) compared with erythrocytes from individuals with sickle cell anemia. Hence, the slower kinetics of hemoglobin aggregation in hemoglobin Setif-containing cells provide an alternate system for studying hemoglobin polymerization and abnormal rheology. C1 UNIV CALIF BERKELEY LAWRENCE BERKELEY LAB,BERKELEY,CA 94720. SYDNEY HOSP,SYDNEY,NSW 2000,AUSTRALIA. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. RP NOGUCHI, CT (reprint author), NIDDKD,BLDG 10,ROOM 9N307,BETHESDA,MD 20892, USA. FU NHLBI NIH HHS [HL31579] NR 28 TC 1 Z9 1 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD FEB PY 1991 VL 36 IS 2 BP 131 EP 139 DI 10.1002/ajh.2830360212 PG 9 WC Hematology SC Hematology GA EX558 UT WOS:A1991EX55800010 PM 2012063 ER PT J AU LAM, NP KENNEDY, PE JAROSINSKI, PF GALLELLI, JF AF LAM, NP KENNEDY, PE JAROSINSKI, PF GALLELLI, JF TI STABILITY OF ZIDOVUDINE IN 5-PERCENT DEXTROSE INJECTION AND 0.9-PERCENT SODIUM-CHLORIDE INJECTION SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article DE ADDITIVES; ANTIVIRALS; DEXTROSE; INCOMPATIBILITIES; INJECTIONS; SODIUM CHLORIDE; STABILITY; STORAGE; TEMPERATURE; VEHICLES; ZIDOVUDINE ID 3'-AZIDO-3'-DEOXYTHYMIDINE; AIDS AB The stability of zidovudine at a concentration of 4 mg/mL in 5% dextrose injection and 0.9% sodium chloride injection in polyvinyl chloride infusion bags stored at room and refrigerated temperatures for up to eight days was studied. Zidovudine was diluted in 5% dextrose injection and in 0.9% sodium chloride injection to a concentration of 4 mg/mL. Six admixtures were prepared with each diluent; three were stored at room temperature (25 +/- 1-degrees-C) and three were refrigerated (4 +/- 1-degrees-C). At 0, 3, 6, 24, 48, 72, and 192 hours, 2-mL aliquots were removed. One milliliter of each aliquot was diluted to a zidovudine concentration of approximately 40-mu-g/mL and assayed in duplicate by a stability-indicating high-performance liquid chromatographic method. Visual inspection was performed at each sampling time for precipitation, turbidity, color change, and gas formation. Sample pH was recorded at 0 and 192 hours. In all admixtures, more than 97% of the initial zidovudine concentration remained throughout the study period. No visual or pH changes were observed. Zidovudine 4 mg/mL in admixtures with 5% dextrose injection or 0.9% sodium chloride injection stored in polyvinyl chloride infusion bags was stable for up to 192 hours (eight days) at room temperature and under refrigeration. C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT PHARM,BLDG 10,ROOM 1D-51,BETHESDA,MD 20892. UNIV ILLINOIS,CHICAGO,IL 60680. NIH,PHARMACEUT DEV SERV,ANALYT LAB,BETHESDA,MD 20892. NR 4 TC 5 Z9 5 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD FEB PY 1991 VL 48 IS 2 BP 280 EP 282 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EV467 UT WOS:A1991EV46700024 PM 2003500 ER PT J AU KINTZEL, PE KENNEDY, PE AF KINTZEL, PE KENNEDY, PE TI STABILITY OF AMPHOTERICIN-B IN 5-PERCENT DEXTROSE INJECTION AT CONCENTRATIONS USED FOR ADMINISTRATION THROUGH A CENTRAL VENOUS LINE SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article DE ADDITIVES; AMPHOTERICIN-B; ANTIFUNGALS; CONCENTRATION; DEXTROSE; INCOMPATIBILITIES; INJECTIONS; STABILITY; STORAGE; TEMPERATURE; VEHICLES AB The stability of amphotericin B in 5% dextrose injection was studied at concentrations used for administration through a central venous line. Amphotericin B 60, 80, and 100 mg was diluted in 50 mL of 5% dextrose injection; final mean +/- S.D. concentrations after adjustment for total volume were 0.92 +/- 0.01, 1.20 +/- 0.03, and 1.40 +/- 0.03 mg/mL, respectively. For each concentration, six admixtures were prepared; of these, three were stored at 25-degrees-C and three at 6-degrees-C. Amphotericin B concentration was tested at 0, 4, 12, 24, and 36 hours by stability-indicating high-performance liquid chromatography. The admixtures were inspected visually at each time point for precipitation, turbidity, gas formation, and color change, and the pH was measured. Concentrations of amphotericin B remained within 3% of initial concentrations at each time point at both storage temperatures. No precipitation, turbidity, gas formation, or color change was observed, and no changes in pH were measured. Amphotericin B in 5% dextrose injection was stable at concentrations of 0.92, 1.20, and 1.40 mg/mL when stored at 6 and 25-degrees-C for up to 36 hours. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NIH,WARREN G MAGNUSON CLIN CTR,PHARMACEUT DEV SERV,ANALYT LAB,BETHESDA,MD 20892. RP KINTZEL, PE (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284, USA. NR 7 TC 14 Z9 14 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD FEB PY 1991 VL 48 IS 2 BP 283 EP 285 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EV467 UT WOS:A1991EV46700025 PM 2003501 ER PT J AU IANNUZZI, MC STERN, RC COLLINS, FS HON, CT HIDAKA, N STRONG, T BECKER, L DRUMM, ML WHITE, MB GERRARD, B DEAN, M AF IANNUZZI, MC STERN, RC COLLINS, FS HON, CT HIDAKA, N STRONG, T BECKER, L DRUMM, ML WHITE, MB GERRARD, B DEAN, M TI 2 FRAMESHIFT MUTATIONS IN THE CYSTIC-FIBROSIS GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID POLYMERASE CHAIN-REACTION; DNA; IDENTIFICATION; POLYMORPHISMS AB Cystic fibrosis (CF) is a recessive disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene. We have identified in exon 7 two frameshift mutations, one caused by a two-nucleotide insertion and the other caused by a one-nucleotide deletion; these mutations-CF1154insTC and CF1213delT, respectively, are predicted to shift the reading frame of the protein and to introduce UAA(ochre) termination codons at residues 369 and 368. C1 UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. CASE WESTERN RESERVE UNIV,SCH MED,DEPT PEDIAT,CLEVELAND,OH 44106. RAINBOW BABIES & CHILDRENS HOSP,CLEVELAND,OH 44106. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD. RP IANNUZZI, MC (reprint author), UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,MSRB 1,ROOM 5520-B,ANN ARBOR,MI 48109, USA. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 FU NCI NIH HHS [N01-CO-74102]; NIDDK NIH HHS [DK 32960, DK2756] NR 14 TC 40 Z9 41 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD FEB PY 1991 VL 48 IS 2 BP 227 EP 231 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA EV744 UT WOS:A1991EV74400007 PM 1990834 ER PT J AU NAVON, R PROIA, RL AF NAVON, R PROIA, RL TI TAY-SACHS DISEASE IN MOROCCAN JEWS - DELETION OF A PHENYLALANINE IN THE ALPHA-SUBUNIT OF BETA-HEXOSAMINIDASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID ASHKENAZI JEWS; EXTENSIVE HOMOLOGY; CHAIN; GENE; SEQUENCE; DEFECT; ACID; CDNA; MUTATION; CLONING AB Tay-Sachs disease is an inherited lysosomal storage disorder caused by defects in the beta-hexosaminidase alpha-subunit gene. The carrier frequency for Tay-Sachs disease is significantly elevated in both the Ashkenazi Jewish and Moroccan Jewish populations but not in other Jewish groups. We have found that the mutations underlying Tay-Sachs disease in Ashkenazi and Moroccan Jews are different. Analysis of a Moroccan Jewish Tay-Sachs patient has revealed an in-frame deletion (DELTA-F) of one of the two adjacent phenylalanine codons that are present at positions 304 and 305 in the alpha-subunit sequence. The mutation impairs the subunit assembly of beta-hexosaminidase A, resulting in an absence of enzyme activity. The Moroccan patient was found also to carry, in the other alpha-subunit allele, a different, and as yet unidentified, mutation which causes a deficit of mRNA. Analysis of obligate carriers from six unrelated Moroccan Jewish families showed that three harbor the DELTA-F mutation, raising the possibility that this defect may be a prevalent mutation in this ethnic group. C1 NIDDKD,GENET & BIOCHEM BRANCH,BLDG 10,ROOM 9D-15,BETHESDA,MD 20892. SAPIR MED CTR,MOLEC GENET UNIT,KFAR SAVA,ISRAEL. TEL AVIV UNIV,SACKLER SCH MED,DEPT HUMAN GENET,TEL AVIV,ISRAEL. RI Proia, Richard/A-7908-2012 NR 30 TC 31 Z9 31 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 FEB PY 1991 VL 48 IS 2 BP 412 EP 419 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA EV744 UT WOS:A1991EV74400026 PM 1825014 ER PT J AU FAHEY, BJ KOZIOL, DE BANKS, SM HENDERSON, DK AF FAHEY, BJ KOZIOL, DE BANKS, SM HENDERSON, DK TI FREQUENCY OF NONPARENTERAL OCCUPATIONAL EXPOSURES TO BLOOD AND BODY-FLUIDS BEFORE AND AFTER UNIVERSAL PRECAUTIONS TRAINING SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID HEALTH-CARE WORKERS; INFECTION; RISK; VIRUS AB This study provides data suggesting that implementation of Universal Precautions had an impact in reducing occupational cutaneous and mucous membrane exposures to potentially infected body fluids. C1 NIAID,WARREN G MAGNUSON CLIN CTR,HOSP EPIDEMIOL SERV,CLIN INVEST LAB,BETHESDA,MD 20892. NIAID,WARREN G MAGNUSON CLIN CTR,OFF DIRECTOR,BETHESDA,MD 20892. NR 22 TC 77 Z9 80 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD FEB PY 1991 VL 90 IS 2 BP 145 EP 153 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA EY990 UT WOS:A1991EY99000002 PM 1996583 ER PT J AU SAAD, MF KNOWLER, WC PETTITT, DJ NELSON, RG CHARLES, MA BENNETT, PH AF SAAD, MF KNOWLER, WC PETTITT, DJ NELSON, RG CHARLES, MA BENNETT, PH TI A 2-STEP MODEL FOR DEVELOPMENT OF NON-INSULIN-DEPENDENT DIABETES SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID IMPAIRED GLUCOSE-TOLERANCE; PIMA-INDIANS; BETA-CELL; MELLITUS; RESISTANCE; SECRETION; OBESITY; HYPERINSULINEMIA; HYPERTRIGLYCERIDEMIA; HYPERGLYCEMIA AB Both insulin resistance and beta-cell dysfunction occur during the development of non-insulin-dependent diabetes mellitus (NIDDM), but controversy exists about which lesion is primary. Based on longitudinal studies in the Pima Indians, a population with the world's highest reported prevalence of NIDDM, a two-step model for development of the disease is proposed. The first step is transition from normal to impaired glucose tolerance, for which insulin resistance is the main determinant, and the second and later step is worsening from impaired glucose tolerance to diabetes, in which beta-cell dysfunction plays a critical role. This hypothesis is consistent with findings from other ethnic groups from many parts of the world. C1 CLEVELAND CLIN EDUC FDN,DEPT BIOSTAT & EPIDEMIOL,CLEVELAND,OH 44106. RP SAAD, MF (reprint author), NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,DIABET & ARTHRITIS EPIDEMIOL SECT,PHOENIX,AZ 85014, USA. RI Nelson, Robert/B-1470-2012 NR 59 TC 208 Z9 216 U1 0 U2 4 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD FEB PY 1991 VL 90 IS 2 BP 229 EP 235 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA EY990 UT WOS:A1991EY99000014 PM 1996593 ER PT J AU WOLF, PH MADANS, JH FINUCANE, FF HIGGINS, M KLEINMAN, JC AF WOLF, PH MADANS, JH FINUCANE, FF HIGGINS, M KLEINMAN, JC TI REDUCTION OF CARDIOVASCULAR-DISEASE RELATED MORTALITY AMONG POSTMENOPAUSAL WOMEN WHO USE HORMONES - EVIDENCE FROM A NATIONAL COHORT SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE POSTMENOPAUSAL; HORMONES; CARDIOVASCULAR; MORTALITY ID NON-CONTRACEPTIVE ESTROGENS; CORONARY HEART-DISEASE; MYOCARDIAL-INFARCTION; REPLACEMENT THERAPY; PROTECTION; MENOPAUSE; RISK AB A national sample of 1944 white menopausal women greater-than-or-equal-to 55 years old from the epidemiologic follow-up of participants in the National Health and Nutrition Examination Survey was reviewed to investigate the role of hormone therapy in altering the risk of death from cardiovascular disease. Women in the study were observed for up to 16 years after the baseline survey in 1971 to 1975. By 1987 631 women had died; 347 of these deaths were due to cardiovascular disease. History of diabetes (relative risk, 2.38; 95% confidence interval 1.73 to 3.26), previous myocardial infarction (relative risk, 2.12; 95% confidence interval 1.56 to 2.86), smoking (relative risk, 2.18; 95% confidence interval, 1.69 to 2.81), and elevated blood pressure (relative risk, 1.49; 95% confidence interval, 1.14 to 1.94) were strong predictors of cardiovascular disease-related death in this cohort. After adjusting for known cardiovascular disease risk factors (smoking, cholesterol, body mass index, blood pressure, previous myocardial infarction, history of diabetes, age) and education, the use of postmenopausal hormones was associated with a reduced risk of death from cardiovascular disease (relative risk, 0.66; 95% confidence interval, 0.48 to 0.90). The same protective effect provided by postmenopausal hormone therapy was seen in women who experienced natural menopause (relative risk, 0.69; 95% confidence interval, 0.45 to 1.06). C1 NICHHD,CONTRACEPT EVALUAT BRANCH,BETHESDA,MD 20892. NHLBI,EPIDEMIOL & BIOMETRY PROGRAM,BETHESDA,MD 20892. NATL CTR HLTH STAT,DIV ANAL,HYATTSVILLE,MD 20782. NR 19 TC 121 Z9 122 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD FEB PY 1991 VL 164 IS 2 BP 489 EP 494 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA EX765 UT WOS:A1991EX76500006 PM 1992690 ER PT J AU LONGNECKER, DS PETTENGILL, OS DAVIS, BH SCHAEFFER, BK ZURLO, J HONG, HL KUHLMANN, ET AF LONGNECKER, DS PETTENGILL, OS DAVIS, BH SCHAEFFER, BK ZURLO, J HONG, HL KUHLMANN, ET TI CHARACTERIZATION OF PRENEOPLASTIC AND NEOPLASTIC LESIONS IN THE RAT PANCREAS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID CORN-OIL GAVAGE; TRANSFORMING GENES; AZASERINE; DIFFERENTIATION; MARKER; DNA AB Nodules of acinar cells with increased proliferative potential develop in the pancreases of carcinogentreated rats and in untreated aged rats. Large nodules are classed as adenomas. Phenotypic and genotypic characteristics of nodule cells were compared with normal pancreas and transplantable acinar cell carcinomas by several methods. Nuclei of acinar cells from normal pancreas, adenomas, and three carcinomas in situ had normal diploid DNA content as determined by flow cytometry. One of two primary carcinomas had a hypodiploid DNA content. Two of three transplantable carcinomas were aneuploid with a DNA content in the tetraploid range. Explants from nodules and adenomas failed to grow in soft agar, whereas several carcinomas were positive in this assay. A primary carcinoma was serially transplanted, but transplantation of nodules or adenomas failed. Transfection of DNA from carcinomas in situ yielded a higher frequency of NIH 3T3 transformants than DNA from adenomas. DNAs from the transformants did not contain ras sequences. These studies indicate that cells from nodules and adenomas have low growth potential and lack critical phenotypic and genotypic characteristics of transformed malignant cells that were present in some primary and transplanted carcinomas. C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PHARMACOL & TOXICOL,HANOVER,NH 03756. NIEHS,CHEM PATHOL BRANCH,RES TRIANGLE PK,NC 27709. RP LONGNECKER, DS (reprint author), DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PATHOL,HANOVER,NH 03756, USA. FU NCI NIH HHS [CA 23108]; NIEHS NIH HHS [ES-03283, ES-03687] NR 26 TC 17 Z9 17 U1 0 U2 1 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 FEB PY 1991 VL 138 IS 2 BP 333 EP 340 PG 8 WC Pathology SC Pathology GA EX434 UT WOS:A1991EX43400009 PM 1992760 ER PT J AU SCHULZ, LO NYOMBA, BL ALGER, S ANDERSON, TE RAVUSSIN, E AF SCHULZ, LO NYOMBA, BL ALGER, S ANDERSON, TE RAVUSSIN, E TI EFFECT OF ENDURANCE TRAINING ON SEDENTARY ENERGY-EXPENDITURE MEASURED IN A RESPIRATORY CHAMBER SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ENERGY BALANCE; EXERCISE TRAINING; INDIRECT CALORIMETRY ID RESTING METABOLIC-RATE; GLUCOSE-INDUCED THERMOGENESIS; DIET-INDUCED THERMOGENESIS; BODY-COMPOSITION; CALORIC RESTRICTION; OBESE WOMEN; EXERCISE; FITNESS; WEIGHT; INDIVIDUALS AB The effect of endurance training on 24-h energy expenditure (EE), basal metabolic rate (BMR), sleeping metabolic rate (SMR), and the thermic effect of food (TEF) was assessed in a respiratory chamber where only spontaneous physical activity (SPA) was allowed. Results from 20 highly trained male endurance athletes (25 +/- 5 yr, 178 +/- 7 cm, 70 +/- 8 kg body wt, 64 +/- 7 kg fat-free mass) were compared with those of 43 untrained males who were matched for age (28 +/- 6 yr), height (175 +/- 5 cm), weight (73 +/- 13 kg), and fat-free mass (62 +/- 8 kg). Subjects were admitted to a metabolic ward, fed a weight-maintenance diet, and refrained from physical activity for at least 2 days before measurements. No significant differences were found with respect to 24-h EE (2,126 +/- 186 vs. 2,154 +/- 245 kcal), BMR (1,808 +/- 342 vs. 1,709 +/- 329 kcal), SMR (1,523 +/- 120 vs. 1,555 +/- 188 kcal), or TEF (24.9 +/- 9.2 vs. 21.3 +/- 6.7% of ingested calories; these values included the energy cost of arousal) between trained and untrained subjects, respectively, before or after adjusting for differences in body composition. Neither the 24-h respiratory quotient nor the level of SPA differed between the two groups. No relationship was found between maximal aerobic capacity and metabolic rate adjusted for differences in fat-free mass and fat mass. These results do not support an effect of fitness level on EE measured under sedentary conditions. Therefore, although physical activity plays an important role in maintaining optimal health and body weight, its effect on calorie output does not extend beyond the cost of the activity and recovery periods. C1 NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,RM 541,PHOENIX,AZ 85016. UNIV WISCONSIN,DEPT HLTH SCI,MILWAUKEE,WI 53201. NR 33 TC 56 Z9 56 U1 1 U2 7 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 FEB PY 1991 VL 260 IS 2 BP E257 EP E261 PN 1 PG 5 WC Physiology SC Physiology GA EY855 UT WOS:A1991EY85500041 PM 1996628 ER PT J AU FLESSNER, MF WALL, SM KNEPPER, MA AF FLESSNER, MF WALL, SM KNEPPER, MA TI PERMEABILITIES OF RAT COLLECTING DUCT SEGMENTS TO NH3 AND NH4+ SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE AMMONIA; AMMONIUM; ACID BASE; PERMEABILITY; RENAL EPITHELIA; KIDNEY ID AMMONIA TRANSPORT; BICARBONATE TRANSPORT; METABOLIC-ACIDOSIS; INNER MEDULLA; KIDNEY; PH; ACIDIFICATION; MEMBRANES; SECRETION; GRADIENT AB We have measured NH3 and NH4+ permeability coefficients in collecting ducts from the cortex, outer medulla, and inner medulla of the rat kidney. Isolated collecting duct segments of the rat were perfused with bicarbonate-buffered solutions containing carbonic anhydrase to eliminate any pH disequilibrium in the tubule lumen. NH3 or NH4+ concentration gradients were set up between the bath and the lumen. By measuring the total CO2 and total ammonia concentrations in the bath, the perfusate, and collected fluid, the NH3 and NH4+ concentrations were determined. Then, using the flow rate in the tubule and the tubule dimensions, we calculated the apparent permeability in each collecting duct segment for NH3 and NH4+. The NH3 permeabilities were as follows: 0.002 cm/s in the inner medullary collecting duct, 0.012 cm/s in the outer medullary collecting duct, and 0.024 cm/s in the cortical collecting duct. The NH4+ permeabilities for all segments were on the order of 10(-5) cm/s or less. The relative permeability values for the two ammonium species are consistent with the view that the secretion observed in vivo in collecting ducts is due to passive diffusion of NH3 from the interstitium to the lumen of the duct, parallel with H+ secretion. RP FLESSNER, MF (reprint author), NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BLDG 10,RM 6N-307,BETHESDA,MD 20892, USA. NR 35 TC 43 Z9 43 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 FEB PY 1991 VL 260 IS 2 BP F264 EP F272 PN 2 PG 9 WC Physiology SC Physiology GA EY856 UT WOS:A1991EY85600088 PM 1996677 ER PT J AU KWON, HM YAMAUCHI, A UCHIDA, S ROBEY, RB GARCIAPEREZ, A BURG, MB HANDLER, JS AF KWON, HM YAMAUCHI, A UCHIDA, S ROBEY, RB GARCIAPEREZ, A BURG, MB HANDLER, JS TI RENAL NA-MYO-INOSITOL COTRANSPORTER MESSENGER-RNA EXPRESSION IN XENOPUS-OOCYTES - REGULATION BY HYPERTONICITY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE OSMOLYTES; MADIN-DARBY CANINE KIDNEY CELLS; PHLORIZIN; PHLORETIN; CYTOCHALASIN-B ID MAJOR ORGANIC OSMOLYTES; INNER MEDULLA; ACTIVE-TRANSPORT; ALDOSE REDUCTASE; RAT; MYOINOSITOL; CELLS; CLONING; CDNA; ACCUMULATION AB Canine renal cells in culture (MDCK cells) accumulate organic osmolytes, including myo-inositol (MI), in response to hypertonic stress. When medium tonicity is increased, intracellular concentration of MI rises because hypertonicity elicits increased uptake of MI via Na-MI cotransporter(s). To study the mechanism for this increase in cotransporter activity, poly(A)+ RNA isolated from MDCK cells maintained in hypertonic or isotonic medium was injected into Xenopus oocytes, and Na-dependent MI uptake was measured 3-5 days later. Poly(A)+ RNA from hypertonic cells induced clear expression of the cotransporter. In contrast, oocytes injected with poly(A)+ RNA isolated from MDCK cells maintained in isotonic medium exhibited cotransporter activity like oocytes injected with water. Upon size fractionation of RNA, peak activity appeared in a fraction that contained poly(A)+ RNA with median size of approximately 4 kilobases. Na-dependent MI uptake by poly(A)+ RNA-injected oocytes was inhibited by both phlorizin and phloretin. We suggest that hypertonicity-induced upregulation of the Na-MI cotransporter involves an increase in mRNA and synthesis of cotransporter protein(s). C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV NEPHROL,217 HUNTERIAN,725 N WOLFE ST,BALTIMORE,MD 21205. NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892. RI Lee-Kwon, Whaseon/D-6021-2011; Uchida, Shinichi/D-1111-2013; Robey, R. Brooks/J-7099-2013 OI Robey, R. Brooks/0000-0001-5059-3965 FU NIDDK NIH HHS [DK-42479] NR 25 TC 41 Z9 41 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 FEB PY 1991 VL 260 IS 2 BP F258 EP F263 PN 2 PG 6 WC Physiology SC Physiology GA EY856 UT WOS:A1991EY85600087 PM 1996676 ER PT J AU WINOKUR, G CORYELL, W AF WINOKUR, G CORYELL, W TI FAMILIAL ALCOHOLISM IN PRIMARY UNIPOLAR MAJOR DEPRESSIVE DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DIAGNOSTIC CRITERIA; SPECTRUM DISEASE; VALIDITY; RELIABILITY; RELATIVES; PROBANDS; LINKAGE AB Objective: Some studies have suggested relationships between depression in probands and alcoholism in relatives. Other studies have not, but some of these have used inappropriate control groups or failed to divide probands by sex. Method: The present study controlled for sex of probands and used several comparison groups to further explore the familial relationship between depression and alcoholism. Diagnoses for 723 directly interviewed relatives of 326 probands with primary unipolar depression were compared to diagnoses in 469 control subjects chosen by an acquaintanceship method to demographically resemble the relatives of affective disorder probands. Diagnoses in the uninterviewed relatives of both control and depressed subjects were used for comparisons as well. Results: Results indicated higher rates of alcoholism in the families of depressed women but not in the families of depressed men. Conclusions: This familial association between alcoholism and depression may be the result of either genetic or environmental factors or an interaction between the two. C1 NIMH,COLLABORAT PROGRAM PSYCHOBIOL DEPRESS CLIN STUDIES,BETHESDA,MD 20892. NR 18 TC 46 Z9 46 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD FEB PY 1991 VL 148 IS 2 BP 184 EP 188 PG 5 WC Psychiatry SC Psychiatry GA EV209 UT WOS:A1991EV20900006 PM 1987815 ER PT J AU CHICHESTER, CH PHILPOT, RM WEIR, AJ BUCKPITT, AR PLOPPER, CG AF CHICHESTER, CH PHILPOT, RM WEIR, AJ BUCKPITT, AR PLOPPER, CG TI CHARACTERIZATION OF THE CYTOCHROME-P-450 MONOOXYGENASE SYSTEM IN NONCILIATED BRONCHIOLAR EPITHELIAL (CLARA) CELLS ISOLATED FROM MOUSE LUNG SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID ALVEOLAR TYPE-II; RABBIT CYTOCHROME-P-450; XENOBIOTIC METABOLISM; MONOCLONAL-ANTIBODIES; ENZYME COMPONENTS; MURINE LUNG; PULMONARY; NAPHTHALENE; CYTOCHROMES-P-450; LIVER AB The nonciliated bronchiolar epithelial (Clara) cell of the mouse is highly susceptible to toxicants that undergo metabolic activation, presumably because this cell type has high levels of cytochrome P-450 monooxygenases. As a first step in futher defining the role of Clara cells in pulmonary xenobiotic activation and detoxication, we have isolated Clara cells (75 to 80% purity) and characterized them morphologically and biochemically. The identity of Clara cells, confirmed by transmission electron microscopy, was based on several features, including abundant agranular endoplasmic reticulum, large mitochondria, and dense secretory granules. Immumocytochemistry of isolated mouse cells showed that the majority were positive with antibbodies against three mahor components of the pulmonary cytochrome P-450 monooxygenase system, cytochrome P-450 usizymes 2 (HB), 5 (IVB), and NADPH cytochrome P-450 redutase, purified from rabbit lung. The isolated cells also showed a positive reacion with an antibody against the cytochrome P-450 isozyme that is active in the steroselective metabolism of naphthalene, cytochrome P-450 mN (mN). Immunocytochemistry usingk the antibody against cytochrome P-450 isozyme 6 (IAI), purified from rabbit lung, showed no reaction in the isolated cells. The presence of intact cytochrome P-450 protein was confirmed by sodium dodecyl sulfate polyacrylamide gell electrophoresis and Western blots of homogenates of isolated cell preparations. The N-demithylation of benzphjetamine and expoxidation of naphthalend occured at easily mesurble rates in incubations of isolated Clara cells. In contrast, diols, quinones, and monohydroxylated benzo(a)pyrene metabolites, analyzed by high performance liquid chromatography, were undetectable in exacts of Clara cells incubated with H-3-labeled substrate. We conclude: 1) cells isolated by this method resemble Clara cells untrastructurally and immunocytochemically, 2) the cells retain cytochrome P-450 monooxygenase activity, 3) the isolation procedure does not degrade proteins fo the cytochrome P-450 enzyme system 4) isolated mouse Clara cell preparations lack the cytochrome P-450 isozyme (IAI) primarily responsible for the metabolism of benzo(a)pyrene, and 5) the isolated cells are capable of metabolizing a cytoxicant for which they are the principal target. C1 UNIV CALIF DAVIS,SCH VET MED,DEPT ANAT,DAVIS,CA 95616. NIEHS,CELLULAR & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. UNIV CALIF DAVIS,SCH MED,DEPT PHARMACOL & TOXICOL,DAVIS,CA 95616. UNIV CALIF DAVIS,SCH MED,OCCUPAT & ENVIRONM HLTH UNIT,DAVIS,CA 95616. FU NIEHS NIH HHS [ES04311] NR 39 TC 57 Z9 57 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD FEB PY 1991 VL 4 IS 2 BP 179 EP 186 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA EY085 UT WOS:A1991EY08500012 PM 1991074 ER PT J AU CHOYKE, PL BEATROUS, TE FRANK, JA AF CHOYKE, PL BEATROUS, TE FRANK, JA TI BONE-SCINTIGRAPHY FOR EVALUATION OF PELVIC PAIN - REPLY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter C1 GLENWOOD REG MED CTR,MONROE,LA 71294. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. RP CHOYKE, PL (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD FEB PY 1991 VL 156 IS 2 BP 407 EP 407 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EU535 UT WOS:A1991EU53500046 ER PT J AU JAFFE, ES AF JAFFE, ES TI INTRODUCTION TO DIAGNOSTIC PROBLEMS IN ANGIOIMMUNOBLASTIC LYMPHADENOPATHY SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Meeting Abstract ID ANGIO-IMMUNOBLASTIC LYMPHADENOPATHY; T-CELL LYMPHOMA; MALIGNANT-LYMPHOMA; FEATURES; DYSPROTEINEMIA; EVOLUTION; DISORDERS C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,BETHESDA,MD 20892. NR 14 TC 1 Z9 1 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 FEB PY 1991 VL 15 IS 2 BP 193 EP 194 DI 10.1097/00000478-199102000-00015 PG 2 WC Pathology; Surgery SC Pathology; Surgery GA EU738 UT WOS:A1991EU73800015 ER PT J AU BALTARO, RJ HOFFMAN, GS SECHLER, JMG SUFFREDINI, AF SHELHAMER, JH FAUCI, AS FLEISHER, TA AF BALTARO, RJ HOFFMAN, GS SECHLER, JMG SUFFREDINI, AF SHELHAMER, JH FAUCI, AS FLEISHER, TA TI IMMUNOGLOBULIN-G ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES ARE PRODUCED IN THE RESPIRATORY-TRACT OF PATIENTS WITH WEGENERS GRANULOMATOSIS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID BRONCHOALVEOLAR LAVAGE; ANTICYTOPLASMIC AUTOANTIBODIES; THERAPEUTIC CONSIDERATIONS; DIAGNOSIS; VASCULITIS; PATHOGENESIS; DISEASE; ALBUMIN; SERUM; FLUID AB Wegener's granulomatosis (WG) is a small-vessel vasculitis of unknown etiology that usually involves the upper and lower respiratory tract and the kidneys. Recently, an association has been made between the presence of serum antineutrophil cytoplasmic antibodies (ANCA) and WG. Because WG frequently involves the lung, we sought to evaluate bronchoalveolar lavage (BAL) fluids obtained from 14 patients with WG for the presence of ANCA. Immunoglobulin (Ig) G ANCA was found in the BAL with the same staining patterns as observed in the serum. Patients with active disease had the highest serum and BAL IgG ANCA titers. IgA or IgM ANCA was not detected in the serum or BAL of these patients. Protein analysis of BAL fluid revealed that patients with active, untreated WG had approximately a fourfold elevation in total protein (41.3 versus 10.5 mg/dl), with a disproportionately greater increase in the ratio of IgG to albumin (BAL IgG index = 1.49, normal = 0.74; p = 0.027). The increase of the IgG index in patients with active WG suggests that local production of IgG ANCA occurs in the lungs. C1 NIAID,CTR CLIN,DEPT CLIN PATHOL,BETHESDA,MD 20892. NIAID,CTR CLIN,DEPT CRIT CARE MED,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NR 35 TC 32 Z9 33 U1 1 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD FEB PY 1991 VL 143 IS 2 BP 275 EP 278 PG 4 WC Respiratory System SC Respiratory System GA EX245 UT WOS:A1991EX24500014 PM 1990940 ER PT J AU HOFFMAN, GS SECHLER, JMG GALLIN, JI SHELHAMER, JH SUFFREDINI, A OGNIBENE, FP BALTARO, RJ FLEISHER, TA LEAVITT, RY TRAVIS, WD BARILE, MF TSOKOS, M HOLMAN, RP STRAUS, SE FAUCI, AS AF HOFFMAN, GS SECHLER, JMG GALLIN, JI SHELHAMER, JH SUFFREDINI, A OGNIBENE, FP BALTARO, RJ FLEISHER, TA LEAVITT, RY TRAVIS, WD BARILE, MF TSOKOS, M HOLMAN, RP STRAUS, SE FAUCI, AS TI BRONCHOALVEOLAR LAVAGE ANALYSIS IN WEGENERS GRANULOMATOSIS - A METHOD TO STUDY DISEASE PATHOGENESIS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID LUNG-DISEASE; ALVEOLAR MACROPHAGES; INFLAMMATION; NEUTROPHILS; DIAGNOSIS; SERUM AB A prospective analysis of bronchoalveolar lavage (BAL) in 13 patients with Wegener's granulomatosis (WG), 20 disease control subjects with idiopathic pulmonary fibrosis (IPF), and 24 normal control subjects was conducted to (1) evaluate the quality of the alveolar inflammatory response associated with active WG; (2) determine whether antineutrophil cytoplasmic antibody (ANCA) is present in alveolar fluid and produced in the lungs of patients with WG; and (3) determine whether inhaled particles or infectious agents may play an etiologic role in WG. BAL in untreated active WG had a marked increase in neutrophils (mean = 42% of total WBC count), and usually in eosinophils (mean = 4%) compared with that in normal control subjects (1.6% neutrophils, 0% eosinophils), and untreated WG in remission (5.9% neutrophils, 0% eosinophils). Disease control subjects with IPF, a process known to be associated with neutrophilic alveolitis, had an increased population of neutrophils (15.4%) and eosinophils (2.7%) in BAL. Leukocyte remnants, as well as intact leukocytes, could be identified within BAL macrophages in the patients with WG and IPF, and rarely in the normal control subjects. Normal subjects and control patients with IPF were all negative for ANCA in serum, whereas ANCA was found in serum and BAL in all patients with active WG who had generalized disease. Protein analysis of BAL revealed a disporportionate increase in the IgG to albumin ratio compared with serum values (IgG index) in patients with active untreated disease. The increase in the IgG index suggests that IgG with ANCA reactivity is produced by pulmonary lymphoid tissue. An infectious agent in BAL was not identified by any of the techniques applied in this study. If an inhaled infectious agent is responsible for the neutrophilic alveolitis of active WG, its presence is either very transient or it is an unusual organism, not identifiable by most routine or research laboratory techniques. The neutrophilia in BAL of active WG contrasts with several other granulomatous lung disease in which increased numbers of lymphocytes are noted. On the basis of observations in our control populations, phagocytosis of neutrophils by macrophages is not, by itself, sufficient to lead to ANCA production. The presence of ANCA distinguishes WG from other diseases that also have a neutrophilic alveolitis. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NCI,DEPT CRIT CARE MED,BETHESDA,MD 20892. NCI,CTR CLIN,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. RP HOFFMAN, GS (reprint author), NIH,CTR BIOL EVALUAT & RES,DIV BACTERIAL PROD,BLDG 10,ROOM 11B-13,BETHESDA,MD 20892, USA. NR 30 TC 45 Z9 45 U1 1 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD FEB PY 1991 VL 143 IS 2 BP 401 EP 407 PG 7 WC Respiratory System SC Respiratory System GA EX245 UT WOS:A1991EX24500036 PM 1990960 ER PT J AU ROM, WN TRAVIS, WD BRODY, AR AF ROM, WN TRAVIS, WD BRODY, AR TI CELLULAR AND MOLECULAR-BASIS OF THE ASBESTOS-RELATED DISEASES SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Review ID PLEURAL MESOTHELIAL CELLS; BRONCHOALVEOLAR LAVAGE FLUID; ARYL-HYDROCARBON HYDROXYLASE; INDUCED PULMONARY FIBROSIS; LOWER RESPIRATORY-TRACT; CHRYSOTILE ASBESTOS; ALVEOLAR MACROPHAGES; GROWTH-FACTOR; MALIGNANT MESOTHELIOMA; CROCIDOLITE ASBESTOS C1 NYU MED CTR, BELLEVUE HOSP, DEPT ENVIRONM MED, NEW YORK, NY 10016 USA. NYU MED CTR, BELLEVUE HOSP, CHEST SERV, NEW YORK, NY 10016 USA. NCI, DIV CANC BIOL & PREVENT, PATHOL LAB, BETHESDA, MD 20892 USA. NIEHS, PULM PATHOBIOL LAB, RES TRIANGLE PK, NC 27709 USA. RP ROM, WN (reprint author), NYU MED CTR, BELLEVUE HOSP, DEPT MED, DIV PULM & CRIT CARE MED, RM 7N24, NEW YORK, NY 10016 USA. NR 164 TC 214 Z9 218 U1 1 U2 4 PU AMER THORACIC SOC PI NEW YORK PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD FEB PY 1991 VL 143 IS 2 BP 408 EP 422 PG 15 WC Respiratory System SC Respiratory System GA EX245 UT WOS:A1991EX24500037 PM 1990961 ER PT J AU GOLDSTEIN, RA AF GOLDSTEIN, RA TI ISOLATION OF COCCIDIOIDES-IMMITIS FROM BRONCHOALVEOLAR LAVAGE IS DIAGNOSTIC OF INFECTION - REPLY SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Letter RP GOLDSTEIN, RA (reprint author), NIAID,DIV ALLERGY IMMUNOL & TRANSPLANTAT,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD FEB PY 1991 VL 143 IS 2 BP 451 EP 451 PG 1 WC Respiratory System SC Respiratory System GA EX245 UT WOS:A1991EX24500046 ER PT J AU DANFORTH, DN FRAKER, DL AF DANFORTH, DN FRAKER, DL TI SPLENECTOMY FOR THE MASSIVELY ENLARGED SPLEEN SO AMERICAN SURGEON LA English DT Article; Proceedings Paper CT 58TH ANNUAL ASSEMBLY OF THE SOUTHEASTERN SURGICAL CONGRESS CY JAN 30, 1990 CL NAPLES, FL SP SE SURG CONGRESS ID EXPERIENCE; LEUKEMIA; RISK AB The experience at the National Cancer Institute from 1955 to 1988 with 46 cases of splenectomy for massive splenomegaly (greater-than-or-equal-to 1,500 grams) was reviewed to assess the indications, pathology, operative, and postoperative course for this procedure. The median age was 51 years. Thirty-one splenectomies (67.4%) were performed for malignancy (chronic lymphocytic leukemia, 11; chronic myelogenous leukemia, 10; lymphoma, 9; hairy cell leukemia, 1), 11 for myeloid metaplasia, and four for other nonmalignant conditions. Indications for splenectomy included hypersplenism (32 patients), symptoms (6), diagnosis (3), and splenic rupture (3). A midline incision (30 patients) was most commonly used. Median operative time was 2 hours, 50 minutes. Median operative blood loss was 1,300 ml (range, 100 ml-60 units). The splenic artery was ligated initially in 16 patients (34.8%) but did not correlate with blood loss or operating time. The median splenic weight was 2,030 grams (range, 1500-5320 gm). The postoperative complication rate was 39.1 per cent (21 complications in 18 patients). This included infection in 10 patients, bleeding in six patients. Six patients required reoperation (bleeding, 4; abscess, 1; small bowel obstruction, 1 patient). The 30-day operative mortality was 19.6 per cent (9 patients). Excluding operative deaths, 35 patients were available for follow-up evaluation. Twenty-nine patients had improvement in parameters for which splenectomy was indicated. Six patients had no change in their course after splenectomy. These findings indicate that many patients with massive splenomegaly benefit from splenectomy, however, the procedure is associated with a high risk for postoperative morbidity and mortality. Careful patient selection and consideration of performing splenectomy earlier in the course of the disease may improve the benefits of the procedure. RP DANFORTH, DN (reprint author), NCI,SURG BRANCH,BLDG 10,ROOM 2B38,BETHESDA,MD 20892, USA. NR 12 TC 25 Z9 26 U1 0 U2 1 PU SOUTHEASTERN SURGICAL CONGRESS PI ATLANTA PA 1776 PEACHTREE RD, NW., SUITE 410N, ATLANTA, GA 30309-2352 SN 0003-1348 J9 AM SURGEON JI Am. Surg. PD FEB PY 1991 VL 57 IS 2 BP 108 EP 113 PG 6 WC Surgery SC Surgery GA EY302 UT WOS:A1991EY30200009 PM 1992865 ER PT J AU ROCCELLA, EJ AF ROCCELLA, EJ TI NATIONAL EDUCATION-PROGRAMS WORKING GROUP-REPORT ON THE MANAGEMENT OF PATIENTS WITH HYPERTENSION AND HIGH BLOOD CHOLESTEROL SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID CORONARY HEART-DISEASE; PRIMARY-PREVENTION TRIAL; SERUM LIPOPROTEIN LEVELS; RISK-FACTORS; FOLLOW-UP; MYOCARDIAL-INFARCTION; ORAL-CONTRACEPTIVES; CARDIOVASCULAR-DISEASE; TRANSPLANT RECIPIENTS; NEPHROTIC SYNDROME AB Cardiovascular diseases are responsible for nearly one of every two deaths in the United States, and have been estimated to cost more than $127 billion annually. Epidemiologic data have shown that persons with fewer or lower levels of the risk factors for cardiovascular disease are less likely to have a cardiovascular event. In addition, the greater the level of any single risk factor, the greater is the chance of incurring disease. Moreover, a combination of risk factors creates a synergistic effect, further increasing risk. Conversely, reducing the number and level of risk factors prevents death and disability from cardiovascular diseases. This report addresses the management of patients with several cardiovascular risk factors, placing a special emphasis on hypertension and high blood cholesterol. Nonpharmacologic therapy, in the form of proper diet, exercise, and smoking cessation, is the foundation for management of both hypertension and high blood cholesterol. Clinicians should use these nondrug measures as definitive or adjunctive therapy. Pharmacologic agents can be very beneficial in managing the risks imposed by elevated levels of blood pressure or blood cholesterol. In selecting medications, it is important to weigh their benefits, costs, and potential untoward effects. Clinicians must consider these issues in managing patients with several risk factors but should not avoid managing any risk factor or quickly dismiss any particular mode of therapy simply because of the potential for adverse effects. RP ROCCELLA, EJ (reprint author), NHLBI,BLDG 31,ROOM 4A05,BETHESDA,MD 20892, USA. NR 89 TC 29 Z9 29 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 FEB 1 PY 1991 VL 114 IS 3 BP 224 EP 237 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA EV339 UT WOS:A1991EV33900011 ER PT J AU HEYES, MP BREW, BJ MARTIN, A PRICE, RW SALAZAR, AM SIDTIS, JJ YERGEY, JA MOURADIAN, MM SADLER, AE KEILP, J RUBINOW, D MARKEY, SP AF HEYES, MP BREW, BJ MARTIN, A PRICE, RW SALAZAR, AM SIDTIS, JJ YERGEY, JA MOURADIAN, MM SADLER, AE KEILP, J RUBINOW, D MARKEY, SP TI QUINOLINIC ACID IN CEREBROSPINAL-FLUID AND SERUM IN HIV-1 INFECTION - RELATIONSHIP TO CLINICAL AND NEUROLOGICAL STATUS SO ANNALS OF NEUROLOGY LA English DT Article ID AIDS DEMENTIA COMPLEX; METHYL-D-ASPARTATE; IMMUNE-DEFICIENCY SYNDROME; CENTRAL NERVOUS-SYSTEM; RAT-BRAIN; HUNTINGTONS-DISEASE; ALZHEIMERS-DISEASE; TRYPTOPHAN; BLOOD AB Quinolinic acid is an "excitotoxic" metabolite and an agonist of N-methyl-D-aspartate receptors. Of patients infected with human immunodeficiency virus type 1 (HIV-1) who were neurologically normal or exhibited only equivocal and subclinical signs of the acquired immunodeficiency syndrome (AIDS) dementia complex, concentrations of quinolinic acid in cerebrospinal fluid (CSF) were increased twofold in patients in the early stages of disease (Walter Reed stages 1 and 2) and averaged 3.8 times above normal in later-stage patients (Walter Reed stages 4 through 6). However, in patients with either clinically overt AIDS dementia complex, aseptic meningitis, opportunistic infections, or neoplasms, CSF levels were elevated over 20-fold and generally paralleled the severity of cognitive and motor dysfunction. CSF concentrations of quinolinic acid were significantly correlated to the severity of the neuropsychological deficits. After treatment of AIDS dementia complex with zidovudine and treatment of the opportunistic infections with specific antimicrobial therapies, CSF levels of quinolinic acid decreased in parallel with clinical neurological improvement. By analysis of the relationship between levels of quinolinic acid in the CSF and serum and integrity of the blood-brain barrier, as measured by the CSF: serum albumin ratio, it appears that CSF levels of quinolinic acid may be derived predominantly from intracerebral sources and perhaps from the serum. While quinolinic acid may be another "marker" of host- and virus-mediated events in the brain, the established excitotoxic effects of quinolinic acid and the magnitude of the increases in CSF levels of the acid raise the possibility that quinolinic acid plays a direct role in the pathogenesis of brain dysfunction associated with HIV-1 infection. C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. MEM SLOAN KETTERING CANC CTR,DEPT NEUROL,NEW YORK,NY 10021. MIL MED CONSORTIUM APPL RETROVIRUS RES,WASHINGTON,DC. NIAAA,CLIN SCI LAB,ANALYT CHEM SECT,ROCKVILLE,MD 20852. NINCDS,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892. UNIFORM SERV UNIV HLTH SCI,WALTER REED ARMY MED CTR,DEPT NEUROL,WASHINGTON,DC. RP HEYES, MP (reprint author), NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BLDG 10,ROOM 3D40,BETHESDA,MD 20892, USA. RI martin, alex/B-6176-2009; Brew, Bruce/J-6513-2012; OI Mouradian, M. Maral/0000-0002-9937-412X FU NINDS NIH HHS [NS-25701] NR 35 TC 520 Z9 529 U1 3 U2 7 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD FEB PY 1991 VL 29 IS 2 BP 202 EP 209 DI 10.1002/ana.410290215 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA EW939 UT WOS:A1991EW93900014 PM 1826418 ER PT J AU GILL, I MUGGIA, FM TERHEGGEN, PMAB MICHAEL, C PARKER, RJ KORTES, V GRUNBERG, S CHRISTIAN, MC REED, E DENENGELSE, L AF GILL, I MUGGIA, FM TERHEGGEN, PMAB MICHAEL, C PARKER, RJ KORTES, V GRUNBERG, S CHRISTIAN, MC REED, E DENENGELSE, L TI DOSE-ESCALATION STUDY OF CARBOPLATIN (DAY-1) AND CISPLATIN (DAY-3) - TOLERANCE AND RELATION TO LEUKOCYTE AND BUCCAL CELL PLATINUM DNA ADDUCTS SO ANNALS OF ONCOLOGY LA English DT Article DE CISPLATIN; CARBOPLATIN; PLATINUM-DNA ADDUCT; PHASE-I ID CIS-DIAMMINEDICHLOROPLATINUM(II); TOXICITY AB Carboplatin and cisplatin have similar antitumor activities but different toxicities. Combining these two analogs may be expected to balance the toxicities and allow higher doses of platinum compounds to be administered with tolerable toxicity. To test this concept, a Phase I trial of carboplatin in combination with cisplatin was performed. Thirty-three eligible patients received carboplatin doses ranging from 200-480 mg/m2 on day 1 and cisplatin doses ranging from 50-100 mg/m2 on day 3 of the 28 day cycle. A 2-day interval ensured no interference in renal excretion of carboplatin by cisplatin. Myelosuppression was the dose limiting toxicity. With the usual full dose of carboplatin, 480 mg/m2, patients tolerated 50 mg/m2 of cisplatin, without apparent additional toxicity. At 100 mg/m2 of cisplatin, non-hematologic as well as hematologic toxicities frequently precluded administration of more than 300 mg/m2 of carboplatin. Platinum-DNA adduct quantitation was done in leukocytes and buccal cells during cycle 1 in most patients. The adduct-specific immunosignal in buccal cells was always increased after carboplatin and in all but one after cisplatin. The level of adducts in buccal cells increased with increasing doses of carboplatin and cisplatin. In leukocytes, measurable levels of adducts were formed after carboplatin with further contribution made by cisplatin but not obviously in a dose dependent fashion. We conclude from the toxicities observed, that combinations of carboplatin with cisplatin may have advantages over either drug alone in certain clinical situations; and that further study of platinum-DNA adducts may shed light on platinum dose-response relationships. C1 UNIV SO CALIF,NORRIS CANC CTR,LOS ANGELES,CA 90089. NCI,INVEST DRUG BRANCH,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. NETHERLANDS CANC INST,DIV CHEM CARCINOGENESIS,1066 CX AMSTERDAM,NETHERLANDS. NR 23 TC 41 Z9 41 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD FEB PY 1991 VL 2 IS 2 BP 115 EP 121 PG 7 WC Oncology SC Oncology GA FA601 UT WOS:A1991FA60100013 PM 2054312 ER PT J AU ELMAWLA, NG MANSOUR, MA EISSA, S ALI, NM ELATTAR, I HAMZA, MR KHALED, H HABBOUBI, N MAGRATH, I ELSEBAI, I AF ELMAWLA, NG MANSOUR, MA EISSA, S ALI, NM ELATTAR, I HAMZA, MR KHALED, H HABBOUBI, N MAGRATH, I ELSEBAI, I TI A RANDOMIZED PILOT-STUDY OF HIGH-DOSE EPIRUBICIN AS NEOADJUVANT CHEMOTHERAPY IN THE TREATMENT OF CANCER OF THE BILHARZIAL BLADDER SO ANNALS OF ONCOLOGY LA English DT Article DE INVASIVE BLADDER CANCER; NEOADJUVANT; EPIRUBICIN AB Seventy-one patients with T2 and T3 bladder cancer were randomized to receive either two courses of epirubicin 120 mg/m2 i.v. push every 21 days pre-operatively, and four additional courses post-operatively (group I = 34 patients), or radical surgery (group II = 37 patients). At median follow-up of 24 months (range 22 months to 38 months) 25 patients from group I and 14 patients from group II are still alive and disease-free. The estimated two-year disease-free survival percentages were 73.5 and 37.9%, respectively (P = 0.05). After initial chemotherapy, resected specimens were subjected to histopathological study of chemotherapeutic effects. Necrosis was detected in 95% of cases with squamous cell carcinoma and in 57.3% of cases with transitional cell carcinoma. We conclude that the benefit which was obtained by pre-operative and post-operative chemotherapy with epirubicin is promising and may represent a significant improvement in the treatment of patients with carcinoma of the bilharzial bladder. C1 FARMITALIA CARLO ERBA SPA,MILAN,ITALY. NCI,BETHESDA,MD 20892. RP ELMAWLA, NG (reprint author), NATL CANC INST,MED ONCOL,CAIRO,EGYPT. NR 7 TC 3 Z9 4 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD FEB PY 1991 VL 2 IS 2 BP 137 EP 140 PG 4 WC Oncology SC Oncology GA FA601 UT WOS:A1991FA60100017 PM 2054316 ER PT J AU SANTINI, G COSER, P CHISESI, T PORCELLINI, A SERTOLI, R CONTU, A VINANTE, O CONGIU, AM CARELLA, AM DAMICO, T PIERLUIGI, D ROSSI, E SCARPATI, D RIZZOLI, V AF SANTINI, G COSER, P CHISESI, T PORCELLINI, A SERTOLI, R CONTU, A VINANTE, O CONGIU, AM CARELLA, AM DAMICO, T PIERLUIGI, D ROSSI, E SCARPATI, D RIZZOLI, V TI AUTOLOGOUS BONE-MARROW TRANSPLANTATION FOR ADVANCED STAGE ADULT LYMPHOBLASTIC LYMPHOMA IN 1ST COMPLETE REMISSION - REPORT OF THE NON-HODGKINS-LYMPHOMA-COOPERATIVE-STUDY-GROUP (NHLCSG) SO ANNALS OF ONCOLOGY LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL CONF ON MALIGNANT LYMPHOMA CY JUN 06-09, 1990 CL LUGANO, SWITZERLAND ID TOTAL-BODY IRRADIATION; MALIGNANT-LYMPHOMA; ACUTE-LEUKEMIA; THERAPY; CHEMOTHERAPY; ABMT AB Thirty-six successive adult patients with lymphoblastic lymphoma entered a study of sequential chemotherapy consisting of an intensive LSA2-L2-type protocol to induce first complete remission. Eighteen patients in first CR (median age 22 years, range 15-51), underwent autologous bone marrow transplantation after receiving a conditioning regimen consisting of cyclophosphamide and total body irradiation. Of these 18 patients, 2 were in stage III and 16 in stage IV; 15 showed mediastinal and 9 bone marrow involvement at diagnosis. The transplant procedure was well tolerated and no treatment-induced deaths occurred. At this time, 14 out of 18 patients are alive and well between 1 and 60 months post transplant (median follow-up time 46 months) with an actuarial disease-free survival of 74%. This phase II study suggests that high-dose chemo-radiotherapy followed by autologous bone marrow transplantation may improve long-term disease-free survival in advanced stage adult lymphoblastic lymphoma. C1 OSPED CIVILE NOALE,DIV ONCOL,NOALE,ITALY. INST RADIOL,GENOA,ITALY. INST HEMATOL,PARMA,ITALY. OSPED SAN MARTINO GENOVA,DIV HEMATOL,GENOA,ITALY. OSPED CIVILE BOLZANO,DIV HEMATOL,BOLZANO,ITALY. OSPED CIVILE,DIV HEMATOL,VICENZA,ITALY. OSPED CIVILE CREMONA,DIV HEMATOL,CREMONA,ITALY. NATL CANC INST,GENOA,ITALY. OSPED CIVILE,DIV ONCOL,SASSARI,ITALY. NR 26 TC 15 Z9 17 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD FEB PY 1991 VL 2 SU 2 BP 181 EP 185 PG 5 WC Oncology SC Oncology GA FB412 UT WOS:A1991FB41200029 PM 2049316 ER PT J AU PLUDA, JM YARCHOAN, R BRODER, S AF PLUDA, JM YARCHOAN, R BRODER, S TI THE OCCURRENCE OF OPPORTUNISTIC NON-HODGKINS-LYMPHOMAS IN THE SETTING OF INFECTION WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS SO ANNALS OF ONCOLOGY LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL CONF ON MALIGNANT LYMPHOMA CY JUN 06-09, 1990 CL LUGANO, SWITZERLAND DE AIDS; IMMUNOSUPPRESSION; LYMPHOMA; PATHOGENESIS; SURVIVAL, THERAPY ID PNEUMOCYSTIS-CARINII PNEUMONIA; HAIRY-CELL LEUKEMIA; ORGAN TRANSPLANT RECIPIENTS; WISKOTT-ALDRICH SYNDROME; AIDS-ASSOCIATED LYMPHOMA; SOFT-TISSUE SARCOMA; ACQUIRED IMMUNODEFICIENCY; HOMOSEXUAL MEN; MALIGNANT-LYMPHOMA; UNITED-STATES AB The incidence of non-Hodgkin's lymphoma (NHL) has increased by over 50% in the United States since 1973. There is epidemiologic evidence that some of this increase is the result of AIDS-related lymphoma and that this component is increasing. Prolonged survival in the setting of a variety of immunodeficiency states is associated with an increased incidence of NHL. The development of antiretroviral therapy and improved therapy for the complications of AIDS has resulted in prolonged survival of patients with AIDS. As these patients survive longer with profound immunodeficiency, they have an increased cumulative risk of developing NHL. This may result in even more AIDS-related NHL in the future than predicted from current epidemiological studies. An increased understanding of the pathogenesis of AIDS-related NHL may lead to means of preventing their occurrence. Also, therapies that may prevent immunodeficiency from developing in HIV-infected patients may reduce the likelihood of NHL developing. Current efforts at treating these lymphomas are aimed at preventing the myelosuppression and immunosuppression associated with current regimens, lymphoma relapses within the central nervous system, and the opportunistic infections associated with treatment of these tumors. Ultimately, the best means of preventing the development of these lymphomas is by preventing infection with HIV. RP PLUDA, JM (reprint author), NCI,CLIN ONCOL KLIN,9000 ROCKVILLE PIKE,BLDG 10,ROOM 13N248,BETHESDA,MD 20892, USA. NR 111 TC 7 Z9 7 U1 1 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD FEB PY 1991 VL 2 SU 2 BP 191 EP 200 PG 10 WC Oncology SC Oncology GA FB412 UT WOS:A1991FB41200031 PM 1646622 ER PT J AU CROWTHER, D SPORN, MB ROBERTS, AB DURIE, BGM AF CROWTHER, D SPORN, MB ROBERTS, AB DURIE, BGM TI WORKSHOP ON GROWTH-FACTORS SO ANNALS OF ONCOLOGY LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL CONF ON MALIGNANT LYMPHOMA CY JUN 06-09, 1990 CL LUGANO, SWITZERLAND ID POSSIBLE SIGNAL TRANSDUCER; COLONY-STIMULATING FACTOR; RECEIVING INTENSIVE CHEMOTHERAPY; CELL LUNG-CANCER; INTERLEUKIN-6 TRIGGERS; MULTIPLE-MYELOMA; PHASE-I/II; ASSOCIATION; RECEPTOR; GP130 AB The 'Workshop on Growth Factors' which took place at the Lugano Lymphoma Conference on June 8, 1990, included a presentation by Michael Sporn on the concept that loss of inhibitory control mechanisms may be important in the development and growth of human cancer. Examples illustrating this were taken from current experimental biology research into transforming growth factor beta (TGF-beta) interactions. Brain Durie presented recent data on the biology of interleukin-6 (IL-6) and its putative role in plasma cell diseases. These studies have culminated in the first clinical study of the role of an antibody to a growth factor as therapy for a human cancer (anti-IL-6 antibody as therapy for patients with myeloma). Derek Crowther presented data concerning the current clinical role of the haematopoietic growth factors in patients undergoing chemotherapy for cancer. Recent clinical research has established the role of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in improving the safety of high-dose or accelerated chemotherapy, and their use is associated with enhanced neutrophil recovery following ablative therapy and bone marrow rescue. This session was followed by the presentation of three papers concerning the use of G-CSF and GM-CSF in association with chemotherapy for patients with malignant lymphoma. C1 CHARING CROSS & WESTMINSTER MED SCH,LONDON,ENGLAND. NCI,BETHESDA,MD 20892. RP CROWTHER, D (reprint author), CHRISTIE HOSP & HOLT RADIUM INST,WILMSLOW RD,MANCHESTER M20 9BX,LANCS,ENGLAND. NR 17 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD FEB PY 1991 VL 2 SU 2 BP 207 EP 211 PG 5 WC Oncology SC Oncology GA FB412 UT WOS:A1991FB41200033 PM 1675582 ER PT J AU MURPHY, SB MAGRATH, IT AF MURPHY, SB MAGRATH, IT TI WORKSHOP ON PEDIATRIC LYMPHOMAS - CURRENT RESULTS AND PROSPECTS SO ANNALS OF ONCOLOGY LA English DT Editorial Material C1 CHILDRENS MEM HOSP,DIV HEMATOL ONCOL,CHICAGO,IL 60614. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. NCI,DIV CANC TREATMENT,PEDIAT ONCOL BRANCH,LYMPHOMA BIOL SECT,BETHESDA,MD 20892. NR 12 TC 10 Z9 10 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD FEB PY 1991 VL 2 SU 2 BP 219 EP 223 PG 5 WC Oncology SC Oncology GA FB412 UT WOS:A1991FB41200035 PM 1675584 ER PT J AU NORTON, JA AF NORTON, JA TI CARCINOEMBRYONIC ANTIGEN - NEW APPLICATIONS FOR AN OLD MARKER SO ANNALS OF SURGERY LA English DT Editorial Material ID COLORECTAL-CANCER; NUDE-MICE; SURVIVAL; ANTIBODY RP NORTON, JA (reprint author), NCI,SURG METAB SECT,SURG BRANCH,BETHESDA,MD 20892, USA. NR 18 TC 17 Z9 21 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD FEB PY 1991 VL 213 IS 2 BP 95 EP 97 DI 10.1097/00000658-199102000-00001 PG 3 WC Surgery SC Surgery GA EX438 UT WOS:A1991EX43800002 PM 1992947 ER PT J AU SINCLAIR, JF MCCAFFREY, J SINCLAIR, PR BEMENT, WJ LAMBRECHT, LK WOOD, SG SMITH, EL SCHENKMAN, JB GUZELIAN, PS PARK, SS GELBOIN, HV AF SINCLAIR, JF MCCAFFREY, J SINCLAIR, PR BEMENT, WJ LAMBRECHT, LK WOOD, SG SMITH, EL SCHENKMAN, JB GUZELIAN, PS PARK, SS GELBOIN, HV TI ETHANOL INCREASES CYTOCHROME-P450IIE, CYTOCHROME-IIB1/2, AND CYTOCHROME-IIIA IN CULTURED RAT HEPATOCYTES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID INDUCIBLE CYTOCHROME-P-450; LIVER CYTOCHROME-P-450; MONOCLONAL-ANTIBODIES; MEDIATED INCREASE; PARA-NITROPHENOL; GROWTH-HORMONE; ACETAMINOPHEN; INDUCTION; HYDROXYLATION; EXPRESSION C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT BIOCHEM,HANOVER,NH 03756. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PHARMACOL,HANOVER,NH 03756. UNIV CONNECTICUT,SCH MED,DEPT PHARMACOL,FARMINGTON,CT 06032. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED,RICHMOND,VA 23298. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP SINCLAIR, JF (reprint author), VET ADM MED CTR,WHITE RIVER JCT,VT 05009, USA. FU NCI NIH HHS [CA 25012]; NIEHS NIH HHS [ES07104]; NIGMS NIH HHS [GM26114] NR 32 TC 73 Z9 73 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 FEB 1 PY 1991 VL 284 IS 2 BP 360 EP 365 DI 10.1016/0003-9861(91)90308-6 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA ET071 UT WOS:A1991ET07100020 PM 1989519 ER PT J AU LIU, G GELBOIN, HV MYERS, MJ AF LIU, G GELBOIN, HV MYERS, MJ TI ROLE OF CYTOCHROME-P450 IA2 IN ACETANILIDE 4-HYDROXYLATION AS DETERMINED WITH CDNA EXPRESSION AND MONOCLONAL-ANTIBODIES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID MUTAGEN ACTIVATION; CYTOCHROMES-P-450; CHROMATOGRAPHY; PURIFICATION C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 21 TC 58 Z9 58 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 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD FEB 1 PY 1991 VL 284 IS 2 BP 400 EP 406 DI 10.1016/0003-9861(91)90315-A PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA ET071 UT WOS:A1991ET07100027 PM 1989524 ER PT J AU STEIN, MB UHDE, TW AF STEIN, MB UHDE, TW TI ENDOCRINE, CARDIOVASCULAR, AND BEHAVIORAL-EFFECTS OF INTRAVENOUS PROTIRELIN IN PATIENTS WITH PANIC DISORDER SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID THYROTROPIN-RELEASING-HORMONE; DEXAMETHASONE SUPPRESSION TEST; PSYCHIATRIC-PATIENTS; HEALTHY-SUBJECTS; DEPRESSED-PATIENTS; THYROID-FUNCTION; TSH RESPONSE; LACTATE PROVOCATION; ANOREXIA-NERVOSA; STIMULATION TEST AB The effects of protirelin administration on the anterior pituitary release of thyrotropin and prolactin were examined in 26 patients with panic disorder and 22 healthy volunteers. There were no differences observed in hormonal responses to protirelin between patients and controls. However, higher Beck Depression inventory scores were associated with smaller baseline-corrected maximal changes in thyrotropin responses. Cardiovascular responses to protirelin did not differ between a subgroup of 15 patients with panic disorder and 15 age- and sex-matched healthy controls. Although protirelin produced robust increases in heart rate and blood pressure, only one patient with panic disorder experienced a panic attack during the infusion. The hormonal findings suggest that the presence of depressive symptoms may have a significant impact on various indexes of neuroendocrine responsivity and should be taken into consideration when looking at biologic measures in patients with panic disorder. The cardiovascular and behavioral findings do not support the hypothesis that all panic-producing stimuli are non-specific and suggest that the induction of physical stimuli may be insufficient to produce panic attacks even in susceptible individuals. C1 NIMH,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS SECT,BLDG 10,ROOM 3S-239,BETHESDA,MD 20892. NR 94 TC 26 Z9 26 U1 2 U2 2 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 FEB PY 1991 VL 48 IS 2 BP 148 EP 156 PG 9 WC Psychiatry SC Psychiatry GA EV899 UT WOS:A1991EV89900007 PM 1899183 ER PT J AU INGRAHAM, LJ BRIDGE, TP PARKER, E BICKHAM, CE MYSLOBODSKY, MS AF INGRAHAM, LJ BRIDGE, TP PARKER, E BICKHAM, CE MYSLOBODSKY, MS TI CEREBRAL SIZE AFFECTS LOCALIZED DENSITY MEASURED BY COMPUTED-TOMOGRAPHY SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter ID BRAIN RATIO; SCHIZOPHRENICS C1 CTR NEUROPSYCHOL,NEWPORT BEACH,CA 92660. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. TEL AVIV UNIV,DEPT PSYCHOL,PSYCHOBIOL RES UNIT,IL-69978 TEL AVIV,ISRAEL. RP INGRAHAM, LJ (reprint author), NIMH,PSYCHOL & PSYCHOPATHOL LAB,9900 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 11 TC 1 Z9 1 U1 2 U2 2 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 FEB PY 1991 VL 48 IS 2 BP 178 EP 179 PG 2 WC Psychiatry SC Psychiatry GA EV899 UT WOS:A1991EV89900011 ER PT J AU SCHMITZ, J DEJONG, J GARNETT, D MOORE, V WAXMAN, R LINNOILA, M ROY, A LAMPARSKI, D AF SCHMITZ, J DEJONG, J GARNETT, D MOORE, V WAXMAN, R LINNOILA, M ROY, A LAMPARSKI, D TI SUBSTANCE-ABUSE AMONG SUBJECTS SEEKING TREATMENT FOR ALCOHOLISM SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter C1 HILLSIDE HOSP,GLEN OAKS,NY 11004. MARYLAND PSYCHIAT RES CTR,BALTIMORE,MD 21228. RP SCHMITZ, J (reprint author), NIAAA,CLIN STUDIES LAB,9000 ROCKVILLE PIKE,BLDG 10,ROOM 3B19,BETHESDA,MD 20892, USA. NR 5 TC 11 Z9 11 U1 1 U2 1 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 FEB PY 1991 VL 48 IS 2 BP 182 EP 183 PG 2 WC Psychiatry SC Psychiatry GA EV899 UT WOS:A1991EV89900015 PM 1989574 ER PT J AU KUMAR, A SCHAPIRO, MB GRADY, CL MATOCHA, MF HAXBY, JV MOORE, AM LUXENBERG, JS STGEORGEHYSLOP, PH ROBINETTE, CD BALL, MJ RAPOPORT, SL AF KUMAR, A SCHAPIRO, MB GRADY, CL MATOCHA, MF HAXBY, JV MOORE, AM LUXENBERG, JS STGEORGEHYSLOP, PH ROBINETTE, CD BALL, MJ RAPOPORT, SL TI ANATOMIC, METABOLIC, NEUROPSYCHOLOGICAL, AND MOLECULAR GENETIC-STUDIES OF 3 PAIRS OF IDENTICAL-TWINS DISCORDANT FOR DEMENTIA OF THE ALZHEIMERS TYPE SO ARCHIVES OF NEUROLOGY LA English DT Article ID DISEASE; CHROMOSOME-21; ABNORMALITIES; ASYMMETRIES; CONCORDANT; TOMOGRAPHY; DIAGNOSIS; AGE AB Three pairs of twins, each with proved monozygosity, were shown to be discordant for dementia of the Alzheimer's type and to have remained discordant for periods of 8 to 11 years. Dementia of the Alzheimer's type was demonstrated by history; serial clinical examinations; serial measurements of cerebral glucose utilization using positron emission tomography and of cerebral ventricular volumes and of rates of change of volumes using quantitative computed tomography; and by serial neuropsychological tests. The results of each of these measures showed no evidence of clinical abnormality in any unaffected twin. DNA markers from the proximal long arm of chromosome 21 did not distinguish between the affected and the unaffected member of any pair of identical twins. Family pedigrees were negative for Alzheimer's disease. The results suggest that environmental or other nongenetic factors contribute to Alzheimer's disease in discordant monozygotic twins, or that some cases arise by a postzygotic somatic mutation. C1 NIA,NEUROSCI LAB,BLDG 10,ROOM 6C103,BETHESDA,MD 20892. NATL RES COUNCIL,NATL ACAD SCI,WASHINGTON,DC 20418. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. UNIV WESTERN ONTARIO,DEPT PATHOL,LONDON N6A 3K7,ONTARIO,CANADA. UNIV WESTERN ONTARIO,DEPT PSYCHIAT,LONDON N6A 3K7,ONTARIO,CANADA. UNIV WESTERN ONTARIO,DEPT CLIN NEUROL SCI,LONDON N6A 3K7,ONTARIO,CANADA. FU NIA NIH HHS [AG-03047-06A1, AG-05134, AG-06865] NR 68 TC 31 Z9 31 U1 3 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD FEB PY 1991 VL 48 IS 2 BP 160 EP 168 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA EX214 UT WOS:A1991EX21400009 PM 1993007 ER PT J AU WEINBERGER, DR GIBSON, R COPPOLA, R JONES, DW MOLCHAN, S SUNDERLAND, T BERMAN, KF REBA, RC AF WEINBERGER, DR GIBSON, R COPPOLA, R JONES, DW MOLCHAN, S SUNDERLAND, T BERMAN, KF REBA, RC TI THE DISTRIBUTION OF CEREBRAL MUSCARINIC ACETYLCHOLINE-RECEPTORS INVIVO IN PATIENTS WITH DEMENTIA - A CONTROLLED-STUDY WITH 123IQNB AND SINGLE PHOTON-EMISSION COMPUTED-TOMOGRAPHY SO ARCHIVES OF NEUROLOGY LA English DT Article ID CHOLINE-ACETYLTRANSFERASE ACTIVITY; ALZHEIMERS-DISEASE; SENILE DEMENTIA; BLOOD-FLOW; HUMAN-BRAIN; POSITRON TOMOGRAPHY; PARKINSONS-DISEASE; BINDING; SUBTYPES; HIPPOCAMPUS AB A high-affinity muscarinic receptor antagonist, IQNB-123 (3-quinuclidinyl-4-iodobenzilate labeled with iodine 123), was used with single photon emission computed tomography to image muscarinic acetylcholine receptors in 14 patients with dementia and in 11 healthy controls. High-resolution single photon emission computed tomographic scanning was performed 21 hours after the intravenous administration of approximately 5 mCi of IQNB. In normal subjects, the images of retained ligand showed a consistent regional pattern that correlated with postmortem studies of the relative distribution of muscarinic receptors in the normal human brain, having high radioactivity counts in the basal ganglia, occipital cortex, and insular cortex, low counts in the thalamus, and virtually no counts in the cerebellum. Eight of 12 patients with a clinical diagnosis of Alzheimer's disease had obvious focal cortical defects in either frontal or posterior temporal cortex. Both patients with a clinical diagnosis of Pick's disease had obvious frontal and anterior temporal defects. A region of interest statistical analysis of relative regional activity revealed a significant reduction bilaterally in the posterior temporal cortex of the patients with Alzheimer's disease compared with controls. This study demonstrates the practicability of acetylcholine receptor imaging with IQNB-123 and single photon emission computed tomography. The data suggest that focal abnormalities in muscarinic binding in vivo may characterize some patients with Alzheimer's disease and Pick's disease, but further studies are needed to address questions about partial volume artifacts and receptor quantification. C1 GEORGE WASHINGTON UNIV,DEPT NUCL MED,WASHINGTON,DC 20052. NIMH,CLIN SCI LAB,GERIATR PSYCHOPHARMACOL UNIT,WASHINGTON,DC 20032. RP WEINBERGER, DR (reprint author), ST ELIZABETH HOSP,NIMH,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. FU NINDS NIH HHS [NS22215] NR 72 TC 130 Z9 132 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD FEB PY 1991 VL 48 IS 2 BP 169 EP 176 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA EX214 UT WOS:A1991EX21400010 PM 1993008 ER PT J AU SEDDON, JM CHRISTEN, WG MANSON, JAE BURING, JE SPERDUTO, RD HENNEKENS, CH AF SEDDON, JM CHRISTEN, WG MANSON, JAE BURING, JE SPERDUTO, RD HENNEKENS, CH TI LOW-DOSE ASPIRIN AND RISKS OF CATARACT IN A RANDOMIZED TRIAL OF US PHYSICIANS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID NUCLEAR AB Observational studies have raised the question of a possible benefit of aspirin on the development of cataract. The Physicians' Health Study, a randomized double-masked placebo-controlled trial among 22 071 male physicians, aged 40 to 84 years, provided the opportunity to collect information about whether low-dose aspirin therapy (325 mg on alternate days) affects the development or extraction of cataract. There were 173 age-related cataracts among those physicians assigned to aspirin therapy and 180 among those given placebo (relative risk, 0.95; 95% confidence interval, 0.74 to 1.22). Cataract extractions were less frequent in the aspirin than in the placebo group, but this difference was not statistically significant (relative risk, 0.80; 95% confidence interval, 0.56 to 1.15). Among younger men (aged 40 to 59 years), the relative risks were 0.62 (95% confidence interval, 0.40 to 0.94) for cataract development and 0.67 (95% confidence interval, 0.38 to 1.31) for cataract extraction. These randomized trial data tend to exclude any large benefit of aspirin. While the overall findings concerning cataract development seem to be null, the data on extraction of age-related cataract, while not statistically significant, cannot exclude a possible small to moderate benefit of alternate-day aspirin therapy on the extraction of age-related cataract. C1 NEI,BETHESDA,MD. MASSACHUSETTS EYE & EAR HOSP,EPIDEMIOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,CHANNING LAB,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PREVENT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA 40360]; NEI NIH HHS [EY 06633]; NHLBI NIH HHS [HL 34595] NR 20 TC 39 Z9 40 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD FEB PY 1991 VL 109 IS 2 BP 252 EP 255 PG 4 WC Ophthalmology SC Ophthalmology GA EX564 UT WOS:A1991EX56400029 PM 1993037 ER PT J AU CHAN, CC NI, M MIELE, L CORDELLAMIELE, E FERRICK, M MUKHERJEE, AB NUSSENBLATT, RB AF CHAN, CC NI, M MIELE, L CORDELLAMIELE, E FERRICK, M MUKHERJEE, AB NUSSENBLATT, RB TI EFFECTS OF ANTIFLAMMINS ON ENDOTOXIN-INDUCED UVEITIS IN RATS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID LIPOCORTIN-I; UTEROGLOBIN; PEPTIDES; REGION AB Antiflammins are phospholipase A2-inhibitory, anti-inflammatory, synthetic oligopeptides derived from the region of the highest amino-acid sequence similarity between uteroglobin and lipocortin I. Endotoxin-induced uveitis is a model for anterior uveitis of the eye, which has been suggested to be induced through phospholipase A2 activation. In a preliminary report we demonstrated that topical administration of antiflammins could inhibit endotoxin-induced uveitis in rats. In this study, the anti-inflammatory effects of antiflammins were compared with those of corticosteroids on endotoxin-induced uveitis as measured by phospholipase A2 enzyme activity, inflammatory cell counts in the aqueous humor, and histopathologic features. Antiflammins are as effective as corticosteroids in their ability to suppress endotoxin-induced uveitis. C1 HOWARD HUGHES MED INST,BETHESDA,MD. NICHHD,HUMAN GENET BRANCH,DEV GENET BRANCH,BETHESDA,MD 20892. RP CHAN, CC (reprint author), NEI,IMMUNOL LAB,BLDG 10,ROOM 10N206,BETHESDA,MD 20892, USA. NR 19 TC 40 Z9 40 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD FEB PY 1991 VL 109 IS 2 BP 278 EP 281 PG 4 WC Ophthalmology SC Ophthalmology GA EX564 UT WOS:A1991EX56400035 PM 1993038 ER PT J AU HENSON, DE AF HENSON, DE TI CANCER-PATIENT STAGING - A PERSPECTIVE SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Editorial Material RP HENSON, DE (reprint author), NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,EXECUT PLAZA N,BETHESDA,MD 20892, USA. NR 5 TC 4 Z9 4 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD FEB PY 1991 VL 115 IS 2 BP 120 EP 121 PG 2 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA EX232 UT WOS:A1991EX23200007 PM 1992975 ER PT J AU ZWEIG, MH CSAKO, G REYNOLDS, JC CARRASQUILLO, JA AF ZWEIG, MH CSAKO, G REYNOLDS, JC CARRASQUILLO, JA TI INTERFERENCE BY IATROGENICALLY INDUCED ANTI-MOUSE IGG ANTIBODIES IN A 2-SITE IMMUNOMETRIC ASSAY FOR THYROTROPIN SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID IMMUNORADIOMETRIC ASSAY; IMMUNOGLOBULIN ANTIBODIES; MONOCLONAL-ANTIBODIES; FACTITIOUS ELEVATION; IMMUNOASSAYS; SPECIFICITY AB Two-site immunometric assays using mouse monoclonal antibodies are gaining increasingly widespread popularity and use. Patients with circulating antimurine immunoglobulin antibodies capable of interfering in these assays have been encountered and described sporadically. Parenteral administration of murine monoclonal antibodies for imaging and therapeutic purposes is increasing and is known to induce human antimurine antibodies frequently. We examined 60 serum samples from 48 individuals who received such murine immunoglobulin to determine whether iatrogenically induced antimurine antibodies could interfere in a two-site (sandwich) immunoradiometric assay for serum thyrotropin. We found that these circulating antibodies can indeed interfere in an "unblocked" assay, but that the interference appears to be suppressed by including nonspecific IgG in the commercial version of the assay kit. C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT NUCL MED,BETHESDA,MD 20892. RP ZWEIG, MH (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,BETHESDA,MD 20892, USA. RI Carrasquillo, Jorge/E-7120-2010 NR 16 TC 4 Z9 4 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD FEB PY 1991 VL 115 IS 2 BP 164 EP 168 PG 5 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA EX232 UT WOS:A1991EX23200018 PM 1992984 ER PT J AU BERLIN, E JUDD, JT NAIR, PP JONES, DY TAYLOR, PR AF BERLIN, E JUDD, JT NAIR, PP JONES, DY TAYLOR, PR TI DIETARY-FAT AND HORMONAL INFLUENCES ON LIPOPROTEIN FLUIDITY AND COMPOSITION IN PREMENOPAUSAL WOMEN SO ATHEROSCLEROSIS LA English DT Article DE DIETARY FAT; HORMONAL INFLUENCE; LIPOPROTEINS; LIPOPROTEIN COMPOSITION; PREMENOPAUSAL WOMEN ID LOW-DENSITY LIPOPROTEIN; ISCHEMIC HEART-DISEASE; RABBIT PLASMA-LIPOPROTEINS; SERUM-LIPOPROTEINS; LIPID FLUIDITY; CHOLESTEROL; ESTROGEN; RATS; TRIGLYCERIDES; MENOPAUSE AB LDL and HDL became more fluid when healthy, free-living, premenopausal women were fed reduced fat diets with higher proportions of polyunsaturated fatty acids. Lipoproteins were isolated from plasma of 31 female subjects fed one of two sets of diets from typical U.S.A. foods with P/S ratios of 0.3 or 1.0. All subjects were fed high-fat diets (40% of energy) for the duration of four menstrual cycles followed by low-fat diets (20% of energy) for the next four cycles. Blood samples were collected during mid-follicular and mid-luteal phases of the fourth menstrual cycle of each diet period to assess interactive dietary and hormonal control of lipoprotein fluidity. LDL was significantly more fluid, as determined by DPH fluorescence, upon reducing fat consumption from 40 to 20% of energy for subjects eating foods with P/S = 1.0 or 0.3. Generally LDL was more fluid during the follicular phase than the luteal phase of the cycles, thus indicating hormonal influences on LDL fluidity. HDL results were similar but not as pronounced as with LDL. Lipoprotein phospholipid (PL) and cholesteryl ester (CE) fatty acyl compositions were also subject to dietary and hormonal influences. Effects were noted in several fatty acids depending upon diet and hormonal state; however, generally diet fat reduction resulted in reduced linoleate and increased oleate contents. Regression analyses showed that fluidity was more dependent upon the lipoprotein cholesterol content than upon fatty acyl composition. C1 NCI,DHHS,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. RP BERLIN, E (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE HUMAN NUTR RES CTR,LIPID NUTR LAB,BLDG 308,ROOM 109,BELTSVILLE,MD 20705, USA. NR 55 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0021-9150 J9 ATHEROSCLEROSIS JI Atherosclerosis PD FEB PY 1991 VL 86 IS 2-3 BP 95 EP 110 DI 10.1016/0021-9150(91)90206-I PG 16 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FC471 UT WOS:A1991FC47100001 PM 1872920 ER PT J AU MUNTANER, C HIGGINS, ST ROACHE, JD HENNINGFIELD, JE AF MUNTANER, C HIGGINS, ST ROACHE, JD HENNINGFIELD, JE TI ETHANOL DECREASES RESPONDING ON BEHAVIOR MAINTAINED UNDER CONCURRENT SCHEDULES OF BOTH POSITIVE REINFORCER PRESENTATION AND AVOIDANCE IN HUMANS SO BEHAVIOURAL PHARMACOLOGY LA English DT Article DE ALCOHOL; HUMANS; CONCURRENT SCHEDULES; AVOIDANCE; OPERANT BEHAVIOR; BEHAVIORAL PHARMACOLOGY; AGGRESSION ID SOCIAL-LEARNING FORMULATIONS; STIMULUS-SHOCK TERMINATION; HUMAN AGGRESSIVE-BEHAVIOR; FOOD PRESENTATION; ALCOHOL-ABUSE; EXPECTANCIES; ACQUISITION; TOLERANCE C1 NIDA,ADDICT RES CTR,CLIN PHARMACOL RES BRANCH,POB 5180,BALTIMORE,MD 21224. UNIV VERMONT,DEPT PSYCHIAT,HUMAN BEHAV PHARMACOL LAB,BURLINGTON,VT 05401. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MENTAL HYG,BALTIMORE,MD 21205. UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,HOUSTON,TX 77030. UNIV TEXAS,HLTH SCI CTR,DEPT BEHAV SCI,HOUSTON,TX 77030. RI Muntaner, C/A-5043-2010 NR 23 TC 1 Z9 1 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0955-8810 J9 BEHAV PHARMACOL JI Behav. Pharmacol. PD FEB PY 1991 VL 2 IS 1 BP 47 EP 56 PG 10 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA FC691 UT WOS:A1991FC69100007 ER PT J AU BIRD, GSJ OLIVER, KG HORSTMAN, DA OBIE, J PUTNEY, JW AF BIRD, GSJ OLIVER, KG HORSTMAN, DA OBIE, J PUTNEY, JW TI RELATIONSHIP BETWEEN THE CALCIUM-MOBILIZING ACTION OF INOSITOL 1,4,5-TRISPHOSPHATE IN PERMEABLE AR4-2J CELLS AND THE ESTIMATED LEVELS OF INOSITOL 1,4,5-TRISPHOSPHATE IN INTACT AR4-2J CELLS SO BIOCHEMICAL JOURNAL LA English DT Article ID PAROTID ACINAR-CELLS; GUINEA-PIG HEPATOCYTES; RADIORECEPTOR ASSAY; RECEPTOR ACTIVATION; PHOSPHATES; CA-2+; METABOLISM; MASS; POLYPHOSPHOINOSITIDES; PHOSPHATIDYLINOSITOL AB Various experimental strategies were employed in an effort to explain the previously reported [Horstman, Takemura & Putney (1988) J. Biol. Chem. 263, 15297-15303] paradoxically high levels of inositol 1,4,5-trisphosphate [(1,4,5)IP3] in resting and substance-P-stimulated AR4-2J cells. The concentration-effect curves for substance-P-induced [H-3](1,4,5)IP3 formation in [H-3]inositol-labelled cells and substance-P-induced increase in intracellular [Ca2+] were essentially superimposable, suggesting that formation of (1,4,5)IP3 is limiting for cellular Ca2+ mobilization. In electrically permeabilized AR4-2J cells, (1,4,5)IP3 and other inositol polyphosphates stimulated Ca2+ release with potencies similar to those reported for other cell types, including the parent pancreatic acinar cell. Compartmentalization of basal (1,4,5)IP3 was suggested by the fact that this material was stable in the presence of antimycin A, although this toxin completely blocked agonist stimulation of phospholipase C. However, subcellular fractionation as well as permeabilization of the cells with Staphylococcus aureus alpha-toxin failed to provide evidence for binding or sequestration of [H-3](1,4,5)IP3 in AR4-2J cells. The density of (1,4,5)IP3 receptors in AR4-2J cells was not sufficiently large to impose non-linearity in the relationship between (1,4,5)IP3 concentration and (1,4,5)IP3-induced Ca2+ release. Thus the apparent high concentrations of (1,4,5)IP3 in resting and stimulated AR4-2J cells are not indicative of atypically low sensitivity or high concentration of (1,4,5)IP3 receptors, nor is there evidence for compartmentalization of (1,4,5)IP3 outside of the cytoplasm in these cells. It is possible that soluble factors in the cytoplasm of AR4-2J cells regulate the free concentration of (1,4,5)IP3 or the sensitivity of receptors to (1,4,5)IP3. C1 NIEHS, CELLULAR & MOLEC PHARMACOL LAB, CALCIUM REGULAT SECT, RES TRIANGLE PK, NC 27709 USA. NR 36 TC 37 Z9 37 U1 0 U2 0 PU PORTLAND PRESS LTD PI LONDON PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND SN 0264-6021 EI 1470-8728 J9 BIOCHEM J JI Biochem. J. PD FEB 1 PY 1991 VL 273 BP 541 EP 546 PN 3 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY139 UT WOS:A1991EY13900007 PM 1705113 ER PT J AU NAKAJIMA, T WANG, RS ELOVAARA, E PARK, SS GELBOIN, HV HIETANEN, E VAINIO, H AF NAKAJIMA, T WANG, RS ELOVAARA, E PARK, SS GELBOIN, HV HIETANEN, E VAINIO, H TI MONOCLONAL ANTIBODY-DIRECTED CHARACTERIZATION OF CYTOCHROME-P450 ISOZYMES RESPONSIBLE FOR TOLUENE METABOLISM IN RAT-LIVER SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID CYTOCHROMES-P-450; BENZENE AB Monoclonal antibodies (MAbs) were used to study the contribution of cytochromes P450IA1/IA2, P450IIB1/IIB2, P450IIC11/IIC6 and P450IIE1 to toluene side-chain (benzyl alcohol, BA, formation) and ring (o- and p-cresol formation) oxidation in liver microsomes from fed, one-day fasted, and phenobarbital (PB)-, 3-methylcholanthrene (MC)- and ethanol-treated rats. All rats were fed synthetic liquid diets. MAb 1-7-1 against P450IA1/IA2 inhibited markedly o-cresol formation and slightly p-cresol formation but not BA formation only in microsomes from MC-treated rats. MAbs 2-66-3, 4-7-1 and 4-29-5 against P450IIB1/IIB2 strongly inhibited BA, o-cresol and p-cresol formation only in PB-induced microsomes. MAb 1-68-11 against P450IIC11/IIC6 inhibited BA formation at high toluene concentration in the following order: fed > fasted > ethanol = MC > PB, and ethanol greater-than-or-equal-to fed = fasted > MC > PB on the basis of the percentage and net amount inhibition, respectively. MAb 1-91-3 against P450IIE1 inhibited BA formation at low toluene concentration, but not at high concentration, in the following order: ethanol > fasted = fed > MC, and ethanol > fasted > fed > MC on the basis of percentage and net inhibition, respectively. MAbs 1-68-11 and 1-91-3 also inhibited p-cresol formation at high and low toluene concentrations, respectively. These results indicate that (i) both P450IIE1 and P450II11/IIC6 are constitutive isozymes mainly responsible for the formation of BA and p-cresol from toluene as low- and high-K(m) isozymes, respectively; (ii) P450IIE1, but not P450IIC11/IIC6, is induced by one-day fasting and ethanol treatment; (iii) both P450IIE1 and P450IIC11/IIC6 are decreased by PB and MC treatments; (iv) P450IIE1 is inhibited by high concentration of toluene; (v) P450IIB1/IIB2 can contribute to the formation of BA, o- and p-cresol from toluene, while P450IAI/IA2 preferentially contributes to the formation of o-cresol. C1 INST OCCUPAT HLTH,DEPT IND HYG & TOXICOL,SF-00250 HELSINKI,FINLAND. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. INT AGCY RES CANC,F-69372 LYONS,FRANCE. RP NAKAJIMA, T (reprint author), SHINSHU UNIV,SCH MED,DEPT HYG,MATSUMOTO,NAGANO 390,JAPAN. NR 21 TC 77 Z9 79 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 FEB 1 PY 1991 VL 41 IS 3 BP 395 EP 404 DI 10.1016/0006-2952(91)90536-E PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EX838 UT WOS:A1991EX83800010 PM 1994898 ER PT J AU KOCER, Z RAUNIO, H PASANEN, M ARVELA, P RAISKILA, T HONKAKOSKI, P LANG, MA NEGISHI, M PELKONEN, O AF KOCER, Z RAUNIO, H PASANEN, M ARVELA, P RAISKILA, T HONKAKOSKI, P LANG, MA NEGISHI, M PELKONEN, O TI COMPARISON BETWEEN COBALT AND PYRAZOLE IN THE INCREASED EXPRESSION OF COUMARIN 7-HYDROXYLASE IN MOUSE-LIVER SO BIOCHEMICAL PHARMACOLOGY LA English DT Note ID SEX-DEPENDENT EXPRESSION; STEROID 15-ALPHA-HYDROXYLASE; II P-45015-ALPHA; MICE; GENE; INDUCTION; REGIOSELECTIVITY; PURIFICATION; METABOLISM; MODIFIER C1 UNIV KUOPIO,DEPT PHARMACOL & TOXICOL,SF-70211 KUOPIO,FINLAND. NIEHS,REPROD & DEV TOXICOL LAB,PHARMACOGENET SECT,RES TRIANGLE PK,NC 27709. UNIV ANKARA,FAC PHARM,DEPT BIOCHEM,ANKARA,TURKEY. RP KOCER, Z (reprint author), UNIV OULU,DEPT PHARMACOL & TOXICOL,SF-90220 OULU,FINLAND. RI Lang, Matti/C-9948-2009; OI Honkakoski, Paavo/0000-0002-4332-3577 NR 24 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 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD FEB 1 PY 1991 VL 41 IS 3 BP 462 EP 465 DI 10.1016/0006-2952(91)90547-I PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EX838 UT WOS:A1991EX83800021 PM 1994904 ER PT J AU FISHEL, R DERBYSHIRE, MK MOORE, SP YOUNG, CSH AF FISHEL, R DERBYSHIRE, MK MOORE, SP YOUNG, CSH TI BIOCHEMICAL-STUDIES OF HOMOLOGOUS AND NONHOMOLOGOUS RECOMBINATION IN HUMAN-CELLS SO BIOCHIMIE LA English DT Article; Proceedings Paper CT MEETING ON REC A AND RELATED PROTEINS : FROM RECOMBINATION TO SOS FUNCTIONS CY SEP 17-21, 1990 CL SACLAY, FRANCE SP CNRS, DEPT BIOL, DUPONT, EUROPEAN DNA REPAIR NETWORK, LIGUE CONTRE CANC, MINIST RECH & TECHNOL FRANCE, TOXICOL GENET, NATL SCI FDN, TRANSGENE, US BIOCHEM DE MAMMALIAN RECOMBINATION; END JOINING; GENE TARGETING; REPLICATION; STRAND EXCHANGE ID DNA-BINDING-PROTEIN; SINGLE-STRANDED-DNA; SACCHAROMYCES-CEREVISIAE; PURIFICATION; REPLICATION; EXCHANGE; INVITRO; ATP AB Purified and partially purified protein fractions from human cells have been developed that promote homologous and nonhomologous recombination reactions in vitro. Homologous pairing of model DNA substrates is catalyzed by the homologous pairing protein HPP-1 in a magnesium-dependent, ATP-independent reaction that requires stoichiometric amounts of the protein. Addition of the human single-strand binding (SSB) holoprotein complex hRP-A reduces the requirement of HPP-1 in the reaction up to 20-fold. Although the combination of homologous pairing and SSB activities is similar to the bacterial strand-exchange process, the numbers, size, and requirements of the human reaction appear to preclude any detailed comparisons. We have used Z-DNA affinity chromatography as a major step in isolation of human recombination proteins and found that the activities appear to elute as a complex form in approximate multiples of 500 kDa. Associated with the homologous recombination complex is a potent blunt-end ligation activity that appears to mimic the nonhomologous joining functions that are frequently seen following transfection of DNA into mammalian cells. A simple scheme for the association of homologous and nonhomologous recombination functions in mammalian cells is discussed. C1 COLUMBIA UNIV,DEPT MICROBIOL,NEW YORK,NY 10032. RP FISHEL, R (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHROMOSOME BIOL LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101]; NIGMS NIH HHS [GM31452] NR 33 TC 17 Z9 17 U1 0 U2 1 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0300-9084 J9 BIOCHIMIE JI Biochimie PD FEB-MAR PY 1991 VL 73 IS 2-3 BP 257 EP 267 DI 10.1016/0300-9084(91)90211-I PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP161 UT WOS:A1991FP16100017 PM 1653033 ER PT J AU LESEM, MD BERRETTINI, WH KAYE, WH JIMERSON, DC AF LESEM, MD BERRETTINI, WH KAYE, WH JIMERSON, DC TI MEASUREMENT OF CSF DYNORPHIN-A-1-8 IMMUNOREACTIVITY IN ANOREXIA-NERVOSA AND NORMAL-WEIGHT BULIMIA SO BIOLOGICAL PSYCHIATRY LA English DT Article ID HUMAN CEREBROSPINAL-FLUID; BETA-ENDORPHIN; FOOD-INTAKE; OPIOID-PEPTIDES; EATING BEHAVIOR; RAT-BRAIN; NALOXONE; RECEPTOR AB Twenty-one patients with anorexia nervosa and 35 normal-weight patients with bulimia underwent a series of CSF studies involving measurement of CSF dynorphin A 1-8 immunoreactivity during hospitalization in an eating-disorder treatment and research program. The control group consisted of 17 healthy volunteers. There were no statistically significant differences in CSF dynorphin A 1-8 measurements among groups or within a group at various stages of treatment. These results regarding dynorphin A 1-8 immunoreactivity are discussed in light of other evidence for altered opiate function in some eating-disorder patients. C1 UNIV PITTSBURGH,DEPT PSYCHIAT,EATING DISORDERS PROGRAM,PITTSBURGH,PA 15260. BETH ISRAEL HOSP,DEPT PSYCHIAT,BOSTON,MA 02215. NIH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. RP LESEM, MD (reprint author), HARRIS CTY PSYCHIAT CTR,DEPT PSYCHIAT,2800 S MACGREGOR WAY,HOUSTON,TX 77021, USA. NR 29 TC 18 Z9 18 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD FEB 1 PY 1991 VL 29 IS 3 BP 244 EP 252 DI 10.1016/0006-3223(91)91286-Z PG 9 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA EX037 UT WOS:A1991EX03700006 PM 1673064 ER PT J AU RUDORFER, MV RISBY, ED OSMAN, OT GOLD, PW POTTER, WZ AF RUDORFER, MV RISBY, ED OSMAN, OT GOLD, PW POTTER, WZ TI HYPOTHALAMIC PITUITARY-ADRENAL AXIS AND MONOAMINE TRANSMITTER ACTIVITY IN DEPRESSION - A PILOT-STUDY OF CENTRAL AND PERIPHERAL EFFECTS OF ELECTROCONVULSIVE-THERAPY SO BIOLOGICAL PSYCHIATRY LA English DT Article ID CORTICOTROPIN-RELEASING-FACTOR; FACTOR-LIKE IMMUNOREACTIVITY; URINARY FREE CORTISOL; CEREBROSPINAL-FLUID; ELECTROCHEMICAL DETECTION; CSF; PLASMA; NOREPINEPHRINE; METABOLITES; HORMONE AB Central and peripheral measures of hypothalamic-pituitary-adrenal (HPA) axis and monoamine neurotransmitter activity were assessed in 8 depressed patients during a medication-free period and again after completion of a course of electroconvulsive therapy (ECT). Seven patients responded fully to ECT. At baseline there was corresponding activation of the HPA and noradrenergic systems, with apparent elevation in cerebrospinal fluid (CSF) concentrations of corticotropin-releasing hormone (CRH) in some patients. Neither CRH nor adrenocorticotropin (ACTH) in CSF changed significantly after ECT, with a mean 10% decline in CSF CRH. Urinary free cortisol (UFC) excretion was high both before and after treatment. Although peripheral noradrenergic hyperreactivity at baseline appeared to normalize with ECT, CSF concentrations of the principal norepinephrine metabolite, 3-methoxy-4-hydroxyphenyl-glycol (MHPG) were unaffected and remained correlated with CSF CRH. In contrast, there were increases in the CSF levels of the main metabolite of serotonin in half the patients. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RP RUDORFER, MV (reprint author), NIMH,CLIN NEUROSCI BRANCH,CLIN PHARMACOL SECT,BLDG 10,ROOM 2D46,BETHESDA,MD 20892, USA. NR 29 TC 27 Z9 27 U1 4 U2 5 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD FEB 1 PY 1991 VL 29 IS 3 BP 253 EP 264 DI 10.1016/0006-3223(91)91287-2 PG 12 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA EX037 UT WOS:A1991EX03700007 PM 1707686 ER PT J AU LAWLOR, BA NEWHOUSE, PA BALKIN, TJ MOLCHAN, SE MELLOW, AM MURPHY, DL SUNDERLAND, T AF LAWLOR, BA NEWHOUSE, PA BALKIN, TJ MOLCHAN, SE MELLOW, AM MURPHY, DL SUNDERLAND, T TI A PRELIMINARY-STUDY OF THE EFFECTS OF NIGHTTIME ADMINISTRATION OF THE SEROTONIN AGONIST, M-CPP, ON SLEEP ARCHITECTURE AND BEHAVIOR IN HEALTHY-VOLUNTEERS SO BIOLOGICAL PSYCHIATRY LA English DT Article ID SLOW-WAVE SLEEP; META-CHLOROPHENYLPIPERAZINE; NEURO-ENDOCRINE; 5-HT2 RECEPTORS; HUMAN-BRAIN; ANTAGONIST; TRAZODONE; SITES; RATS; MCPP AB The effects of m-chlorophenylpiperazine (m-CPP) (0.5 mg/kg) on sleep architecture and behavior were examined in six healthy volunteers following a single oral dose of the drug in a randomized, double-blind, placebo-controlled study. m-CPP reduced total sleep time (TST) and sleep efficiency in all subjects. Slow-wave sleep (SWS) and rapid-eye-movement (REM) sleep were decreased and stage 1 sleep was prolonged in a majority of subjects. Prominent behavioral and psychological effects were reported in five out of six subjects following m-CPP (but not following placebo) that interfered with sleep. The sleep disruption and behavioral activation following nighttime administration of m-CPP contrasts with the sedative properties of its parent compound, trazodone, suggesting that the hypnotic effect of trazodone is not related to the agonist profile of its metabolite, m-CPP. C1 WALTER REED ARMY MED CTR,DEPT BEHAV BIOL,WASHINGTON,DC 20307. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. UNIV MICHIGAN,DEPT PSYCHIAT,ANN ARBOR,MI 48109. UNIV VERMONT,COLL MED,DEPT PSYCHIAT,NEUROSCI RES UNIT,BURLINGTON,VT. RP LAWLOR, BA (reprint author), CUNY MT SINAI SCH MED,DEPT PSYCHIAT,DIV GERIATR PSYCHIAT,1 GUSTAVE L LEVY PL,NEW YORK,NY 10029, USA. RI Newhouse, Paul/J-4597-2014 NR 26 TC 42 Z9 44 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD FEB 1 PY 1991 VL 29 IS 3 BP 281 EP 286 DI 10.1016/0006-3223(91)91290-8 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA EX037 UT WOS:A1991EX03700010 PM 2015332 ER PT J AU CASANOVA, MF AF CASANOVA, MF TI BASAL GANGLIA MINERALIZATION IN SCHIZOPHRENIA - RESPONSE SO BIOLOGICAL PSYCHIATRY LA English DT Letter RP CASANOVA, MF (reprint author), NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,WASHINGTON,DC 20032, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD FEB 1 PY 1991 VL 29 IS 3 BP 297 EP 297 DI 10.1016/0006-3223(91)91295-3 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA EX037 UT WOS:A1991EX03700015 ER PT J AU SHEA, C WILLIAMSON, JC AF SHEA, C WILLIAMSON, JC TI A FLUOROMETRIC MICROTITER ASSAY FOR THE RAPID ENUMERATION OF ADHERENT BACTERIA SO BIOTECHNIQUES LA English DT Note C1 NCI,FREDERICK & CANC RES FACIL,PROGRAM RESOURCES INC,CELL & MOLEC STRUCT LAB,FREDERICK,MD 21702. RP SHEA, C (reprint author), UNIV ALABAMA,DEPT MICROBIOL,BOX 870334,TUSCALOOSA,AL 35487, USA. NR 2 TC 2 Z9 2 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 FEB PY 1991 VL 10 IS 2 BP 177 EP 177 PG 1 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX833 UT WOS:A1991EX83300009 PM 1711870 ER PT J AU BRUGGEMANN, EP CHAUDHARY, V GOTTESMAN, MM PASTAN, I AF BRUGGEMANN, EP CHAUDHARY, V GOTTESMAN, MM PASTAN, I TI PSEUDOMONAS EXOTOXIN FUSION PROTEINS ARE POTENT IMMUNOGENS FOR RAISING ANTIBODIES AGAINST P-GLYCOPROTEIN SO BIOTECHNIQUES LA English DT Article ID ESCHERICHIA-COLI; MULTIDRUG RESISTANCE; GLUTAMIC ACID-553; RNA-POLYMERASE; ACTIVE-SITE; DOMAIN-II; EXPRESSION; AERUGINOSA; GENE; CELLS AB Antibodies to specific regions of human P-glycoprotein have been difficult to obtain. We developed a method to express in E. coli fusions between Pseudomonas exotoxin and specific regions of human P-glycoprotein. We used the polymerase chain reaction to amplify the desired regions of MDR1 cDNA and to introduce appropriate restriction sites. These fragments were cloned into the 3' end of the Pseudomonas exotoxin gene. With this system we produced large amounts of fusion proteins for immunizations, and we obtained positive rabbit antiserum against P-glycoprotein with most of these antigens. We now have a comprehensive panel of polyclonal antibodies against P-glycoprotein. This system should be generally useful to raise antibodies against other eukaryotic proteins that are difficult to prepare in large quantities. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 44 TC 43 Z9 43 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 FEB PY 1991 VL 10 IS 2 BP 202 EP 209 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EX833 UT WOS:A1991EX83300018 PM 1676289 ER PT J AU WIEDER, R CORNETTA, K KESSLER, SW ANDERSON, WF AF WIEDER, R CORNETTA, K KESSLER, SW ANDERSON, WF TI INCREASED EFFICIENCY OF RETROVIRAL-MEDIATED GENE-TRANSFER AND EXPRESSION IN PRIMATE BONE-MARROW PROGENITORS AFTER 5-FLUOROURACIL INDUCED HEMATOPOIETIC SUPPRESSION AND RECOVERY SO BLOOD LA English DT Article ID HUMAN ADENOSINE-DEAMINASE; COLONY-FORMING CELLS; STEM-CELLS; ANTIGEN EXPRESSION; GENERATION-AGE; DNA-SYNTHESIS; W/WV MICE; VIRAL-DNA; MOUSE; VIRUS C1 NHLBI,MOLEC HEMATOL BRANCH,BLDG 10,ROOM 7D18,BETHESDA,MD 20892. USN,MED RES INST,DEPT IMMUNOBIOL & TRANSPLANTAT,BETHESDA,MD 20814. NR 46 TC 28 Z9 28 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 FEB 1 PY 1991 VL 77 IS 3 BP 448 EP 455 PG 8 WC Hematology SC Hematology GA EV332 UT WOS:A1991EV33200004 PM 1846760 ER PT J AU DICHEK, DA NUSSBAUM, O DEGEN, SJF ANDERSON, WF AF DICHEK, DA NUSSBAUM, O DEGEN, SJF ANDERSON, WF TI ENHANCEMENT OF THE FIBRINOLYTIC-ACTIVITY OF SHEEP ENDOTHELIAL-CELLS BY RETROVIRAL VECTOR-MEDIATED GENE-TRANSFER SO BLOOD LA English DT Article ID TISSUE PLASMINOGEN-ACTIVATOR; ADENOSINE-DEAMINASE; MONOCLONAL-ANTIBODY; RAPID INHIBITOR; FACTOR-IX; THERAPY; EXPRESSION; SECRETION; RELEASE; PA C1 UNIV CINCINNATI,CHILDRENS HOSP,RES FDN,DEPT PEDIAT,CINCINNATI,OH 45221. RP DICHEK, DA (reprint author), NHLBI,MOLEC HEMATOL BRANCH,BLDG 10,ROOM 7D-18,BETHESDA,MD 20892, USA. NR 59 TC 42 Z9 43 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 FEB 1 PY 1991 VL 77 IS 3 BP 533 EP 541 PG 9 WC Hematology SC Hematology GA EV332 UT WOS:A1991EV33200016 PM 1899348 ER PT J AU SCHWAB, G SIEGALL, CB AARDEN, LA NECKERS, LM NORDAN, RP AF SCHWAB, G SIEGALL, CB AARDEN, LA NECKERS, LM NORDAN, RP TI CHARACTERIZATION OF AN INTERLEUKIN-6-MEDIATED AUTOCRINE GROWTH LOOP IN THE HUMAN MULTIPLE-MYELOMA CELL-LINE, U266 SO BLOOD LA English DT Article ID STIMULATORY FACTOR-II; MESSENGER-RNA; COMPLEMENTARY-DNA; DIFFERENTIATION; INTERLEUKIN-HP1; EXPRESSION; INVITRO; ACID; PLASMACYTOMAS; PROLIFERATION C1 NCI,MED BRANCH,TUMOR CELL BIOL SECT,BETHESDA,MD 20892. NETHERLANDS RED CROSS,BLOOD TRANSFUS SERV,CENT LAB,AMSTERDAM,NETHERLANDS. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 40 TC 158 Z9 160 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 1 PY 1991 VL 77 IS 3 BP 587 EP 593 PG 7 WC Hematology SC Hematology GA EV332 UT WOS:A1991EV33200022 PM 1991169 ER PT J AU COHEN, LG MEER, J TARKKA, I BIERNER, S LEIDERMAN, DB DUBINSKY, RM SANES, JN JABBARI, B BRANSCUM, B HALLETT, M AF COHEN, LG MEER, J TARKKA, I BIERNER, S LEIDERMAN, DB DUBINSKY, RM SANES, JN JABBARI, B BRANSCUM, B HALLETT, M TI CONGENITAL MIRROR MOVEMENTS - ABNORMAL ORGANIZATION OF MOTOR PATHWAYS IN 2 PATIENTS SO BRAIN LA English DT Article ID SOMATOSENSORY EVOKED-POTENTIALS; CORTICAL POTENTIALS; INTACT MAN; HYPOGONADOTROPIC HYPOGONADISM; TRANSCRANIAL STIMULATION; ELECTRICAL-STIMULATION; CEREBRAL POTENTIALS; CORTEX STIMULATION; VERTEBRAL ARTERY; FINGER MOVEMENTS AB We studied 2 patients with congenital mirror movements by means of various neurophysiological and metabolic techniques, including mapping of motor evoked potentials to transcranial electrical and magnetic stimulation, premovement and somatosensory evoked potentials, kinematics of voluntary movements, muscle reflexes, and positron emission tomography (PET). Abnormalities in maps of motor and premovement potentials and in PET scans were consistent with a bilateral representation of hand muscles in the motor cortex, the existence of physiologically active connections capable of conducting fast efferent volleys from the motor cortex to ipsilateral muscles, the presence of mirror EMG activity in either hand with intended voluntary movement of the other hand, the absence of mirrored EMG responses from wrist flexors and extensors to mechanical perturbation of the contralateral wrist, and normal scalp distribution of somatosensory evoked potentials to right and left median nerve stimulation. Our findings are consistent with aberrant organization of motor representation areas and corticospinal pathways with ipsilateral as well as contralateral control of voluntary movement. RP COHEN, LG (reprint author), NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BLDG 10,ROOM 5N226,BETHESDA,MD 20892, USA. NR 81 TC 120 Z9 126 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 FEB PY 1991 VL 114 BP 381 EP 403 DI 10.1093/brain/114.1.381 PN 1B PG 23 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FC628 UT WOS:A1991FC62800003 PM 2004248 ER PT J AU COHEN, LG BANDINELLI, S FINDLEY, TW HALLETT, M AF COHEN, LG BANDINELLI, S FINDLEY, TW HALLETT, M TI MOTOR REORGANIZATION AFTER UPPER LIMB AMPUTATION IN MAN - A STUDY WITH FOCAL MAGNETIC STIMULATION SO BRAIN LA English DT Article ID CORTICOSPINAL AXONS; NERVE INJURY; HUMAN-BRAIN; CORTEX; REPRESENTATION; ADULT; ORGANIZATION; MUSCLES; RATS; PATTERNS AB To evaluate reorganization in motor pathways following amputation, we studied motor evoked potentials (MEPs) to transcranial magnetic stimulation in 7 patients with unilateral upper limb amputations, a patient with congenital absence of a hand, and 10 normal subjects. Electromyographic recordings were made from biceps and deltoid muscles immediately proximal to the stump and the same contralateral muscles. Magnetic stimulation was delivered by a Cadwell MES-10 magnetic stimulator through a 'figure eight' magnetic coil over scalp positions separated by 1-2.5 cm. Maximal M responses were elicited by peripheral nerve stimulation at Erb's point. The amplitude of MEPs was expressed both as absolute values and as a percentage of maximal responses to peripheral nerve stimulation. Threshold for activation of muscles ipsilateral and contralateral to the stump and the region of excitable scalp positions were also determined in 7 patients. Magnetic scalp stimulation induced a sensation of movement in the missing hand or fingers in the patients with acquired amputation, but failed to do so in the patient with congenital absence of a limb. It evoked larger MEPs, recruited a larger percentage of the motoneuron pool, and elicited MEPs at lower intensities of stimulation in muscles ipsilateral to the stump than in contralateral muscles. Muscles ipsilateral to the stump could be activated from a larger area than those contralateral to the stump. These results are compatible with cortical or spinal reorganization in adult human motor pathways targeting muscles proximal to the stump after amputations. C1 KESSLER INST REHABIL,W ORANGE,NJ. RP COHEN, LG (reprint author), NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,HUMAN CORTICAL PHYSIOL UNIT,BLDG 10,BETHESDA,MD 20892, USA. NR 54 TC 389 Z9 393 U1 1 U2 12 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 FEB PY 1991 VL 114 BP 615 EP 627 DI 10.1093/brain/114.1.615 PN 1B PG 13 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FC628 UT WOS:A1991FC62800017 PM 2004259 ER PT J AU SIRIGU, A GRAFMAN, J BRESSLER, K SUNDERLAND, T AF SIRIGU, A GRAFMAN, J BRESSLER, K SUNDERLAND, T TI MULTIPLE REPRESENTATIONS CONTRIBUTE TO BODY KNOWLEDGE PROCESSING - EVIDENCE FROM A CASE OF AUTOTOPAGNOSIA SO BRAIN LA English DT Article ID PARTS; LOCALIZATION AB Body schema disturbances were studied in a 62-yr-old woman with Alzheimer's disease. She was severely impaired in verbal and nonverbal tasks requiring her to localize body parts (on her own body, the examiner's body or a doll's body) even though she correctly named the same parts when pointed at by the examiner. Pointing responses were misdirected mainly to parts contiguous with the target area and, to a lesser extent, to functionally equivalent body parts. We also found that the patient was able to define body part names functionally but not spatially. In another series of tasks, and in contrast to the above results, performances were normal when small objects, attached to the patient's body, served as pointing targets. Furthermore, on subsequent testing she pointed correctly at the remembered position of these objects. The fact that the same point in 'body space' is localized correctly when it corresponds to an external object and erroneously when it corresponds to a body part contradicts the idea of the body schema as a unitary function. Learning the position of objects on the body surface requires access to some form of body-reference system on which this information can be mapped. We argue that such a system can be available in autotopagnosia and is independent from the visuospatial representations of the body structure that are postulated to be damaged or inaccessible in this syndrome. An integrated account of the present results and of those reported by other authors suggests that multiple levels of representation (e.g., sensorimotor, visuospatial, semantic) are involved in the organization of body knowledge. C1 NIMH,GERIATR PSYCHOPHARMACOL UNIT,BETHESDA,MD 20892. RP SIRIGU, A (reprint author), NINCDS,COGNIT NEUROSCI SECT,BLDG 10,ROOM 5C422,BETHESDA,MD 20892, USA. OI Grafman, Jordan H./0000-0001-8645-4457 NR 13 TC 154 Z9 156 U1 1 U2 14 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 FEB PY 1991 VL 114 BP 629 EP 642 DI 10.1093/brain/114.1.629 PN 1B PG 14 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FC628 UT WOS:A1991FC62800018 PM 2004260 ER PT J AU RICHFIELD, EK AF RICHFIELD, EK TI QUANTITATIVE AUTORADIOGRAPHY OF THE DOPAMINE UPTAKE COMPLEX IN RAT-BRAIN USING [H-3] GBR-12935 - BINDING CHARACTERISTICS SO BRAIN RESEARCH LA English DT Article DE DOPAMINE TRANSPORTER; QUANTITATIVE AUTORADIOGRAPHY; COCAINE RECEPTOR; DOPAMINE LESION; BINDING PARAMETER; DOPAMINE UPTAKE PHARMACOLOGY ID CENTRAL NERVOUS-SYSTEM; H-3 COCAINE BINDING; TRANSPORT COMPLEX; NONHUMAN-PRIMATES; UPTAKE SITES; UPTAKE INHIBITOR; CEREBRAL-CORTEX; CAUDATE-PUTAMEN; INVIVO BINDING; MOUSE STRIATUM AB The dopamine uptake complex was examined in the rat central nervous system using [H-3]GBR 12935 and in vitro quantitative autoradiography to determine all binding data. [H-3]GBR 12935 labels two unique binding sites, the dopamine uptake complex and a piperazine acceptor site. These two sites differ in their pharmacologic properties, anatomical distributions, densities, and response to lesions. Using appropriate binding conditions, [H-3]GBR 12935 can be used to specifically label the dopamine uptake complex. [H-3]GBR 12935 labeled a single binding site with characteristics of the dopamine uptake complex when mazindol (25-mu-M) was used as a blank. The specific binding and autoradiographic appearance of [H-3]GBR 12935 to the dopamine uptake complex was improved by including trans-flupentixol (0.75-mu-M) to displace binding to a previously described piperazine acceptor site, recently determined to be a site on cytochrome P450IID1. Binding was saturable and reversible to the dopamine uptake complex. The equilibrium dissociation constant (1.4 +/- 0.7 nM), maximal number of binding sites (6.0 +/- 1.3 pmol/mg protein), and Hill coefficient (1.1 +/- 0.1) of [H-3]GBR 12935 in rat striatum using mazindol to define non-specific binding was not significantly altered by the inclusion of trans-flupentixol (0.75-mu-M). Using GBR 12909 as a blank produced a greater maximal number of binding sites (8.4 +/- 2.3 pmol/mg protein), but no significant difference in the equilibrium dissociation constant (1.6 +/- 0.3 nM) or Hill coefficient (1.1 +/- 0.1). A series of drugs that bind to the dopamine uptake complex displaced [H-3]GBR 12935 in a rank order consistent with other binding and behavioral studies of this complex. The rank order of these drugs was GBR 12909 > mazindol > nomifensine > benztropine > desipramine > amphetamine > dopamine; all these drugs displayed a Hill coefficient near one and were best modeled as a single site. Cocaine and WIN 35,428 (a cocaine congener) were unique in their competition for [H-3]GBR 12935 binding, displaying biphasic curves, low Hill coefficients, and were best modeled as two site fits. Lesioning of the dopaminergic median forebrain bundle resulted in a dramatic loss of the dopamine uptake complex in the striatum, nucleus accumbens, olfactory tubercle, and substantia nigra. Other dopaminergic projection areas were decreased to a lesser extent. Striatal ibotenate lesions did not decrease the density of the dopamine uptake complex, despite a large decrease in the dopamine D1 receptor. [H-3]GBR 12935 can be used as an effective ligand to label the dopamine uptake complex for quantitative autoradiographic studies. It offers a number of advantages over previous autoradiographic assays for this complex including high specificity (> 95% specific binding in rat striatum), high sensitivity (detection of mazindol displaceable sites in the cerebral cortex), low background (comparable to film background), and low cost. This assay also supports the existence of two binding sites for cocaine on the dopamine uptake complex. The exact nature and differences between these two cocaine sites remains to be determined. C1 NIMH,FUNCT NEUROANAT UNIT,BETHESDA,MD 20892. RP RICHFIELD, EK (reprint author), UNIV ROCHESTER,MONROE COMMUNITY HOSP,NEUROL UNIT,435 E HENRIETTA RD,ROCHESTER,NY 14620, USA. NR 60 TC 71 Z9 72 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 FEB 1 PY 1991 VL 540 IS 1-2 BP 1 EP 13 DI 10.1016/0006-8993(91)90486-F PG 13 WC Neurosciences SC Neurosciences & Neurology GA EY794 UT WOS:A1991EY79400001 PM 1829013 ER PT J AU WOZNIAK, KM PERT, A MELE, A LINNOILA, M AF WOZNIAK, KM PERT, A MELE, A LINNOILA, M TI FOCAL APPLICATION OF ALCOHOLS ELEVATES EXTRACELLULAR DOPAMINE IN RAT-BRAIN - A MICRODIALYSIS STUDY SO BRAIN RESEARCH LA English DT Article DE ETHANOL; DOPAMINE; CORPUS STRIATUM; NUCLEUS ACCUMBENS; MICRODIALYSIS ID FREELY MOVING RATS; ETHANOL-INDUCED STIMULATION; SYNAPTOSOMAL CALCIUM-UPTAKE; STRIATAL DOPAMINE; NEUROTRANSMITTER RELEASE; HIPPOCAMPAL-NEURONS; MESOLIMBIC SYSTEM; NUCLEUS ACCUMBENS; SUBSTANTIA-NIGRA; CAUDATE-NUCLEUS AB Dopaminergic systems are thought to play a major role in the stimulant and reinforcing properties of drugs of abuse, including ethanol. The present study describes the effects of local perfusion with ethanol (and other alcohols) on extracellular dopamine in the striatum and nucleus accumbens. Following the establishment of basal dopamine levels (2-3 h), various concentrations of ethanol in artificial CSF (0.01-10% v/v) were slowly perfused through a microdialysis probe. Each dose of ethanol was found to increase dopamine concentrations in both the striatum and nucleus accumbens. This increase was dose-related in the striatum. The exclusion of calcium and inclusion of 12.5 mM magnesium in the perfusion medium prevented, or greatly attenuated the ethanol-induced dopamine (DA) release. Thus, the release of DA by ethanol is exocytotic in nature and involves calcium-dependent processes. The other alcohols tested, namely methanol and butanol, demonstrated a structure-activity relationship together with ethanol, in their ability to increase extracellular DA. The relative potency was butanol > ethanol > methanol. The diffusion of ethanol into the brain tissue was investigated following perfusion through the probe. Relatively low concentrations of ethanol were found in striatal tissue during perfusion and they declined rapidly with time, following the removal of ethanol from the perfusate. The concentrations of ethanol achieved in brain tissue following focal application through the microdialysis probe were relevant to human intoxication. C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. RP WOZNIAK, KM (reprint author), NIAAA,DICBR,CLIN STUDIES LAB,BLDG 10-3B19,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Mele, Andrea/E-7741-2015 NR 76 TC 137 Z9 137 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 FEB 1 PY 1991 VL 540 IS 1-2 BP 31 EP 40 DI 10.1016/0006-8993(91)90489-I PG 10 WC Neurosciences SC Neurosciences & Neurology GA EY794 UT WOS:A1991EY79400004 PM 2054625 ER PT J AU ZHANG, WQ HUDSON, PM SOBOTKA, TJ HONG, JS TILSON, HA AF ZHANG, WQ HUDSON, PM SOBOTKA, TJ HONG, JS TILSON, HA TI EXTRACELLULAR CONCENTRATIONS OF AMINO-ACID TRANSMITTERS IN VENTRAL HIPPOCAMPUS DURING AND AFTER THE DEVELOPMENT OF KINDLING SO BRAIN RESEARCH LA English DT Note DE KINDLING; VENTRAL HIPPOCAMPUS; BRAIN DIALYSIS; AMINO ACID ID PREPYRIFORM CORTEX; NMDA RECEPTORS; GRANULE CELLS; ASPARTATE; RELEASE; RATS; ANTAGONISTS; GLUTAMATE; SEIZURE; STIMULATION AB This study examined the possible involvement of amino acid release from ventral hippocampus in the establishment and maintenance of kindling in rats. Release of amino acids from ventral hippocampus was measured by microdialysis coupled with high-performance liquid chromatography. Samples were obtained by microdialysis perfusion of freely moving animals receiving deep prepiriform cortex (DPC) electrical stimulation. Samples of perfusate were collected before, during and after kindling was established. DPC kindling stimulation significantly increased concentrations of glutamate (Glu) and glycine (Gly) in perfusate from ventral hippocampus during kindling. Increased basal release of Glu was evident up to 30 days after the last electrical stimulation. We conclude that release of Glu and Gly in the ventral hippocampus may play an important role during establishment, but not in maintenance of kindling. C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,POB 12233,RES TRIANGLE PK,NC 27709. US FDA,WASHINGTON,DC 20204. NR 37 TC 48 Z9 49 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 FEB 1 PY 1991 VL 540 IS 1-2 BP 315 EP 318 DI 10.1016/0006-8993(91)90527-3 PG 4 WC Neurosciences SC Neurosciences & Neurology GA EY794 UT WOS:A1991EY79400042 PM 1675918 ER PT J AU GOZES, Y BRENNEMAN, DE FRIDKIN, M ASOFSKY, R GOZES, I AF GOZES, Y BRENNEMAN, DE FRIDKIN, M ASOFSKY, R GOZES, I TI A VIP ANTAGONIST DISTINGUISHES VIP RECEPTORS ON SPINAL-CORD CELLS AND LYMPHOCYTES SO BRAIN RESEARCH LA English DT Note DE VASOACTIVE INTESTINAL PEPTIDE; SPINAL CORD CELL CULTURE; LYMPHOCYTE; VASOACTIVE INTESTINAL RECEPTOR; VASOACTIVE INTESTINAL PEPTIDE RECEPTOR ANTAGONIST ID VASOACTIVE INTESTINAL PEPTIDE; T-CELLS; LYMPHOBLASTS; POLYPEPTIDE; AFFINITY; BINDING AB Vasoactive intestinal peptide (VIP) is a neuropeptide which also interacts with cells of the immune system. The paucity of specific VIP receptor antagonists has hampered studies of possible receptor heterogeneity and of VIP function. To aid in achieving these goals, a new VIP antagonist, a hybrid between neurotensin and VIP, has been synthesized. This peptide interacted with VIP receptors on spinal cord cells with an affinity 10-fold greater than VIP itself. In contrast, 1000-fold higher concentrations of the antagonist were required to displace labeled VIP from its receptor on lymphoid cells as compared to VIP itself, suggesting VIP receptor heterogeneity between immune and spinal cord cells. C1 NICHHD,DEV NEUROBIOL LAB,NEUROCHEM UNIT,BLDG 36,ROOM 2A21,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. ISRAEL INST BIOL RES,IL-70450 NESS ZIONA,ISRAEL. WEIZMANN INST SCI,DEPT ORGAN CHEM,IL-76100 REHOVOT,ISRAEL. TEL AVIV UNIV,SACKLER SCH MED,DEPT CHEM PATHOL,TEL AVIV,ISRAEL. NR 15 TC 61 Z9 61 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 FEB 1 PY 1991 VL 540 IS 1-2 BP 319 EP 321 DI 10.1016/0006-8993(91)90528-4 PG 3 WC Neurosciences SC Neurosciences & Neurology GA EY794 UT WOS:A1991EY79400043 PM 1647246 ER PT J AU SAITO, K LACKNER, A MARKEY, SP HEYES, MP AF SAITO, K LACKNER, A MARKEY, SP HEYES, MP TI CEREBRAL-CORTEX AND LUNG INDOLEAMINE-2,3-DIOXYGENASE ACTIVITY IS INCREASED IN TYPE-D RETROVIRUS INFECTED MACAQUES SO BRAIN RESEARCH LA English DT Note DE INDOLEAMINE-2,3-DIOXYGENASE; CEREBRAL CORTEX; LUNG; EXCITOTOXIN; TYPE-D RETROVIRUS; SIMIAN ACQUIRED IMMUNE DEFICIENCY SYNDROME; KYNURENINE PATHWAY ID HUMAN IMMUNODEFICIENCY VIRUS; CENTRAL NERVOUS-SYSTEM; AIDS DEMENTIA COMPLEX; QUINOLINIC ACID; KYNURENIC ACID; INDOLEAMINE 2,3-DIOXYGENASE; TRYPTOPHAN DEGRADATION; CEREBROSPINAL-FLUID; TOXOPLASMA-GONDII; GAMMA-INTERFERON AB Increased concentrations of the neuroactive kynurenine pathway metabolites, quinolinic acid (QUIN) and kynurenic acid (KYNA), occur in the CSF of humans infected with the human immunodeficiency virus and macaques infected with retroviruses, including the D/1/ California serotype. In the present study, increased activity of indoleamine-2,3-dioxygenase (IDO), the first enzyme of the kynurenine pathway, occurred in cerebral cortex and lung of macaques with clinical SAIDS. Such increases provide a mechanism to accelerate the formation of kynurenine pathway metabolites in both systemic tissues and the central nervous system. C1 NIMH,CLIN SCI LAB,ANALYT BIOCHEM LAB,BLDG 10,ROOM 3D40,BETHESDA,MD 20892. UNIV CALIF DAVIS,CALIF REG PRIMATE RES CTR,DAVIS,CA 95616. FU NCRR NIH HHS [RR00169, RR00039]; NIAID NIH HHS [AI20573] NR 33 TC 47 Z9 47 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 FEB 1 PY 1991 VL 540 IS 1-2 BP 353 EP 356 DI 10.1016/0006-8993(91)90536-5 PG 4 WC Neurosciences SC Neurosciences & Neurology GA EY794 UT WOS:A1991EY79400051 PM 1647247 ER PT J AU KHACHATURIAN, H KWAK, SP SCHAFER, MKH WATSON, SJ AF KHACHATURIAN, H KWAK, SP SCHAFER, MKH WATSON, SJ TI PROOPIOMELANOCORTIN MESSENGER-RNA AND PEPTIDE COEXPRESSION IN THE DEVELOPING RAT PITUITARY SO BRAIN RESEARCH BULLETIN LA English DT Article DE PITUITARY; DEVELOPMENT; POMC; ACTH; GENE EXPRESSION; MESSENGER RNA ID INSITU HYBRIDIZATION HISTOCHEMISTRY; PROOPIOMELANOCORTIN GENE-EXPRESSION; CENTRAL NERVOUS-SYSTEM; BETA-ENDORPHIN; PRENATAL DEVELOPMENT; POSTNATAL ONTOGENY; CONTAINING NEURONS; BRAIN; GLAND; ENKEPHALIN AB Pro-opiomelanocortin (POMC) is synthesized in both the pituitary gland and the brain. Various peptide products of this precursor, namely beta-endorphin. ACTH and alpha-MSH are co-localized in the anterior lobe corticotrophs, all intermediate lobe cells and in hypothalamic neurons. Messenger RNA (mRNA) for POMC has further been shown to exist in these tissues. In this study, we have shown that POMC mRNA, and peptide accumulation as detected by in situ hybridization and immunocytochemistry, respectively, occur simultaneously within the rat pituitary gland during ontogeny and that their maturation occurs in parallel during prenatal and early postnatal development. C1 NIMH,NEUROIMAGING & APPL NEUROSCI RES BRANCH,ROCKVILLE,MD 20857. RP KHACHATURIAN, H (reprint author), UNIV MICHIGAN,MENTAL HLTH RES INST,205 WASHTENAW PL,ANN ARBOR,MI 48109, USA. FU NIADDK NIH HHS [AM34933]; NIDA NIH HHS [DA02265] NR 52 TC 6 Z9 6 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PD FEB PY 1991 VL 26 IS 2 BP 195 EP 201 DI 10.1016/0361-9230(91)90226-A PG 7 WC Neurosciences SC Neurosciences & Neurology GA EX060 UT WOS:A1991EX06000002 PM 1849441 ER PT J AU FOERSTER, A LEWIS, S OWEN, M MURRAY, R AF FOERSTER, A LEWIS, S OWEN, M MURRAY, R TI PREMORBID ADJUSTMENT AND PERSONALITY IN PSYCHOSIS - EFFECTS OF SEX AND DIAGNOSIS SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article ID PREMORBID ADJUSTMENT; SCHIZOPHRENIA; AGE; CHILDREN; DISORDER AB Pre-morbid schizoid and schizotypal traits and social adjustment were assessed blind to diagnosis by interviewing the mothers of 73 consecutively admitted patients with DSM-III schizophrenia or affective psychosis. Analysis of factors associated with pre-morbid deficits showed a highly significant interaction of diagnosis with sex, such that schizophrenic men showed much greater pre-morbid impairment than either schizophrenic women or men with affective disorder. Poor pre-morbid adjustment predicted an early age at first admission. The results can be explained by a neurodevelopmental disorder in some schizophrenic males. C1 CHARING CROSS & WESTMINSTER MED SCH,ACAD DEPT PSYCHIAT,LONDON W6 8RP,ENGLAND. KINGS COLL HOSP,ACAD DEPT PSYCHOL MED,LONDON SE5 8AF,ENGLAND. NIMH,BETHESDA,MD 20892. INST PSYCHIAT,LONDON SE5 8AF,ENGLAND. RI turton, miranda/F-4682-2011; OI murray, robin/0000-0003-0829-0519 NR 32 TC 154 Z9 158 U1 0 U2 0 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD FEB PY 1991 VL 158 BP 171 EP 176 DI 10.1192/bjp.158.2.171 PG 6 WC Psychiatry SC Psychiatry GA EX397 UT WOS:A1991EX39700004 PM 2012907 ER PT J AU STRONG, MJ HUDSON, AJ ALVORD, WG AF STRONG, MJ HUDSON, AJ ALVORD, WG TI FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS, 1850-1989 - A STATISTICAL-ANALYSIS OF THE WORLD LITERATURE SO CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES LA English DT Article ID MOTOR NEURON DISEASE; PARKINSONISM-DEMENTIA; GUAM; ALS; PROGNOSIS AB We present clinical and pathologic data on four previously unreported familial ALS pedigrees and review and analyze by descriptive and exploratory statistical techniques all published cases of familial ALS (1850-1989). In contrast to the age-dependent incidence of sporadic ALS, the age of onset of familial ALS is normally distributed about a mean of 45.7 years (std. dev. 11.3 years). Survival curves for the familial ALS data also demonstrate a skewed distribution with a median survival time of 24 months with 74% surviving at 12 months, 48% at 24 months and 23% surviving at 60 months. The patient characteristics of age at onset of disease, sex and focus of disease onset are unrelated variables and age at onset of disease is the only predictor of survival (Cox's proportional hazard model, chi-square 14.74, p = 0.0001). By applying accelerated failure time models with a log-normal baseline distribution, estimated probabilities for survival adjusted by age at onset were calculated. It was found that the older the age at disease onset, the shorter the survival. C1 NIH,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. UNIV WESTERN ONTARIO,DEPT CLIN NEUROL SCI,LONDON N6A 3K7,ONTARIO,CANADA. NCI,FREDERICK CANC RES FACIL,DATA MANAGEMENT SERV INC,FREDERICK,MD 21701. RI Strong, Michael/H-9689-2012 NR 104 TC 62 Z9 62 U1 0 U2 2 PU CANADIAN J NEUROL SCI INC PI CALGARY PA PO BOX 4220, STATION C EDITORIAL & SUBSCRIPTION SERV, CALGARY AB T2T 5N1, CANADA SN 0317-1671 J9 CAN J NEUROL SCI JI Can. J. Neurol. Sci. PD FEB PY 1991 VL 18 IS 1 BP 45 EP 58 PG 14 WC Clinical Neurology SC Neurosciences & Neurology GA EZ416 UT WOS:A1991EZ41600007 PM 2036615 ER PT J AU GOFFMAN, T TOCHNER, Z GLATSTEIN, E AF GOFFMAN, T TOCHNER, Z GLATSTEIN, E TI PRIMARY-TREATMENT OF LARGE AND MASSIVE ADULT SARCOMAS WITH IODODEOXYURIDINE AND AGGRESSIVE HYPERFRACTIONATED IRRADIATION SO CANCER LA English DT Article ID SOFT-TISSUE; CELLS; BUDR AB For a decade, the authors have experimented with treatment for unresectable adult soft tissue and bony sarcomas. Over the last 6 years, they have combined hyperfractionated radiation therapy and intravenous iododeoxyuridine as a radiosensitizer, in regimens designed to minimize toxicity and permit delivery of aggressive radiation therapy. Patients with solitary lesions and those with metastasis (38%) were treated in the hope of both potential cure in some and durable palliation in others. The most formidable of these cancers have been those that are large or massive, often requiring five or more fields and extensive treatment planning. The authors report results from 36 patients with large unresectable sarcomas (tumors ranging from 5 to 35 cm; average 14 cm) treated with hyperfractionated radiation therapy, with a minimum follow-up of 1 year, follow-up of 4 or more years (in 50%), or follow-up until death. Overall local control has been 60%, with control of 66% of lesions from 5 to 9 cm, 63% of those from 10 to 14 cm, 63% of those from 15 to 19 cm, and 57% of those greater than 20 to 40 cm. Morbidity has been modest. This experience compares favorably with the authors' earlier trials with misonidazole, and toxicity has been reduced considerably. RP GOFFMAN, T (reprint author), NCI,RADIAT ONCOL BRANCH,ROOM B3B69,BLDG 10,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 9 TC 39 Z9 40 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD FEB 1 PY 1991 VL 67 IS 3 BP 572 EP 576 DI 10.1002/1097-0142(19910201)67:3<572::AID-CNCR2820670308>3.0.CO;2-D PG 5 WC Oncology SC Oncology GA EU100 UT WOS:A1991EU10000007 PM 1985751 ER PT J AU SHIFFMAN, S CASSILETH, BR BLACK, BL BUXBAUM, J CELENTANO, DD CORCORAN, RD GRITZ, ER LASZLO, J LICHTENSTEIN, E PECHACEK, TF PROCHASKA, J SCHOLEFIELD, PG AF SHIFFMAN, S CASSILETH, BR BLACK, BL BUXBAUM, J CELENTANO, DD CORCORAN, RD GRITZ, ER LASZLO, J LICHTENSTEIN, E PECHACEK, TF PROCHASKA, J SCHOLEFIELD, PG TI NEEDS AND RECOMMENDATIONS FOR BEHAVIOR RESEARCH IN THE PREVENTION AND EARLY DETECTION OF CANCER SO CANCER LA English DT Article; Proceedings Paper CT 2ND WORKSHOP ON METHODOLOGY IN BEHAVIORAL AND PSYCHOSOCIAL CANCER RESEARCH CY DEC 05-08, 1989 CL SANTA MONICA, CA SP AMER CANC SOC, DEPT RES, AMER CANC SOC, DEPT SERV & REHAB AB Because life-style patterns affect many cancer risks, research on health-risk behavior and behavior change is critical to cancer prevention. This report recommends priorities for the next decade of psychosocial research on cancer prevention and detection. The leading priority for future research is to fill gaps in basic knowledge left by the rush to intervention and outcome studies. Such research must be theoretically driven and should aim to develop broad principles applicable to diverse health behaviors. Studies that include relevant process data on various stages of behavior change are considered more desirable than simple outcome studies. Epidemiologic investigations should be expanded to include measures of relevant behaviors, so that their impact on clinical outcomes might be established. More research is needed on lay perception of health risks and on individual and health-system barriers to effective cancer prevention and detection. Studies that address the needs of minority and underprivileged populations are crucial. Funding agencies' narrow categorical mandates impede interdisciplinary research on multiple risk factors and their interactions; these boundaries must be relaxed to promote such approaches. Funding agencies should also consider basic research as a long-term investment towards the development of effective interventions. C1 UNIV PENN,CANC CONTROL PROGRAM,PHILADELPHIA,PA 19104. AMER CANC SOC,RES DEPT,ATLANTA,GA. NYU,SCH MED,DEPT MED,NEW YORK,NY 10003. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT HLTH POLICY & MANAGEMENT,BALTIMORE,MD 21218. AMER CANC SOC,DEPT PUBL EDUC,ATLANTA,GA. UNIV CALIF LOS ANGELES,JONSSON COMPREHENS CANC CTR,LOS ANGELES,CA 90024. OREGON RES INST,EUGENE,OR 97403. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. UNIV RHODE ISL,DEPT PSYCHOL,KINGSTON,RI 02881. NATL CANC INST CANADA,TORONTO M5S 2V7,ONTARIO,CANADA. RP SHIFFMAN, S (reprint author), UNIV PITTSBURGH,DEPT PSYCHOL,4015 OHARA ST,PITTSBURGH,PA 15260, USA. NR 5 TC 8 Z9 8 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD FEB 1 PY 1991 VL 67 IS 3 SU S BP 800 EP 804 DI 10.1002/1097-0142(19910201)67:3+<800::AID-CNCR2820671408>3.0.CO;2-M PG 5 WC Oncology SC Oncology GA FL822 UT WOS:A1991FL82200007 PM 1986848 ER PT J AU REDD, WH SILBERFARB, PM ANDERSEN, BL ANDRYKOWSKI, MA BOVBJERG, DH BURISH, TG CARPENTER, PJ CLEELAND, C DOLGIN, M LEVY, SM MITNICK, L MORROW, GR SCHOVER, LR SPIEGEL, D STEVENS, J AF REDD, WH SILBERFARB, PM ANDERSEN, BL ANDRYKOWSKI, MA BOVBJERG, DH BURISH, TG CARPENTER, PJ CLEELAND, C DOLGIN, M LEVY, SM MITNICK, L MORROW, GR SCHOVER, LR SPIEGEL, D STEVENS, J TI PHYSIOLOGICAL AND PSYCHOBEHAVIORAL RESEARCH IN ONCOLOGY SO CANCER LA English DT Article; Proceedings Paper CT 2ND WORKSHOP ON METHODOLOGY IN BEHAVIORAL AND PSYCHOSOCIAL CANCER RESEARCH CY DEC 05-08, 1989 CL SANTA MONICA, CA SP AMER CANC SOC, DEPT RES, AMER CANC SOC, DEPT SERV & REHAB ID METASTATIC BREAST-CANCER; ADJUVANT CHEMOTHERAPY; SOCIAL RELATIONSHIPS; ANTICIPATORY NAUSEA; FOLLOW-UP; SURVIVAL; WOMEN; PREVALENCE; MORTALITY; DISORDERS AB A major thrust in research in psychosocial oncology is the study of the interaction of psychologic and physiologic variables. This discussion reviews the current status and future directions of such research. Areas addressed include pain, nausea and vomiting with chemotherapy, sexuality, effects of cancer on psychologic and neuropsychologic function, impact of psychologic factors on cancer and its treatment, and psychoneuroimmunology. In addition, specific recommendations for strategies to facilitate research in these areas of psychosocial oncology are proposed. C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PSYCHIAT,HANOVER,NH 03756. OHIO STATE UNIV,DEPT PSYCHOL,COLUMBUS,OH 43210. OHIO STATE UNIV,DEPT OBSTET & GYNECOL,COLUMBUS,OH 43210. UNIV KENTUCKY,COLL MED,DEPT BEHAV SCI,LEXINGTON,KY 40506. VANDERBILT UNIV,PROVOSTS OFF,NASHVILLE,TN 37240. UNIV ROCHESTER,MED CTR,DEPT PSYCHIAT,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT PEDIAT,ROCHESTER,NY 14642. UNIV WISCONSIN,SCH MED,PAIN RES GRP,MADISON,WI 53706. CHILDRENS HOSP,DIV HEMATOL & ONCOL,LOS ANGELES,CA 90027. UNIV PITTSBURGH,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA 15261. NIMH,HLTH & BEHAV RES BRANCH,BETHESDA,MD 20892. UNIV ROCHESTER,CTR CANC,BEHAV MED UNIT,ROCHESTER,NY 14627. CLEVELAND CLIN EDUC FDN,DEPT UROL,CLEVELAND,OH 44106. STANFORD UNIV,MED CTR,SCH MED,DEPT PSYCHIAT & BEHAV SCI,STANFORD,CA 94305. AMER CANC SOC,ATLANTA,GA. RP REDD, WH (reprint author), MEM SLOAN KETTERING CANC CTR,DEPT NEUROL,BOX 547,1275 YORK AVE,NEW YORK,NY 10021, USA. NR 52 TC 45 Z9 45 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD FEB 1 PY 1991 VL 67 IS 3 SU S BP 813 EP 822 DI 10.1002/1097-0142(19910201)67:3+<813::AID-CNCR2820671411>3.0.CO;2-W PG 10 WC Oncology SC Oncology GA FL822 UT WOS:A1991FL82200010 PM 1986851 ER PT J AU MORECKI, S KARSON, E CORNETTA, K KASID, A AEBERSOLD, P BLAESE, RM ANDERSON, WF ROSENBERG, SA AF MORECKI, S KARSON, E CORNETTA, K KASID, A AEBERSOLD, P BLAESE, RM ANDERSON, WF ROSENBERG, SA TI RETROVIRUS-MEDIATED GENE-TRANSFER INTO CD4+ AND CD8+ HUMAN T-CELL SUBSETS DERIVED FROM TUMOR-INFILTRATING LYMPHOCYTES AND PERIPHERAL-BLOOD MONONUCLEAR-CELLS SO CANCER IMMUNOLOGY IMMUNOTHERAPY LA English DT Article ID HEMATOPOIETIC PROGENITOR CELLS; HUMAN ADENOSINE-DEAMINASE; MURINE LEUKEMIA-VIRUS; METASTATIC MELANOMA; ANTITUMOR-ACTIVITY; EXPRESSION; INTERLEUKIN-2; EFFICIENCY; VECTOR; IMMUNOTHERAPY AB Studies were undertaken to test the susceptibility of individual T cell subpopulations to retroviral-mediated gene transduction. Gene transfer into human tumor-infiltrating lymphocytes (TIL) or peripheral blood mononuclear cells (PBMC) was carried out by transduction with an amphotropic murine retroviral vector (LNL6 or N2) containing the bacterial neo(R) gene. The presence of the neo(R) gene in the TIL population was demonstrated by Southern blot analysis, detection of the enzymatic activity of the gene product and by the ability of transduced TIL to proliferate in high concentrations of G418, a neomycin analog that is toxic to eukaryotic cells. The presence of the neo(R) gene in TIL did not alter their proliferation or interleukin-2 dependence compared to nontransduced TIL. The differential susceptibility of CD4+ and CD8+ lymphoid cells to the retro-virus-mediated gene transfer was then tested. Transduction of heterogeneous TIL cultures containing both CD4+ and CD8+ cells resulted in gene insertion into both T cell subsets with no preferential transduction frequency into either CD4+ or CD8+ cells. In other experiments highly purified CD4+ and CD8+ T cell subpopulations from either TIL or PBMC could be successfully transduced with the neo(R) gene as demonstrated by Southern blot analysis and detection of the gene product neophosphotransferase activity. No such activity or vector DNA could be detected in controls of nontransduced cells. In these highly purified cell subsets the distinctive T cell phenotypic markers were continually expressed after transduction, G418 selection and long-term growth. Clinical trials have begun in patients with advanced cancer using heterogeneous populations of CD4+ and CD8+ gene-modified TIL. C1 NCI,SURG BRANCH,BLDG 10,ROOM 2B42,BETHESDA,MD 20892. NCI,METAB BRANCH,BETHESDA,MD 20892. NHLBI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 35 TC 30 Z9 30 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-7004 J9 CANCER IMMUNOL IMMUN JI Cancer Immunol. Immunother. PD FEB PY 1991 VL 32 IS 6 BP 342 EP 352 DI 10.1007/BF01741329 PG 11 WC Oncology; Immunology SC Oncology; Immunology GA EV435 UT WOS:A1991EV43500002 PM 2007247 ER PT J AU KIMES, BW CAIROLI, V FREIREICH, EJ KARP, J YANG, SS AF KIMES, BW CAIROLI, V FREIREICH, EJ KARP, J YANG, SS TI TRAINING IN CLINICAL RESEARCH IN ONCOLOGY SO CANCER RESEARCH LA English DT Editorial Material C1 NCI,DIV CANC BIOL & DIAG,CTR TRAINING & RESOURCES PROGRAM,EXECUT PLAZA N,SUITE 308,BETHESDA,MD 20892. NR 6 TC 8 Z9 8 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 1 PY 1991 VL 51 IS 3 BP 753 EP 756 PG 4 WC Oncology SC Oncology GA EV569 UT WOS:A1991EV56900001 PM 1988114 ER PT J AU USUI, N MIMNAUGH, EG SINHA, BK AF USUI, N MIMNAUGH, EG SINHA, BK TI A ROLE OF THE INTERLEUKIN-1 RECEPTOR IN THE SYNERGISTIC ANTITUMOR EFFECTS OF HUMAN INTERLEUKIN 1 ALPHA AND ETOPOSIDE AGAINST HUMAN-MELANOMA CELLS SO CANCER RESEARCH LA English DT Article ID RECOMBINANT HUMAN INTERLEUKIN-1-ALPHA; TUMOR NECROSIS FACTOR; HIGH-AFFINITY; IRREVERSIBLE BINDING; MICHAELIS-MENTEN; TOPOISOMERASE-II; KINETIC SYSTEMS; CYTO-TOXICITY; DNA CLEAVAGE; T-CELLS AB To investigate the possibility that anticancer drugs combined with cytokines may show increased activity, human tumor cells were treated with combinations of human recombinant interleukin 1-alpha (rIL-1-alpha) and etoposide (VP-16). The cytotoxicity of these combinations was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay using rIL-1-alpha-sensitive A375-C6 melanoma cells and A375-C5 cells, a clonal variant line that is resistant to IL-1-alpha. Data were analyzed for synergism by the median effect principle of T-C. Chou and P. Talalay (J. Biol. Chem., 252: 6438-6442, 1977). At a dose ratio of VP-16 to rIL-1-alpha of 12 nM: 1 unit/ml in either simultaneous or sequential exposure (VP-16 first), the calculated combination index values indicated synergistic cytotoxicity toward both A375-C6 cells and A375-C5 cells. IL-1-alpha treatment 24 h prior to VP-16 exposure had no advantage over simultaneous treatment. Surface IL-1-alpha receptors on both A375-C6 and A375-C5 cells were measured using I-125-radiolabeled rIL-1-alpha binding; A375-C6 cells had 701 +/- 128 (SD) receptor molecules/cell and A375-C5 cells only had 58 +/- 33 receptor molecules/cell. The dissociation constants for IL-1-alpha were similar in both cell types (19 +/- 6 pM for A375-C6 and 17 +/- 2 pM for A375-C5). The specific binding of rIL-1-alpha to the surface IL-1-alpha receptors of both sensitive and resistant cells was significantly increased in a dose-dependent fashion by the prior treatment with VP-16 (1.75-fold on A375-C6 cells and 3.5-fold on A375-C5 cells). VP-16 also enhanced the internalization of receptor-bound rIL-1-alpha, suggesting that a possible mechanism of the synergistic cytotoxicity of rIL-1-alpha and VP-16 might be related to the modulation of rIL-1-alpha receptors by VP-16, resulting in increased internalization of rIL-1-alpha. C1 NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,ENGN SCI BRANCH,BETHESDA,MD 20892. NR 43 TC 27 Z9 27 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 1 PY 1991 VL 51 IS 3 BP 769 EP 774 PG 6 WC Oncology SC Oncology GA EV569 UT WOS:A1991EV56900004 PM 1824825 ER PT J AU LEDOUX, SP THANGADA, M BOHR, VA WILSON, GL AF LEDOUX, SP THANGADA, M BOHR, VA WILSON, GL TI HETEROGENEOUS REPAIR OF METHYLNITROSOUREA-INDUCED ALKALI-LABILE SITES IN DIFFERENT DNA-SEQUENCES SO CANCER RESEARCH LA English DT Article ID DIHYDROFOLATE-REDUCTASE GENE; HAMSTER OVARY CELLS; ACTIVE GENE; CARCINOGENESIS; STREPTOZOTOCIN; MUTAGENESIS; SPECIFICITY; MECHANISMS; ALKYLATION; EFFICIENT AB The repair of DNA damage induced by methylnitrosourea (MNU) in restriction fragments containing the dihydrofolate reductase (DHFR) gene in Chinese hamster ovary cells was compared to that in equal size restriction fragments containing a nontranscribed flanking sequence 3' to the DHFR gene or the c-fos gene. Following exposure to 10(-3) M MNU, restriction fragments containing either the DHFR gene or the 3' flanking sequence had similar amounts of alkali labile sits, approximately 2 sites/restriction fragment. Fragments encompassing the c-fos gene had less than 2 breaks/fragment. Twenty-four h after exposure to MNU a consistent, but slight and not statistically significant, difference was seen with more adducts removed from the DHFR gene than the 3' flanking sequence. No repair was detected in the c-fos containing fragments. In addition, the repair of N7-methylguanine in the overall genome was assessed by use of a P-32 end labeling technique. Seventy % of this major alkylation product was repaired after 24 h. These findings establish that repair heterogeneity occurs in Chinese hamster ovary cells after exposure to MNU. C1 UNIV SO ALABAMA,DEPT STRUCT & CELLULAR BIOL,MOBILE,AL 36688. NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. FU NIEHS NIH HHS [ES00150, ES05446, ES03456] NR 24 TC 37 Z9 37 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 FEB 1 PY 1991 VL 51 IS 3 BP 775 EP 779 PG 5 WC Oncology SC Oncology GA EV569 UT WOS:A1991EV56900005 PM 1899045 ER PT J AU FERNSTEN, PD PRIMUS, FJ GREINER, JW SIMPSON, JF SCHLOM, J AF FERNSTEN, PD PRIMUS, FJ GREINER, JW SIMPSON, JF SCHLOM, J TI CHARACTERIZATION OF THE COLORECTAL CARCINOMA-ASSOCIATED ANTIGEN DEFINED BY MONOCLONAL-ANTIBODY D612 SO CANCER RESEARCH LA English DT Article ID TUMOR-ASSOCIATED GLYCOPROTEIN; CARCINOEMBRYONIC ANTIGEN; SURFACE-ANTIGEN; CELL-SURFACE; TISSUE DISTRIBUTION; ADULT FECES; EXPRESSION; PROTEINS; CANCER; DETERMINANTS AB Monoclonal antibody (MAb) D612 recognizes an antigen expressed on the cell surface of normal and malignant gastrointestinal epithelium. It is a murine IgG2a/kappa which has been previously shown to mediate killing of human colon carcinoma cells using human effector cells (which could be enhanced in the presence of interleukin-2). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analyses of MAb D612 immunoprecipitates of extracts of L[S-35]methionine-,L-[H-3]leucine-, and D-[H-3]glucosamine-labeled human colon carcinoma cells showed that the D612 antigen is a M(r) 48,000 glycoprotein. Similar estimates of molecular mass were obtained from SDS-PAGE analyses of MAb D612 immunoprecipitates of radioiodinated extracts of surgically resected colon carcinoma and adjacent normal colonic mucosa. D612 antigen was not detectable in immunoprecipitates of supernatant media from radiolabeled cell cultures, suggesting that the antigen is not readily shed from the surface of cultured cells. The D612 antigen was shown to be clearly distinct from previously described gastrointestinal carcinoma-associated glycoproteins: the D612 antigen shows a migration pattern of SDS-PAGE distinct from those of the antigens recognized by MAbs KS1/4 and GA733, and reciprocal immunodepletion analyses of D-pH-3]glucosamine-labeled colon carcinoma cells utilizing MAbs D612 and GA733 revealed no cross-reactivity between these antibodies. Similarly, competitive binding studies between MAbs 17-1A and KS1/4 and MAb D612 revealed no similarity between the epitopes recognized by MAb D612 and MAbs 17-1A and KS1/4. MAbs D612 and 17-1A were also titered in immunoperoxidase staining assays on serial frozen sections of normal and malignant colon. MAb D612 showed a higher titer of immunostaining reactivity with both normal and malignant colon than did MAb 17-1A. MAb D612 showed roughly equivalent immunostaining titers against normal and malignant colon; whereas MAb 17-1A showed a higher titer of immunostaining reactivity against the normal colon tissue than against the malignant colon. Flow cytometric analysis of phosphatidylinositol-specific phospholipase C-treated colon carcinoma cells revealed no loss of D612 antigen from the cell surface, suggesting that the mechanism of attachment of the D612 antigen to the cell surface does not involve linkage to a phosphatidylinositol glycan. Radioiodination of the D612 antigen in a plasma membrane-enriched cell fraction by the photoactivatable carbenegenerating reagent, 3-(trifluoromethyl)-3-(m[I-125]iodophenyl)diazirine, suggests that the D612 antigen polypeptide penetrates the lipid bilayer of the plasma membrane. It has been determined by Scatchard analysis that the number of binding sites for MAb D612 on the LS-174T human colorectal carcinoma cell line is 4.8 X 10(5). MAb D612 was found to have a K(A) of approximately 1.3 X 10(9) M-1. C1 NCI,TUMOR IMMUNOL & BIOL,BLDG 10,RM 8B07,BETHESDA,MD 20892. NR 58 TC 14 Z9 14 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 FEB 1 PY 1991 VL 51 IS 3 BP 926 EP 934 PG 9 WC Oncology SC Oncology GA EV569 UT WOS:A1991EV56900031 PM 1988133 ER PT J AU CIARDIELLO, F DONO, R KIM, N PERSICO, MG SALOMON, DS AF CIARDIELLO, F DONO, R KIM, N PERSICO, MG SALOMON, DS TI EXPRESSION OF CRIPTO, A NOVEL GENE OF THE EPIDERMAL GROWTH-FACTOR GENE FAMILY, LEADS TO INVITRO TRANSFORMATION OF A NORMAL MOUSE MAMMARY EPITHELIAL-CELL LINE SO CANCER RESEARCH LA English DT Note ID FACTOR-ALPHA CDNA; RAT FIBROBLASTS; HUMAN-BREAST; TGF-ALPHA; HA-RAS; ONCOGENE; INDUCTION; RECEPTOR; CANCER AB cripto is a gene encoding an epidermal growth factor-related protein that is expressed in undifferentiated embryonal carcinoma cells. To ascertain if cripto is capable of functioning as a transforming gene, a full-length human cripto complementary DNA under the transcriptional control of the Rous sarcoma virus long terminal repeat has been cotransfected with the selectable pSV2neo marker plasmid into immortalized mouse NOG-8 mammary epithelial cells. Several neomycin-resistant clones were isolated that express high levels of a specific cripto 4.5-kilobase mRNA transcript and possess multiple copies of cripto plasmid DNA. NOG-8 cells that express cripto are able to clone in soft agar and exhibit an approximately 3-fold increase in their anchorage-dependent growth in serum-free medium as compared to the neo-transfected NOG-8 cells. However, non of the cripto-expressing NOG-8 clones are able to form tumors in nude mice. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BLDG 10,ROOM 5B39,BETHESDA,MD 20892. CNR,INT INST GENET & BIOPHYS,I-80125 NAPLES,ITALY. RI DONO, ROSANNA/I-7821-2016; OI Ciardiello, Fortunato/0000-0002-3369-4841 NR 19 TC 102 Z9 102 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 FEB 1 PY 1991 VL 51 IS 3 BP 1051 EP 1054 PG 4 WC Oncology SC Oncology GA EV569 UT WOS:A1991EV56900052 PM 1846316 ER PT J AU JIAO, J ZIELENSKA, M ANDERSON, MW GLICKMAN, BW AF JIAO, J ZIELENSKA, M ANDERSON, MW GLICKMAN, BW TI MUTATIONAL SPECIFICITIES OF ENVIRONMENTAL CARCINOGENS IN THE LACI GENE OF ESCHERICHIA-COLI .4. THE TOBACCO-SPECIFIC NITROSAMINE 4-(METHYLNITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE SO CARCINOGENESIS LA English DT Article ID F344 RATS; N-NITROSAMINES; CHEMICAL CARCINOGENESIS; DNA METHYLATION; A/J MICE; 4-(N-METHYL-N-NITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE; N'-NITROSONORNICOTINE; INDUCTION; MUTAGENESIS; METABOLISM AB We have determined the mutational specificity of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) by the characterization of 58 induced Escherichia coli lacI(-d) mutants at the DNA sequence level. Metabolic activation of NNK was carried out using the S9 fraction from Aroclor 1254-treated rats. G:C --> A:T transitions dominated the spectrum, accounting for 55% of the mutations recovered. The other base substitutions recovered include three A:T --> G:C transitions as well as two A:T --> T:A, three A:T --> C:G, five G:C --> C:G and five G:C --> T:A transversions. Other classes of mutational events included two deletions, three duplications and three frameshifts. The complexity of the NNK mutational spectrum appears consistent with a model that this compound induces mutations by both the methylation and the pyridoloxobutylation of DNA. C1 YORK UNIV,DEPT BIOL,4700 KEELE ST,N YORK M3J 1P3,ONTARIO,CANADA. NIEHS,RES TRIANGLE PK,NC 27709. NR 37 TC 14 Z9 14 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD FEB PY 1991 VL 12 IS 2 BP 221 EP 224 DI 10.1093/carcin/12.2.221 PG 4 WC Oncology SC Oncology GA EW904 UT WOS:A1991EW90400011 PM 1995189 ER PT J AU DEVEREUX, TR ANDERSON, MW BELINSKY, SA AF DEVEREUX, TR ANDERSON, MW BELINSKY, SA TI ROLE OF RAS PROTOONCOGENE ACTIVATION IN THE FORMATION OF SPONTANEOUS AND NITROSAMINE-INDUCED LUNG-TUMORS IN THE RESISTANT C3H MOUSE SO CARCINOGENESIS LA English DT Article ID STRAIN-A MOUSE; CHEMICAL CARCINOGENESIS; B6C3F1 MOUSE; A/J MICE; DNA; ONCOGENES; HEPATOCARCINOGENESIS; MUTAGENESIS; METABOLISM; KINETICS AB The role of ras activation in the formation of spontaneous and chemically induced tumors was evaluated in the C3H mouse, a strain that has a low incidence of spontaneous lung tumors. Lung tumors were induced in C3H mice by treatment with 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), 50 mg/kg, or nitrosodimethylamine (NDMA), 3 mg/kg for 7 weeks (3 times/week, i.p.). Eleven tumors from each treatment group were evaluated for activated ras genes by direct sequencing and oligonucleotide hybridization to slot blots of amplified DNA from these tumors. An activated K-ras gene was detected in 100% of NDMA- and NNK-induced lung tumors, and the activating mutation detected in all samples was a GC to AT transition (GGT to GAT) in codon 12. In contrast, only 40% of the seven spontaneous lung tumors analyzed contained an activated K-ras gene and the mutations identified were not localized to either a specific base or codon. Both NNK and NDMA can be activated via alpha-hydroxylation to methylating agents. The GC to AT mutation observed in codon 12 in the nitrosamine-induced tumors is consistent with the formation of an O6-methylguanine (O6MG) adduct. Similar concentrations (13-15 pmoles/mu-mol deoxyguanosine) of this promutagenic adduct were detected in lungs during treatment with either NNK or NDMA. Thus, both these nitrosamines appear to activate the K-ras gene in lung through a direct genotoxic mechanism involving the formation of the O6MG adduct. The frequency of K-ras activation was similar in chemically induced lung tumors from the sensitive A/J strain and the C3H mouse, indicating that susceptibility for neoplasia in these strains is not related to the ability to activate this gene. Although tumors were induced in lung from 100% of C3H mice following chronic carcinogen exposure, both the size and the multiplicity was significantly less, while latency was longer than that observed in the A/J mouse. These differences could not be attributed to an altered propensity for DNA damage, but rather suggest that genetic loci which regulate clonal expansion and growth of initiated cells play a major role in the susceptibility of pulmonary neoplasia. RP DEVEREUX, TR (reprint author), NIEHS,MOLEC TOXICOL LAB,RES TRIANGLE PK,NC 27709, USA. NR 35 TC 99 Z9 99 U1 1 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD FEB PY 1991 VL 12 IS 2 BP 299 EP 303 DI 10.1093/carcin/12.2.299 PG 5 WC Oncology SC Oncology GA EW904 UT WOS:A1991EW90400022 PM 1995195 ER PT J AU CRESPI, CL PENMAN, BW STEIMEL, DT GELBOIN, HV GONZALEZ, FJ AF CRESPI, CL PENMAN, BW STEIMEL, DT GELBOIN, HV GONZALEZ, FJ TI THE DEVELOPMENT OF A HUMAN CELL-LINE STABLY EXPRESSING HUMAN CYP3A4 - ROLE IN THE METABOLIC-ACTIVATION OF AFLATOXIN-B1 AND COMPARISON TO CYP1A2 AND CYP2A3 SO CARCINOGENESIS LA English DT Article ID NIFEDIPINE OXIDASE; MUTATION ASSAYS; HUMAN-LIVER; GENE; TRANSFECTION; SEQUENCE; CDNA AB We have developed a human lymphoblastoid cell line, designated 3A4/Hol, which stably expresses human CYP3A4 cDNA. This cell line exhibited testosterone 6beta-hydroxylase activity, produced immunologically detectable CYP3A4 protein and was more sensitive to the cytotoxicity and mutagenicity of the carcinogenic mycotoxin aflatoxin B1 (AFB1) than was the parent cell line. The concentration-response for AFB1 cytotoxicity and mutagenicity in 3A4/Hol cells was compared to the responses of isogenic cell lines expressing comparable levels of human CYP1A2 (1A2/Hyg cells) and human CYP2A3 (2A3/Hyg cells). 1A2/Hyg cells were 3- to 6-fold more sensitive than 3A4/Hol cells to AFB1-induced mutation. 3A4/Hol cells were 10- to 15-fold more sensitive to AFB1-induced mutation than 2A3/Hyg cells. The differences in mutagenicity were supported by the relative binding of [H-3]AFB1 to cellular DNA. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP CRESPI, CL (reprint author), GENTEST CORP,6 HENSHAW ST,WOBURN,MA 01801, USA. FU NIEHS NIH HHS [N44-ES-71001] NR 19 TC 108 Z9 111 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD FEB PY 1991 VL 12 IS 2 BP 355 EP 359 DI 10.1093/carcin/12.2.355 PG 5 WC Oncology SC Oncology GA EW904 UT WOS:A1991EW90400031 PM 1899812 ER PT J AU ROSENTHAL, DS STEINERT, PM CHUNG, S HUFF, CA JOHNSON, J YUSPA, SH ROOP, DR AF ROSENTHAL, DS STEINERT, PM CHUNG, S HUFF, CA JOHNSON, J YUSPA, SH ROOP, DR TI A HUMAN EPIDERMAL DIFFERENTIATION-SPECIFIC KERATIN GENE IS REGULATED BY CALCIUM BUT NOT NEGATIVE MODULATORS OF DIFFERENTIATION IN TRANSGENIC MOUSE KERATINOCYTES SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID SQUAMOUS-CELL CARCINOMAS; RETINOIC ACID RECEPTOR; VITAMIN-A; TERMINAL DIFFERENTIATION; EPITHELIAL-CELLS; EXPRESSION; TUMORS; 12-O-TETRADECANOYLPHORBOL-13-ACETATE; IDENTIFICATION; ANTIBODIES AB Keratins K1 and K10 represent the major differentiation products of the maturing epidermal keratinocytes. Primary epidermal cell cultures from newborn K1 transgenic mice containing a 12-kilobase human K1 genomic fragment were established in order to examine the expression of both human and mouse K1 in the presence of known modulators of epidermal differentiation. Elevated levels of Ca2+ in the culture medium induced both mouse K1 and human K1. Supplementing the medium with retinoic acid or 12-O-tetradecanoylphorbol-13-acetate or introducing a Harvey viral ras oncogene (v-ras(Ha)) into the cells completely suppressed mouse K1 but not human K1. Our results suggest that: (a) the human 12-kilobase insert contains all the necessary cis-acting elements to respond to the Ca2+ signal, and (b) other cis-acting elements, not present within this insert, may function independently to regulate the response of K1 to retinoids, 12-O-tetradecanoylphorbol-13-acetate, and v-ras(Ha) transformation. This transgenic model provides an approach to identify elements required for the regulation of an epidermal differentiation-specific gene. C1 BAYLOR UNIV,DEPT CELL BIOL,HOUSTON,TX 77030. BAYLOR UNIV,DEPT DERMATOL,HOUSTON,TX 77030. NCI,DEPT DERMATOL,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. RP ROSENTHAL, DS (reprint author), NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892, USA. NR 29 TC 57 Z9 57 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD FEB PY 1991 VL 2 IS 2 BP 107 EP 113 PG 7 WC Cell Biology SC Cell Biology GA EY544 UT WOS:A1991EY54400005 PM 1712625 ER PT J AU BOTO, WMO BROWN, L CHREST, J ADLER, WH AF BOTO, WMO BROWN, L CHREST, J ADLER, WH TI DISTINCT MODULATORY EFFECTS OF BRYOSTATIN-1 AND STAUROSPORINE ON THE BIOSYNTHESIS AND EXPRESSION OF THE HIV RECEPTOR PROTEIN (CD4) BY T-CELLS SO CELL REGULATION LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; TUMOR PROMOTERS; RIBONUCLEIC-ACID; PHORBOL ESTERS; HTLV-III/LAV; KINASE-C; INFECTIVITY; BINDING; ANTIGEN; FUSION AB A family of structurally related macrocyclic lactones, bryostatins, have recently been shown to display several intriguing pharmacologic properties. Bryostatins are biosynthetic products of bryozoa phyllum of marine animals. To extend the analyses of the biological activities of these highly unusual biosynthetic animal products, we have examined the effect of bryostatin 1 (bryo-1) on the steady-state expression of the human immunodeficiency virus receptor, CD4, by normal peripheral blood T lymphocytes. Incubation of the cells with 5 nM bryo-1 caused a substantial loss of CD4 from the cell surface, as analyzed by flow cytometry using anti-CD4 monoclonal antibody. The modulation of CD4 expression by bryo-1 was not due to a cytotoxicity effect: in the culture conditions where it modulated CD4, bryo-1 also stimulated the expression of the interleukin 2 gene, as indicated by northern blot hybridization. In addition, incubation of the lymphocytes with nanomolar amounts of protein kinase C antagonist, staurosporine, resulted in the inhibition of the bryo-1-induced modulation of CD4 expression. The results of radioimmunoprecipitation analysis of detergent lysates of [S-35] methionine-labeled lymphocytes strongly suggest that bryo-1 inhibits the glycosylation and expression of CD4 in a manner similar to that of tunicamycin. C1 ADDICT RES & TREATMENT CORP,BROOKLYN,NY 11201. NIA,CLIN IMMUNOL SECT,BALTIMORE,MD 21224. RP BOTO, WMO (reprint author), CUNY CITY COLL,DEPT BIOL,NEW YORK,NY 10031, USA. FU NCRR NIH HHS [RR03060-04] NR 32 TC 16 Z9 17 U1 0 U2 3 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1044-2030 J9 CELL REGUL PD FEB PY 1991 VL 2 IS 2 BP 95 EP 103 PG 9 WC Cell Biology SC Cell Biology GA EZ581 UT WOS:A1991EZ58100002 PM 1863603 ER PT J AU WEISS, GH AF WEISS, GH TI DIFFUSION IN DISORDERED MEDIA - DISCUSSION SO CHEMOMETRICS AND INTELLIGENT LABORATORY SYSTEMS LA English DT Discussion ID TIME RANDOM-WALK; RANDOM ENVIRONMENT; TRANSPORT; LATTICES; SOLIDS C1 NIH, BETHESDA, MD 20892 USA. NR 18 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-7439 EI 1873-3239 J9 CHEMOMETR INTELL LAB JI Chemometrics Intell. Lab. Syst. PD FEB PY 1991 VL 10 IS 1-2 BP 123 EP 126 DI 10.1016/0169-7439(91)80041-N PG 4 WC Automation & Control Systems; Chemistry, Analytical; Computer Science, Artificial Intelligence; Instruments & Instrumentation; Mathematics, Interdisciplinary Applications; Statistics & Probability SC Automation & Control Systems; Chemistry; Computer Science; Instruments & Instrumentation; Mathematics GA FC580 UT WOS:A1991FC58000015 ER PT J AU HIGGINS, M KELLER, JB WAGENKNECHT, LE TOWNSEND, MC SPARROW, D JACOBS, DR HUGHES, G AF HIGGINS, M KELLER, JB WAGENKNECHT, LE TOWNSEND, MC SPARROW, D JACOBS, DR HUGHES, G TI PULMONARY-FUNCTION AND CARDIOVASCULAR RISK FACTOR RELATIONSHIPS IN BLACK AND IN WHITE YOUNG MEN AND WOMEN - THE CARDIA STUDY SO CHEST LA English DT Article ID CHRONIC RESPIRATORY-DISEASE; CORONARY HEART-DISEASE; LUNG-FUNCTION; MORTALITY; ADULTS; POPULATION; FRAMINGHAM; PREDICTOR; SYMPTOMS; DEATH AB Pulmonary function is known to be related inversely to incidence of coronary heart disease, congestive heart failure, chronic obstructive lung disease, lung cancer, and death from all causes. Reasons for some of these associations are poorly understood. Relationships between cardiovascular disease risk factors and pulmonary function were examined in 5,115 18- to 30-year-old black and white male and female participants in the study of Coronary Artery Risk Development in Young Adults (CARDIA). Forced expiratory volume in 1 s adjusted for height (FEV1/Ht2) was significantly lower in smokers than nonsmokers and in persons who reported shortness of breath; FEV1/Ht2 was correlated positively with a history of strenuous physical activity, duration of exercise on the treadmill, and high-density lipoprotein cholesterol. It was associated negatively with skinfold thicknesses, serum triglycerides, fasting serum insulin, and the Cook Medley scale of hostility. The association between pulmonary function and heart disease risk may reflect associations with physical fitness, vigor, fatness, and lipid profiles, as well as with cigarette smoking. RP HIGGINS, M (reprint author), NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,FED BLDG,RM 2C08,BETHESDA,MD 20892, USA. NR 30 TC 47 Z9 51 U1 0 U2 3 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD FEB PY 1991 VL 99 IS 2 BP 315 EP 322 DI 10.1378/chest.99.2.315 PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA EW488 UT WOS:A1991EW48800014 PM 1989788 ER PT J AU LUDEMANN, PM AF LUDEMANN, PM TI GENERALIZED DISCRIMINATION OF POSITIVE FACIAL EXPRESSIONS BY 7-MONTH-OLD AND 10-MONTH-OLD INFANTS SO CHILD DEVELOPMENT LA English DT Article ID EMOTIONAL EXPRESSIONS; RECOGNITION; PERCEPTION; FACE RP LUDEMANN, PM (reprint author), NICHHD,BLDG 31,ROOM B2B15,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 28 TC 24 Z9 24 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0009-3920 J9 CHILD DEV JI Child Dev. PD FEB PY 1991 VL 62 IS 1 BP 55 EP 67 DI 10.1111/j.1467-8624.1991.tb01514.x PG 13 WC Psychology, Educational; Psychology, Developmental SC Psychology GA EX934 UT WOS:A1991EX93400004 PM 2022138 ER PT J AU FOX, NA KIMMERLY, NL SCHAFER, WD AF FOX, NA KIMMERLY, NL SCHAFER, WD TI ATTACHMENT TO MOTHER ATTACHMENT TO FATHER - A METAANALYSIS SO CHILD DEVELOPMENT LA English DT Article ID TRADITIONAL SWEDISH FAMILIES; COMPONENT PROCESS ANALYSIS; INFANT-MOTHER; STRANGE SITUATION; PENNSYLVANIA INFANT; DEVELOPMENT PROJECT; 1ST YEAR; SECURITY; TEMPERAMENT; BEHAVIOR C1 NICHHD,BETHESDA,MD 20892. RP FOX, NA (reprint author), UNIV MARYLAND,INST CHILD STUDY,COLLEGE PK,MD 20742, USA. FU NICHD NIH HHS [HD 17899] NR 48 TC 168 Z9 173 U1 4 U2 31 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0009-3920 J9 CHILD DEV JI Child Dev. PD FEB PY 1991 VL 62 IS 1 BP 210 EP 225 DI 10.1111/j.1467-8624.1991.tb01526.x PG 16 WC Psychology, Educational; Psychology, Developmental SC Psychology GA EX934 UT WOS:A1991EX93400016 PM 1827064 ER PT J AU GORE, JM SLOAN, M PRICE, TR RANDALL, AMY BOVILL, E COLLEN, D FORMAN, S KNATTERUD, GL SOPKO, G TERRIN, ML AF GORE, JM SLOAN, M PRICE, TR RANDALL, AMY BOVILL, E COLLEN, D FORMAN, S KNATTERUD, GL SOPKO, G TERRIN, ML TI INTRACEREBRAL HEMORRHAGE, CEREBRAL INFARCTION, AND SUBDURAL-HEMATOMA AFTER ACUTE MYOCARDIAL-INFARCTION AND THROMBOLYTIC THERAPY IN THE THROMBOLYSIS IN MYOCARDIAL-INFARCTION STUDY - THROMBOLYSIS IN MYOCARDIAL-INFARCTION, PHASE-II, PILOT AND CLINICAL-TRIAL SO CIRCULATION LA English DT Article DE CLINICAL TRIALS; THROMBOLYSIS; CEREBROVASCULAR ACCIDENT; TISSUE-TYPE PLASMINOGEN ACTIVATOR, RECOMBINANT ID TISSUE PLASMINOGEN-ACTIVATOR; LEFT-VENTRICULAR FUNCTION; STREPTOKINASE; COMPLICATIONS; SURVIVAL; STROKE; SIZE AB In the Thrombolysis in Myocardial Infarction, Phase II pilot and clinical trial, 908 patients [326 (35.9%) in the pilot study and 582 (64.0%) in the randomized study] were treated with 150 mg recombinant tissue-type plasminogen (rt-PA) activator in combination with heparin and aspirin, and 3,016 patients [64 (2.1%) in the pilot study and 2,952 (97.9%) in the randomized study] were treated with 100 mg rt-PA in combination with heparin and aspirin. Adverse neurological events occurred in 23 patients treated with 150 mg rt-PA (2.5%) [nine cerebral infarctions (1.0%), 12 intracerebral hemorrhages (1.3%), and two subdural hematomas (0.2%)] and in 33 patients treated with 100 mg rt-PA (1.1%) [20 cerebral infarctions (0.7%), 11 intracerebral hemorrhages (0.4%), and two subdural hematomas (0.1%)]. The difference in adverse neurological events observed comparing the two rt-PA regimens was primarily due to a higher frequency of intracerebral bleeding among patients treated with 150 mg rt-PA (1.3% versus 0.4%, p < 0.01). Patients with recent (within 6 months) histories of stroke were not eligible for the study, and patients with any history of cerebrovascular disease were declared ineligible early in the study. The small number of patients (89, or 2.3%) with any history of neurological disease, intermittent cerebral ischemic attacks, or stroke who were enrolled before the stricter eligibility criteria were imposed or on the basis of incomplete baseline information experienced an increased frequency of intracerebral hemorrhage compared with patients without such histories (3.4% versus 0.5%). Mortality at 6 weeks after presentation among 23 patients who had intracerebral hemorrhage was 47.8%. Intracerebral hemorrhage is a severe but infrequent complication of rt-PA therapy for acute myocardial infarction. The combined frequency of intracerebral hemorrhage, subdural hematoma, and cerebral infarction after treatment with 100 mg rt-PA is comparable to that observed in other trials with thrombolytic agents in acute myocardial infarction. C1 UNIV VERMONT,BURLINGTON,VT. MARYLAND MED RES INST,BALTIMORE,MD. NHLBI,BETHESDA,MD 20892. RP GORE, JM (reprint author), UNIV MASSACHUSETTS,SCH MED,DIV CARDIOVASC MED,55 LAKE AVE N,WORCESTER,MA 01655, USA. FU NHLBI NIH HHS [HL-38460, HL-35058] NR 41 TC 261 Z9 262 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1991 VL 83 IS 2 BP 448 EP 459 PG 12 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EW940 UT WOS:A1991EW94000008 PM 1899364 ER PT J AU PROBSTFIELD, JL MARGITIC, SE FURBERG, CD AF PROBSTFIELD, JL MARGITIC, SE FURBERG, CD TI METHODOLOGIC ISSUES FACING STUDIES OF ATHEROSCLEROTIC CHANGE SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 FEB PY 1991 VL 83 IS 2 BP 726 EP 726 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EW940 UT WOS:A1991EW94000090 ER PT J AU SHARRETT, AR AF SHARRETT, AR TI INVASIVE VS NONINVASIVE STUDIES OF RISK-FACTORS AND ATHEROSCLEROSIS SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 FEB PY 1991 VL 83 IS 2 BP 726 EP 726 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EW940 UT WOS:A1991EW94000087 ER PT J AU ROSSOUW, JE BANGDIWALA, SI RIFKIND, BM AF ROSSOUW, JE BANGDIWALA, SI RIFKIND, BM TI LOW PLASMA-CHOLESTEROL AND MORTALITY - THE LIPID RESEARCH CLINICS FOLLOW-UP-STUDY SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,LIPID METAB ATHEROGENESIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 FEB PY 1991 VL 83 IS 2 BP 727 EP 727 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EW940 UT WOS:A1991EW94000092 ER PT J AU SUH, I SHATEN, J CUTLER, JA KULLER, LH AF SUH, I SHATEN, J CUTLER, JA KULLER, LH TI ALCOHOL AND CORONARY HEART-DISEASE MORTALITY IN THE MULTIPLE RISK FACTOR INTERVENTION TRIAL - THE ROLE OF HIGH-DENSITY-LIPOPROTEIN CHOLESTEROL SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1991 VL 83 IS 2 BP 731 EP 731 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EW940 UT WOS:A1991EW94000108 ER PT J AU BILD, DE RUTAN, GH HERMANSON, B TELL, GS KITTNER, SJ LABAW, F AF BILD, DE RUTAN, GH HERMANSON, B TELL, GS KITTNER, SJ LABAW, F TI PREVALENCE OF AND FACTORS RELATED TO ORTHOSTATIC HYPOTENSION AMONG THE ELDERLY - RESULTS FROM THE CARDIOVASCULAR HEALTH STUDY (CHS) SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. RI Tell, Grethe/G-5639-2015 OI Tell, Grethe/0000-0003-1386-1638 NR 0 TC 3 Z9 3 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 FEB PY 1991 VL 83 IS 2 BP 732 EP 732 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EW940 UT WOS:A1991EW94000112 ER PT J AU EMANCIPATOR, K AF EMANCIPATOR, K TI URINE AND SERUM PREGNANCY TESTS COMPARED SO CLINICAL CHEMISTRY LA English DT Letter RP EMANCIPATOR, K (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,BLDG 10,ROOM 2C407,BETHESDA,MD 20892, USA. NR 5 TC 1 Z9 2 U1 0 U2 1 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 FEB PY 1991 VL 37 IS 2 BP 302 EP 303 PG 2 WC Medical Laboratory Technology SC Medical Laboratory Technology GA EY835 UT WOS:A1991EY83500043 PM 1993349 ER PT J AU ZEIGLER, D LYNCH, SA MUIR, J BENJAMIN, J MAX, M AF ZEIGLER, D LYNCH, SA MUIR, J BENJAMIN, J MAX, M TI TRANSDERMAL CLONIDINE VS PLACEBO IN PAINFUL DIABETIC NEUROPATHY SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 132 EP 132 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000037 ER PT J AU LIEBERMAN, R KATZPER, M COOPER, M MYERS, C BURKE, G SANANTHANAN, L PECK, C AF LIEBERMAN, R KATZPER, M COOPER, M MYERS, C BURKE, G SANANTHANAN, L PECK, C TI BAYESIAN (BAY) PK CONCENTRATION CONTROLLED TRIALS (CCT) OF SURAMIN (SUR) ANTICANCER THERAPY SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 US FDA,CDER,ROCKVILLE,MD 20857. NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 155 EP 155 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000128 ER PT J AU FUDALA, PJ JOHNSON, RE HEISHMAN, SJ HENNINGFIELD, JE AF FUDALA, PJ JOHNSON, RE HEISHMAN, SJ HENNINGFIELD, JE TI EVALUATION OF THE ABUSE LIABILITY OF NALMEFENE SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIDA,ADDICT RES CTR,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 167 EP 167 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000178 ER PT J AU DIONNE, RA DOBBINS, KR HARGREAVES, KM AF DIONNE, RA DOBBINS, KR HARGREAVES, KM TI EVALUATION OF A KAPPA-OPIOID AGONIST, SPIRADOLINE, IN COMPARISON TO MORPHINE AND PLACEBO IN THE ORAL-SURGERY MODEL SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIDR,NAB,CLIN PHARMACOL UNIT,BETHESDA,MD 20892. NR 0 TC 21 Z9 21 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 183 EP 183 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000240 ER PT J AU GEORGE, DT LINNOILA, M AF GEORGE, DT LINNOILA, M TI EFFECTS OF GLUCOSE ON LACTATE INFUSIONS IN PANIC PATIENTS SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIAAA,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 184 EP 184 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000246 ER PT J AU MASANA, M MANJI, H BITRAN, J POTTER, WZ AF MASANA, M MANJI, H BITRAN, J POTTER, WZ TI LITHIUMS EFFECTS ON ADENYLATE-CYCLASE - AN INVIVO MICRODIALYSIS STUDY SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIMH,NSB,CLIN PHARMACOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 186 EP 186 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000251 ER PT J AU AWEEKA, FT GAMBERTOGLIO, J VANDERHORST, C JACOBSON, MA AF AWEEKA, FT GAMBERTOGLIO, J VANDERHORST, C JACOBSON, MA TI PHARMACOKINETICS (PK) OF CONCOMITANTLY ADMINISTERED FOSCARNET (F) AND ZIDOVUDINE (Z) IN THE TREATMENT OF PATIENTS WITH AIDS SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,SAN FRANCISCO,CA 94110. UNIV N CAROLINA,CHAPEL HILL,NC 27514. NIAID,ACTG,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 198 EP 198 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000301 ER PT J AU ADAIR, SF FREIFELD, AG DEKKER, CL SAVARESE, B TIGGES, M BURKE, RL STRAUS, SE AF ADAIR, SF FREIFELD, AG DEKKER, CL SAVARESE, B TIGGES, M BURKE, RL STRAUS, SE TI RECOMBINANT HERPES-SIMPLEX TYPE 2 GLYCOPROTEIN-D VACCINE IN CLINICAL-PHARMACOLOGY TRIAL SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 CHIRON CORP,EMERYVILLE,CA. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 200 EP 200 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000307 ER PT J AU JOHNSON, RE FUDALA, PJ JAIN, RB JAFFE, JH AF JOHNSON, RE FUDALA, PJ JAIN, RB JAFFE, JH TI BUPRENORPHINE - 1ST PHASE-II CLINICAL-TRIAL FOR THE TREATMENT OF OPIOID DEPENDENCE SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 201 EP 201 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000311 ER PT J AU KINTZEL, PE CALIS, KA AF KINTZEL, PE CALIS, KA TI RECOMBINANT INTERLEUKIN-2 - A BIOLOGICAL RESPONSE MODIFIER SO CLINICAL PHARMACY LA English DT Review AB The chemical properties, pharmacology, immunology, pharmacokinetics, clinical trials, adverse effects, and dosage and administration of recombinant interleukin-2 are reviewed. Recombinant interleukin-2 is an immunomodulating agent that stimulates the proliferation, activation, and differentiation of T and B cells, natural killer cells, and thymocytes. Two recombinant interleukin-2 products, aldesleukin and teceleukin, have been extensively studied. Most clinical experience with recombinant interleukin-2 has involved the treatment of renal cell carcinoma, melanoma, and colorectal cancer with a National Cancer Institute protocol. Patients with renal cell cancer and melanoma, who historically respond poorly to conventional therapy, have responded to therapy with recombinant interleukin-2. Recombinant interleukin-2 has been administered alone and in combination with lymphokine-activated killer cells, tumor-infiltrating lymphocytes, and interferons alfa and beta. In addition, the effect of dosage, administration rate, dosage schedule, route of administration, and cyclophosphamide pretreatment have been investigated. The adverse effects of recombinant interleukin-2 are generally reversible but are frequently severe and dose-related. Dose-limiting adverse effects include hypotension, edema, and renal dysfunction. Since hemodynamic monitoring and supportive care are essential, recombinant interleukin-2 should be administered in a critical-care setting by trained personnel. Recombinant interleukin-2 represents an advance in the therapy of renal cell cancer and melanoma and offers a new approach to the treatment of other refractory or recurrent malignancies. C1 NIH,DRUG INFORMAT SERV,BLDG 10,ROOM 1N257,BETHESDA,MD 20892. NR 0 TC 23 Z9 24 U1 0 U2 1 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0278-2677 J9 CLIN PHARMACY PD FEB PY 1991 VL 10 IS 2 BP 110 EP 128 PG 19 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EW594 UT WOS:A1991EW59400006 PM 2009728 ER PT J AU CASTILLO, C LILLIOJA, S AF CASTILLO, C LILLIOJA, S TI TECHNIQUE FOR THE COLLECTION OF PERIPHERAL LYMPH IN HUMANS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,CDNS,PHOENIX,AZ. RI Lillioja, Stephen/A-8185-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1991 VL 39 IS 1 BP A118 EP A118 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA ET786 UT WOS:A1991ET78600647 ER PT J AU SARRET, Y KLEINMAN, HK WOODLEY, DT AF SARRET, Y KLEINMAN, HK WOODLEY, DT TI THE PEPTIDE (CISKVAVS-NH2) NEAR THE AMINO TERMINUS OF THE LAMININ-A CHAIN MARKEDLY INHIBITS HUMAN KERATINOCYTE LOCOMOTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 STANFORD UNIV,DEPT DERMATOL,STANFORD,CA 94305. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1991 VL 39 IS 1 BP A19 EP A19 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA ET786 UT WOS:A1991ET78600106 ER PT J AU WONG, RA ALEXANDER, RB ROSENBERG, SA GUZE, PA AF WONG, RA ALEXANDER, RB ROSENBERG, SA GUZE, PA TI INVIVO PROLIFERATION OF ADOPTIVELY TRANSFERRED TUMOR INFILTRATING LYMPHOCYTES IN MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,HOWARD HUGHES MED INST,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1991 VL 39 IS 1 BP A33 EP A33 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA ET786 UT WOS:A1991ET78600184 ER PT J AU RIEVES, RD SHELHAMER, JH AF RIEVES, RD SHELHAMER, JH TI FIBEROPTIC BRONCHOSCOPY IN THE ICU SO COMPLICATIONS IN SURGERY LA English DT Article DE BRONCHOSCOPY; IMMUNOSUPPRESSION; KAPOSIS SARCOMA; PNEUMOCYSTIS-CARINII; PNEUMONIA AB Fiberoptic bronchoscopy has assumed a crucial role in the management of critically ill patients with respiratory failure. Bronchoscopy may include obtaining bronchial washings, brushings, biopsy, and lavage. The morbidity and mortality associated with the procedure is low. RP RIEVES, RD (reprint author), NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SCP COMMUNICATIONS INC PI NEW YORK PA 134 W 29TH ST, NEW YORK, NY 10001-5304 SN 1053-749X J9 COMPLICATION SURG JI Complicat. Surg. PD FEB PY 1991 VL 10 IS 2 BP 40 EP 44 PG 5 WC Surgery SC Surgery GA EX317 UT WOS:A1991EX31700009 ER PT J AU TYLER, EC HORTON, MR KRAUSE, PR AF TYLER, EC HORTON, MR KRAUSE, PR TI A REVIEW OF ALGORITHMS FOR MOLECULAR SEQUENCE COMPARISON SO COMPUTERS AND BIOMEDICAL RESEARCH LA English DT Review ID SIMILARITY SEARCHES; NUCLEIC-ACID; METRICS RP TYLER, EC (reprint author), NIAID,DIV COMP RES & TECHNOL,BETHESDA,MD 20892, USA. RI Tyler-Kabara, Elizabeth/H-4930-2013 OI Tyler-Kabara, Elizabeth/0000-0003-3286-1094 NR 26 TC 10 Z9 10 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 0010-4809 J9 COMPUT BIOMED RES JI Comput. Biomed. Res. PD FEB PY 1991 VL 24 IS 1 BP 72 EP 96 DI 10.1016/0010-4809(91)90014-N PG 25 WC Computer Science, Interdisciplinary Applications; Medical Informatics SC Computer Science; Medical Informatics GA EV542 UT WOS:A1991EV54200005 PM 2004526 ER PT J AU POLLACK, MM ALEXANDER, SR CLARKE, N RUTTIMANN, UE TESSELAAR, HM BACHULIS, AC AF POLLACK, MM ALEXANDER, SR CLARKE, N RUTTIMANN, UE TESSELAAR, HM BACHULIS, AC TI IMPROVED OUTCOMES FROM TERTIARY CENTER PEDIATRIC INTENSIVE-CARE - A STATEWIDE COMPARISON OF TERTIARY AND NONTERTIARY CARE FACILITIES SO CRITICAL CARE MEDICINE LA English DT Article DE QUALITY OF HEALTH CARE; QUALITY ASSURANCE; HEALTH CARE; QUALITY CONTROL; PATIENT OUTCOME ASSESSMENT; OUTCOME ASSESSMENT; HEALTH CARE; REGIONAL HEALTH PLANNING (REGIONALIZATION); INTENSIVE CARE; CRITICAL CARE; PEDIATRICS; SEVERITY OF ILLNESS ID INTERVENTION SCORING SYSTEM; SURGICAL VOLUME; HOSPITAL VOLUME; TRAUMA SYSTEM; ORANGE COUNTY; MORTALITY; IMPACT; UNIT; EFFICIENCY; VALIDATION AB Objective: To compare outcomes from pediatric intensive care in hospitals with different levels of resources. Design: Prospective, blinded comparison of outcome and care Setting: Tertiary (n = 3) and nontertiary (n = 71) hospitals in Oregon and southwestern Washington. Patients: All critically ill children admitted with respiratory failure and head trauma for 6 months. Measurements and Main Results: Severity of illness adjusted mortality rates were determined using admission day, physiologic profiles (Pediatric Risk of Mortality score) and care modalities were assessed daily. The crude mortality rate of the tertiary patients was four times higher than for the nontertiary patients (23.4% vs. 6.0%, p < .0001). In the tertiary patients, the numbers of outcomes were accurately predicted by physiologic profiles (observed: 30 deaths and 98 survivors; predicted: 29.3 deaths and 98.7 survivors, z = -.25, p > .4). However, for the nontertiary patients, the number of the deaths were significantly different than predicted (observed: 20 deaths and 315 survivors; predicted: 14.4 deaths and 320.6 survivors, z = -2.08, p < .05). The odds ratios of dying in a nontertiary vs. a tertiary facility were about 1.1, 2.3, and 8 (p < .05) for mortality risk groups of <5%, 5% to 30%, and >30%. Patients in tertiary facilities received more (p < .05) invasive (e.g., arterial catheters) and complex (e.g., mechanical ventilation) care, whereas patients in nontertiary facilities received more (p < .05) labor-intensive care (e.g., hourly vital signs). Conclusions: Care of the most seriously ill children in tertiary pediatric ICUs could improve their chances of survival. C1 OREGON DEPT HUMAN RESOURCES,DIV HLTH,EMERGENCY MED SERV,PORTLAND,OR. GEORGE WASHINGTON UNIV,SCH MED,WASHINGTON,DC 20052. NATL INST HLTH,WASHINGTON,DC. RP POLLACK, MM (reprint author), CHILDRENS HOSP,NATL MED CTR,NATL MED CTR,DEPT CRIT CARE MED,111 MICHIGAN AVE NW,WASHINGTON,DC 20010, USA. FU ORS NIH HHS [OR851115-015-2] NR 41 TC 182 Z9 187 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD FEB PY 1991 VL 19 IS 2 BP 150 EP 159 DI 10.1097/00003246-199102000-00007 PG 10 WC Critical Care Medicine SC General & Internal Medicine GA EW990 UT WOS:A1991EW99000007 PM 1796932 ER PT J AU HERMAN, DC SUFFREDINI, AF PARILLO, JE PALESTINE, AG AF HERMAN, DC SUFFREDINI, AF PARILLO, JE PALESTINE, AG TI OCULAR PERMEABILITY AFTER SYSTEMIC ADMINISTRATION OF ENDOTOXIN IN HUMANS SO CURRENT EYE RESEARCH LA English DT Article ID INDUCED UVEITIS; FLUORESCEIN; INHIBITION; DISEASE AB Acute anterior uveitis in response to the administration of systemic gram-negative endotoxin was studied in humans. The blood-aqueous barrier was evaluated in eight normal human subjects at 8 or 24 hours after systemic administration of purified gram-negative endotoxin. No significant changes in the blood-aqueous barrier were found, as evaluated by permeability to fluorescein, number of aqueous cells, flare, or intraocular pressure, despite profound endotoxin-induced cardiac, pulmonary, and circulatory effects. Gram-negative endotoxin does not appear to affect the human blood-aqueous barrier in doses that can safely be given to humans. C1 NIH,CTR CLIN,DEPT CRIT CARE MED,BETHESDA,MD 20892. NEI,IMMUNOL LAB,BETHESDA,MD 20892. RP HERMAN, DC (reprint author), MAYO CLIN & MAYO FDN,DEPT OPHTHALMOL,200 1ST ST SW,ROCHESTER,MN 55905, USA. NR 33 TC 6 Z9 6 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD FEB PY 1991 VL 10 IS 2 BP 121 EP 126 DI 10.3109/02713689109001739 PG 6 WC Ophthalmology SC Ophthalmology GA FD351 UT WOS:A1991FD35100002 PM 2036803 ER PT J AU Sellers, JR AF Sellers, James R. TI Regulation of cytoplasmic and smooth muscle myosin SO CURRENT OPINION IN CELL BIOLOGY LA English DT Article AB Phosphorylation is commonly the regulator of smooth muscle and cytoplasmic myosins, but the site and mechanism of this regulation varies widely between different species and between myosin types. C1 NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA. RP Sellers, JR (reprint author), NHLBI, Mol Cardiol Lab, NIH, Bldg 10,Room 8N202, Bethesda, MD 20892 USA. NR 62 TC 166 Z9 166 U1 0 U2 2 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0955-0674 EI 1879-0410 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD FEB PY 1991 VL 3 IS 1 BP 98 EP 104 DI 10.1016/0955-0674(91)90171-T PG 7 WC Cell Biology SC Cell Biology GA V39FV UT WOS:000209397800014 PM 1854490 ER PT J AU METZGER, H AF METZGER, H TI FC-RECEPTORS AND MEMBRANE IMMUNOGLOBULIN SO CURRENT OPINION IN IMMUNOLOGY LA English DT Article ID NATURAL-KILLER CELLS; SINGLE AMINO-ACID; TRANSFECTED CELLS; IGG FC; GAMMA-RIII; EXPRESSION; HETEROGENEITY; ISOFORMS; CD16; PRODUCTS AB This year there have been three major highlights in this field: genetic sequencing of the principal Fc receptors has been completed; new proteins associated with both Fc-gamma receptors and B-cell membrane immunoglobulins have been identified; and there has been an initial analysis of structural-functional relationships in these receptors using genetic engineering. RP METZGER, H (reprint author), NIAMSD,CHEM IMMUNOL SECT,ARTHRITIS & RHEUMATISM BRANCH,BETHESDA,MD 20892, USA. NR 39 TC 12 Z9 12 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 FEB PY 1991 VL 3 IS 1 BP 40 EP 46 DI 10.1016/0952-7915(91)90074-B PG 7 WC Immunology SC Immunology GA FA867 UT WOS:A1991FA86700008 PM 1828949 ER PT J AU FISHER, C BYERS, MR IADAROLA, MJ POWERS, EA AF FISHER, C BYERS, MR IADAROLA, MJ POWERS, EA TI PATTERNS OF EPITHELIAL EXPRESSION OF FOS PROTEIN SUGGEST IMPORTANT ROLE IN THE TRANSITION FROM VIABLE TO CORNIFIED CELL DURING KERATINIZATION SO DEVELOPMENT LA English DT Article DE C-FOS; PROTOONCOGENE; KERATINIZATION; CELL DEATH; DIFFERENTIATION ID GENE-EXPRESSION; DNA-BINDING; TERMINAL DIFFERENTIATION; MUTANT MOUSE; EPIDERMIS; IDENTIFICATION; TRANSCRIPTION; PROFILAGGRIN; ACTIVATION; KERATINS AB An antibody directed against the DNA-binding region of c-fos was used to localize the distribution of cells positive for Fos protein in epithelial tissues. The antibody consistently bound to the nuclei of epithelial cells in the late stages of differentiation, just prior to cornification. The epidermis, palate, buccal mucosa, gingiva, tongue, forestomach and vagina in estrus all produced this type of labelling, suggesting a burst of expression immediately before cell death and cornification. The differentiating cells of the hair follicle, including the hair and inner root sheath, were also labelled. Non-keratinized tissues including junctional epithelium, embryonic epidermis and diestrus vaginal epithelium showed little or no Fos labelling. With the onset of keratinization at 18 days gestation or with induction of estrus in ovariectomized mice with estradiol benzoate, the epidermis and vagina expressed Fos protein in the manner typical for keratinized tissues. The Er/Er mutant epidermis, a tissue that is blocked in its ability to keratinize, overexpresses Fos with Fos-positive cells appearing in virtually every cell layer. Gel shift analysis demonstrates the presence of a functional AP-1 complex in epidermal extracts that is recognized by our antibody. Our data suggest that the expression of Fos is intricately related to epithelial cell differentiation, especially in relation to the process of cornification and cell death. C1 UNIV WASHINGTON,DEPT ANESTHESIOL,SEATTLE,WA 98195. NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. RP FISHER, C (reprint author), UPJOHN CO,7235-25-10,KALAMAZOO,MI 49001, USA. FU NICHD NIH HHS [HD 24443]; NIDCR NIH HHS [DE 05159] NR 36 TC 77 Z9 78 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD FEB PY 1991 VL 111 IS 2 BP 253 EP 258 PG 6 WC Developmental Biology SC Developmental Biology GA FA073 UT WOS:A1991FA07300001 PM 1909952 ER PT J AU PERKINS, AS MERCER, JA JENKINS, NA COPELAND, NG AF PERKINS, AS MERCER, JA JENKINS, NA COPELAND, NG TI PATTERNS OF EVI-1 EXPRESSION IN EMBRYONIC AND ADULT TISSUES SUGGEST THAT EVI-1 PLAYS AN IMPORTANT REGULATORY ROLE IN MOUSE DEVELOPMENT SO DEVELOPMENT LA English DT Article DE EVI-1; ZINC-FINGER PROTEIN; MOUSE EMBRYOGENESIS; TRANSCRIPTION FACTORS; PROTOONCOGENES; MYELOID LEUKEMOGENESIS ID HOMEOBOX GENE; DEVELOPING LIMBS; DNA FRAGMENTS; AGAROSE GELS; PROTEIN; CELL; RNA; EMBRYOGENESIS; HYBRIDIZATION; DOMAINS AB Evi-l is a putative protooncogene first identified as a common site of retroviral integration in murine myeloid leukemias. It encodes a 145 x 10(3) M(r) nuclear DNA-binding protein that contains ten zinc-finger motifs separated into two domains, as well as an acidic domain. These features suggest that Evi-l encodes a transcriptional regulatory protein. In Drosophila, zinc-finger proteins such as Kruppel are involved in body plan patterning, and exhibit a spatially restricted pattern of expression in the embryo. To determine if Evi-l may be involved in morphogenetic processes in the mouse embryo, we have performed in situ hybridization and Northern blot analysis on embryonic and adult mouse tissues to delineate the spatial and temporal pattern of Evi-l expression. Our results show that Evi-l is expressed at high levels in a few tissues in the embryo and is widely expressed, albeit at generally low levels, in the adult. Regions that exhibit high-level expression in the embryo include: the urinary system and the Mullerian ducts; the bronchial epithelium of the lung; focal areas within the nasal cavities; the endocardial cushions and truncus swellings in the heart; and the developing limbs. Expression in the limb occurs at the highest levels from 9.5 to 12.5 days, is present in both hind and forelimbs, is absent at the apical ectodermal ridge, and does not appear to establish a gradient. This pattern of expression in the limb is reminiscent of other putative transcriptional factors such as Hox-5.2 and retinoic acid receptor-gamma, consistent with the hypothesis that particular combinations or networks of transcriptional regulatory proteins are required for morphogenesis. Overall, these results suggest that Evi-l plays an important role in mouse development. RP PERKINS, AS (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701, USA. FU NCI NIH HHS [N01-CO-74101] NR 36 TC 73 Z9 75 U1 0 U2 4 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 FEB PY 1991 VL 111 IS 2 BP 479 EP 487 PG 9 WC Developmental Biology SC Developmental Biology GA FA073 UT WOS:A1991FA07300019 PM 1893871 ER PT J AU PERRIS, R KROTOSKI, D LALLIER, T DOMINGO, C SORRELL, JM BRONNERFRASER, M AF PERRIS, R KROTOSKI, D LALLIER, T DOMINGO, C SORRELL, JM BRONNERFRASER, M TI SPATIAL AND TEMPORAL CHANGES IN THE DISTRIBUTION OF PROTEOGLYCANS DURING AVIAN NEURAL CREST DEVELOPMENT SO DEVELOPMENT LA English DT Article DE PROTEOGLYCANS; HYALURONAN; NEURAL CREST; AVIAN EMBRYO; CELL MIGRATION; EXTRACELLULAR MATRIX ID EXTRACELLULAR-MATRIX ORGANIZATION; PIGMENT CELL-MIGRATION; MONOCLONAL-ANTIBODY; SULFATE PROTEOGLYCANS; CHONDROITINASE ABC; HYALURONIC-ACID; CHICK-EMBRYO; GLYCOSAMINOGLYCANS; FIBRONECTIN; LAMININ AB In this study, we describe the distribution of various classes of proteoglycans and their potential matrix ligand, hyaluronan, during neural crest development in the trunk region of the chicken embryo. Different types of chondroitin and keratan sulfate proteoglycans were recognized using a panel of monoclonal antibodies produced against specific epitopes on their glycosaminoglycan chains. A heparan sulfate proteoglycan was identified by an antibody against its core protein. The distribution of hyaluronan was mapped using a biotinylated fragment that corresponds to the hyaluronan-binding region of cartilage proteoglycans. Four major patterns of proteoglycan immunoreactivity were observed. (1) Chondroitin-6-sulfate-rich proteoglycans and certain keratan sulfate proteoglycans were absent from regions containing migrating neural crest cells, but were present in interstitial matrices and basement membranes along prospective migratory pathways such as the ventral portion of the sclerotome. Although initially distributed uniformly along the rostrocaudal extent of the sclerotome, these proteoglycans became rearranged to the caudal portion of the sclerotome with progressive migration of neural crest cells through the rostral sclerotome and their aggregation into peripheral ganglia. (2) A subset of chondroitin/keratan sulfate proteoglycans bearing primarily unsulfated chrondroitin chains was observed exclusively in regions where neural crest cells were absent or delayed from entering, such as the perinotochordal and subepidermal spaces. (3) A subset of chondroitin/keratan sulfate proteoglycans was restricted to the perinotochordal region and, following gangliogenesis, was arranged in a metameric pattern corresponding to the sites where presumptive vertebral arches form. (4) Certain keratan sulfate proteoglycans and a heparan sulfate proteoglycan were observed in basement membranes and in an interstitial matrix uniformly distributed along the rostrocaudal extent of the sclerotome. After gangliogenesis, the neural crest-derived dorsal root and sympathetic ganglia contained both these proteoglycan types, but were essentially free of other chondroitin/keratan-proteoglycan subsets. Hyaluronan generally colocalized with the first set of proteoglycans, but also was concentrated around migrating neural crest cells and was reduced in neural crest-derived ganglia. These observations demonstrate that proteoglycans have diverse and dynamic distributions during times of neural crest development and chondrogenesis of the presumptive vertebrae. In general, chondroitin/keratan sulfate proteoglycans are abundant in regions where neural crest cells are absent, and their segmental distribution inversely correlates with that of neural crest-derived ganglia. C1 NICHHD,ROCKVILLE,MD. UNIV CALIF BERKELEY,DEPT CELL & MOLEC BIOL,BERKELEY,CA 94720. CASE WESTERN RESERVE UNIV,DEPT BIOL,CLEVELAND,OH 44106. RP PERRIS, R (reprint author), UNIV CALIF IRVINE,CTR DEV BIOL,IRVINE,CA 92717, USA. RI Lallier, Thomas/K-5977-2015; OI Domingo, Carmen/0000-0003-0987-1841 FU NICHD NIH HHS [HD-15527] NR 47 TC 140 Z9 141 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD FEB PY 1991 VL 111 IS 2 BP 583 EP 599 PG 17 WC Developmental Biology SC Developmental Biology GA FA073 UT WOS:A1991FA07300029 PM 1893876 ER PT J AU PARALKAR, VM VUKICEVIC, S REDDI, AH AF PARALKAR, VM VUKICEVIC, S REDDI, AH TI TRANSFORMING GROWTH-FACTOR-BETA TYPE-1 BINDS TO COLLAGEN-IV OF BASEMENT-MEMBRANE MATRIX - IMPLICATIONS FOR DEVELOPMENT SO DEVELOPMENTAL BIOLOGY LA English DT Article ID EXTRACELLULAR-MATRIX; EXPRESSION; CELLS; PROTEOGLYCANS; INVITRO; DIFFERENTIATION; PROLIFERATION; FIBROBLASTS; STIMULATION; OSTEOGENIN C1 NIDR,BONE CELL BIOL SECT,BLDG 30,ROOM 211,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 38 TC 235 Z9 238 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD FEB PY 1991 VL 143 IS 2 BP 303 EP 308 DI 10.1016/0012-1606(91)90081-D PG 6 WC Developmental Biology SC Developmental Biology GA EV512 UT WOS:A1991EV51200011 PM 1991553 ER PT J AU COLLIER, E GORDEN, P AF COLLIER, E GORDEN, P TI O-LINKED OLIGOSACCHARIDES ON INSULIN-RECEPTOR SO DIABETES LA English DT Article ID DENSITY LIPOPROTEIN RECEPTOR; GROWTH-FACTOR; GLYCOSYLATION; MUTANT; CARBOHYDRATE; CELLS; BIOSYNTHESIS; PATIENT; BINDING AB The insulin receptor, an integral membrane glycoprotein, is synthesized as a single-chain precursor that is cleaved to produce two mature subunits, both of which contain N-linked oligosaccharide chains and covalently linked fatty acids. We report that the beta-subunit also contains O-linked oligosaccharides. The proreceptor, alpha-subunit, and beta-subunit were labeled with [H-3]mannose and [H-3]galactose in the presence or absence of an inhibitor of O-linked glycosylation. Tryptic peptides from each component were separated by reverse-phase high-performance liquid chromatography. N- and O-linked oligosaccharide chains were identified on these peptides by specific enzymatic digestions. The proreceptor and alpha-subunit contained only N-linked oligosaccharides, whereas the beta-subunit contained both N- and O-linked oligosaccharides. The O-linked oligosaccharide chains were attached to a single tryptic fraction of the beta-subunit, which also contained N-linked chains. This fraction was further localized to the NH2-terminal tryptic peptide of the beta-subunit by specific immunoprecipitation with an anti-peptide antibody with specificity for this region. Binding of insulin and autophosphorylation of the beta-subunit were not dependent on O-linked glycosylation, because cells grown in the presence of the inhibitor exhibited a normal dose response to insulin. Therefore, the insulin receptor contains O-linked oligosaccharides on the NH2-terminal tryptic peptide of the beta-subunit, and these O-linked oligosaccharides are not necessary to the binding or autophosphorylation function of the receptor. RP COLLIER, E (reprint author), NIDDKD,DIABET BRANCH,BLDG 10,RM 85 243,BETHESDA,MD 20892, USA. NR 30 TC 28 Z9 28 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD FEB PY 1991 VL 40 IS 2 BP 197 EP 203 DI 10.2337/diabetes.40.2.197 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EU663 UT WOS:A1991EU66300005 PM 1991570 ER PT J AU ROTH, BJ SAYPOL, JM HALLETT, M COHEN, LG AF ROTH, BJ SAYPOL, JM HALLETT, M COHEN, LG TI A THEORETICAL CALCULATION OF THE ELECTRIC-FIELD INDUCED IN THE CORTEX DURING MAGNETIC STIMULATION SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE MAGNETIC STIMULATION; ELECTRIC FIELD; CORTEX ID NERVE STIMULATION; HUMAN-BRAIN; SYSTEM AB We present a mathematical model for calculating the electric field induced in the head during magnetic stimulation of the cortex. The electric field arises from 2 sources: (1) the changing magnetic field creates an electric field in the tissue by electromagnetic induction, and (2) a charge distribution arises on the surface of the head and produces its own electrostatic field. A 3-sphere model is used to represent the brain, skull and scalp. The electric field as a function of the coil position, shape and orientation is computed numerically. The charge distribution partially shields the brain from the stimulus. The electric field is insensitive to the skull conductivity, in contrast with electrical stimulation using surface electrodes. Different coil shapes and orientations are considered, and a figure-of-eight coil is shown to deliver the largest and most focal stimulus. C1 NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,HUMAN CORT PHYSIOL UNIT,BETHESDA,MD 20892. RP ROTH, BJ (reprint author), NINCDS,DIV RES SERV,BIOMED ENGN & INSTRUMENTAT BRANCH,BLDG 13,ROOM 3W13,BETHESDA,MD 20892, USA. RI Roth, Bradley/A-4920-2008 NR 29 TC 232 Z9 240 U1 1 U2 8 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD FEB PY 1991 VL 81 IS 1 BP 47 EP 56 DI 10.1016/0168-5597(91)90103-5 PG 10 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA FA301 UT WOS:A1991FA30100007 PM 1705219 ER PT J AU CLARK, DJ FELSENFELD, G AF CLARK, DJ FELSENFELD, G TI FORMATION OF NUCLEOSOMES ON POSITIVELY SUPERCOILED DNA SO EMBO JOURNAL LA English DT Article DE HISTONE OCTAMER; NEGATIVE SUPERCOILS; NUCLEOSOME; POSITIVE SUPERCOILS ID RNA-POLYMERASE TRANSCRIBES; RICH HISTONE KERNEL; CORE PARTICLES; GENE-TRANSCRIPTION; GLOBIN GENE; BETA-GLOBIN; CHROMATIN; INITIATION; TEMPLATE; INVITRO AB A transcribing RNA polymerase is though to generate positive supercoils in front of the advancing transcription complex and negative supercoils behind. We have examined the possibility that positive supercoils might destabilize nucleosomes, facilitating transcription. We show that histone octamers bind to positively supercoiled DNA, and that after the complex is relaxed, 'classical' nucleosomes are present. We tested the possibility that nucleosomes on positively supercoiled DNA are in an altered (presumably more open) conformation, but revert to the classical structure only on release of this stress. However, circular dichroic spectra, and chemical cross-linking and modification of core histones, all suggest that the complexes initially formed on positively supercoiled DNA are classical nucleosomes. Although such structures are stable, their formation requires the plasmid to become more positively supercoiled, resulting in greater superhelical stress. In contrast, formation of nucleosomes on negatively supercoiled DNA relieves superhelical stress. In an exchange experiment in which equilibrium is achieved, nucleosomes transfer from positively to negatively supercoiled DNA, as predicted from the supercoiling free energies of the reactions. This suggests a mechanism for transcription of a gene assembled into chromatin, in which octamers are sequentially transferred from the region in front of the polymerase to the region behind. RP CLARK, DJ (reprint author), NIDDKD,MOLEC BIOL LAB,BLDG 2,ROOM 301,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 47 TC 110 Z9 110 U1 0 U2 5 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD FEB PY 1991 VL 10 IS 2 BP 387 EP 395 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EX360 UT WOS:A1991EX36000018 PM 1991452 ER PT J AU JOHNSON, AE COIRINI, H INSEL, TR MCEWEN, BS AF JOHNSON, AE COIRINI, H INSEL, TR MCEWEN, BS TI THE REGULATION OF OXYTOCIN RECEPTOR-BINDING IN THE VENTROMEDIAL HYPOTHALAMIC NUCLEUS BY TESTOSTERONE AND ITS METABOLITES SO ENDOCRINOLOGY LA English DT Article ID MALE COPULATORY-BEHAVIOR; FEMALE RAT-BRAIN; ANTAGONIST D(CH2)5TYR(ME)-ORN8-VASOTOCIN; ANDROGEN RECEPTORS; ESTROGEN-TREATMENT; PENILE ERECTION; TIME COURSE; PITUITARY; CELLS; 5ALPHA-DIHYDROTESTOSTERONE AB Oxytocin (OT) receptor binding in the ventromedial hypothalamic nucleus is regulated by testosterone (T) in male rats. However, T is metabolized in the brain, and many of the central effects of T are mediated by its metabolites. The experiments reported here were designed to determine whether T affects OT receptor binding directly or through the action of its metabolites 17-beta-estradiol and 5-alpha-dihydrotestosterone. Adult male rats were either sham operated or castrated and treated 1 week later with T propionate (TP), 17-beta-estradiol benzoate (EB), dihydrotestosterone benzoate (DHTB), DHTB plus EB, or oil. OT receptor binding was assessed autoradiographically using [I-125]d(CH2)5[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT. In addition, seminal vesicle weights were measured as an index of androgenic activity. These experiments showed that TP and DHBT plus EB increased OT receptor binding in the ventromedial hypothalamic nucleus to the levels in intact males. Treatment with EB alone partially reinstated binding to the levels in intact males, while DHTB treatment was without effect. Castrated males treated with either TP or DHBT had seminal vesicle weights comparable to those of gonadally intact males and greater than those of animals in all other steroid conditions, indicating that sufficient levels of circulating steroids were attained in these groups. These data suggest that the induction of hypothalamic OT receptor binding by T is the result of the combined actions of estradiol and dihydrotestosterone. However, the mechanism underlying this interaction is unknown. C1 NIMH,CLIN SCI LAB,COMPARAT STUDIES BRAIN & BEHAV SECT,POOLESVILLE,MD 20837. ROCKEFELLER UNIV,NEUROENDOCRINOL LAB,NEW YORK,NY 10021. FU NINDS NIH HHS [NS-07080] NR 41 TC 53 Z9 53 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 FEB PY 1991 VL 128 IS 2 BP 891 EP 896 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300036 PM 1846593 ER PT J AU FONTANA, JA BURROWSMEZU, A CLEMMONS, DR LEROITH, D AF FONTANA, JA BURROWSMEZU, A CLEMMONS, DR LEROITH, D TI RETINOID MODULATION OF INSULIN-LIKE GROWTH FACTOR-BINDING PROTEINS AND INHIBITION OF BREAST-CARCINOMA PROLIFERATION SO ENDOCRINOLOGY LA English DT Article ID CANCER CELL-LINES; HUMAN AMNIOTIC-FLUID; IGF-I; ACID RECEPTOR; FACTOR-BETA; 2 FORMS; 4-HYDROXYTAMOXIFEN; IDENTIFICATION; INVITRO; CULTURE AB Retinoids induce cellular differentiation and inhibit cellular proliferation. Proliferation of human breast carcinoma cells in vitro is markedly inhibited by these compounds. On the other hand, insulin-like growth factors (IGFs) and their receptors seem to be involved in the growth of certain breast carcinoma cells by autocrine or paracrine effects. Since the effects of both IGF-I and IGF-II may be modulated by specific binding proteins (IGF-BPs) we examined the possibility that one mechanism by which retinoic acid may inhibit cancer growth is by an alteration in these BPs, thereby blocking IGF's growth effect. Retinoic acid (RA; 1-mu-M) completely blocked the effect of IGF-I (50 ng/ml) on enhancing proliferation on MCF-7 cells in culture. this effect of RA was not associated with any significant change in specific IGF-I-binding sites on these cells. RA induced a 3-fold increase in IGF-binding activity in conditioned medium, measured using a polyethylene glycol-immunoglobulin precipitation assay and a charcoal absorption assay. This increase was associated with the appearance of 42- and 46-kDa IGF-BPs on ligand blotting. The effect of RA on these IGF-BPs was time and concentration dependent. In contrast, during some experiments the 27- and 36-kDa BPs actually decreased. These findings support the hypothesis that RA may inhibit the growth of certain breast carcinoma cells by increasing the secretion of certain IGF-BPs, which could directly modulate the growth effect of IGFs. C1 UNIV MARYLAND,DEPT MED,BALTIMORE,MD 21201. VET ADM MED CTR,BALTIMORE,MD 21202. UNIV N CAROLINA,SCH MED,DEPT MED,CHAPEL HILL,NC 27514. NIDDKD,DIABET BRANCH,BETHESDA,MD 20982. RP FONTANA, JA (reprint author), UNIV MARYLAND,CTR CANC,ROOM S9D05,22 S GREENE ST,BALTIMORE,MD 21201, USA. OI Fontana, Joseph/0000-0003-3829-3358 NR 48 TC 113 Z9 113 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 FEB PY 1991 VL 128 IS 2 BP 1115 EP 1122 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300066 PM 1703480 ER PT J AU SAJI, M KOHN, LD AF SAJI, M KOHN, LD TI INSULIN AND INSULIN-LIKE GROWTH FACTOR-I INHIBIT THYROTROPIN-INCREASED IODIDE TRANSPORT IN SERUM-DEPLETED FRTL-5 RAT-THYROID CELLS - MODULATION OF ADENOSINE-3',5'-MONOPHOSPHATE SIGNAL ACTION SO ENDOCRINOLOGY LA English DT Article ID TYROSINE AMINOTRANSFERASE; THYROGLOBULIN GENE; ADENYLYL CYCLASE; MESSENGER-RNA; DNA-SYNTHESIS; CYCLIC-AMP; STIMULATION; ADENOSINE-3',5'-MONOPHOSPHATE; TRANSCRIPTION; EXPRESSION AB Insulin enhances the ability of TSH to induce iodide uptake in FRTL-5 rat thyroid cells maintained in 5% serum; however, in cells maintained in 0.2% serum, insulin inhibits the ability of TSH to induce iodide uptake. Since the inhibitory action of insulin is duplicated by 100-fold lower concentrations of insulin-like growth factor-I (IGF-I), inhibition appears to be mediated by the IGF-I receptor. Insulin and IGF-I inhibit the action of a cAMP analog to induce iodide uptake in a manner identical to TSH, but do not inhibit basal or TSH-increased cAMP levels; inhibition, thus, results from regulation of cAMP signal action rather cAMP signal generation. Inhibition is associated with a more than 2-fold decrease in the maximum velocity of iodide influx, a less than 15% change in the rate of iodide efflux, and no change in the K(m) for iodide influx, i.e. inhibition effectively results from a decrease in the number of iodide porters. The inhibitory aaction of insulin/IGF-I is not additive with hydrocortisone, which, under the same conditions, also inhibits TSH- or cAMP-induced iodide porter activity. Actinomycin-D, given 24 h after TSH, superinduces TSH-induced iodide porter activity and abolishes the inhibition by insulin, IGF-I, and/or hydrocortisone; a similar paradoxical effect of actinomycin-D under these conditions has been explained by its ability to inhibit the action of a cAMP-induced factor that increases mRNA degradation. The inhibitory actions of insulin, IGF-I, and hydrocortisone on cAMP-induced iodide porter activity contrast with their simultaneous and synergistic stimulation of the transcriptional action of cAMP on DNA and thyroglobulin synthesis under these conditions. C1 NIDDKD,DEPT BIOCHEM METAB,BIOCHEM & METAB LAB,CELL REGULAT SECT,BLDG 10,ROOM 9B13,BETHESDA,MD 20892. RI Saji, Motoyasu/E-4007-2011 NR 49 TC 21 Z9 22 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 FEB PY 1991 VL 128 IS 2 BP 1136 EP 1143 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300069 PM 1846578 ER PT J AU DYM, M LAMSAMCASALOTTI, S JIA, MC KLEINMAN, HK PAPADOPOULOS, V AF DYM, M LAMSAMCASALOTTI, S JIA, MC KLEINMAN, HK PAPADOPOULOS, V TI BASEMENT-MEMBRANE INCREASES G-PROTEIN LEVELS AND FOLLICLE-STIMULATING-HORMONE RESPONSIVENESS OF SERTOLI-CELL ADENYLYL CYCLASE ACTIVITY SO ENDOCRINOLOGY LA English DT Article ID GTP-BINDING PROTEIN; BETA-SUBUNIT; KINASE-C; EXTRACELLULAR-MATRIX; ALPHA-SUBUNIT; RAT; LAMININ; IDENTIFICATION; FORSKOLIN; DIFFERENTIATION AB On a basement membrane substrate, Sertoli cells in culture have been shown to assume a phenotype similar to that of the in vivo differentiated cells. Sertoli cells from 10-day-old rats were cultured on plastic and on different extracellular matrix substrates [laminin, a reconstituted basement membrane (Matrigel), and a synthetic laminin peptide containing the arginine-glycine-aspartic acid (RGD) tripeptide sequence] to investigate the effects of the extracellular matrix on FSH responsiveness. Both laminin and Matrigel markedly enhanced the cAMP response to FSH and cholera toxin, indicating modifications at the level of guanine nucleotide-binding regulatory (G) proteins. Furthermore, Sertoli cells grown on either of these two substrates responded to physiological levels of FSH (25-50 ng/ml), whereas pharmacological levels of FSH (500 ng/ml) were required for cells grown on either plastic or on the RGD-containing laminin peptide. Immunoblotting of Sertoli cell plasma membranes with antibodies directed against the alpha-subunit of the stimulatory G-protein (Gs-alpha) of adenylyl cyclase indicated that Sertoli cell culture on either laminin or Matrigel increased the amounts of Gs-alpha. These results were further confirmed by immunoprecipitating the Gs-alpha protein from the particulate fraction of [S-35] methionine metabolically labeled Sertoli cells. However, Northern blot analysis using a cDNA probe for Gs-alpha did not demonstrate changes in gene expression when Sertoli cells were grown on the various substrates. Immunofluorescent studies revealed that the Gs complex of adenylyl cyclase was preferentially located at the base of the Sertoli cells at the site of contact with the extracellular matrix. These data suggest that culture of epithelial Sertoli cells on basement membrane substrates enhances the Gs complex of adenylyl cyclase and the cAMP response to FSH, consistent with the more differentiated morphology and function of the cells. C1 GEORGETOWN UNIV,MED CTR,SCH MED,DEPT ANAT & CELL BIOL,3900 RESERVOIR RD NW,WASHINGTON,DC 20007. NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. OI Papadopoulos, Vassilios/0000-0002-1183-8568 FU NICHD NIH HHS [HD-16260] NR 66 TC 54 Z9 54 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 FEB PY 1991 VL 128 IS 2 BP 1167 EP 1176 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300073 PM 1846579 ER PT J AU YANG, YWH ROBBINS, AR NISSLEY, SP RECHLER, MM AF YANG, YWH ROBBINS, AR NISSLEY, SP RECHLER, MM TI THE CHICK-EMBRYO FIBROBLAST CATION-INDEPENDENT MANNOSE 6-PHOSPHATE RECEPTOR IS FUNCTIONAL AND IMMUNOLOGICALLY RELATED TO THE MAMMALIAN INSULIN-LIKE GROWTH FACTOR-II (IGF-II) MAN 6-P RECEPTOR BUT DOES NOT BIND IGF-II SO ENDOCRINOLOGY LA English DT Article ID MULTIPLICATION-STIMULATING ACTIVITY; HAMSTER OVARY CELLS; LYSOSOMAL-ENZYME; POLYACRYLAMIDE GELS; LIGAND INTERACTIONS; FILM DETECTION; LIVER-CELLS; HUMAN-SERUM; PROTEINS; CLONING AB The insulin-like growth factor-II (IGF-II)/Mannose 6-P receptor (Man 6-P) is a multifunctional receptor that binds two unrelated ligands, IGF-II and lysosomal enzymes that contain Man 6-P recognition markers. Although this receptor has been extensively characterized in mammalian cells, binding of radiolabeled IGF-II to this receptor in avian cells and tissues has not been reported. In the present study, we demonstrate that chick embryo fibroblasts (CEFs) bind and internalize lysosomal enzymes in a Man 6-P-inhibitable fashion, and possess a protein immunologically related to the mammalian IGF-II/Man 6-P receptor that binds lysosomal enzymes with man 6-P recognition markers but does not bind IGF-II. 1) When lysates of biosynthetically labeled CEFs were affinity-purified on beta-galactosidase-Sepharose, an approximately 250 kilodalton protein was observed in the Man 6-P eluate but not in the Glc 1-P or mannose eluates, that was precipitated by antisera to purified rat and bovine IGF-II/Man 6-P receptors, but not by nonimmune serum . 2) When CEFs were incubated with [s-35] proteins enriched in lysosomal enzymes, Man 6-P inhibited binding (0 C) and uptake (34 C) in a dose-dependent fashion. Binding was unchanged in the absence of divalent cations. At low sugar concentrations, binding and uptake were inhibited selectively by Man 6-P and the conformationally similar sugar phosphate, Fru 1-P, a specificity similar to that of mammalian cation-independent Man 6-P receptors. 3) When affinity-purified lysates from biosynthetically labeled CEFs were incubated with antiserum to the rat IGF-II/Man 6-P receptor, a 245 kilodalton protein was immunoprecipitated from lysates that had been affinity purified on beta-galactosidase-Sepharose but not after purification on IGF-II-Sepharose. By contrast, truncated IGF-II/Man 6-P receptor, presumably internalized from the fetal bovine serum used to feed the cells, was purified from lysates of unlabeled CEFs on IGF-II-Sepharose. Thus, CEFs possess a cation-independent Man 6-P receptor that is similar in size and immunological reactivity to the mammalian IGF-II/Man 6-P receptor, and binds and internalizes lysosomal enzymes but, unlike the mammalian receptor, does not bind IGF-II. C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NCI,METAB BRANCH,BETHESDA,MD 20892. RP YANG, YWH (reprint author), NIDDKD,MOLEC CELLULAR & NUTR ENDOCRINOL BRANCH,BLDG 10,ROOM 8D-08,BETHESDA,MD 20892, USA. NR 69 TC 38 Z9 39 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 FEB PY 1991 VL 128 IS 2 BP 1177 EP 1189 PG 13 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300074 PM 1846580 ER PT J AU NORDBERG, GF MAHAFFEY, KR FOWLER, BA AF NORDBERG, GF MAHAFFEY, KR FOWLER, BA TI INTERNATIONAL WORKSHOP ON LEAD IN BONE - IMPLICATIONS FOR DOSIMETRY AND TOXICOLOGY - INTRODUCTION AND SUMMARY SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Editorial Material C1 UNIV MARYLAND,PROGRAM TOXICOL,660 W REDWOOD ST,BALTIMORE,MD 21201. UMEA UNIV,DEPT ENVIRONM HYG,S-90187 UMEA,SWEDEN. NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 22 Z9 23 U1 1 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD FEB PY 1991 VL 91 BP 3 EP 7 PG 5 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA FD604 UT WOS:A1991FD60400001 PM 1674907 ER PT J AU HE, RY BREITMAN, TR AF HE, RY BREITMAN, TR TI RETINOIC ACID INHIBITS SODIUM BUTYRATE-INDUCED MONOCYTIC DIFFERENTIATION OF HL60 CELLS WHILE SYNERGISTICALLY INDUCING GRANULOCYTOID DIFFERENTIATION SO EUROPEAN JOURNAL OF HAEMATOLOGY LA English DT Article DE BUTYRATES; CELL DIFFERENTIATION; DRUG SYNERGY; LEUKEMIA; TRETINOIN ID ACUTE PROMYELOCYTIC LEUKEMIA; HL-60 CELLS; LINE HL-60; ENDOGENOUS COMPOUND; HUMAN-BLOOD; INDUCTION; CULTURE; PROLIFERATION; METHYLATION; MATURATION AB The human myeloid leukemia cell line HL60 is an in vitro model to study myeloid differentiation. HL60 cells differentiate along different cell type lineages in response to a variety of compounds. The direction of differentiation is usually inducer-specific. However, the response of HL60 cells to sodium n-butyrate (NaB) is pleiotropic. NaB induces HL60 along the monocytic, neutrophilic, eosinophilic, and basophilic pathways. In this study we saw that physiologic concentrations of all-trans-retinoic acid (RA) switched the direction of NaB-induced differentiation from monocytic to granulocytic. We showed previously (Breitman & He, Cancer Res 1990: 50: 6268-6273) that combinations of RA and NaB synergistically induce HL60 to cells that reduce nitrobule tetrazolium. The present study shows that this synergy was even greater if the parameter measured was mature granulocytes. Our results raise the possibility that the endogenous RA in the serum used to grow cells in culture may affect the direction of differentiation of HL60 cells induced by NaB. Furthermore, our results may provide additional rationale for the use of combinations of RA and NaB in the treatment of some leukemias. C1 NCI,DEV THERAPEUT PROGRAM,DIV CANC TREATMENT,BIOL CHEM LAB,BLDG 37,ROOM 5D-02,BETHESDA,MD 20892. NR 48 TC 22 Z9 22 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-4441 J9 EUR J HAEMATOL JI Eur. J. Haematol. PD FEB PY 1991 VL 46 IS 2 BP 93 EP 100 PG 8 WC Hematology SC Hematology GA EZ306 UT WOS:A1991EZ30600005 PM 1995327 ER PT J AU PROUST, JJ SHAPER, NL BUCHHOLZ, MA NORDIN, AA AF PROUST, JJ SHAPER, NL BUCHHOLZ, MA NORDIN, AA TI T-CELL ACTIVATION IN THE ABSENCE OF INTERLEUKIN-2 (IL2) RESULTS IN THE INDUCTION OF HIGH-AFFINITY IL-2 RECEPTOR UNABLE TO TRANSMIT A PROLIFERATIVE SIGNAL SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID LYMPHOCYTES-T; GROWTH-FACTOR; BETA-CHAIN; ANTIGENIC-STIMULATION; MURINE INTERLEUKIN-2; BINDING-PROTEIN; CROSS-LINKING; ALPHA-CHAIN; EXPRESSION; COMPLEX AB Although interleukin 2 (IL 2) clearly up-regulates the expression of the p55 chain of the IL 2 receptor (IL 2R) little is known about its role in the induction of the high-affinity IL 2R. Resting T lymphocytes were induced to express IL 2R under experimental conditions in which IL2 production was not induced or was prevented. Under these conditions high- and low-affinity IL 2R were easily demonstrated by Scatchard analysis. Northern blot analysis confirmed the accumulation of p55 specific mRNA and the absence of the IL 2 transcript. High-affinity IL 2R induced in the complete absence of IL 2 were unable to transmit a proliferative response unless exposed to extremely high concentrations of IL 2. The addition of picomolar amounts of recombinant IL 2 or the initiation of endogenous IL 2 production during the induction period restored the functionality of high-affinity IL 2R. Also, T cells induced to generate IL 2 displayed functional high-affinity IL 2R even in the presence of monoclonal antibodies blocking extracellular IL2 and IL2R. These results indicate that the presence of IL 2 during the early phase of T cell activation is an absolute requirement for the induction of fully operational high-affinity IL 2R and that low amounts of intracellular IL 2 are sufficient to confer functional properties to these receptors. The data also suggest that an intracellular as well as an extracellular high-affinity structure, expressed as a consequence of cell activation, is responsible for conferring competence to the high-affinity IL 2R involved in IL2-dependent proliferation. C1 NIA,GERONTOL RES CTR,CLIN IMMUNOL SECT,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,CTR ONCOL,BALTIMORE,MD 21205. NR 52 TC 20 Z9 21 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD FEB PY 1991 VL 21 IS 2 BP 335 EP 341 DI 10.1002/eji.1830210214 PG 7 WC Immunology SC Immunology GA FA425 UT WOS:A1991FA42500013 PM 1999222 ER PT J AU HOLE, NJK YOUNGCOOPER, GO MAGE, RG AF HOLE, NJK YOUNGCOOPER, GO MAGE, RG TI MAPPING OF THE DUPLICATED RABBIT IMMUNOGLOBULIN-CHI LIGHT CHAIN LOCUS SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID KAPPA-GENE EXPRESSION; MOUSE LAMBDA-GENES; BASILEA RABBITS; STABLE INTEGRATION; TOPOISOMERASE-II; MESSENGER-RNA; INTRONIC MAR; ENHANCER; SEQUENCE; SITES AB The rabbit has two isotypic forms of the immunoglobulin aleph light chain, K1 and K2, which probably arose by duplication. In the normal rabbit, only traces of K2 light chains are produced. However, K2 levels are elevated in allotype-suppressed rabbits and in the Basilea strain which does not produce K1 because of a K1 mRNA splice site mutation. Previous cloning and sequencing showed that each isotype has its own set of J aleph genes but it was not known whether the two isotypes utilize shared or separate sets of V aleph genes. In addition, although genetic linkage of allotypes associated with the K1 and K2 genes has been demonstrated, physical linkage had not been previously demonstrated by overlapping cosmid or phage clones. We used pulsed field and transverse alternating field electrophoresis to obtain megabase maps and to estimate the size of the duplication of the rabbit aleph light chain locus. We found that the two C aleph genes are about 1 megabase apart. One explanation for the poor expression of K2, could be great physical distance from V aleph genes. However, we found that there are V aleph, J aleph and C aleph 2 genes within a approximately 105-kb fragment. Thus, physical distance of V aleph from C aleph 2 may not be the basis for poor K2 expression. C1 NIAID,IMMUNOL LAB,IMMUNOL LAB,BLDG 10,11-N-311,BETHESDA,MD 20892. NR 33 TC 16 Z9 16 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD FEB PY 1991 VL 21 IS 2 BP 403 EP 409 DI 10.1002/eji.1830210223 PG 7 WC Immunology SC Immunology GA FA425 UT WOS:A1991FA42500022 PM 1671838 ER PT J AU ALLEGRUCCI, M YOUNGCOOPER, GO ALEXANDER, CB NEWMAN, BA MAGE, RG AF ALLEGRUCCI, M YOUNGCOOPER, GO ALEXANDER, CB NEWMAN, BA MAGE, RG TI PREFERENTIAL REARRANGEMENT IN NORMAL RABBITS OF THE 3' VHA ALLOTYPE GENE THAT IS DELETED IN ALICIA MUTANTS - SOMATIC HYPERMUTATION CONVERSION MAY PLAY A MAJOR ROLE IN GENERATING THE HETEROGENEITY OF RABBIT HEAVY-CHAIN VARIABLE REGION SEQUENCES SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTIBODY DIVERSITY; IMMUNOGLOBULIN; CHICKEN; ORGANIZATION; RESTRICTION; EXPRESSION; REPERTOIRE; SEGMENTS; DNA; LYMPHOCYTES AB The rabbit is unique in having well-defined allotypes in the variable region of the heavy chain. Products of the V(H)a locus, (with alleles a1, a2, and a3), account for the majority of the serum immunoglobulins. A small percentage of the serum immunoglobulins are a-negative. In 1986, Kelus and Weiss described a mutation that depressed the expression of the Ig V(H) a2 genes in an a1/a2 rabbit. From this animal the Alicia rabbit strain was developed and the mutation was termed ali. We previously showed, using Southern analysis and the transverse alternating field electrophoresis technique, that the difference between the ali rabbit and normal is a relative small deletion including some of the most 3' V(H) genes. The most J(H) proximal 3' V(H)1 genes in DNA from normal rabbits of a1, a2 and a3 haplotypes encode a1, a2 and a3 molecules respectively, and it has been suggested that these genes are responsible for allelic inheritance of V(H)a allotypes. The present study suggests that the 3' end of the V(H) locus probably plays a key role in regulation of V(H) gene expression in rabbits because V(H) gene(s) in this region are the target(s) of preferential VDJ rearrangements. This raises the possibility that mechanisms such as somatic gene conversion and hypermutation are at work to generate the antibody repertoire in this species. Our data support the view that the 3' V(H)1 gene may be the preferred target for rearrangement in normal rabbits, and for the normal chromosome in heterozygous ali animals. However, homozygous ali rabbits with a deletion that removed the a2-encoding V(H)1 on both chromosomes do survive, rearrange other V(H) genes and produce normal levels of immunoglobulins as well as a significant percentage of B cells which bear the a2 allotype. This challenges the view that one V(H) gene, V(H)1, is solely responsible for the inheritance pattern of V(H)a allotypes. C1 NIAID,IMMUNOL LAB,BLDG 10,11-N-311,BETHESDA,MD 20892. OI Allegrucci, Massimo/0000-0002-1147-3802 NR 43 TC 41 Z9 41 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD FEB PY 1991 VL 21 IS 2 BP 411 EP 417 DI 10.1002/eji.1830210224 PG 7 WC Immunology SC Immunology GA FA425 UT WOS:A1991FA42500023 PM 1999224 ER PT J AU TAKEYA, M YOSHIMURA, T LEONARD, EJ KATO, T OKABE, H TAKAHASHI, K AF TAKEYA, M YOSHIMURA, T LEONARD, EJ KATO, T OKABE, H TAKAHASHI, K TI PRODUCTION OF MONOCYTE CHEMOATTRACTANT PROTEIN-1 BY MALIGNANT FIBROUS HISTIOCYTOMA - RELATION TO THE ORIGIN OF HISTIOCYTE-LIKE CELLS SO EXPERIMENTAL AND MOLECULAR PATHOLOGY LA English DT Article ID SOFT-TISSUE TUMORS; BLOOD MONONUCLEAR LEUKOCYTES; AMINO-ACID ANALYSIS; PARAFFIN SECTIONS; MONOCLONAL-ANTIBODIES; CHEMOTACTIC FACTOR; EXPRESSION; ANTIGENS; IMMUNOPEROXIDASE; PURIFICATION C1 NCI,IMMUNOBIOL LAB,IMMUNOPATHOL SECT,FREDERICK,MD 21701. SHIGA UNIV,SCH MED,DEPT LAB MED,OTSU,SHIGA 52021,JAPAN. RP TAKEYA, M (reprint author), KUMAMOTO UNIV,SCH MED,DEPT PATHOL 2,2-2-1 HONJO,KUMAMOTO 860,JAPAN. NR 42 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 0014-4800 J9 EXP MOL PATHOL JI Exp. Mol. Pathol. PD FEB PY 1991 VL 54 IS 1 BP 61 EP 71 DI 10.1016/0014-4800(91)90044-X PG 11 WC Pathology SC Pathology GA EY951 UT WOS:A1991EY95100007 PM 1847338 ER PT J AU HARRISON, ET LUYTEN, FP REDDI, AH AF HARRISON, ET LUYTEN, FP REDDI, AH TI OSTEOGENIN PROMOTES REEXPRESSION OF CARTILAGE PHENOTYPE BY DEDIFFERENTIATED ARTICULAR CHONDROCYTES IN SERUM-FREE MEDIUM SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID DIFFERENTIATED COLLAGEN PHENOTYPE; MONOLAYER-CULTURE; CELL-SHAPE; GROWTH; INVITRO; STIMULATION; EXPRESSION; CHONDROGENESIS; FIBROBLAST; SPINNER RP HARRISON, ET (reprint author), NIDR,CELLULAR DEV & ONCOL LAB,BONE CELL BIOL SECT,BETHESDA,MD 20892, USA. NR 30 TC 33 Z9 34 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD FEB PY 1991 VL 192 IS 2 BP 340 EP 345 DI 10.1016/0014-4827(91)90050-5 PG 6 WC Oncology; Cell Biology SC Oncology; Cell Biology GA EU287 UT WOS:A1991EU28700003 PM 1988283 ER PT J AU CAI, DC WEBBER, MM DE LUCA, LM AF CAI, DC WEBBER, MM DE LUCA, LM TI RETINOIDS ENHANCE LECTIN BINDING TO GP130, A GLYCOPROTEIN OF NIH-3T3 CELLS - CORRELATION WITH CELL-GROWTH AND ADHESION SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID TRANSFORMED MOUSE FIBROBLASTS; BIOLOGICAL-ACTIVITY; ACID RECEPTOR; IDENTIFICATION; SIALYLTRANSFERASE; DIFFERENTIATION; GLYCOSYLATION; DERIVATIVES; CARCINOMA; LINE C1 NCI, CELLULAR CARCIOOGENESIS & TUMOR PROMOT LAB, BLDG 37, ROOM 3A17, BETHESDA, MD 20892 USA. NR 27 TC 15 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD FEB PY 1991 VL 192 IS 2 BP 366 EP 372 DI 10.1016/0014-4827(91)90053-W PG 7 WC Oncology; Cell Biology SC Oncology; Cell Biology GA EU287 UT WOS:A1991EU28700006 PM 1988285 ER PT J AU SIEBER, KP HUBER, M KASLOW, D BANKS, SM TORII, M AIKAWA, M MILLER, LH AF SIEBER, KP HUBER, M KASLOW, D BANKS, SM TORII, M AIKAWA, M MILLER, LH TI THE PERITROPHIC MEMBRANE AS A BARRIER - ITS PENETRATION BY PLASMODIUM-GALLINACEUM AND THE EFFECT OF A MONOCLONAL-ANTIBODY TO OOKINETES SO EXPERIMENTAL PARASITOLOGY LA English DT Article DE PLASMODIUM-GALLINACEUM; AEDES-AEGYPTI; MALARIA; MOSQUITOS; OOKINETES; PERITROPHIC MEMBRANE; MIDGUT ID TRANSMISSION-BLOCKING ANTIBODIES; ANOPHELES-STEPHENSI LISTON; MALARIA PARASITE; AEDES-AEGYPTI; SEXUAL STAGES; MOSQUITOS; IMMUNIZATION; MIDGUT; FALCIPARUM; ANTIGENS C1 CASE WESTERN RESERVE UNIV,INST PATHOL,CLEVELAND,OH 44106. RP SIEBER, KP (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [AI-10645] NR 29 TC 81 Z9 83 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 0014-4894 J9 EXP PARASITOL JI Exp. Parasitol. PD FEB PY 1991 VL 72 IS 2 BP 145 EP 156 DI 10.1016/0014-4894(91)90132-G PG 12 WC Parasitology SC Parasitology GA EY211 UT WOS:A1991EY21100003 PM 2009919 ER PT J AU PIMENTA, PFP SARAIVA, EMB SACKS, DL AF PIMENTA, PFP SARAIVA, EMB SACKS, DL TI THE COMPARATIVE FINE-STRUCTURE AND SURFACE GLYCOCONJUGATE EXPRESSION OF 3 LIFE STAGES OF LEISHMANIA-MAJOR SO EXPERIMENTAL PARASITOLOGY LA English DT Article DE LEISHMANIA; METACYCLIC; ULTRASTRUCTURE; CELL SURFACE, LIPOPHOSPHOGLYCAN; GP63; IMMUNOCYTOCHEMISTRY; LOGARITHMIC PHASE PROMASTIGOTE (LP); METACYCLIC PROMASTIGOTE (MP); PEANUT AGGLUTININ (PNA); LIPOPHOSPHOGLYCAN (LPG); ELECTRON MICROSCOPIC (EM); DULBECCOS PHOSPHATE-BUFFERED SALINE (D-PBS) ID MEXICANA-AMAZONENSIS; MONOCLONAL-ANTIBODIES; DEVELOPMENTAL STAGES; ACID-PHOSPHATASE; PROMASTIGOTES; MACROPHAGES; MEMBRANE; DONOVANI; LIPOPHOSPHOGLYCAN; IDENTIFICATION RP PIMENTA, PFP (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA. NR 31 TC 99 Z9 102 U1 1 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4894 J9 EXP PARASITOL JI Exp. Parasitol. PD FEB PY 1991 VL 72 IS 2 BP 191 EP 204 DI 10.1016/0014-4894(91)90137-L PG 14 WC Parasitology SC Parasitology GA EY211 UT WOS:A1991EY21100008 PM 2009923 ER PT J AU ZIGLER, JS RAO, PV AF ZIGLER, JS RAO, PV TI ENZYME CRYSTALLINS AND EXTREMELY HIGH PYRIDINE-NUCLEOTIDE LEVELS IN THE EYE LENS SO FASEB JOURNAL LA English DT Article DE CRYSTALLINE LENS; ENZYME/CRYSTALLINS; PYRIDINE NUCLEOTIDE LEVELS AB Taxon-specific crystallins are proteins present in high abundance in the lens of phylogenetically restricted groups of animals. Recently it has been found that these proteins are actually enzymes which the lens has apparently adopted to serve as structural proteins. Most of these proteins have been shown to be identical to, or related to, oxidoreductases. In guinea pig lens, which contains zeta-crystallin, a protein with an NADPH-dependent oxidoreductase activity, the levels of both NADPH and NADP+ are extremely high and correlate with the concentration of zeta-crystallin. We report here nucleotide assays on lenses from vertebrates containing other enzyme/crystallins. In each case where the enzyme/crystallin is a pyridine nucleotide-binding protein the level of that particular nucleotide is extremely high in the lens. The presence of an enzyme/crystallin does not affect the lenticular concentrations of those nucleotides which are not specifically bound. The possibility that nucleotide binding may be a factor in the selection of some enzymes to serve as enzyme/crystallins is considered. RP ZIGLER, JS (reprint author), NEI,MECHANISMS OCULAR DIS LAB,9000 ROCKVILLE PIKE,BLDG 6,RM 237,BETHESDA,MD 20892, USA. NR 12 TC 46 Z9 46 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB PY 1991 VL 5 IS 2 BP 223 EP 225 PG 3 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA EZ002 UT WOS:A1991EZ00200013 PM 2004667 ER PT J AU CHHABRA, RS HUFF, JE HASEMAN, JK ELWELL, MR PETERS, AC AF CHHABRA, RS HUFF, JE HASEMAN, JK ELWELL, MR PETERS, AC TI CARCINOGENICITY OF PARA-CHLOROANILINE IN RATS AND MICE SO FOOD AND CHEMICAL TOXICOLOGY LA English DT Article ID ANIMAL CARCINOGENICITY; ANILINE AB p-Chloroaniline (PCA), a dye intermediate, was evaluated for potential long-term toxicity and carcinogenicity. Groups of 50 F344/N rats of each sex were given by gavage PCA hydrochloride in deionized water at doses of 0, 2, 6 or 18 mg/kg body weight, 5 days/wk for 103 wk. Groups of 50 male and female B6C3F1 mice of each sex were given 0, 3, 10 or 30 mg/kg on the same schedule. In general, body weights and survival were unaffected by PCA administration. In rats the group given 18 mg/kg had mild haemolytic anaemia and slight increases in methaemoglobin at various times during the study. Fibrosis of the spleen was significantly increased in all PCA-treated groups of male rats and in the 18-mg/kg group of female rats. Sarcomas of the spleen occurred in male rats, their incidence being 0/49, 1/50, 3/50 and 38/50 in control low-, mid- and high-dose groups, respectively. There was a slightly increased incidence of pheochromocytomas of the adrenal gland in both male and female rats. Dosed groups of male mice had increased incidences of hepatocellular adenomas or carcinomas (11/50, 21/49, 20/50 and 21/50 in controls, low- mid- and high-dose groups, respectively). Haemangiosarcomas of the liver or spleen were also increased in the high-dose group (incidences of 4/50, 4/49, 1/50 and 10/50 in controls, low-, mid- and high-dose groups, respectively). In conclusion, PCA was carcinogenic in male rats and male mice. C1 BATTELLE MEM INST,COLUMBUS,OH 43201. RP CHHABRA, RS (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 29 TC 42 Z9 45 U1 0 U2 4 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 FEB PY 1991 VL 29 IS 2 BP 119 EP 124 DI 10.1016/0278-6915(91)90166-5 PG 6 WC Food Science & Technology; Toxicology SC Food Science & Technology; Toxicology GA FF438 UT WOS:A1991FF43800007 PM 2010141 ER PT J AU KAPLAN, N HUDSON, RR IIZUKA, M AF KAPLAN, N HUDSON, RR IIZUKA, M TI THE COALESCENT PROCESS IN MODELS WITH SELECTION, RECOMBINATION AND GEOGRAPHIC SUBDIVISION SO GENETICAL RESEARCH LA English DT Article ID DROSOPHILA-MELANOGASTER; ALCOHOL-DEHYDROGENASE; POLYMORPHISM; POPULATION; LOCUS AB A population genetic model with a single locus at which balancing selection acts and many linked loci at which neutral mutations can occur is analysed using the coalescent approach. The model incorporates geographic subdivision with migration, as well as mutation, recombination, and genetic drift of neutral variation. It is found that geographic subdivision can affect genetic variation even with high rates of migration, providing that selection is strong enough to maintain different allele frequencies at the selected locus. Published sequence data from the alcohol dehydrogenase locus of Drosophila melanogaster are found to fit the proposed model slightly better than a similar model without subdivision. C1 UNIV CALIF IRVINE,DEPT ECOL & EVOLUT BIOL,IRVINE,CA 92717. CHIKUSHI JOGAKUEN JR COLL,GEN EDUC COURSE,DAZAIFU,FUKUOKA 81801,JAPAN. RP KAPLAN, N (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 14 TC 25 Z9 25 U1 0 U2 3 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0016-6723 J9 GENET RES JI Genet. Res. PD FEB PY 1991 VL 57 IS 1 BP 83 EP 91 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA FE839 UT WOS:A1991FE83900012 PM 1904048 ER PT J AU ENG, CM KOZAK, CA BEAUDET, AL ZOGHBI, HY AF ENG, CM KOZAK, CA BEAUDET, AL ZOGHBI, HY TI MAPPING OF MULTIPLE SUBUNITS OF THE NEURONAL NICOTINIC ACETYLCHOLINE-RECEPTOR TO CHROMOSOME-15 IN MAN AND CHROMOSOME-9 IN MOUSE SO GENOMICS LA English DT Article ID CENTRAL NERVOUS-SYSTEM; GENE FAMILY; FUNCTIONAL EXPRESSION; ALPHA-SUBUNIT; LINKAGE; ONCOGENE; BETA-2; BRAIN C1 BAYLOR UNIV,DEPT PEDIAT,HOUSTON,TX 77030. BAYLOR UNIV,HOWARD HUGHES MED INST,HOUSTON,TX 77030. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RP ENG, CM (reprint author), BAYLOR UNIV,INST MOLEC GENET,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. FU NICHD NIH HHS [KH11HD00684] NR 27 TC 34 Z9 34 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 FEB PY 1991 VL 9 IS 2 BP 278 EP 282 DI 10.1016/0888-7543(91)90253-B PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA EU767 UT WOS:A1991EU76700009 PM 2004777 ER PT J AU OVNIC, M TEPPERMAN, K MEDDA, S ELLIOTT, RW STEPHENSON, DA GRANT, SG GANSCHOW, RE AF OVNIC, M TEPPERMAN, K MEDDA, S ELLIOTT, RW STEPHENSON, DA GRANT, SG GANSCHOW, RE TI CHARACTERIZATION OF A MURINE CDNA-ENCODING A MEMBER OF THE CARBOXYLESTERASE MULTIGENE FAMILY SO GENOMICS LA English DT Article ID AMINO-ACID SEQUENCE; MOUSE MUS-MUSCULUS; 60-KILODALTON GLYCOPROTEIN ESTERASE; 2ND TRIMERIC CARBOXYLESTERASE; LIVER MICROSOMAL-MEMBRANES; RECOMBINANT INBRED STRAINS; HOUSE MOUSE; MESSENGER-RNA; BETA-GLUCURONIDASE; 60-KDA PROTEINS C1 NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. UNIV CALIF LAWRENCE LIVERMORE NATL LAB,DIV BIOMED SCI,LIVERMORE,CA 94550. UNIV CINCINNATI,DEPT BIOL SCI,CINCINNATI,OH 45221. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT MOLEC & CELLULAR BIOL,BUFFALO,NY 14263. RP OVNIC, M (reprint author), CHILDRENS HOSP MED CTR,INST DEV RES,ELLAND & BETHESDA AVE,CINCINNATI,OH 45229, USA. RI Grant, Stephen/D-6984-2014 OI Grant, Stephen/0000-0002-9236-0913 FU NIDDK NIH HHS [DK 14770]; NIGMS NIH HHS [GM 36366, GM 28464] NR 55 TC 60 Z9 61 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 FEB PY 1991 VL 9 IS 2 BP 344 EP 354 DI 10.1016/0888-7543(91)90263-E PG 11 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA EU767 UT WOS:A1991EU76700019 PM 1840565 ER PT J AU KEIR, WJ KOZAK, CA CHAKRABORTI, A DEITRICH, RA SIKELA, JM AF KEIR, WJ KOZAK, CA CHAKRABORTI, A DEITRICH, RA SIKELA, JM TI THE CDNA SEQUENCE AND CHROMOSOMAL LOCATION OF THE MURINE GABA(A)ALPHA-1 RECEPTOR GENE SO GENOMICS LA English DT Note ID GAMMA-AMINOBUTYRIC ACID; SUBUNIT MESSENGER-RNAS; NICOTINIC ACETYLCHOLINE-RECEPTOR; GABAA RECEPTOR; DIFFERENTIAL DISTRIBUTION; BENZODIAZEPINE RECEPTORS; BOVINE CEREBELLUM; GLYCINE RECEPTOR; ION CHANNELS; EXPRESSION C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RP KEIR, WJ (reprint author), UNIV COLORADO,HLTH SCI CTR,ALCOHOL RES CTR,DEPT PHARMACOL,DENVER,CO 80262, USA. FU NIAAA NIH HHS [AA03527, AA00093] NR 42 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 0888-7543 J9 GENOMICS JI Genomics PD FEB PY 1991 VL 9 IS 2 BP 390 EP 395 DI 10.1016/0888-7543(91)90272-G PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA EU767 UT WOS:A1991EU76700028 PM 1848528 ER PT J AU JENKINS, NA JUSTICE, MJ GILBERT, DJ CHU, ML COPELAND, NG AF JENKINS, NA JUSTICE, MJ GILBERT, DJ CHU, ML COPELAND, NG TI NIDOGEN ENTACTIN (NID) MAPS TO THE PROXIMAL END OF MOUSE CHROMOSOME-13 LINKED TO BEIGE (BG) AND IDENTIFIES A NEW REGION OF HOMOLOGY BETWEEN MOUSE AND HUMAN-CHROMOSOMES SO GENOMICS LA English DT Note ID AMINO-ACID SEQUENCE; GAMMA-CHAIN; GENE; RECEPTOR; CELLS C1 THOMAS JEFFERSON UNIV,JEFFERSON INST MOLEC MED,DEPT BIOCHEM & MOLEC BIOL,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON INST MOLEC MED,DEPT DERMATOL,PHILADELPHIA,PA 19107. RP JENKINS, NA (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101, 5F32CA 08853-02]; NIAMS NIH HHS [P01 AR 38923] NR 16 TC 28 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 0888-7543 J9 GENOMICS JI Genomics PD FEB PY 1991 VL 9 IS 2 BP 401 EP 403 DI 10.1016/0888-7543(91)90275-J PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA EU767 UT WOS:A1991EU76700031 PM 1672300 ER PT J AU LEBOWITZ, BD AF LEBOWITZ, BD TI HANDBOOK OF AGING AND THE SOCIAL-SCIENCES - BINSTOCK,RH, GEORGE,LK SO GERONTOLOGIST LA English DT Book Review RP LEBOWITZ, BD (reprint author), NIMH,MENTAL DISORDERS AGING RES BRANCH,ROCKVILLE,MD 20815, USA. NR 1 TC 4 Z9 4 U1 0 U2 0 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD FEB PY 1991 VL 31 IS 1 BP 138 EP 140 PG 3 WC Gerontology SC Geriatrics & Gerontology GA FJ237 UT WOS:A1991FJ23700023 ER PT J AU SHANKAR, S LANZA, E AF SHANKAR, S LANZA, E TI DIETARY FIBER AND CANCER PREVENTION SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID LARGE BOWEL-CANCER; COLO-RECTAL CANCER; COLORECTAL-CANCER; BREAST-CANCER; CELL-PROLIFERATION; OVARIAN-CANCER; FECAL MUTAGENS; BILE-ACIDS; METABOLIC EPIDEMIOLOGY; DIVERTICULAR-DISEASE RP SHANKAR, S (reprint author), NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892, USA. NR 124 TC 21 Z9 21 U1 0 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD FEB PY 1991 VL 5 IS 1 BP 25 EP 41 PG 17 WC Oncology; Hematology SC Oncology; Hematology GA EZ506 UT WOS:A1991EZ50600004 PM 1851150 ER PT J AU DORGAN, JF SCHATZKIN, A AF DORGAN, JF SCHATZKIN, A TI ANTIOXIDANT MICRONUTRIENTS IN CANCER PREVENTION SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID DIETARY VITAMIN-A; COLO-RECTAL CANCER; URINARY-BLADDER CARCINOGENESIS; AZO-DYE HEPATOCARCINOGENESIS; SUPPLEMENTAL BETA-CAROTENE; UTERINE CERVICAL DYSPLASIA; SPONTANEOUS MAMMARY-TUMORS; EPITHELIAL OVARIAN-CANCER; POLY-UNSATURATED FAT; PAST MEDICAL HISTORY RP DORGAN, JF (reprint author), NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892, USA. NR 209 TC 86 Z9 87 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD FEB PY 1991 VL 5 IS 1 BP 43 EP 68 PG 26 WC Oncology; Hematology SC Oncology; Hematology GA EZ506 UT WOS:A1991EZ50600005 PM 2026568 ER PT J AU WEINDRUCH, R ALBANES, D KRITCHEVSKY, D AF WEINDRUCH, R ALBANES, D KRITCHEVSKY, D TI THE ROLE OF CALORIES AND CALORIC RESTRICTION IN CARCINOGENESIS SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID INDUCED MAMMARY TUMORIGENESIS; CHEMICALLY-INDUCED MAMMARY; COLON CANCER RISK; DIETARY RESTRICTION; ENERGY-INTAKE; COLORECTAL-CANCER; PHYSICAL-ACTIVITY; FOOD RESTRICTION; TUMOR PROMOTION; GROWTH-FACTOR C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. NCI,BETHESDA,MD 20892. WISTAR INST,PHILADELPHIA,PA 19104. RP WEINDRUCH, R (reprint author), UNIV WISCONSIN,INST AGING,425 HENRY MALL,ROOM 330,MADISON,WI 53706, USA. RI Albanes, Demetrius/B-9749-2015 NR 78 TC 48 Z9 48 U1 4 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD FEB PY 1991 VL 5 IS 1 BP 79 EP 89 PG 11 WC Oncology; Hematology SC Oncology; Hematology GA EZ506 UT WOS:A1991EZ50600007 PM 2026570 ER PT J AU LANGSTEIN, HN NORTON, JA AF LANGSTEIN, HN NORTON, JA TI MECHANISMS OF CANCER CACHEXIA SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID TUMOR-NECROSIS-FACTOR; TOTAL PARENTERAL-NUTRITION; HIGH-FAT DIET; FACTOR-ALPHA; GAMMA-INTERFERON; FOOD-INTAKE; MALIGNANT DISEASE; FACTOR CACHECTIN; COMMON MEDIATOR; BEARING MICE C1 NCI,SURG BRANCH,SURG METAB SECT,BLDG 10,ROOM 2B07,BETHESDA,MD 20892. NR 108 TC 128 Z9 131 U1 2 U2 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD FEB PY 1991 VL 5 IS 1 BP 103 EP 123 PG 21 WC Oncology; Hematology SC Oncology; Hematology GA EZ506 UT WOS:A1991EZ50600009 PM 2026566 ER PT J AU RESCAN, PY CLEMENT, B YAMADA, Y GLAISE, D SEGUIREAL, B GUGUENGUILLOUZO, C GUILLOUZO, A AF RESCAN, PY CLEMENT, B YAMADA, Y GLAISE, D SEGUIREAL, B GUGUENGUILLOUZO, C GUILLOUZO, A TI EXPRESSION OF LAMININ AND ITS RECEPTOR LBP-32 IN HUMAN AND RAT HEPATOMA-CELLS SO HEPATOLOGY LA English DT Article ID BASEMENT-MEMBRANE COMPONENTS; HEPATOCELLULAR-CARCINOMA; EXTRACELLULAR-MATRIX; MULTIDOMAIN PROTEIN; IV COLLAGEN; A-CHAIN; LIVER; HEPATOCYTES; FIBRONECTIN; INVITRO AB Dramatic cellular changes that occur during hepatocarcinogenesis are associated with major alterations in extracellular matrix formation and in the relationships between cells and their microenvironment. We have studied the expression of laminin, the major noncollagenous glycoprotein of basement membrane, and the laminin receptor 32 kD laminin-binding protein in two rat (Faza 967 and HTC) and two human (HepG2 and HBGC2) hepatoma cell lines that express a variety of liver-specific functions. Laminin was found in the rough endoplasmic reticulum of these cells when the indirect immunoperoxidase method and electron microscopic examination were used. Radiolabeled laminin, immunoprecipitated from both media and cell extracts, was resolved by electrophoresis on sodium dodecyl sulfate gel in two major polypeptides that comigrated with the A and B subunits from Engelbreth-Holm-Swarm tumor laminin. Immunoblot analysis showed that the Mr = 400,000 polypeptide did not correspond to the A subunit of laminin. Northern blot analyses demonstrated large amounts of B1 and B2 mRNAs but no A chain mRNA. We conclude that the tumor cells produce the laminin B chains only. In contrast, normal adult hepatocytes from either man or rat lacked laminin mRNAs, whereas in 1-day primary culture, B chain mRNAs became detectable. The steady-state level of 32 kD laminin-binding protein mRNA was 10-fold and threefold higher in rat hepatoma cells than in freshly isolated and 1-day cultured normal rat hepatocytes, respectively. In human hepatocytes, the steady-state levels of 32 kD laminin-binding protein mRNAs varied depending on the donor and never reached the level of the human hepatoma cells. Subsequently, Faza, HTC and HepG2 cells, which were selected for their ability to grow on soft agar, were injected into the flank of nude mice and formed solid tumors with no formation of secondary tumors. The tumors contained laminin in sparse deposits between adjacent cells and accumulated around vessels. None of the hepatoma cell lines studied was found to penetrate a reconstituted basement membrane using a chemoinvasion assay with a Boyden chamber. Our data show that hepatoma cells produce the B chains of laminin and express a high level of receptor 32 kD laminin-binding protein mRNA. However these properties appear to be insufficient for these cells to form metastases in vivo. C1 HOP PONTCHAILLOU,UNITE RECH HEPATOL,INSERM,U49,F-35033 RENNES,FRANCE. NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. RI Clement, Bruno/E-5546-2016 NR 41 TC 18 Z9 19 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 FEB PY 1991 VL 13 IS 2 BP 289 EP 296 DI 10.1016/0270-9139(91)92442-B PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FA551 UT WOS:A1991FA55100013 PM 1847349 ER PT J AU BONOW, RO AF BONOW, RO TI LEFT-VENTRICULAR DIASTOLIC FUNCTION IN HYPERTROPHIC CARDIOMYOPATHY SO HERZ LA English DT Article ID MYOCARDIAL PERFUSION ABNORMALITIES; PULSED DOPPLER ECHOCARDIOGRAPHY; ISOVOLUMIC RELAXATION PERIOD; PRESSURE-VOLUME RELATIONS; MAMMALIAN HEART; INTRACELLULAR CALCIUM; CARDIAC-HYPERTROPHY; VERAPAMIL THERAPY; INDUCED ISCHEMIA; BLOCKING-AGENTS AB Impaired diastolic function of the hypertrophied and stiffened left ventricle is a characteristic feature of hypertrophic cardiomyopathy (Figure 1). Altered left ventricular filling dynamics and reduced left ventricular distensibility or increased left ventricular diastolic chamber stiffness are associated with reduced left ventricular stroke volume, increased left ventricular filling pressures and compressive effects on the coronary microcirculation. These factors contribute importantly to the clinical presentation of many patients, including symptoms of fatigue, dyspnea and angina pectoris. Reduced distensibility results both from factors determining the passive elastic properties of the ventricular chamber (including severity of hypertrophy, fibrosis and cellular disarray) and from factors influencing the rate and extent of active left ventricular relaxation (Figure 2). The factors contributing to impaired relaxation in hypertrophic cardiomyopathy are mediated via either inactivation dependent or load-dependent mechanisms. In laboratory animals, compromise of myocardial inactivation results in a persistent increase in intracellular calcium concentration and in prolonged interaction of the contractile proteins. Additionally, there is evidence for an increased number of active receptors for calcium antagonists and, lastly, for myocardial ischemia (Figure 3). Load-dependent mechanisms include diminished wall tension at the opening of the mitral valve, changes in afterload, contractility and coronary flow. Other factors are nonuniform and asynchronous regional ventricular function due to differing increases in thickness of the ventricular walls and ischemia (Figure 4). Calcium channel blockers exert a favorable influence on left ventricular relaxation and filling (Figure 5); verapamil and diltiazem are preferable to nifedipine. Verapamil increases left ventricular stroke volume without an increase in the end-diastolic pressure (Figure 6), reduces regional asynchrony if present, and leads to a more homogeneous regional diastolic filling (Figure 4). Adrenergic stimulation with isoproterenol can have a favorable effect in relaxation and the diastolic pressure-volume relationship in spite of the left ventricular outflow tract gradient and increase in myocardial ischemia because of more favorable loading conditions (Figure 8). Isoproterenol also clearly reduced regional systolic dyssynchrony; it is not a clinically usefull drug for treatment of obstructive hypertrophic cardiomyopathy, however. Other substances capable of favorably influencing myocardial relaxation or reducing ventricular asynchrony have been shown to be beneficial in the treatment of hypertrophic cardiomyopathy. RP BONOW, RO (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 57 TC 19 Z9 20 U1 0 U2 0 PU URBAN & VOGEL PI MUNICH PA LINDWURMSTRASSE 95, D-80337 MUNICH, GERMANY SN 0340-9937 J9 HERZ JI Herz PD FEB PY 1991 VL 16 IS 1 BP 13 EP 21 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FN092 UT WOS:A1991FN09200002 PM 2026381 ER PT J AU ROSENBRONSON, S LONG, EO AF ROSENBRONSON, S LONG, EO TI AN UNUSUAL FORM OF ALTERNATIVE SPLICING IN THE HLA-DNA GENE SO IMMUNOGENETICS LA English DT Article ID LYMPHOBLASTOID-CELLS; CHAIN GENES; BETA-CHAINS; CLASS-I; EXPRESSION; DQ; POLYMORPHISM; PROTEINS; DISTINCT; ALPHA AB The HLA-DNA gene of the human major histocompatibility complex (MHC) produces RNA transcripts of unusual size compared to the 1.3 kilobase (kb) transcripts of other class II genes. Several cDNA clones derived from HLA-DNA transcripts were isolated, including a full-length 3.5 kb cDNA named DN1. Sequence analysis of DN1 demonstrated that the 3.5 kb transcript is fully spliced, contains a long 3' untranslated region, and encodes an apparently normal class II alpha chain. Two other cDNA clones, DN2 and DN7, revealed an alternative splice that resulted from the use of a splice acceptor upstream of the second exon encoding the alpha-1 domain. The translation product of this alternative transcript would share the signal sequence of the DN-alpha chain but would otherwise be unrelated. Removal of the signal sequence would yield a highly basic peptide of 42 amino acids. RNA was prepared by in vitro transcription of DN1 and DN2, and was used to direct protein synthesis in a rabbit reticulocyte system. The product of DN1 had an apparent relative mass of 25 000, whereas the product of DN2 was a peptide with a relative mass of about 6000. The alternatively spliced RNA represents about 1/10 of the transcripts from the HLA-DNA gene in the cells tested, which included transformed B-cell lines as well as normal blood cells and thymus cells. C1 NIAID,IMMUNOGENET LAB,BLDG 4,ROOM 213,BETHESDA,MD 20892. RI Long, Eric/G-5475-2011 OI Long, Eric/0000-0002-7793-3728 NR 28 TC 8 Z9 8 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD FEB PY 1991 VL 33 IS 2 BP 124 EP 131 PG 8 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA EZ766 UT WOS:A1991EZ76600008 PM 1999352 ER PT J AU FANGER, MW SEGAL, DM ROMETLEMONNE, JL AF FANGER, MW SEGAL, DM ROMETLEMONNE, JL TI BISPECIFIC ANTIBODIES AND TARGETED CELLULAR CYTOTOXICITY SO IMMUNOLOGY TODAY LA English DT Editorial Material AB The Second International Conference on Bispecific Antibodies (BsAbs) and Targeted Cellular Cytotoxicity* considered how targeted cytotoxicity can be used (1) to increase understanding of the general mechanisms of cellular cytotoxicity and (2) clinically in the treatment of cancer and infections disease. BsAbs, the main mediators of targeted cellular cytotoxicity, can be made by chemical crosslinking, by fusing hybridoma cells and by molecular genetic approaches. BsAbs bind to target cells via one V region and trigger molecules such as T-cell receptors (TCRs) or FcR for IgG (Fc-gamma-R) on cytotoxic cells via their other V region. This linking of triggering structures to target cells induces target cells lysis and provides important clues to the signals used to elicit the lytic process. C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. CTR NATL TRANSFUS SANGUINE,F-91943 LES ULIS,FRANCE. RP FANGER, MW (reprint author), DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT MICROBIOL,HANOVER,NH 03756, USA. NR 0 TC 56 Z9 56 U1 0 U2 1 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 FEB PY 1991 VL 12 IS 2 BP 51 EP 54 DI 10.1016/0167-5699(91)90156-N PG 4 WC Immunology SC Immunology GA EW189 UT WOS:A1991EW18900001 PM 1676265 ER PT J AU DURUM, SK QUINN, DG MUEGGE, K AF DURUM, SK QUINN, DG MUEGGE, K TI NEW CYTOKINES AND RECEPTORS MAKE THEIR DEBUT IN SAN-ANTONIO SO IMMUNOLOGY TODAY LA English DT Editorial Material AB Two exciting developments were reported at the recent Seventh International Lymphokine Workshop*. First, a number of recently cloned cytokines and cytokine receptors were described, proving that there is still a great deal to be learned about the most fundamental aspects of cell-cell communication. Second, advances were reported in the understanding of post-receptor signalling at both cytoplasmic and nuclear levels. C1 NCI,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. ST THOMAS HOSP,INST DERMATOL,LONDON SE1 7EH,ENGLAND. RP DURUM, SK (reprint author), NCI,BIOL RESPONSE MODIFIERS PROGRAM,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702, USA. NR 0 TC 14 Z9 14 U1 0 U2 0 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 FEB PY 1991 VL 12 IS 2 BP 54 EP 57 DI 10.1016/0167-5699(91)90157-O PG 4 WC Immunology SC Immunology GA EW189 UT WOS:A1991EW18900002 PM 1676266 ER PT J AU TAYLOR, CE FAUNTLEROY, MB STASHAK, PW BAKER, PJ AF TAYLOR, CE FAUNTLEROY, MB STASHAK, PW BAKER, PJ TI ANTIGEN-SPECIFIC SUPPRESSOR T-CELLS RESPOND TO RECOMBINANT INTERLEUKIN-2 AND OTHER LYMPHOKINES SO INFECTION AND IMMUNITY LA English DT Article ID III PNEUMOCOCCAL POLYSACCHARIDE; ANTIBODY-PRODUCING CELLS; PLAQUE-FORMING CELLS; LOW-DOSE PARALYSIS; CELLULAR LEVEL; B-CELLS; EXPRESSION; ACTIVATION; INVITRO; IL-2 AB Previous studies have shown that transfer of whole spleen cell populations obtained from primed donors or transfer of purified T cells enriched for suppressor activity (Ts) to recipient mice decreased the antibody response to pneumococcal polysaccharide type III (SSS-III) when the animals were simultaneously immunized with SSS-III. In the present studies, such suppression of the antibody response was transferred with 10- to 100-fold fewer primed spleen cells when the cells were treated in vitro with recombinant interleukin-2 (rIL-2) before transfer; spleen cells from naive mice or mice primed with an unrelated antigen (dextran) and then treated with rIL-2 did not cause suppression of the antibody response to SSS-III, thereby eliminating the possibility of nonspecific carryover effects induced by rIL-2. In vivo administration of rIL-2 at the time of immunization with an optimally immunogenic dose of SSS-III resulted in significant (P < 0.05) suppression of the antibody response relative to that of control animals, suggesting that IL-2 augments the clonal expansion of Ts cells in vivo. Further, the ability of passively administered anti-IL-2 receptor antibody to inhibit generation of Ts cells in vivo is consistent with such a view. Spleen cells from primed animals treated with rIL-4, rIL-5, or gamma interferon--but not those from primed animals treated with rIL-6--likewise were able to transfer suppression of the antibody response with fewer cells than those required when primed cells not treated with lymphokines were used. Thus, these studies indicate that Ts cell activity is greatly influenced by lymphokines produced by helper T cells. The studies also suggest that these lymphokines are required during activation and/or clonal expansion of Ts cells. RP TAYLOR, CE (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK 2 RES FACIL,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 28 TC 13 Z9 13 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 FEB PY 1991 VL 59 IS 2 BP 575 EP 579 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EU973 UT WOS:A1991EU97300016 PM 1824762 ER PT J AU DEVI, SJN SCHNEERSON, R EGAN, W VANN, WF ROBBINS, JB SHILOACH, J AF DEVI, SJN SCHNEERSON, R EGAN, W VANN, WF ROBBINS, JB SHILOACH, J TI IDENTITY BETWEEN POLYSACCHARIDE ANTIGENS OF MORAXELLA-NONLIQUEFACIENS, GROUP-B NEISSERIA-MENINGITIDIS, AND ESCHERICHIA-COLI K1 (NON-O ACETYLATED) SO INFECTION AND IMMUNITY LA English DT Article ID CAPSULAR POLYSACCHARIDE; ANTISERUM AGAR; SEROGROUP IDENTIFICATION; ACID; MENINGOCOCCI; POLYSIALOGLYCOPROTEINS; PATHOGENESIS; ANTIBODY AB A surface polysaccharide antigen of Moraxella nonliquefaciens, reported to be cross-reactive with the capsular polysaccharides of group B Neisseria meningitidis and Escherichia coli K1 (K. Bovre, K. Bryn, O. Closs, N. Hagen and L.O. Froholm, NIPH Ann. 6:65-73,1983), was isolated, purified, and characterized chemically, immunologically, and by nuclear magnetic resonance. This polysaccharide was shown to be a linear homopolymer of alpha(2-->8)-linked N-acetylneuraminic acid, identical to the capsular polysaccharide of group B N. meningitidis and O-acetyl-negative variants of E. coli K1. C1 US FDA,CTR DRUGS & BIOL,DIV BIOCHEM & BIOPHYS,BETHESDA,MD 20892. US FDA,DIV BACTERIAL PROD,BETHESDA,MD 20892. NID,BETHESDA,MD 20892. RP DEVI, SJN (reprint author), NICHHD,DEV & MOLEC IMMUN LAB,BETHESDA,MD 20892, USA. NR 40 TC 35 Z9 36 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD FEB PY 1991 VL 59 IS 2 BP 732 EP 736 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EU973 UT WOS:A1991EU97300043 PM 1898915 ER PT J AU TSAI, CM GAZDAR, AF PERNG, RP KRAMER, BS AF TSAI, CM GAZDAR, AF PERNG, RP KRAMER, BS TI SCHEDULE-DEPENDENT INVITRO COMBINATION EFFECTS OF METHOTREXATE AND 5-FLUOROURACIL IN HUMAN TUMOR-CELL LINES SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID METASTATIC COLORECTAL-CARCINOMA; SEQUENTIAL METHOTREXATE; RANDOMIZED TRIAL; CYTO-TOXICITY; NECK-CANCER; COLORIMETRIC ASSAY; PHASE-II; CHEMOTHERAPY; FLUOROURACIL; HYPOXANTHINE AB Because of conflicting reports of clinical synergy, we used the tetrazolium-based colorimetric (MTT) assay to test in vitro combination effects of methotrexate (MTX) plus 5-fluorouracil (FUra) in 4 schedules on 2 human non-small-cell lung cancer cell lines (adenocarcinoma, NCI-H23; bronchoalveolar-cell carcinoma, NCI-H358), and 1 human colorectal adenocarcinoma cell line (SNU-C1). The complete 3 dimensional set of isoboles in the dose range under study was generated by a microcomputer-based method. We found that the combination effects of 8-hr sequential FUra-MTX, simultaneous administration of MTX-FUra, and 8-hr sequential MTX-FUra were clearly antagonistic for all 3 cell lines. In contrast, the combination cytotoxic effects of 24-hr sequential MTX-FUra were much more active. Our in vitro model thus clearly shows that MTX-FUra interactions are highly schedule-dependent. This provides a rational basis for testing sequential MTX-FUra with a longer administration interval than usually employed clinically. C1 NATL NAVAL MED CTR, NCI, NAVY MED ONCOL BRANCH, BETHESDA, MD 20814 USA. UNIFORMED SERV UNIV HLTH SCI, BETHESDA, MD 20814 USA. RP TSAI, CM (reprint author), VET GEN HOSP TAIPEI, DEPT CHEST, TAIPEI 11217, TAIWAN. NR 41 TC 9 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD FEB 1 PY 1991 VL 47 IS 3 BP 401 EP 407 DI 10.1002/ijc.2910470316 PG 7 WC Oncology SC Oncology GA FA210 UT WOS:A1991FA21000015 PM 1847123 ER PT J AU LARSON, DB LYONS, JS HOHMANN, AA BEARDSLEY, RS HIDALGO, J AF LARSON, DB LYONS, JS HOHMANN, AA BEARDSLEY, RS HIDALGO, J TI PSYCHOTROPICS PRESCRIBED TO THE UNITED-STATES ELDERLY IN THE EARLY AND MID 1980S - PRESCRIBING PATTERNS OF PRIMARY CARE PRACTITIONERS, PSYCHIATRISTS, AND OTHER PHYSICIANS SO INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article DE PRIMARY CARE; PSYCHIATRISTS; PSYCHOTROPIC MEDICATIONS; ELDERLY ID MENTAL-HEALTH-SERVICES; DRUG-USE; DISORDERS; HOMES; RISK C1 NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. UNIV MARYLAND,COLLEGE PK,MD 20742. MARYLAND DEPT HLTH & MENTAL HYG,BALTIMORE,MD 21201. RP LARSON, DB (reprint author), NIMH,BIOMET & CLIN APPL BRANCH,ROOM 18C 14,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 48 TC 11 Z9 11 U1 2 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0885-6230 J9 INT J GERIATR PSYCH JI Int. J. Geriatr. Psychiatr. PD FEB PY 1991 VL 6 IS 2 BP 63 EP 70 DI 10.1002/gps.930060204 PG 8 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA EZ764 UT WOS:A1991EZ76400003 ER PT J AU NOMIZU, M INAGAKI, Y YAMASHITA, T OHKUBO, A OTAKA, A FUJII, N ROLLER, PP YAJIMA, H AF NOMIZU, M INAGAKI, Y YAMASHITA, T OHKUBO, A OTAKA, A FUJII, N ROLLER, PP YAJIMA, H TI 2-STEP HARD ACID DEPROTECTION CLEAVAGE PROCEDURE FOR SOLID-PHASE PEPTIDE-SYNTHESIS SO INTERNATIONAL JOURNAL OF PEPTIDE AND PROTEIN RESEARCH LA English DT Article DE HUMAN ENDOTHELIN; HF; NIN-FORMYLTRYPTOPHAN; SOLID PHASE PEPTIDE SYNTHESIS; TRIMETHYLSILYL BROMIDE (TMSBR); TRIMETHYLSILYL TRIFLUOROMETHANESULFONATE (TMSOTF); 2-STEP HARD ACID DEPROTECTION CLEAVAGE PROCEDURE; UROTENSIN-II ID VASOCONSTRICTOR PEPTIDE; UROTENSIN-II; REAGENT; TRIFLUOROMETHANESULFONATE; SEQUENCE AB A new two-step deprotection/cleavage procedure for t-butoxycarbonyl (Boc) based solid phase peptide synthesis is reported. First the protective groups are removed from 4-(oxymethyl)-phenylacetamidomethyl (PAM) resin attached peptide with the weak hard acid, trimethylsilyl bromide-thioanisole/trifluoroacetic acid (TFA). In the second step, the peptide is cleaved from the resin with a stronger hard acid such as trimethylsilvl trifluoromethanesulfonate in TFA or with HF. The method is also shown to deformylate N(in)-formyltryptophan moiety efficiently. The usefulness of this procedure for practical solid phase peptide synthesis is demonstrated by comparison with other deprotection methods in the synthesis of urotensin II and human endothelin. C1 KIRIN BREWERY CO LTD,CENT LABS KEY TECHNOL,MAEBASHI,GUNMA,JAPAN. KIRIN BREWERY CO LTD,PHARMACEUT LAB,MAEBASHI,GUNMA,JAPAN. KYOTO UNIV,FAC PHARMACEUT SCI,KYOTO 606,JAPAN. RP NOMIZU, M (reprint author), NCI,MED CHEM LAB,BLDG 37,RM 5C02,BETHESDA,MD 20892, USA. NR 23 TC 23 Z9 23 U1 0 U2 5 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0367-8377 J9 INT J PEPT PROT RES JI Int. J. Pept. Protein Res. PD FEB PY 1991 VL 37 IS 2 BP 145 EP 152 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY124 UT WOS:A1991EY12400009 PM 2019476 ER PT J AU FAIRCHILD, CR COWAN, KH AF FAIRCHILD, CR COWAN, KH TI MULTIDRUG RESISTANCE - A PLEIOTROPIC RESPONSE TO CYTOTOXIC DRUGS - KEYNOTE ADDRESS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT 3RD INTERNATIONAL CONF ON THE INTERACTION OF RADIATION THERAPY AND SYSTEMIC THERAPY CY MAR 10-12, 1990 CL MONTEREY, CA DE MULTIDRUG RESISTANCE; XENOBIOTIC RESISTANCE; P-GLYCOPROTEIN; GLUTATHIONE S-TRANSFERASE; HYPEROPLASTIC LIVER NODULES ID GLUTATHIONE-S-TRANSFERASE; BREAST CANCER-CELLS; P-GLYCOPROTEIN GENE; BACTERIAL TRANSPORT PROTEINS; DOUBLE-MINUTE CHROMOSOMES; ESTROGEN-RECEPTOR CONTENT; BINDING PROTEIN; HEPATOCYTE NODULES; CROSS-RESISTANCE; DNA-SEQUENCES AB Tumor cells exposed in tissue culture to one of several different classes of antineoplastic agents, including anthracyclines, vinca alkaloids, epipodophyllotoxins, and certain antitumor antibiotics, can develop resistance to the selecting agent and cross resistance to the other classes of agents. This phenomena of multidrug resistance is generally associated with decreased drug accumulation and overexpression of a membrane glycoprotein. This membrane protein, referred to as P-glycoprotein, apparently acts as an energy-dependent drug efflux pump. Multidrug resistance in human MCF-7 breast cancer cells selected for resistance to adriamycin (AdrR MCF-7) is associated with amplification and overexpression of the mdr 1 gene which encodes P-glycoprotein. A number of other changes are also seen in this resistant cell line including alterations in Phase I and Phase II drug metabolizing enzymes. Similar biochemical changes occur in a rat model for hepatocellular carcinogenesis and are associated in that system with broad spectrum resistance to hepatotoxins. The similar changes in these two models of resistance suggests that these changes might be part of a battery of genes whose expression can be altered in response to cytotoxic stress, thus rendering the cell resistant to a wide variety of cytotoxic agents. RP FAIRCHILD, CR (reprint author), NCI,DIV CANC TREATMENT,MED BRANCH,BLDG 10,12C112,BETHESDA,MD 20892, USA. NR 79 TC 16 Z9 17 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD FEB PY 1991 VL 20 IS 2 BP 361 EP 367 PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA EW196 UT WOS:A1991EW19600034 PM 1671383 ER PT J AU ZAHARKO, DS KELLEY, JA TOMASZEWSKI, JE HEGEDUS, L HARTMAN, NR AF ZAHARKO, DS KELLEY, JA TOMASZEWSKI, JE HEGEDUS, L HARTMAN, NR TI CYCLOPENTENYL CYTOSINE - INTERSPECIES PREDICTIONS BASED ON RODENT PLASMA AND URINE KINETICS SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE CYCLOPENTENYL CYTOSINE; INTERSPECIES; PHARMACOKINETICS; TOXICITY ID CYTIDINE; TRIPHOSPHATE; ANTITUMOR; ANALOG AB A hybrid compartmental-physiological model for cyclopentenyl cytosine (CPE-C) is designed on the basis of early limited rodent pharmacokinetic data. Application of model independent pharmacokinetics and biochemical knowledge was first used to conceptualize such a model. The approach was to scale the physiological parameters of the model (compartmental clearances) and keep constant the anatomic parameters of the model (compartment volumes). Scaling of physiological mechanisms was based on body weight/surface area ratios. Using these principles, simulations with the model can reasonably anticipate the in vivo behavior of (CPE-C) in several species (mouse, rat, dog). The model is useful in understanding species differences in pharmacokinetic behavior of CPE-C. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,TOXICOL BRANCH,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,ANAESTHESIOL LAB,BETHESDA,MD 20892. RP ZAHARKO, DS (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,PHARMACOL BRANCH,EXECUT PLAZA N,ROOM 841,BETHESDA,MD 20892, USA. NR 19 TC 9 Z9 9 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PD FEB PY 1991 VL 9 IS 1 BP 9 EP 17 PG 9 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA EZ122 UT WOS:A1991EZ12200002 PM 2026489 ER PT J AU CHAN, PC HUFF, J HASEMAN, JK ALISON, R PREJEAN, JD AF CHAN, PC HUFF, J HASEMAN, JK ALISON, R PREJEAN, JD TI CARCINOGENESIS STUDIES OF DICHLORVOS IN FISCHER RATS AND B6C3F1 MICE SO JAPANESE JOURNAL OF CANCER RESEARCH LA English DT Article DE DICHLORVOS; CARCINOGENESIS; RATS; MICE ID 2,2-DICHLOROVINYL DIMETHYL-PHOSPHATE; SISTER-CHROMATID EXCHANGES; CORN-OIL GAVAGE; ANIMAL CARCINOGENICITY; ALKYLATING PROPERTIES; ABERRATIONS; REGRESSION; CHEMICALS; INDUCTION; EXPOSURE AB Dichlorvos (dichlorovinyl dimethyl phosphoric acid ester) is a cholinesterase inhibitor used widely as a contact and stomach insecticide for control of internal and external parasites. Carcinogenesis studies were conducted by administering dichlorvos in corn oil by gavage 5 times a week for 103 weeks to groups of 50 male and 50 female Fischer rats at 0, 4, or 8 mg/kg body weight, to groups of 50 male B6C3F1 mice at 0, 10, or 20 mg/kg, and to groups of 50 female B6C3F1 mice at 0, 20, or 40 mg/kg. During the course of the studies, body weights and survival rates of the male and female rats and mice were not different from those of their respective controls; females of both species appeared to gain more weight than controls. Neoplasms induced by dichlorvos included adenomas of the exocrine pancreas (male rats), mononuclear cell leukemia (male rats), and squamous cell papilloma of the forestomach (male and female mice; two other female mice had squamous cell carcinomas). Lesions observed in female rats that may have been due to dichlorvos administration included adenomas of the exocrine pancreas and fibroadenomas of the mammary gland. The results demonstrated that dichlorvos is carcinogenic for Fischer rats and B6C3F1 mice. C1 SO RES INST,BIRMINGHAM,AL 35255. RP CHAN, PC (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 54 TC 19 Z9 21 U1 0 U2 0 PU JAPANESE CANCER ASSOCIATION PI TOKYO PA EDITORIAL OFFICE 7TH FLOOR, JOHKOH BLDG 2-23-11, KOISHIKAWA, TOKYO 112, JAPAN SN 0910-5050 J9 JPN J CANCER RES JI Jpn. J. Cancer Res. PD FEB PY 1991 VL 82 IS 2 BP 157 EP 164 PG 8 WC Oncology SC Oncology GA EY812 UT WOS:A1991EY81200006 PM 1900819 ER PT J AU HOOLEY, JM RICHTERS, JE AF HOOLEY, JM RICHTERS, JE TI ALTERNATIVE MEASURES OF EXPRESSED EMOTION - A METHODOLOGICAL AND CAUTIONARY NOTE SO JOURNAL OF ABNORMAL PSYCHOLOGY LA English DT Note ID PSYCHIATRIC-PATIENTS; FAMILY FACTORS; RELAPSE; REPLICATION; RELATIVES C1 NIMH,ROCKVILLE,MD 20857. RP HOOLEY, JM (reprint author), HARVARD UNIV,DEPT PSYCHOL,33 KIRKLAND ST,CAMBRIDGE,MA 02138, USA. RI Hooley, Jill/A-3945-2013; OI Hooley, Jill/0000-0002-1162-3540; Richters, John/0000-0002-6780-1828 NR 16 TC 28 Z9 28 U1 0 U2 1 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0021-843X J9 J ABNORM PSYCHOL JI J. Abnorm. Psychol. PD FEB PY 1991 VL 100 IS 1 BP 94 EP 97 DI 10.1037/0021-843X.100.1.94 PG 4 WC Psychology, Clinical; Psychology, Multidisciplinary SC Psychology GA EX407 UT WOS:A1991EX40700013 PM 2005278 ER PT J AU RAPHAEL, GD BARANIUK, JN KALINER, MA AF RAPHAEL, GD BARANIUK, JN KALINER, MA TI HOW AND WHY THE NOSE RUNS SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID INDUCED NASAL SECRETIONS; GENE-RELATED PEPTIDE; PATHO-PHYSIOLOGY; INDUCED RHINORRHEA; RHINITIS; LOCALIZATION; LACTOFERRIN; MUCOSA; ANTIHISTAMINE; PROVOCATION C1 NIAID,CLIN INVEST LAB,ALLERG DIS SECT,BLDG 1,11C207,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 47 TC 77 Z9 78 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD FEB PY 1991 VL 87 IS 2 BP 457 EP 467 DI 10.1016/0091-6749(91)90001-5 PG 11 WC Allergy; Immunology SC Allergy; Immunology GA EX987 UT WOS:A1991EX98700001 PM 1993805 ER PT J AU KEAHEY, TM INDRISANO, J WHITE, MV KALINER, MA AF KEAHEY, TM INDRISANO, J WHITE, MV KALINER, MA TI ANALYSES OF MICROVASCULAR PERMEABILITY IN RESPONSE TO MEDIATORS OF IMMEDIATE HYPERSENSITIVITY SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID VASCULAR-PERMEABILITY; HISTAMINE; SITES; RAT AB Mediator-induced changes in microvascular permeability were studied in rodent skin. To monitor these changes, Evan's blue dye, iodinated rat albumin and IgG, and tritiated neutral dextran molecules having different molecular radii were used. After intradermal injections of serotonin, histamine, and bradykinin, the degree of radiolabeled tracer efflux was determined by measuring the extent of blueing and the level of radioactivity in skin biopsy specimens. Although the mediators varied in potency on a molar basis (serotonin > bradykinin > histamine), the efflux resulting from each was similar. Furthermore, kinetic studies revealed that each of these vasoactive agents caused a marked but transient increase in macromolecular permeability that lasted less than 30 minutes. To determine the pore size created and the effect of charge on the transudation of macromolecules into the interstitium, fractions of neutral [H-3]dextrans with a known molecular size (average radii, 12 and 4.4 nm, respectively) were infused either singly or in combination with I-125-labeled rat albumin and/or IgG before intradermal injection of serotonin, histamine, bradykinin, or compound 48/80. Regardless of the mediator used, no differences could be demonstrated in macromolecular efflux, as indicated by either the molecular size of the charge of the tracer used. Thus, all mediators of immediate hypersensitivity reactions that were studied produce venular gaps > 12 nm in addition to displaying similar vasopermeable characteristics. C1 NIAID,CLIN INVEST LAB,ALLERG DIS SECT,BETHESDA,MD 20892. NR 17 TC 7 Z9 7 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD FEB PY 1991 VL 87 IS 2 BP 586 EP 594 DI 10.1016/0091-6749(91)90019-K PG 9 WC Allergy; Immunology SC Allergy; Immunology GA EX987 UT WOS:A1991EX98700018 PM 1993817 ER PT J AU HIGUCHI, M DIAMANTSTEIN, T OSAWA, H CASPI, RR AF HIGUCHI, M DIAMANTSTEIN, T OSAWA, H CASPI, RR TI COMBINED ANTI-INTERLEUKIN-2 RECEPTOR AND LOW-DOSE CYCLOSPORINE THERAPY IN EXPERIMENTAL AUTOIMMUNE UVEORETINITIS SO JOURNAL OF AUTOIMMUNITY LA English DT Article ID ADJUVANT-INDUCED ARTHRITIS; RETINAL S-ANTIGEN; T-CELL LINES; INTERLEUKIN-2 RECEPTOR; ENCEPHALOMYELITIS EAE; SELECTIVE IMMUNOSUPPRESSION; TARGETED THERAPY; ANTIBODY; RATS; IMMUNOTHERAPY C1 NEI,IMMUNOL LAB,NIH BLDG 10,ROOM 10N216,BETHESDA,MD 20892. FREE UNIV BERLIN,KLINIKUM STEGLITZ,INST IMMUNOL,W-1000 BERLIN 45,GERMANY. NR 23 TC 16 Z9 16 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0896-8411 J9 J AUTOIMMUN JI J. Autoimmun. PD FEB PY 1991 VL 4 IS 1 BP 113 EP 124 DI 10.1016/0896-8411(91)90011-Z PG 12 WC Immunology SC Immunology GA EZ847 UT WOS:A1991EZ84700010 PM 1827711 ER PT J AU CATT, KJ HUNYADY, L BALLA, T AF CATT, KJ HUNYADY, L BALLA, T TI 2ND MESSENGERS DERIVED FROM INOSITOL LIPIDS SO JOURNAL OF BIOENERGETICS AND BIOMEMBRANES LA English DT Review DE PHOSPHOINOSITIDES; INOSITOL-PHOSPHATES; PHOSPHOLIPASE-C; CA-MOBILIZATION; G-PROTEINS; INOSITOL-TRISPHOSPHATE-RECEPTOR; TYROSINE KINASES ID ADRENAL GLOMERULOSA CELLS; NUCLEOTIDE-BINDING PROTEIN; ANGIOTENSIN-II RECEPTORS; ISLET-ACTIVATING PROTEIN; PHOSPHOLIPASE-C ACTIVITY; EPIDERMAL GROWTH-FACTOR; GUANINE-NUCLEOTIDE; PERTUSSIS-TOXIN; PLASMA-MEMBRANE; 3T3 CELLS AB Many hormones, growth factors, and neurotransmitters stimulate their target cells by promoting the hydrolysis of plasma-membrane phosphoinositides to form the two second messengers, diacylglycerol and inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]. In such cells, ligand-receptor interaction stimulates specific phospholipases that are activated by guanyl nucleotide regulatory G proteins or tyrosine phosphorylation. In many cells, the initial rise in cytoplasmic calcium due to Ins(1,4,5)P3-induced mobilization of calcium from agonist-sensitive stores is followed by a sustained phase of cytoplasmic calcium elevation that maintains the target-cell response, and is dependent on influx of extracellular calcium. Numerous inositol phosphates are formed during metabolism of the calcium-mobilizing messenger, inositol 1,4,5-trisphosphate [Ins(1,4,5)P3)], to lower and higher phosphorylated derivatives. The cloning of several phospholipase-C isozymes, as well as the Ins(1,4,5)P3-5 kinase and the Ins(1,4,5)P3 receptor, have clarified several aspects of the diversity and complexity of the phosphoinositide-calcium signaling system. In addition to their well-established roles in hormonal activation of cellular responses such as secretion and contraction, phospholipids and their hydrolysis products have been increasingly implicated in the actions of growth factors and oncogenes on cellular growth and proliferation. RP CATT, KJ (reprint author), NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892, USA. NR 135 TC 26 Z9 26 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0145-479X J9 J BIOENERG BIOMEMBR JI J. Bioenerg. Biomembr. PD FEB PY 1991 VL 23 IS 1 BP 7 EP 27 PG 21 WC Biophysics; Cell Biology SC Biophysics; Cell Biology GA EW523 UT WOS:A1991EW52300002 PM 2010435 ER PT J AU EASTELL, R YERGEY, AL VIEIRA, NE CEDEL, SL KUMAR, R RIGGS, BL AF EASTELL, R YERGEY, AL VIEIRA, NE CEDEL, SL KUMAR, R RIGGS, BL TI INTERRELATIONSHIP AMONG VITAMIN-D METABOLISM, TRUE CALCIUM-ABSORPTION, PARATHYROID FUNCTION, AND AGE IN WOMEN - EVIDENCE OF AN AGE-RELATED INTESTINAL RESISTANCE TO 1,25-DIHYDROXYVITAMIN-D ACTION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID PHOSPHORUS-METABOLISM; LIQUID-CHROMATOGRAPHY; OSTEOPOROTIC PATIENTS; ELDERLY SUBJECTS; DIETARY CALCIUM; RENAL-FUNCTION; ADVANCING AGE; BONE-DENSITY; 25-HYDROXYVITAMIN-D3; MALABSORPTION AB We studied the mechanism of impaired calcium absorption with aging in 51 healthy women whose ages ranged from 26 to 88 years. Serum concentrations of 1,25-dihydroxyvitamin D [11,25-(OH)2D, mean of four measurements per subject] increased with age by 22% (P < 0.05) but, by split-point analysis, plateaued or decreased slightly after age 65. In a subset of 20 subjects, [H-3]1,25-(OH)2D3 kinetic analysis showed that this increase with age resulted from both increased production and decreased metabolic clearance of 1,25-(OH)2D. Despite the increase in serum 1,25-(OH)2D concentration, true calcium absorption did not change with age. The expected inverse correlation between true fractional calcium absorption and dietary calcium intake, however, was easily demonstrated (r = 0.66, P < 0.001). Serum intact parathyroid hormone (PTH) increased with age by 35% (P < 0.02) and serum bone gla protein (BGP, osteocalcin) increased by 47% (P < 0.001); the increases in serum PTH and serum BGP were directly correlated (r = 0.32, P < 0.05). The data are consistent with the following hypothetical model: (1) intestinal resistance to 1,25-(OH)2D action accounts for the increase in serum 1,25-(OH)2D concentrations with aging with no change in true calcium absorption; (2) this results in a compensatory increase in PTH secretion and in 1,25-(OH)2D production that prevents true calcium absorption from decreasing; (3) the previously described defect in 25-hydroxyvitamin D (25-OHD) 1-alpha-hydroxylase activity in aging animals and humans accounts for the leveling off in serum 1,25-(OH)2D concentration after age 65 years; and (4) the secondary hyperparathyroidism leads to increased bone turnover and thus contributes to age-related bone loss. C1 MAYO CLIN & MAYO FDN,ENDOCRINE RES UNIT,200 1ST ST SW,ROCHESTER,MN 55905. NICHHD,METAB ANAL & MASS SPECTROSCOPY SECT,BETHESDA,MD 20205. MAYO CLIN & MAYO FDN,DEPT HLTH SCI RES,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,NEPHROL RES UNIT,ROCHESTER,MN 55905. RI Eastell, Richard/G-5851-2011 OI Eastell, Richard/0000-0002-0323-3366 FU NCRR NIH HHS [RR-00585]; NIA NIH HHS [AG-04875]; NIDDK NIH HHS [R01 DK025409, R01 DK058546] NR 45 TC 133 Z9 134 U1 0 U2 4 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD FEB PY 1991 VL 6 IS 2 BP 125 EP 132 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GN783 UT WOS:A1991GN78300004 PM 2028834 ER PT J AU LIPPINCOTTSCHWARTZ, J GLICKMAN, J DONALDSON, JG ROBBINS, J KREIS, TE SEAMON, KB SHEETZ, MP KLAUSNER, RD AF LIPPINCOTTSCHWARTZ, J GLICKMAN, J DONALDSON, JG ROBBINS, J KREIS, TE SEAMON, KB SHEETZ, MP KLAUSNER, RD TI FORSKOLIN INHIBITS AND REVERSES THE EFFECTS OF BREFELDIN-A ON GOLGI MORPHOLOGY BY A CAMP-INDEPENDENT MECHANISM SO JOURNAL OF CELL BIOLOGY LA English DT Article ID CELL-FREE SYSTEM; ENDOPLASMIC-RETICULUM; INTRACELLULAR-TRANSPORT; SECRETORY PROTEINS; ANTIGEN RECEPTOR; RAT HEPATOCYTES; COMPLEX; IDENTIFICATION; MEMBRANES; APPARATUS AB Brefeldin A (BFA) causes rapid redistribution of Golgi proteins into the ER, leaving no definable Golgi apparatus, and blocks transport of proteins into post-Golgi compartments in the cell. In this study we follow the disassembly of the Golgi apparatus in BFA-treated, living cells labeled with NBD-ceramide and demonstrate that forskolin can both inhibit and reverse this process. Long, tubular processes labeled with NBD-ceramide were observed emerging from Golgi elements and extending out to the cell periphery in cells treated with BFA for 5 min. With longer incubations in BFA, the NBD label was dispersed in a fine reticular pattern characteristic of the ER. Treatment with forskolin inhibited these effects of BFA as well as BFA's earliest morphologic effect on the Golgi apparatus: the redistribution to the cytosol of a 110-kD Golgi peripheral membrane protein. In addition, forskolin could reverse BFA's block in protein secretion. Forskolin inhibition of BFA's effects was dose dependent and reversible. High concentrations of BFA could overcome forskolin's inhibitory effect, suggesting forskolin and BFA interact in a competitive fashion. Remarkably, in cells already exposed to BFA, forskolin could reverse BFA's effects causing the 110-kD Golgi peripheral membrane protein to reassociate with Golgi membrane and juxtanuclear Golgi complexes to reassemble. Neither membrane permeant cAMP analogues nor cAMP phosphodiesterase inhibitors could replicate or enhance forskolin's inhibition of BFA. 1,9-Dideoxyforskolin, which does not activate adenylyl cyclase, was equally as effective as forskolin in antagonizing BFA. A derivative of forskolin, 7-HPP-forskolin, that is less potent than forskolin at binding to adenylyl cyclase, was also equally effective as forskolin in antagonizing BFA. In contrast a similar derivative, 6-HPP-forskolin, that is equipotent with forskolin at binding to adenylyl cyclase, did not inhibit BFA's effects. These results suggest that forskolin acts as a competitive antagonist to BFA, using a cAMP-independent mechanism to prevent and reverse the morphologic effects induced by BFA. C1 WASHINGTON UNIV,SCH MED,DEPT CELL BIOL & PHYSIOL,ST LOUIS,MO 63110. US FDA,CTR BIOL EVALUAT & RES,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. EUROPEAN MOLEC BIOL LAB,W-6900 HEIDELBERG,GERMANY. RP LIPPINCOTTSCHWARTZ, J (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 33 TC 79 Z9 79 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD FEB PY 1991 VL 112 IS 4 BP 567 EP 577 DI 10.1083/jcb.112.4.567 PG 11 WC Cell Biology SC Cell Biology GA EX920 UT WOS:A1991EX92000005 PM 1847146 ER PT J AU DONALDSON, JG LIPPINCOTTSCHWARTZ, J KLAUSNER, RD AF DONALDSON, JG LIPPINCOTTSCHWARTZ, J KLAUSNER, RD TI GUANINE-NUCLEOTIDES MODULATE THE EFFECTS OF BREFELDIN-A IN SEMIPERMEABLE CELLS - REGULATION OF THE ASSOCIATION OF A 110-KD PERIPHERAL MEMBRANE-PROTEIN WITH THE GOLGI-APPARATUS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID GTP-BINDING PROTEIN; ENDOPLASMIC-RETICULUM; INTRACELLULAR-TRANSPORT; SECRETORY PROTEINS; RAT HEPATOCYTES; FREE SYSTEM; YEAST; COMPLEX; STACK; RECONSTITUTION AB The release of a 110-kD peripheral membrane protein from the Golgi apparatus is an early event in brefeldin A (BFA) action, preceding the movement of Golgi membrane into the ER. ATP depletion also causes the reversible redistribution of the 110-kD protein from Golgi membrane into the cytosol, although no Golgi disassembly occurs. To further define the effects of BFA on the association of the 110-kD protein with the Golgi apparatus we have used filter perforation techniques to produce semipermeable cells. All previously observed effects of BFA, including the rapid redistribution of the 110-kD protein and the movement of Golgi membrane into the ER, could be reproduced in the semipermeable cells. The role of guanine nucleotides in this process was investigated using the nonhydrolyzable analogue of GTP, GTP-gamma-S. Pretreatment of semipermeable cells with GTP-gamma-S prevented the BFA-induced redistribution of the 110-kD protein from the Golgi apparatus and movement of Golgi membrane into the ER. GTP-gamma-S could also abrogate the observed release of the 110-kD protein from Golgi membranes which occurred in response to ATP depletion. Additionally, when the 110-kD protein had first been dissociated from Golgi membranes by ATP depletion, GTP-gamma-S could restore Golgi membrane association of the 110-kD protein, but not if BFA was present. All of these effects observed with GTP-gamma-S in semipermeable cells could be reproduced in intact cells treated with AlF4-. These results suggest that guanine nucleotides regulate the dynamic association/dissociation of the 110-kD protein with the Golgi apparatus and that BFA perturbs this process by interfering with the association of the 110-kD protein with the Golgi apparatus. RP DONALDSON, JG (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 37 TC 171 Z9 172 U1 1 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD FEB PY 1991 VL 112 IS 4 BP 579 EP 588 DI 10.1083/jcb.112.4.579 PG 10 WC Cell Biology SC Cell Biology GA EX920 UT WOS:A1991EX92000006 PM 1993732 ER PT J AU WILDER, RL CASE, JP CROFFORD, LJ KUMKUMIAN, GK LAFYATIS, R REMMERS, EF SANO, H STERNBERG, EM YOCUM, DE AF WILDER, RL CASE, JP CROFFORD, LJ KUMKUMIAN, GK LAFYATIS, R REMMERS, EF SANO, H STERNBERG, EM YOCUM, DE TI ENDOTHELIAL-CELLS AND THE PATHOGENESIS OF RHEUMATOID-ARTHRITIS IN HUMANS AND STREPTOCOCCAL CELL-WALL ARTHRITIS IN LEWIS RATS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE NEUROENDOCRINE; CYTOKINES; ADHESION; TRANSIN; STROMELYSIN; COLLAGENASE ID TRANSFORMATION-ASSOCIATED METALLOPROTEINASE; TRANSIN STROMELYSIN EXPRESSION; GROWTH FACTOR-BETA; ADHESION MOLECULE-1; CYCLOSPORIN-A; SYNOVIUM; LOCALIZATION; SYNOVIOCYTES; INHIBITION; TISSUES AB Endothelial cells play a fundamental role in the pathogenesis of chronic inflammatory arthritis in humans such as rheumatoid arthritis (RA), as well as experimental animal models such as streptococcal cell wall (SCW) arthritis in LEW/N) rats. This review summarizes data in support of this concept. The earliest apparent abnormalities in synovial tissues of patients with RA and Lewis rats with SCW arthritis appear to reflect microvascular endothelial cell activation or injury. At the molecular level, the abnormalities include enhanced expression by endothelial cells of activation markers such as class II major histocompatibility complex antigens, phosphotyrosine, leukocyte adhesion molecules, oncoproteins such as c-Fos and c-Myc, and metalloproteinases such as collagenase and transin/stromelysin. The development of severe, chronic, destructive arthritis is dependent upon thymic-derived lymphocytes and is accompanied by tumorlike proliferation of cells in the synovial connective tissue stroma (blood vessels and fibroblastlike cells), which results in resorptive destruction of bone and cartilage. Multiple criteria support the analogy to a neoplastic process. Paracrine and autocrine factors such as interleukin-1 (IL-1), platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-beta), and heparin-binding fibroblast growth factors (HBGF, FGF) appear to play important roles in the generation of these lesions. Finally, in addition to the autocrine and paracrine regulatory factors, neuroendocrine factors, particularly the hypothalamic-pituitary-adrenal axis, appear to be involved in the counterregulation of the inflammatory process. The counterregulatory effects are mediated, in part, by inhibition of endothelial cell activation by corticosteroids. C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NCI,CHEMOPREVENT,BETHESDA,MD 20892. UNIV ARIZONA,ARIZONA HLTH SCI CTR,TUCSON,AZ 85724. RP WILDER, RL (reprint author), NIAMSD,ARTHRIT & RHEUMATISM BRANCH,BLDG 10,ROOM 9N240,BETHESDA,MD 20892, USA. RI Crofford, Leslie/J-8010-2013 NR 34 TC 31 Z9 31 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB PY 1991 VL 45 IS 2 BP 162 EP 166 DI 10.1002/jcb.240450207 PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV781 UT WOS:A1991EV78100006 PM 2055944 ER PT J AU MILNE, GWA AF MILNE, GWA TI VERY BROAD MARKUSH CLAIMS - A SOLUTION OR A PROBLEM - PROCEEDINGS OF A ROUND-TABLE DISCUSSION HELD ON AUGUST 29, 1990 SO JOURNAL OF CHEMICAL INFORMATION AND COMPUTER SCIENCES LA English DT Discussion RP MILNE, GWA (reprint author), NCI,BETHESDA,MD 20892, USA. NR 4 TC 4 Z9 5 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0095-2338 J9 J CHEM INF COMP SCI JI J. Chem. Inf. Comput. Sci. PD FEB PY 1991 VL 31 IS 1 BP 9 EP 30 DI 10.1021/ci00001a003 PG 22 WC Chemistry, Multidisciplinary; Computer Science, Information Systems; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA EZ409 UT WOS:A1991EZ40900004 PM 2026664 ER PT J AU KLING, MA ROY, A DORAN, AR CALABRESE, JR RUBINOW, DR WHITFIELD, HJ MAY, C POST, RM CHROUSOS, GP GOLD, PW AF KLING, MA ROY, A DORAN, AR CALABRESE, JR RUBINOW, DR WHITFIELD, HJ MAY, C POST, RM CHROUSOS, GP GOLD, PW TI CEREBROSPINAL-FLUID IMMUNOREACTIVE CORTICOTROPIN-RELEASING HORMONE AND ADRENOCORTICOTROPIN SECRETION IN CUSHINGS-DISEASE AND MAJOR DEPRESSION - POTENTIAL CLINICAL IMPLICATIONS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID BETA-ENDORPHIN; IMMUNOCYTOCHEMICAL LOCALIZATION; BIOCHEMICAL MANIFESTATIONS; CORTISOL SECRETION; SYNTHETIC ACTH; GROWTH-HORMONE; BRAIN-STEM; FEMALE RAT; FACTOR CRF; STRESS AB To explore whether possible differences in central nervous system neuromodulators contribute to the differential presentation of affective symptomatology in Cushing's disease and major depression, we examined the levels of immunoreactive CRH and ACTH in the cerebrospinal fluid (CSF) of 11 patients with Cushing's disease, a patient with ectopic ACTH secretion, 34 patients with major depression, and 60 healthy subjects. We elected to measure these peptides not only because both are classically involved in pituitary-adrenal regulation, but also because their primarily arousal-producing and anorexigenic behavioral effects in experimental animals suggest that they may play a role in the symptom complex of depressive syndromes. We also explored whether the CSF levels of these peptides were more helpful in determining the often difficult differential diagnosis between major depression and Cushing's disease than the plasma ACTH response to ovine CRH, a currently used but somewhat insensitive laboratory means of distinguishing these disorders. CSF levels of immunoreactive CRH and ACTH were significantly lower in Cushing's disease patients [21.9 +/- 2.7 and 15.4 +/- 1.8 pg/mL, (mean +/- SEM), respectively] compared to patients with major depression [38.4 +/- 2.3 pg/mL (P < 0.01) and 24.5 +/- 1.6 pg/mL (P < 0.01), respectively] and controls [38.4 +/- 1.6 pg/mL (P < 0.001) and 26.3 +/- 1.1 pg/mL (P < 0.001), respectively]. The coexistence of high plasma ACTH and low CSF ACTH in Cushing's disease yielded a CSF/plasma ACTH ratio consistently less than that in depressed patients, with only 2 of 31 subjects comprising both groups showing values that overlapped. In contrast, 9 of the combined patients showed ACTH responses to ovine CRH that overlapped. These data suggest that differences in centrally directed CRH secretion may account for the differential presentation of the dysphoric syndromes seen in major depression and Cushing's disease. Hence, the classic form of major depression (melancholia), is often associated with evidence of pathological hyperarousal, such as intense anxiety, sleeplessness, and anorexia, while that of Cushing's disease is associated with evidence of pathological hypoarousal, including hyperphagia, fatigue, and inertia. Moreover, measurement of the CSF/plasma ACTH ratio may serve as a clinically useful adjunct to the ovine CRH stimulation test and other laboratory measures in determining the differential diagnosis between major depression and Cushing's disease. C1 NIMH, CLIN NEUROSCI BRANCH, BETHESDA, MD 20892 USA. NIMH, BIOL PSYCHIAT BRANCH, BETHESDA, MD 20892 USA. NIA, NEUROSCI LAB, BETHESDA, MD 20892 USA. NICHHD, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. RP KLING, MA (reprint author), NIMH, CTR CLIN, DIV INTRAMURAL RES PROGRAM, CLIN NEUROENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. RI Kling, Mitchel/F-4152-2010 OI Kling, Mitchel/0000-0002-2232-1409 NR 68 TC 135 Z9 136 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD FEB PY 1991 VL 72 IS 2 BP 260 EP 271 PG 12 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EX403 UT WOS:A1991EX40300006 PM 1846869 ER PT J AU KAMP, GA MANASCO, PK BARNES, KM JONES, J ROSE, SR HILL, SC CUTLER, GB AF KAMP, GA MANASCO, PK BARNES, KM JONES, J ROSE, SR HILL, SC CUTLER, GB TI LOW GROWTH-HORMONE LEVELS ARE RELATED TO INCREASED BODY-MASS INDEX AND DO NOT REFLECT IMPAIRED GROWTH IN LUTEINIZING-HORMONE-RELEASING HORMONE AGONIST-TREATED CHILDREN WITH PRECOCIOUS PUBERTY SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID SEX STEROID-SECRETION; ANALOG THERAPY; SOMATIC GROWTH; OBESITY; DEFICIENCY; HEIGHT; MATURATION; DYNAMICS; GIRLS AB To test the hypothesis that GH deficiency might explain the low growth velocity of some LHRH agonist (LHRHa)-treated children with central precocious puberty, we measured stimulated (n = 81) and spontaneous (n = 32) GH levels during or after LHRHa treatment. GH stimulation tests in the children who were receiving LHRHa treatment were performed after 2 days of ethinyl estradiol administration. Thirty-one of 81 children (38%) who underwent GH stimulation tests had subnormal responses (less-than-or-equal-to 7-mu-g/L) to all tests administered (at least 2 stimuli), including 22 of 67 (33%) who had precocious puberty that was idiopathic or associated with hypothalamic hamartoma. Eleven of 32 children (34%) who underwent measurement of the mean nighttime spontaneous GH level had levels below the normal range for prepubertal children (< 1.2-mu-g/L). Despite the high incidence of subnormal GH levels, there appeared to be no relationship between the GH levels of these children and their growth characteristics. The height, growth velocity, bone maturation rate, predicted height, and insulin-like growth factor-I levels were not different between the children with low GH levels and the children with normal GH levels. Conversely, the GH levels were not different between the children with subnormal growth rates and the children with normal growth rates. Thus, variation in the growth rates of these LHRHa-treated children with central precocious puberty could not be explained by variation in the stimulated or spontaneous secretion of GH. In attempting to understand the high incidence of low GH levels in children with precocious puberty, we examined the relationship between GH level and body mass index (BMI). Both the stimulated (r = -0.33; P < 0.002) and the spontaneous (r = -0.61; P < 0.0002) GH levels were inversely related to BMI. Moreover, the children with precocious puberty as a group had significantly elevated BMI [1.2 +/- 0.1 (+/- SE) SD units] compared to normal children of the same age (P < 0.0001). Thus, increased body mass may explain the high incidence of subnormal GH levels in these patients, and normative GH levels adjusted for body mass are needed before it can be concluded that the apparently subnormal GH levels in LHRHa-treated children with precocious puberty are in fact low. C1 NIEHS, MOLEC & INTERGRAT NEUROSCI LAB, RES TRIANGLE PK, NC 27709 USA. RP KAMP, GA (reprint author), NICHHD, CTR CLIN, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10-N-262, BETHESDA, MD 20892 USA. NR 39 TC 43 Z9 43 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD FEB PY 1991 VL 72 IS 2 BP 301 EP 307 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EX403 UT WOS:A1991EX40300012 PM 1991801 ER PT J AU VOGELMEIER, C HUBBARD, RC FELLS, GA SCHNEBLI, HP THOMPSON, RC FRITZ, H CRYSTAL, RG AF VOGELMEIER, C HUBBARD, RC FELLS, GA SCHNEBLI, HP THOMPSON, RC FRITZ, H CRYSTAL, RG TI ANTINEUTROPHIL ELASTASE DEFENSE OF THE NORMAL HUMAN RESPIRATORY EPITHELIAL SURFACE PROVIDED BY THE SECRETORY LEUKOPROTEASE INHIBITOR SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ALPHA-1-ANTITRYPSIN; ANTIPROTEASE; BRONCHOALVEOLAR LAVAGE ID LEUKOCYTE PROTEASE INHIBITOR; BRONCHOALVEOLAR LAVAGE FLUIDS; STABLE PROTEINASE-INHIBITOR; AMINO-ACID SEQUENCE; ALPHA-1-PROTEINASE INHIBITOR; HUMAN-LUNG; POLYMORPHONUCLEAR LEUKOCYTES; BRONCHIAL INHIBITOR; HUSI-I; ANTILEUKOPROTEASE AB Secretory leukoprotease inhibitor (SLPI), a 12-kD nonglycosylated serine antiprotease with a high capacity for inhibiting neutrophil elastase (NE), is produced by cells of mucosal surfaces including the human lung. The molar concentrations of SLPI in total respiratory tract epithelial lining fluid (ELF) were 56 +/- 10% that of alpha-1-antitrypsin, suggesting SLPI may be more important for the anti-NE protection of the pulmonary epithelial surface than previously thought. However, evaluation demonstrated that SLPI in respiratory ELF was only one-third functional. Studies aerosolizing recombinant SLPI (rSLPI) to sheep demonstrated that in the short term, neither aerosolization and alveolar deposition nor the lavage procedure inactivated the SLPI molecule. In vitro studies with rSLPI demonstrated that exposure to oxidants did not modify the form of the molecule, while exposure to oxidants and NE caused the molecule to be cleaved from 12 to 8 kD. Consistent with this, evaluation of SLPI in lavage fluid of individuals with cystic fibrosis (a condition with oxidants and NE on the respiratory epithelium) showed that the SLPI was degraded. However, evaluation of SLPI in normal ELF by molecular sieve analysis and Western analysis demonstrated an intact 12-kD molecule, suggesting that the partial inactivation of SLPI in normals in vivo is not because it is complexed to NE or exposed to oxidants + NE. Together, these observations demonstrate that SLPI is present in large amounts in respiratory ELF, but since the majority of the SLPI is inactive, it likely does not play a significant role in protecting the normal respiratory epithelium, except perhaps in the upper airways where the levels of SLPI are the highest. C1 CIBA GEIGY AG,CH-4002 BASEL,SWITZERLAND. SYNERGEN,BOULDER,CO. UNIV MUNICH,DEPT CLIN CHEM & CLIN BIOCHEM,W-8000 MUNICH 2,GERMANY. RP VOGELMEIER, C (reprint author), NHLBI,PULM BRANCH,BLDG 10,ROOM 6D03,BETHESDA,MD 20892, USA. NR 37 TC 153 Z9 157 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB PY 1991 VL 87 IS 2 BP 482 EP 488 DI 10.1172/JCI115021 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EW295 UT WOS:A1991EW29500015 PM 1671391 ER PT J AU KAHN, BB SHULMAN, GI DEFRONZO, RA CUSHMAN, SW ROSSETTI, L AF KAHN, BB SHULMAN, GI DEFRONZO, RA CUSHMAN, SW ROSSETTI, L TI NORMALIZATION OF BLOOD-GLUCOSE IN DIABETIC RATS WITH PHLORIZIN TREATMENT REVERSES INSULIN-RESISTANT GLUCOSE-TRANSPORT IN ADIPOSE-CELLS WITHOUT RESTORING GLUCOSE TRANSPORTER GENE-EXPRESSION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE EUGLYCEMIA; HEXOSE TRANSPORT; GLUCOSE UTILIZATION; MESSENGER RNA ID PRIMARY CULTURED ADIPOCYTES; SKELETAL-MUSCLE; 3T3-L1 ADIPOCYTES; MESSENGER-RNA; DIFFERENTIAL REGULATION; CHRONIC HYPERGLYCEMIA; DEPENDENT REGULATION; RESPONSIVE TISSUES; INTRACELLULAR POOL; SENSITIVE METHOD AB Evidence is emerging for a direct role of glucose, independent of changes in insulin, in the regulation of cellular glucose transport and glucose utilization in vivo. In this study we investigate potential cellular and molecular mechanisms for this regulatory effect of glucose by determining how normalization of glycemia without insulin therapy in diabetic rats influences 3-O-methylglucose transport and the expression and translocation of two genetically distinct species of glucose transporters (GTs) in adipose cells. These results are compared with alterations in glucose transport in adipose cells is decreased 50% in parallel with reduced insulin-mediated glucose disposal in vivo. Levels of adipose/muscle GTs measured by immunoblotting are decreased in adipose cell subcellular membrane fractions, as are the corresponding mRNA levels assessed by Northern blotting of total adipose cell RNA. Normalization of blood glucose in diabetic rats with phlorizin, which impairs renal tubular glucose reabsorption and thus enhances glucose excretion, restores insulin-stimulated glucose transport in adipose cells and insulin-mediated glucose disposal in vivo. Importantly, levels of the adipose/muscle GT protein remain 43% reduced in the low-density microsomes in the basal state and 46% reduced in the plasma membranes in the insulin-stimulated state. Adipose/muscle GT mRNA levels remain approximately 50% depressed. Levels of the HepG2/brain GT protein and mRNA are unaltered by diabetes or phlorizin treatment. Thus, changes in ambient glucose independent of changes in ambient insulin can regulate the glucose transport response to insulin in isolated adipose cells and changes in responsiveness parallel alterations in glucose uptake in vivo. Since this effect can occur without alteration in the expression of the two species of glucose transporters present in adipose cells or in their translocation to the plasma membrane in response to insulin, it may result from changes in GT functional activity. C1 BETH ISRAEL HOSP,DEPT MED,HARVARD THORNDIKE LAB,BOSTON,MA 02215. CHARLES A DANA RES INST,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. YALE UNIV,DEPT MED,NEW HAVEN,CT 06510. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV DIABET,SAN ANTONIO,TX 78284. NIDDKD,MOLEC CELLULAR & NUTR ENDOCRINOL BRANCH,EXPTL DIABET METAB & NUTR SECT,BETHESDA,MD 20892. FU NIA NIH HHS [AG-00294]; NIDDK NIH HHS [DK-40936, R01 DK040936] NR 62 TC 150 Z9 150 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB PY 1991 VL 87 IS 2 BP 561 EP 570 DI 10.1172/JCI115031 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EW295 UT WOS:A1991EW29500025 PM 1991839 ER PT J AU THOMPSON, HL BURBELO, PD GABRIEL, G YAMADA, Y METCALFE, DD AF THOMPSON, HL BURBELO, PD GABRIEL, G YAMADA, Y METCALFE, DD TI MURINE MAST-CELLS SYNTHESIZE BASEMENT-MEMBRANE COMPONENTS - A POTENTIAL ROLE IN EARLY FIBROSIS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE MAST CELL; BASEMENT MEMBRANE; FIBROSIS; WOUND HEALING ID LINES PRODUCE LYMPHOKINES; COLONY-STIMULATING FACTOR; FC-EPSILON-RI; MULTIDOMAIN PROTEIN; PULMONARY FIBROSIS; CALCIUM IONOPHORES; GLOBULAR DOMAIN; CROSS-LINKAGE; GROWTH-FACTOR; LAMININ AB Mast cells are resident in tissues, particularly in association with endothelial and epithelial cell basement membranes, and increase at sites of inflammation, injury, and fibrosis. Although mast cells are known to both release and generate proinflamatory molecules in response to inflammatory stimuli, little is known as their normal biologic functions. Here we demonstrate IL-3-dependent mouse PT18 mast cells, mouse bone marrow-derived mast cells, and rat basophilic leukemia cells express large amounts of mRNA for collagen IV, laminin, and heparan sulfate proteoglycan. Western blot analysis confirmed that mast cells synthesize and secrete significant amounts collagen IV and laminin B1 and B2 chains. These data suggest that mast cells may contribute to normal tissue repair and/or the early overproduction of basement membrane components seen in a variety of fibrotic conditions. C1 NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. RP THOMPSON, HL (reprint author), NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BLDG 10,ROOM 11C208,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Burbelo, Peter/B-1027-2009 NR 38 TC 61 Z9 62 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB PY 1991 VL 87 IS 2 BP 619 EP 623 DI 10.1172/JCI115038 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EW295 UT WOS:A1991EW29500032 PM 1991845 ER PT J AU ELBADRY, OM HELMAN, LJ CHATTEN, J STEINBERG, SM EVANS, AE ISRAEL, MA AF ELBADRY, OM HELMAN, LJ CHATTEN, J STEINBERG, SM EVANS, AE ISRAEL, MA TI INSULIN-LIKE GROWTH FACTOR-II-MEDIATED PROLIFERATION OF HUMAN NEUROBLASTOMA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PARACRINE; AUTOCRINE; ADRENAL; DEVELOPMENT; EOSINOPHIL ID DEOXYRIBONUCLEIC-ACID SYNTHESIS; NEURO-BLASTOMA CELLS; FACTOR MESSENGER-RNA; HUMAN-BREAST CANCER; HUMAN-FETAL; HUMAN-FETUS; GENE-EXPRESSION; IGF-I; MONOCLONAL-ANTIBODY; HORMONAL-REGULATION AB Neuroblastoma is an embryonal tumor that typically arises in cells of the developing adrenal medulla. IGF-II mRNA is expressed at high levels in the adrenal cortex before birth but it is not detectable until after birth in the adrenal medulla. Neuroblastoma cell lines corresponding to early adrenal medullary precursors did not express IGF-II, although all three cell lines we tested were growth stimulated by IGF-II. Cell lines corresponding to more mature adrenal medullary cells expressed IGF-II, and one, SK-N-AS, grows by an IGF-II autocrine mechanism (J. Clin. Invest. 84:829-839) El-Badry, Romanus, Helman, Cooper, Rechler, and Israel. 1989. An examination of human neuroblastoma tumor tissues for IGF-II gene expression using in situ hybridization histochemistry revealed that IGF-II is expressed by tumor cells in only 5 of 21 neuroblastomas, but is detectable in cells of nonmalignant tissues including adrenal cortical cells, stromal fibroblasts, and eosinophils in all 21 tumors. These findings indicate that IGF-II may function as an autocrine growth factor for some neuroblastomas and as a paracrine growth factor for others. They suggest that the growth regulatory pathway utilized by neuroblastoma mimic those used in the precursor cell type from which individual tumors arise. C1 NCI,PEDIAT BRANCH,MOLEC GENET SECT,BETHESDA,MD 20892. NCI,CLIN ONCOL PROGRAM,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. CHILDRENS HOSP PHILADELPHIA,DEPT PATHOL,PHILADELPHIA,PA 19104. CHILDRENS HOSP PHILADELPHIA,DEPT PEDIAT,PHILADELPHIA,PA 19104. NR 49 TC 123 Z9 123 U1 0 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB PY 1991 VL 87 IS 2 BP 648 EP 657 DI 10.1172/JCI115042 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EW295 UT WOS:A1991EW29500036 PM 1991849 ER PT J AU KIDA, Y NYOMBA, BL BOGARDUS, C MOTT, DM AF KIDA, Y NYOMBA, BL BOGARDUS, C MOTT, DM TI DEFECTIVE INSULIN-RESPONSE OF CYCLIC ADENOSINE MONOPHOSPHATE-DEPENDENT PROTEIN-KINASE IN INSULIN-RESISTANT HUMANS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE GLYCOGEN SYNTHASE; PROTEIN PHOSPHORYLATION; MUSCLE ID RABBIT SKELETAL-MUSCLE; GLYCOGEN-SYNTHASE PHOSPHATASE; PHOSPHORYLATION STATE; HORMONAL-REGULATION; AMP; GLUCOSE; METABOLISM; INVIVO; INHIBITION; ACTIVATION AB Insulin-stimulated glycogen synthase activity in human muscle correlates with insulin-mediated glucose disposal is reduced in insulin-resistant subjects. Inhibition of the cyclic AMP-dependent protein kinase (A-kinase) is considered as a possible mechanism of insulin action for glycogen synthase activation. In this study, we investigated the the time course of insulin action on human muscle A-kinase activity during a 2-h insulin infusion in 13 insulin-sensitive (group S) and 7 insulin-resistant subjects (group R). Muscle biopsies were obtained from quadriceps femoris muscle at times 0, 10, 20, 40, and 120 min. Insulin infusion resulted in significant inhibition of A-kinase activity at 20 and/or 40 min using 0.2, 0.6, and 1.0-mu-M cyclic AMP in group S. A-kinase activities both before and after insulin administration were lower in group S than in group R using o.6-mu-M cyclic AMP. The decrease in apparent affinity for cyclic AMP during insulin infusion was larger for group S compared with Group R. Glycogen synthase activity increased significantly after insulin infusion in both groups and was higher in group S compared with group R. The data suggest that a defective response of A-kinase to insulin in insulin-resistant subjects could contribute to their reduced insulin stimulation of skeletal muscle glycogen synthase. RP MOTT, DM (reprint author), NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,ROOM 541,PHOENIX,AZ 85016, USA. NR 59 TC 31 Z9 31 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB PY 1991 VL 87 IS 2 BP 673 EP 679 DI 10.1172/JCI115045 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EW295 UT WOS:A1991EW29500039 PM 1846879 ER PT J AU HURLEY, DM ACCILI, D STRATAKIS, CA KARL, M VAMVAKOPOULOS, N RORER, E CONSTANTINE, K TAYLOR, SI CHROUSOS, GP AF HURLEY, DM ACCILI, D STRATAKIS, CA KARL, M VAMVAKOPOULOS, N RORER, E CONSTANTINE, K TAYLOR, SI CHROUSOS, GP TI POINT MUTATION CAUSING A SINGLE AMINO-ACID SUBSTITUTION IN THE HORMONE BINDING DOMAIN OF THE GLUCOCORTICOID RECEPTOR IN FAMILIAL GLUCOCORTICOID RESISTANCE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE POLYMERASE CHAIN REACTION; SEQUENCING; HYPERCORTISOLEMIA ID PRIMARY CORTISOL RESISTANCE; DEXAMETHASONE 21-MESYLATE; FUNCTIONAL DOMAINS; GENE; DNA; EXPRESSION; POLYMERASE; CLONING; PATIENT; CELLS AB Familial glucocorticoid resistance is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations in the absence of stigmata of Cushing's syndrome. Our previous studies of the first reported kindred showed a two-to threefold reduction in glucocorticoid receptor-ligand binding affinity in the propositus, and a lesser reduction in affinity in his mildy affected son and nephew. Glucocorticoid receptor cDNA from these three patients was amplified by polymerase chain reaction and sequenced. The cDNA nucleotide sequence was normal, except for nucleotide 2054, which substituted valine for aspartic acid at amino acid residue 641. The propositus was homozygous while the other relatives were heterozygous for the mutation. COS-7 monkey kidney cells were cotransfected with expression vectors for either wild type or Val 641-mutant receptors, together with the reporter plasmid pMMTV-CAT. Dexamethasone increased chloramphenicol acetyltransferase activity in cells expressing wild type receptor, but had no effect in cells expressing wild type receptor, but had no effect in cells expressing Val 641-mutant receptors, despite similar receptor concentrations, as indicated by Western blotting. The binding affinity for dexamethasone of the Val 641-mutant receptor was threefold lower than that of the wild type receptor. These results suggest that glucocorticoid resistance in this family is due to a point mutation in the steroid-binding domain of the glucocorticoid receptor. C1 NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10N262,BETHESDA,MD 20892. NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. NR 39 TC 271 Z9 285 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB PY 1991 VL 87 IS 2 BP 680 EP 686 DI 10.1172/JCI115046 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EW295 UT WOS:A1991EW29500040 PM 1704018 ER PT J AU SIMPSON, WJ BURGDORFER, W SCHRUMPF, ME KARSTENS, RH SCHWAN, TG AF SIMPSON, WJ BURGDORFER, W SCHRUMPF, ME KARSTENS, RH SCHWAN, TG TI ANTIBODY TO A 39-KILODALTON BORRELIA-BURGDORFERI ANTIGEN (P39) AS A MARKER FOR INFECTION IN EXPERIMENTALLY AND NATURALLY INOCULATED ANIMALS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID LYME-DISEASE SPIROCHETE; LINKED IMMUNOSORBENT ASSAYS; WHITE-FOOTED MICE; UNITED-STATES; CLINICAL MANIFESTATIONS; PEROMYSCUS-LEUCOPUS; IMMUNOBLOT ANALYSIS; SURVEILLANCE; COMPONENTS; COYOTES AB Borrelia burgdorferi expresses a conserved, species-specific 39-kDa protein (P39) that can stimulate antibodies during human infection. To confirm that anti-P39 antibodies are produced consistently in animals exposed to infectious spirochetes, white-footed mice, Peromyscus leucopus, and laboratory white mice, Mus musculus (strain BALB/c), were experimentally inoculated with either infectious or noninfectious B. burgdorferi and the antibody response to P39 was determined by immunoblot at 21 days postinoculation. All mice inoculated with approximately 10(7) infectious B. burgdorferi produced anti-P39 antibodies and were cultured positive for this spirochete. Mice inoculated with similar numbers of activated or viable noninfectious B. burgdorferi still producing P39 did not induce anti-P39 antibodies. By contrast, putative antiflagellin antibodies were detected in < 18% of the infected animals, which supports the notion that antibody reactive with flagellin may not be reliable as a marker for B. burgdorferi exposure as was originally thought. Mice infected with B. burgdorferi following exposure to ticks (Ixodes dammini) produced anti-P39 antibodies, no later than 7 days postinfection, indicating that P39 is an effective immunogen in natural infections. Notably, anti-P39 antibodies were the predominant B. burgdorferi reactive antibodies detected early in the infection. Our results indicate that anti-P39 antibodies are produced in response to an active infection and are therefore reliable markers for infection in experimentally and naturally inoculated animals. RP SIMPSON, WJ (reprint author), NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,ARTHROPOD BORNE DIS SECT,HAMILTON,MT 59840, USA. NR 42 TC 73 Z9 75 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD FEB PY 1991 VL 29 IS 2 BP 236 EP 243 PG 8 WC Microbiology SC Microbiology GA ET578 UT WOS:A1991ET57800003 PM 2007630 ER PT J AU NUGENT, RP KROHN, MA HILLIER, SL AF NUGENT, RP KROHN, MA HILLIER, SL TI RELIABILITY OF DIAGNOSING BACTERIAL VAGINOSIS IS IMPROVED BY A STANDARDIZED METHOD OF GRAM STAIN INTERPRETATION SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID CHLAMYDIA-TRACHOMATIS; INFECTION; ASSOCIATIONS AB The purpose of the study was to examine intercenter variability in the interpretation of Gram-stained vaginal smears from pregnant women. The intercenter reliability of individual morphotypes identified on the vaginal smear was evaluated by comparing them with those obtained at a standard center. A new scoring system that uses the most reliable morphotypes from the vaginal smear was proposed for diagnosing bacterial vaginosis. This scoring system was compared with the Spiegel criteria for diagnosing bacterial vaginosis. The scoring system (0 to 10) was described as a weighted combination of the following morphotypes: lactobacilli, Gardnerella vaginalis or bacteroides (small gram-variable rods or gram-negative rods), and curved gram-variable rods. By using the Spearman rank correlation to determine intercenter variability, gram-positive cocci had poor agreement (0.23); lactobacilli (0.65), G. vaginalis (0.69), and bacteroides (0.57) had moderate agreement; and small (0.74) and curved (0.85) gram-variable rods had good agreement. The reliability of the 0 to 10 scoring system was maximized by not using gram-positive cocci, combining G. vaginalis and bacteroides morphotypes, and weighting more heavily curved gram-variable-rods. For comparison with the Spiegel criteria, a score of 7 or higher was considered indicative of bacterial vaginosis. The standardized score had improved intercenter reliability (r = 0.82) compared with the Spiegel criteria (r = 0.61). The standardized score also facilitates future research concerning bacterial vaginosis because it provides gradations of the disturbance of vaginal flora which may be associated with different levels of risk for pregnancy complications. C1 UNIV WASHINGTON,DEPT EPIDEMIOL,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT OBSTET & GYNECOL,SEATTLE,WA 98195. RP NUGENT, RP (reprint author), NICHHD,PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH,EXECUT PLAZA N,BETHESDA,MD 20892, USA. FU NICHD NIH HHS [HD3-2832, HD3-2833, HD3-2834] NR 17 TC 1474 Z9 1570 U1 9 U2 58 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 FEB PY 1991 VL 29 IS 2 BP 297 EP 301 PG 5 WC Microbiology SC Microbiology GA ET578 UT WOS:A1991ET57800014 PM 1706728 ER PT J AU LONGO, DL RUSSO, A DUFFEY, PL HUBBARD, SM GLATSTEIN, E HILL, JB JAFFE, ES YOUNG, RC DEVITA, VT AF LONGO, DL RUSSO, A DUFFEY, PL HUBBARD, SM GLATSTEIN, E HILL, JB JAFFE, ES YOUNG, RC DEVITA, VT TI TREATMENT OF ADVANCED-STAGE MASSIVE MEDIASTINAL HODGKINS-DISEASE - THE CASE FOR COMBINED MODALITY TREATMENT SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID BONE-MARROW TRANSPLANTATION; PROGNOSTIC-SIGNIFICANCE; COMBINATION CHEMOTHERAPY; INTENSIVE CHEMOTHERAPY; STANFORD EXPERIENCE; PLUS RADIOTHERAPY; ABVD CHEMOTHERAPY; IRRADIATION; MOPP; INVOLVEMENT C1 NCI,DIV CANC TREATMENT,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 47 TC 69 Z9 69 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD FEB PY 1991 VL 9 IS 2 BP 227 EP 235 PG 9 WC Oncology SC Oncology GA EV470 UT WOS:A1991EV47000006 PM 1988570 ER PT J AU RUDORFER, MV SHERER, MA LANE, EA GOLDEN, RN LINNOILA, M POTTER, WZ AF RUDORFER, MV SHERER, MA LANE, EA GOLDEN, RN LINNOILA, M POTTER, WZ TI ACUTE NORADRENERGIC EFFECTS OF DESIPRAMINE IN DEPRESSION SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID LIQUID-CHROMATOGRAPHIC ASSAY; PLASMA NOREPINEPHRINE LEVELS; CLONIDINE; KINETICS; PHARMACOLOGY; YOHIMBINE; RESPONSES; BLOCKERS; ILLNESS; HUMANS AB As a probe of the noradrenegic system in depression, single oral doses of the tricyclic antidepressant desipramine (100 mg) and placebo were administered to unipolar and bipolar depressed patients and healthy volunteers. Plasma concentrations of norephinephrine (NE) were determined 2-3 hours after dosing, with subjects in supine and upright positions. On the placebo day plasma NE was low in a subset of bipolar patients; both groups of depressives demonstrated an exaggerated increase in plasma NE upon standing. After desipramine dosing, the orthostatic procedure resulted in even greater relative increments in plasma NE in both patient groups, with no change in volunteers. These data are consistent with noradrenergic dysregulation in depression. C1 NIAAA,DIV INTRAMURAL CLIN & BIOL RES,CLIN STUDIES LAB,ROCKVILLE,MD 20852. RP RUDORFER, MV (reprint author), NIMH,CLIN NEUROSCI BRANCH,CLIN PHARMACOL SECT,BLDG 10,ROOM 2D46,BETHESDA,MD 20892, USA. NR 41 TC 3 Z9 3 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 FEB PY 1991 VL 11 IS 1 BP 22 EP 27 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA EX693 UT WOS:A1991EX69300004 PM 2040714 ER PT J AU WOERNER, MG KANE, JM LIEBERMAN, JA ALVIR, J BERGMANN, KJ BORENSTEIN, M SCHOOLER, NR MUKHERJEE, S ROTROSEN, J RUBINSTEIN, M BASAVARAJU, N AF WOERNER, MG KANE, JM LIEBERMAN, JA ALVIR, J BERGMANN, KJ BORENSTEIN, M SCHOOLER, NR MUKHERJEE, S ROTROSEN, J RUBINSTEIN, M BASAVARAJU, N TI THE PREVALENCE OF TARDIVE-DYSKINESIA SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID RATING-SCALE AB A total of 2250 subjects from psychiatric and geriatric settings was examined for abnormal involuntary movements by the same team of trained raters employing a standard examination technique and rating scale. "Spontaneous" dyskinesia rates were 1.3% among 400 healthy elderly people surveyed at senior citizens centers, 4.8% among medical geriatric inpatients and ranged from 0 to 2% among psychiatric patients never exposed to neuroleptics. For samples of neuroleptic-treated patients, prevalence rates ranged from 13.3% among patients at a voluntary psychiatric hospital to 36.1% among state hospital patients. Logistic regression analyses revealed a large effect of age on tardive dyskinesia prevalence and an interaction of age with sex. Among younger subjects, men had higher rates; among subjects over age 40, rates were higher for women. Edentulousness and presence of other neurological disorders were possible contributors to high rates for the elderly. Even with control for age, sex and duration of neuroleptic exposure, prevalence differed markedly across study site. C1 LONG ISL JEWISH MED CTR,DEPT NEUROL,GLEN OAKS,NY 11004. NIMH,PHARMACOL & SOMAT TREATMENTS RES BRANCH,BETHESDA,MD 20892. CREEDMOOR PSYCHIAT CTR,QUEENS VILLAGE,NY. VET ADM MED CTR,NEW YORK,NY 10010. PARKER INST GERIATR CARE,NEW HYDE PK,NY. RP WOERNER, MG (reprint author), HILLSIDE HOSP,DEPT PSYCHIAT,GLEN OAKS,NY 11004, USA. FU NIMH NIH HHS [MH-00537, MH-41960]; PHS HHS [2 78-81-0032] NR 18 TC 98 Z9 98 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 FEB PY 1991 VL 11 IS 1 BP 34 EP 42 PG 9 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA EX693 UT WOS:A1991EX69300006 PM 1674949 ER PT J AU KIVIPELTO, L RUBENSTEIN, J YANG, HYT PANULA, P AF KIVIPELTO, L RUBENSTEIN, J YANG, HYT PANULA, P TI ONTOGENY OF THE F8FAMIDE-LIKE (MORPHINE-MODULATING) PEPTIDES IN THE CENTRAL-NERVOUS-SYSTEM OF RATS SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE BRAIN; SPINAL CORD; IMMUNOHISTOCHEMISTRY; RADIOIMMUNOASSAY ID CONTAINING NEURON SYSTEM; VASOACTIVE INTESTINAL POLYPEPTIDE; LOWER BRAIN-STEM; IMMUNOHISTOCHEMICAL ANALYSIS; SUBSTANCE-P; SPINAL-CORD; ENKEPHALIN; IMMUNOREACTIVITY; NEUROPEPTIDE; NEUROTENSIN AB FLFQPQRF-NH2 (F8Famide; FMRFamide-like peptide; morphine-modulating peptide) is a peptide isolated from bovine brain. It has some opiate analgesia modulating effects. In an adult rat central nervous system, F8Famide-like immunoreactivity is found in high concentrations in the posterior pituitary, hypothalamus, pons, medulla, and dorsal spinal cord. By using immunohistochemistry and radioimmunoassay, we studied the development of the F8Famide-immunoreactive system in the rat central nervous system during the ontogeny. F8Famide-immoreactive fibers and terminals first appeared in the median eminence on the twentieth embryonal day. Postnatally the F8Famide-immunoreactive system developed rapidly both in the brain and spinal cord, the immunoreactive structures having an adultlike distribution by the age of 1 week. A transient increase of the F8Famide-immunoreactive material was observed during the third and fourth postnatal weeks. By the age of 4 weeks, the F8Famide-containing neuronal system was adultlike both in distribution and quantity. The results suggest that the F8Famide-like peptides may act as neurotransmitters or neuromodulators from the time of their appearance in the brain and spinal cord. The early appearance and the distribution of the F8Famide-like immunoreactivity suggest that these peptides may participate, in addition to nociceptive mechanisms, in the regulation of blood pressure, feeding behaviour, and endocrine functions. C1 UNIV HELSINKI,DEPT ANAT,SILTAVUORENPENGER 20A,SF-00170 HELSINKI 17,FINLAND. UNIV HELSINKI,DEPT ANAT,SF-00170 HELSINKI 17,FINLAND. ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. NR 44 TC 23 Z9 23 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD FEB 1 PY 1991 VL 304 IS 1 BP 14 EP 33 DI 10.1002/cne.903040103 PG 20 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA EU460 UT WOS:A1991EU46000002 PM 1673130 ER PT J AU MOULDER, K ROBERTS, K SHEVACH, EM COLIGAN, JE AF MOULDER, K ROBERTS, K SHEVACH, EM COLIGAN, JE TI THE MOUSE VITRONECTIN RECEPTOR IS A T-CELL ACTIVATION ANTIGEN SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID AMINO-ACID SEQUENCE; ALPHA-SUBUNIT; FIBRONECTIN RECEPTOR; SURFACE RECEPTOR; BETA-SUBUNIT; ADHESION; INTEGRINS; LFA-1; IDENTIFICATION; PROTEINS AB In this report, we demonstrate that the T cell activation antigen, recognized by monoclonal antibody H9.2B8, is the murine homologue of the vitronectin receptor (VNR) and, thereby, we provide initial evidence that VNR is expressed on lymphoid cells. VNR is expressed on a variety of T cell lines, tumors, and Con A-activated splenocytes, but not resting T cells, and is capable of binding to the extracellular matrix proteins fibronectin, fibrinogen, and vitronectin, via the tripeptide sequence RGD. There was no evidence of novel beta chains pairing with the VNR alpha chain, as has been demonstrated in some human cells. In view of recent studies demonstrating that this molecule functions as an accessory molecule in T cell activation, the VNR may play an important role in mouse T cell functions. C1 NIAID,BIOL RESOURCES BRANCH,BLDG 4,ROOM 413,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 27 TC 55 Z9 55 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD FEB 1 PY 1991 VL 173 IS 2 BP 343 EP 347 DI 10.1084/jem.173.2.343 PG 5 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EV175 UT WOS:A1991EV17500008 PM 1703206 ER PT J AU RELLAHAN, BL BLUESTONE, JA HOULDEN, BA COTTERMAN, MM MATIS, LA AF RELLAHAN, BL BLUESTONE, JA HOULDEN, BA COTTERMAN, MM MATIS, LA TI JUNCTIONAL SEQUENCES INFLUENCE THE SPECIFICITY OF GAMMA/DELTA T-CELL RECEPTORS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID GAMMA; DELTA; DISTINCT; LYMPHOCYTES; THYMOCYTES; REGION; CHAIN AB T lymphocytes bearing the gamma/delta T cell receptor (TCR-gamma/delta) express a limited number of germline variable gene segments, generating receptor sequence diversity primarily through junctional mechanisms. To examine the role of V(D)J junctional sequences in antigen recognition by TCR-gamma/delta, we derived an alloreactive murine TCR-gamma/delta-+ T cell line, LKD1, specific for the I-A(d) class II major histocompatibility complex (MHC) molecule, and compared its receptor with that expressed by a previously characterized class II MHC alloreactive T cell line, LBK5, specific for I-E(k,b,s,) Ia molecules. Both LKD1 and LBK5 express receptors encoded by rearranged V-gamma-1.2J-gamma-2 and V-delta-5D-delta-2J-delta-1 gene elements, differing in sequence only in the V(D)J junctional regions of the gamma and delta genes. These results demonstrate that junctionally encoded sequences corresponding to the putative third complementarity determining region can influence the antigen specificity of TCR-gamma/delta. C1 NCI,MOLEC IMMUNOREGULAT LAB,BIOL RESPONSE PROGRAM,BLDG 560,ROOM 31-33,FREDERICK,MD 21702. US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,BETHESDA,MD 20892. UNIV CHICAGO,BEN MAY INST,DEPT PATHOL,COMM IMMUNOL,CHICAGO,IL 60637. OI Damschroder, Melissa/0000-0001-9453-6532 FU NIAID NIH HHS [1R01 AI-26847] NR 14 TC 30 Z9 30 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD FEB 1 PY 1991 VL 173 IS 2 BP 503 EP 506 DI 10.1084/jem.173.2.503 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EV175 UT WOS:A1991EV17500028 PM 1703211 ER PT J AU PANTALEO, G BUTINI, L GRAZIOSI, C POLI, G SCHNITTMAN, SM GREENHOUSE, JJ GALLIN, JI FAUCI, AS AF PANTALEO, G BUTINI, L GRAZIOSI, C POLI, G SCHNITTMAN, SM GREENHOUSE, JJ GALLIN, JI FAUCI, AS TI HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) INFECTION IN CD4+ LYMPHOCYTES-T GENETICALLY DEFICIENT IN LFA-1 - LFA-1 IS REQUIRED FOR HIV-MEDIATED CELL-FUSION BUT NOT FOR VIRAL TRANSMISSION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID HTLV-III/LAV ENVELOPE; SYNCYTIUM FORMATION; RECEPTOR; GLYCOPROTEIN; ANTIGEN AB In the present study, we demonstrated that expression of the LFA-1 molecule is necessary for cell fusion and syncytia formation in human immunodeficiency virus (HIV)-infected CD4+ T lymphocytes. In contrast, the lack of expression of LFA-1 does not influence significantly cell-to-cell transmission of HIV. In fact, LFA-1- T lymphocytes obtained from a leukocyte adhesion deficiency patient were unable to fuse and form syncytia when infected with HIV-1 or HIV-2, despite the fact that efficiency of HIV infection (i.e., virus entry, HIV spreading, and levels of virus replication) was comparable with that observed in LFA-1+ T lymphocytes. In addition, we provide evidence that LFA-1 by mediating cell fusion contributes to the depletion of HIV-infected CD4+ T lymphocytes in vitro. C1 NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. RP PANTALEO, G (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B 13,BETHESDA,MD 20892, USA. RI Pantaleo, Giuseppe/K-6163-2016 NR 16 TC 122 Z9 122 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD FEB 1 PY 1991 VL 173 IS 2 BP 511 EP 514 DI 10.1084/jem.173.2.511 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EV175 UT WOS:A1991EV17500030 PM 1671082 ER PT J AU WEGHORST, CM HENNEMAN, JR WARD, JM AF WEGHORST, CM HENNEMAN, JR WARD, JM TI DOSE-RESPONSE OF HEPATIC AND RENAL DNA SYNTHETIC RATES TO CONTINUOUS EXPOSURE OF BROMODEOXYURIDINE (BRDU) VIA SLOW-RELEASE PELLETS OR OSMOTIC MINIPUMPS IN MALE B6C3F1 MICE SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article ID DEOXYRIBONUCLEOSIDE TRIPHOSPHATE POOLS; TUMOR PROMOTION; CELL-PROLIFERATION; CARCINOGENESIS; IRRADIATION; INITIATION; EXPRESSION; THYMIDINE; LIVER AB We studied the use of acute and chronic 5-bromo-2'-deoxy-uridine (BrdU) administration for detection of DNA-synthesizing cells in the liver and kidney of B6C3F1 male mice. Six-week-old mice were exposed to BrdU either acutely with a single-pulse (IP) injection 1 hr before sacrifice or chronically with the use of slow-release pellets or osmotic minipumps at one of four BrdU dose rates. Pellets (2.5, 10, 25, and 50 mg) and minipumps (2.5 and 10 mg equivalents) were implanted subcutaneously on the backs of the animals 4 or 7 days before sacrifice). BrdU incorporation into DNA was determined by immunohistochemistry using an anti-BrdU antibody. Mice chronically exposed to BrdU demonstrated increased levels of nuclear labeling compared with those receiving a single-pulse injection. No time-related increases in nuclear labeling were detected in hepatocytes or renal tubule cells of mice exposed to BrdU pellets and in the kidneys of mice receiving BrdU minipumps at the 7-day compared with the 4-day time point. In some cases, the labeling indices at 7 days were significantly decreased compared with those at 4 days. In contrast, a time-related increase in nuclear labeling was seen in hepatocytes and Kupffer cells of mice exposed to BrdU minipumps. Therefore, the method used to administer BrdU chronically to the animal appears to play an important role in presenting the true proliferative scenario in cell kinetic studies. Our findings also provide evidence for an effect of BrdU on normal proliferation rates in these tissues. C1 NCI,DIV CANC ETIOL,COMPARAT CARCINOGENESIS LAB,BETHESDA,MD 20892. RP WEGHORST, CM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21701, USA. FU NCI NIH HHS [N01-CO-74102] NR 29 TC 40 Z9 40 U1 0 U2 1 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 FEB PY 1991 VL 39 IS 2 BP 177 EP 184 PG 8 WC Cell Biology SC Cell Biology GA EX524 UT WOS:A1991EX52400003 PM 1987261 ER PT J AU MAO, SY VARINBLANK, N EDIDIN, M METZGER, H AF MAO, SY VARINBLANK, N EDIDIN, M METZGER, H TI IMMOBILIZATION AND INTERNALIZATION OF MUTATED IGE RECEPTORS IN TRANSFECTED CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID BASOPHILIC LEUKEMIA-CELLS; IMMUNOGLOBULIN-E; CYTOPLASMIC DOMAIN; LATERAL DIFFUSION; HIGH-AFFINITY; MAST-CELLS; SEROTONIN RELEASE; SMALL OLIGOMERS; FC-RECEPTORS; COATED PITS AB Earlier studies have shown that the mast cell receptor IgE (FcepsilonRI) for is expressed on COS-7 cells transfected with the cDNA for each of the three types of subunits that form the tetrameric, alpha-beta-gamma-2, receptor. Although such transfected COS cells fail to exhibit some of the early biochemical perturbations initiated by aggregation of the receptor on normal mast cells and related tumor lines, we show here that other characteristics of the endogenous FcepsilonRI are retained. Thus, the unaggregated transfected wild-type receptors were found to have a restricted translational diffusion similar to that observed for endogenous receptors on mast cells as assessed by fluorescence photobleaching and recovery. Similarly, as with endogenous receptors, the mobility of transfected receptors was sharply reduced when the receptors were aggregated by reaction with small oligomers of IgE. In addition, aggregation of the transfected FcepsilonRI caused them to be internalized by the COS cells by a cytochalasin-sensitive mechanism, albeit at a considerably slower rate than was seen with endogenous receptors on mast cells or with transfected receptors in a line of receptor-deficient mast cells. We also examined the mobility and internalization before and after aggregation, of some 13 different combinations of receptor subunit mutants in which one or more of the five cytoplasmic domains of the receptor had been truncated. Our results show that whatever interactions between the receptor and cellular components may account for the phenomena we studied, such interactions do not critically depend upon the bulk of the cytoplasmic domains of the receptor. C1 JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218. RP MAO, SY (reprint author), NIAMS,BLDG 10,RM 9N228,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [AI14584] NR 67 TC 37 Z9 37 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 FEB 1 PY 1991 VL 146 IS 3 BP 958 EP 966 PG 9 WC Immunology SC Immunology GA EU926 UT WOS:A1991EU92600025 PM 1824851 ER PT J AU CHAROENVIT, Y MELLOUK, S COLE, C BECHARA, R LEEF, MF SEDEGAH, M YUAN, LF ROBEY, FA BEAUDOIN, RL HOFFMAN, SL AF CHAROENVIT, Y MELLOUK, S COLE, C BECHARA, R LEEF, MF SEDEGAH, M YUAN, LF ROBEY, FA BEAUDOIN, RL HOFFMAN, SL TI MONOCLONAL, BUT NOT POLYCLONAL, ANTIBODIES PROTECT AGAINST PLASMODIUM-YOELII SPOROZOITES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CIRCUMSPOROZOITE PROTEIN; FALCIPARUM SPOROZOITES; BERGHEI SPOROZOITES; MALARIA SPOROZOITES; SYNTHETIC PEPTIDES; SUBUNIT VACCINES; MURINE MALARIA; IMMUNOGENICITY; RECOMBINANT; GENE AB One of the primary strategies for malaria vaccine development has been to design subunit vaccines that induce protective levels of antibodies against the circumsporozoite (CS) protein of malaria sporozoites. In the Plasmodium yoelii mouse model system such vaccines have been uniformly unsuccessful in protecting against sporozoite-induced malaria. To demonstrate that antibodies to P. yoelii CS protein could provide protection we established a passive transfer model. Passive transfer of Navy yoelii sporozoite 1 (NYS1), an IgG3 mAb against the P. yoelii CS protein, protected 100% of mice against challenge with 5000 P. yoelii sporozoites. Binding of NYS1 to sporozoites was inhibited by incubation with (QGPGAP)2, a synthetic peptide derived from the repeat region of the P. yoelii CS protein, indicating that the epitope on sporozoites recognized by this mAb was included within this peptide. The levels of antibodies to (QGPGAP)2 by ELISA, and to sporozoites by indirect fluorecent antibody test and CS precipitation reaction were similar in sera from mice that received NYS1 in passive transfer and were protected against challenge with 5000 sporozoites, and from mice that had been immunized with subunit vaccines containing (QGPGAP)2 but were not protected against challenge with 40-200 sporozoites. To determine if antibody avidity, not absolute concentration could explain the striking differences in protection, we established a thiocyanate elution assay. The results suggest that NYS1, the protective mAb, has a lower avidity for (QGPGAP)2 and for sporozoites than do the vaccine-induced antibodies. Although the results of the conventional antibody assays did not correlate with protection, sera from the protected animals inhibited sporozoite development in mouse hepatocyte cultures significantly more than did the sera from the unprotected, subunit vaccine-immunized animals, correlating with protection. The data clearly demonstrate that antibodies to the CS protein can protect against intense sporozoite infection. Improved understanding of the differences between protective mAb and nonprotective polyclonal antibodies will be important in the further development of malaria vaccines. C1 USN,MED RES INST,DEPT INFECT DIS,BETHESDA,MD 20889. NIDR,BETHESDA,MD 20892. NR 30 TC 98 Z9 98 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 1 PY 1991 VL 146 IS 3 BP 1020 EP 1025 PG 6 WC Immunology SC Immunology GA EU926 UT WOS:A1991EU92600033 PM 1988490 ER PT J AU PENDURTHI, TK SCHLOM, J PRIMUS, FJ AF PENDURTHI, TK SCHLOM, J PRIMUS, FJ TI HUMAN LYMPHOKINE-ACTIVATED KILLER-CELLS AUGMENT IMMUNOTHERAPY OF HUMAN COLON-CARCINOMA XENOGRAFTS WITH MONOCLONAL-ANTIBODY D612 SO JOURNAL OF IMMUNOTHERAPY LA English DT Article ID HUMAN-TUMOR GROWTH; CELLULAR CYTO-TOXICITY; EFFECTOR-CELLS; HUMAN-MELANOMA; DISIALOGANGLIOSIDES GD2; NEUROECTODERMAL ORIGIN; MALIGNANT-MELANOMA; COMBINED THERAPY; NEURO-BLASTOMA; TARGET ANTIGEN AB The tumoricidal properties of an anti-human colon carcinoma monoclonal antibody (MAb), designated D612 (IgG2a), alone and in combination with IL-2-activated human lymphocytes were investigated in athymic mice bearing LS-174T colon tumor xenografts. Treatment of mice bearing LS-174T tumors (1 day, s.c.) with a single i.v. dose of 400-mu-g of D612 alone resulted in a significant inhibition of tumor growth. Lower doses of D612 had an intermediate effect on tumor growth. Similar inhibition of tumor growth was obtained when D612 was administered in three doses of 400 or 800-mu-g each during the first week after tumor implantation. Mouse macrophages but not splenocytes mediated antibody-dependent cellular cytotoxicity with D612, suggesting that tumor inhibition was due to the participation of host macrophages with D612. Human lymphokine-activated killer (LAK) cells were generated by incubating human peripheral blood mononuclear cells (PBLs) from normal donors with 100 U/ml of IL-2 for 24 h. An administration of human LAK cells did not significantly inhibit the growth of the human xenograft tumor. Adoptive transfer of a single dose of human LAK cells (2 x 10(7), i.v.) into mice treated with a suboptimal dose of D612 (200-mu-g) significantly inhibited tumor growth compared to that obtained with either D612 or LAK cells alone. Similar results were obtained with three doses of D612 plus human LAK cells although there was a tendency for multiple doses of LAK cells alone to show some antitumor effects. LAK cells or PBLs had similar antitumor activities when used in conjunction with D612. When larger established tumors were treated, single or multiple doses of D612 or LAK cells alone were without effect; however, LAK cells plus D612 elicited significant growth inhibition. These results demonstrate that the tumoricidal properties of LAK cells and the D612 MAb can be augmented when used together in the immunotherapy of human colon cancer xenografts. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BLDG 10,ROOM 8B07,BETHESDA,MD 20892. NR 41 TC 13 Z9 13 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD FEB PY 1991 VL 10 IS 1 BP 2 EP 12 DI 10.1097/00002371-199102000-00002 PG 11 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA EY347 UT WOS:A1991EY34700001 PM 2012797 ER PT J AU KORMAN, NJ EYRE, RW ZONE, J STANLEY, JR AF KORMAN, NJ EYRE, RW ZONE, J STANLEY, JR TI DRUG-INDUCED PEMPHIGUS - AUTOANTIBODIES DIRECTED AGAINST THE PEMPHIGUS ANTIGEN COMPLEXES ARE PRESENT IN PENICILLAMINE AND CAPTOPRIL-INDUCED PEMPHIGUS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Note ID HUMAN EPIDERMAL-CELLS; FOLIACEUS; VULGARIS; ACANTHOLYSIS; INDUCTION; MECHANISM; PROTEIN; PATIENT; CULTURE; IGG AB Pemphigus is an autoimmune blistering disease characterized by circulating autoantibodies directed against the keratinocyte cell surface. The two variants, pemphigus foliaceus and pemphigus vulgaris, can be distinguished at the molecular level by immunochemical studies. The large majority of patients with pemphigus develop the disease spontaneously; however, there is a small group of patients who develop pemphigus after treatment with certain medications, of which penicillamine and captopril are the best documented. Most patients with drug-induced pemphigus have circulating and/or tissue bound epidermal cell surface autoantibodies; however, the molecular specificity of these autoantibodies has not been studied. We performed immunoprecipitation studies utilizing extracts of I-125-labeled suction blister epidermis and the sera of three patients with drug-induced pemphigus foliaceus (two due to penicillamine an done due to captopril) and one patient with captopril-induced pemphigus vulgaris. We found that the three patients with drug-induced pemphigus foliaceus had circulating autoantibodies that are directed against the pemphigus foliaceus antigen complex and that the one patient with drug-induced pemphigus vulgaris had circulating autoantibodies that are directed against the pemphigus vulgaris antigen complex. The study demonstrates that autoantibodies specificity, on a molecular level, as do autoantibodies from other pemphigus patients. C1 NCI, DERMATOL BRANCH, BLDG 10, ROOM 12N238, BETHESDA, MD 20892 USA. UNIV UTAH, SCH MED, DEPT MED DERMATOL, SALT LAKE CITY, UT 84112 USA. NR 21 TC 67 Z9 67 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0022-202X EI 1523-1747 J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD FEB PY 1991 VL 96 IS 2 BP 273 EP 276 DI 10.1111/1523-1747.ep12464471 PG 4 WC Dermatology SC Dermatology GA EV774 UT WOS:A1991EV77400021 PM 1991988 ER PT J AU THURKAUF, A DECOSTA, B BERGER, P PAUL, S RICE, KC AF THURKAUF, A DECOSTA, B BERGER, P PAUL, S RICE, KC TI SYNTHESIS OF TRITIATED 1-[2-(DIPHENYLMETHOXY)ETHYL]-4-[3-(3-AZIDOPHENYL)PROPYL]PIPERAZINE ([H-3]-META AZIDO GBR-12935), A PHOTOAFFINITY LIGAND FOR THE DOPAMINE REUPTAKE SITE SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE COCAINE; DOPAMINE REUPTAKE; GBR-12935; 1-[2-(DIPHENYLMETHOXY)ETHYL]-4-[3-PHENYLPROPYL]PIPERAZINE; 1-[2-(DIPHENYLMETHOXY)ETHYL]-4-[3-(3-AZIDOPHENYL)PROPYL]PIPERAZINE; TRITIUM ID COCAINE AB A tritiated photoaffinity ligand for the dopamine reuptake transporter protein, 1-[2-(diphenylmethoxy) ethyl]-4-[3-(3-azidophenyl)-2,3-ditritiopropyl]piperazine, of specific activity 41.8 Ci/mmol, was prepared in six steps starting from 1-[2-(diphenylmethoxy)ethyl] piperazine. C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. RP THURKAUF, A (reprint author), NIDDKD,MED CHEM LAB,BETHESDA,MD 20892, USA. NR 9 TC 6 Z9 6 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 FEB PY 1991 VL 29 IS 2 BP 125 EP 129 DI 10.1002/jlcr.2580290202 PG 5 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA EW862 UT WOS:A1991EW86200001 ER PT J AU DECOSTA, BR AF DECOSTA, BR TI SYNTHESIS OF HIGH SPECIFIC ACTIVITY (3,4-[H-3]CYCLOHEXYL)-N-[1(2-BENZO[B]THIENYL)CYCLOHEXYL]PIPERIDINE ([H-3]BTCP) - A SELECTIVE PROBE FOR THE DOPAMINE-REUPTAKE COMPLEX SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE [H-3]BTCP; RADIOLIGAND; DOPAMINE REUPTAKE COMPLEX; CYCLOHEXANE-1,4-DIONE MONOETHYLENE KETAL; BENZO[B]THIOPHENE; N-[4-(2-BENZO[B]THIENYL)CYCLOHEXENYL]PIPERIDINE; CATALYTIC TRITIATION ID NUCLEUS ACCUMBENS; PHENCYCLIDINE; HYPERACTIVITY; BINDING; LESIONS; SITES AB High specific activity [H-3]BTCP, a radioligand for the dopamine-reuptake complex was synthesized in 7-steps starting with the readily available starting materials, cyclohexane-1,4-dione monoethylene ketal and benzo[b]thiophene; the tritium label was introduced in the final step on the 3- and 4- positions of the cyclohexyl ring by catalytic tritiation of N-[4-(2-benzo[b]thienyl)cyclohexenyl]piperidine to give [H-3]BTCP in 7.3% yield with a specific activity of 29.8 Ci/mmol (51.4% isotopic incorporation). RP DECOSTA, BR (reprint author), NIDDKD,MED CHEM LAB,BETHESDA,MD 20892, USA. NR 16 TC 5 Z9 5 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 FEB PY 1991 VL 29 IS 2 BP 165 EP 173 DI 10.1002/jlcr.2580290207 PG 9 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA EW862 UT WOS:A1991EW86200006 ER PT J AU KREEL, B RUBIN, JS JAFFE, ES AF KREEL, B RUBIN, JS JAFFE, ES TI PSEUDOLYMPHOMA OF THE PARAPHARYNGEAL SPACE SO JOURNAL OF LARYNGOLOGY AND OTOLOGY LA English DT Article DE PHARYNGEAL NEOPLASMS; PSEUDOLYMPHOMA ID PULMONARY LYMPHOID NEOPLASMS; LUNG AB A case report of pseudolymphoma of the parapharyngeal space is presented, together with a literature review of pseudolymphoma and management suggestions for such lesions when they occur in the head and neck. To the best of the authors' knowledge, this represents the first case report of pseudolymphoma presenting within the parapharyngeal space. The key to management of these lesions is based on accurate diagnosis, with differentiation of pseudolymphoma from lymphocytic lymphoma, the disease process which it mimics. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT OTORHINOLARYNGOL,BRONX,NY 10461. NCI,HEMATOPATHOL SECT,BETHESDA,MD 20892. NR 14 TC 0 Z9 0 U1 0 U2 0 PU HEADLEY BROTHERS LTD PI ASHFORD PA INVICTA PRESS, ASHFORD, KENT, ENGLAND TN24 8HH SN 0022-2151 J9 J LARYNGOL OTOL JI J. Laryngol. Otol. PD FEB PY 1991 VL 105 IS 2 BP 137 EP 140 DI 10.1017/S0022215100115178 PG 4 WC Otorhinolaryngology SC Otorhinolaryngology GA FB350 UT WOS:A1991FB35000019 PM 2013727 ER PT J AU KAY, LE IKURA, M ZHU, G BAX, A AF KAY, LE IKURA, M ZHU, G BAX, A TI 4-DIMENSIONAL HETERONUCLEAR TRIPLE-RESONANCE NMR OF ISOTOPICALLY ENRICHED PROTEINS FOR SEQUENTIAL ASSIGNMENT OF BACKBONE ATOMS SO JOURNAL OF MAGNETIC RESONANCE LA English DT Note ID MULTIPLE QUANTUM COHERENCE; SPECTROSCOPY; SPECTRA; NOE; PROTON RP KAY, LE (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA. NR 26 TC 44 Z9 44 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 0022-2364 J9 J MAGN RESON PD FEB 1 PY 1991 VL 91 IS 2 BP 422 EP 428 DI 10.1016/0022-2364(91)90208-B PG 7 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA EV483 UT WOS:A1991EV48300021 ER PT J AU PACKARD, B ROSENSHTRAUKH, L STRAUSS, HC AF PACKARD, B ROSENSHTRAUKH, L STRAUSS, HC TI THE 5TH UNITED-STATES USSR SYMPOSIUM ON SUDDEN CARDIAC DEATH SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Editorial Material C1 CARDIOL RES CTR, INST EXPTL CARDIOL, CARDIAC ELECTROPHYSIOL LAB, MOSCOW, USSR. DUKE UNIV, MED CTR, MED & PHARMACOL, DURHAM, NC 27710 USA. RP PACKARD, B (reprint author), NHLBI, SCI PROGRAM OPERAT, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD FEB PY 1991 VL 23 SU 1 BP 1 EP 2 DI 10.1016/0022-2828(91)90017-G PG 2 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA FD095 UT WOS:A1991FD09500001 ER PT J AU LAVENDER, P CLARK, AJL BESSER, GM REES, LH AF LAVENDER, P CLARK, AJL BESSER, GM REES, LH TI VARIABLE METHYLATION OF THE 5'-FLANKING DNA OF THE HUMAN PROOPIOMELANOCORTIN GENE SO JOURNAL OF MOLECULAR ENDOCRINOLOGY LA English DT Article ID BETA-LIPOTROPIN PRECURSOR; MESSENGER RIBONUCLEIC-ACID; PROOPIOMELANOCORTIN GENE; NONPITUITARY TISSUES; CYTOSINE METHYLATION; TRANSCRIPTION; EXPRESSION; BINDING; PROMOTER; RNA AB The pro-opiomelanocortin gene is widely expressed in human tissues, although both transcriptional initiation sites and regulation appear to be tissue specific. In order to determine how promoter and enhancer choice is effected, we have studied the methylation pattern of the gene in a number of normal tissues, tumours and cell lines. Variability of this pattern was observed in the 5'-flanking DNA, particularly at the HpaII site located at -304 bp upstream from the pituitary CAP site. This site was generally methylated in tissues likely to express the predominant extrapituitary (800 nucleotide) message, while in tissues known to express the normal pituitary (1150 nucleotide) message and longer species, a tendency towards undermethylation was observed. Although the sites at which variable methylation occurs did not correspond to established binding sites for regulatory proteins, many of these regions remain to be determined and thus it is possible that methylation may be influential in the tissue-specific regulation of this gene. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. ST BARTHOLOMEWS HOSP,DEPT ENDOCRINOL,LONDON EC1A 7BE,ENGLAND. RP LAVENDER, P (reprint author), ST BARTHOLOMEWS HOSP,DEPT CHEM ENDOCRINOL,LONDON EC1A 7BE,ENGLAND. NR 32 TC 8 Z9 8 U1 0 U2 0 PU J ENDOCRINOLOGY LTD PI BRISTOL PA 17/18 THE COURTYARD, WOODLANDS, ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ SN 0952-5041 J9 J MOL ENDOCRINOL JI J. Mol. Endocrinol. PD FEB PY 1991 VL 6 IS 1 BP 53 EP 61 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EW856 UT WOS:A1991EW85600006 PM 2015057 ER PT J AU FUCHTBAUER, EM AF FUCHTBAUER, EM TI MOLECULAR-BIOLOGY OF EARLY MYOGENESIS SO JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY LA English DT Meeting Abstract ID EXPRESSION C1 NICHHD,BETHESDA,MD 20892. NR 8 TC 0 Z9 0 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0142-4319 J9 J MUSCLE RES CELL M JI J. Muscle Res. Cell Motil. PD FEB PY 1991 VL 12 IS 1 BP 72 EP 72 PG 1 WC Cell Biology SC Cell Biology GA EW837 UT WOS:A1991EW83700012 ER PT J AU KRAFT, T YU, LC BRENNER, B AF KRAFT, T YU, LC BRENNER, B TI KINETICS OF WEAK-BINDING CROSSBRIDGE-INTERACTION WITH ACTIN IN THE PRESENCE OF CA++ IN SKINNED RABBIT PSOAS FIBERS MEASURED BY MECHANICAL AND X-RAY-DIFFRACTION EXPERIMENTS SO JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY LA English DT Meeting Abstract C1 UNIV ULM,DEPT GEN PHYSIOL,W-7900 ULM,GERMANY. NIH,PHYS BIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0142-4319 J9 J MUSCLE RES CELL M JI J. Muscle Res. Cell Motil. PD FEB PY 1991 VL 12 IS 1 BP 98 EP 98 PG 1 WC Cell Biology SC Cell Biology GA EW837 UT WOS:A1991EW83700109 ER PT J AU GLICK, ID BURTI, L SUZUKI, K SACKS, M AF GLICK, ID BURTI, L SUZUKI, K SACKS, M TI EFFECTIVENESS IN PSYCHIATRIC-CARE .1. A CROSS-NATIONAL-STUDY OF THE PROCESS OF TREATMENT AND OUTCOMES OF MAJOR DEPRESSIVE DISORDER SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article AB Recent research suggests that, despite the development of effective psychiatric treatment, there is marked underuse of care. This pilot study had the objective of dissecting the process of care in an attempt to understand outcomes for patients with major affective disorder and for their families. Twenty-four patients with a DSM-III diagnosis of major affective disorder were identified 12 to 18 months after hospital admission in three countries (Italy, Japan, and the United States). The patients, their families, and their doctors were interviewed separately and then together, using instruments measuring delivery of treatment (using an ideal treatment criteria set) and percentage of achievement of treatment goals. These measures were then (using parametric and nonparametric statistics) correlated with resolution of the index episode and the patient's global outcome (using the Global Assessment Scale). The data demonstrated that physicians delivered about half (52%) and, subsequently, achieved about half (54%) of what would be considered ideal care to patients and other family members. The mean resolution of the index episode at follow-up was only 3.0 (on a 0- to 5-point scale). There was a significant positive association between the most important outcome measure, i.e., the resolution of the episode, and the achievement of treatment goals for both the patient (p < .07) and the family (p < .005). Patients and families with the best resolutions received significantly more good treatment than those with the worst resolutions (p < .02), most notably with regard to medication (p < .002). C1 NIMH,ROCKVILLE,MD 20857. UNIV VERONA,INST PSICHIATRIA,I-37100 VERONA,ITALY. NATL INST MENTAL HLTH,SOCIAL PSYCHIAT,ICHIKAWA,JAPAN. RP GLICK, ID (reprint author), CORNELL UNIV,MED CTR,COLL MED,DEPT PSYCHIAT,NEW YORK,NY 10021, USA. NR 18 TC 14 Z9 14 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD FEB PY 1991 VL 179 IS 2 BP 55 EP 63 DI 10.1097/00005053-199102000-00001 PG 9 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA EX951 UT WOS:A1991EX95100001 PM 1990072 ER PT J AU FISZMAN, ML ZUDDAS, A MASANA, MI BARKER, JL DIPORZIO, U AF FISZMAN, ML ZUDDAS, A MASANA, MI BARKER, JL DIPORZIO, U TI DOPAMINE SYNTHESIS PRECEDES DOPAMINE UPTAKE IN EMBRYONIC RAT MESENCEPHALIC NEURONS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE EMBRYONIC; NIGRO-STRIATAL; DOPAMINE ID IMMUNO-CYTOCHEMICAL LOCALIZATION; STRIATAL TARGET-CELLS; SERUM-FREE MEDIUM; SUBSTANTIA-NIGRA; TYROSINE-HYDROXYLASE; INVITRO MATURATION; MONOAMINE NEURONS; PRENATAL ONTOGENY; BRAIN; DOPAMINE AB We have measured [H-3]dopamine ([H-3]DA) uptake and tyrosine hydroxylase-immunopositive immunostaining in cells acutely dissociated from the embryonic ventral mesencephalon (MSC). DA and its metabolites as well as catechol-O-methyltransferase (COMPT) and monoamine oxidase (MAO) activities were determined in homogenates taken from the MSC and striatum (STR). In the embryonic ventral MSC measurable DA and tyrosine hydroxylase (TH) immunostaining were present as early as embryonic day (E) 12.5. At E14 the number of TH+ neurons was about 50% of the values at E18. In the MSC, DA concentration increased sharply at E16 and reached a plateau before birth that was 10-fold lower than adult values. In the STR, DA was first detected at E16, suggesting that DA fibers reach the STR at this embryonic stage. High-affinity DA uptake appeared in the MSC only at E16, concomitantly with the arrival of DA fibers in the STR, increased sharply between E16 and E18, and reached a plateau before birth. This uptake mechanism was not selective for catecholamine uptake inhibitors. Thus, DA synthesis in the MSC preceded the onset of high-affinity uptake mechanism, which could be correlated to the beginning of striatal DA innervation. Measurable MAO and COMT activities were detected as early as E13 (MSC) and E15 (STR), but not DA metabolites, which appeared later. We conclude that the high-affinity DA uptake mechanism in MSC DA neurons develops coincident with the arrival of DA fibers to the STR. The sharp increase of DA uptake between E16 and E18 is due only in part to an increase in the number of TH+ cells. These results support the hypothesis that in vivo the target STR neurons regulate the maturation of MSC DA cells. C1 CNR, INT INST GENET & BIOPHYS, VIA MARCONI 12, I-80125 NAPLES, ITALY. NINCDS, NEUROPHYSIOL LAB, BETHESDA, MD 20892 USA. NINCDS, CLIN NEUROSCI BRANCH, BETHESDA, MD 20892 USA. UNIV BUENOS AIRES, FAC MED, IST BIOL CELLULAR, BUENOS AIRES, ARGENTINA. NIMH, CLIN NEUROSCI BRANCH, BETHESDA, MD 20892 USA. IST FARMACOL, SCUOLA, ITALY. NR 31 TC 46 Z9 49 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0022-3042 EI 1471-4159 J9 J NEUROCHEM JI J. Neurochem. PD FEB PY 1991 VL 56 IS 2 BP 392 EP 399 DI 10.1111/j.1471-4159.1991.tb08164.x PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA ET732 UT WOS:A1991ET73200005 PM 1671084 ER PT J AU FUKAMAUCHI, F HOUGH, C CHUANG, DM AF FUKAMAUCHI, F HOUGH, C CHUANG, DM TI EXPRESSION AND AGONIST-INDUCED DOWN-REGULATION OF MESSENGER-RNAS OF M2-MUSCARINIC AND M3-MUSCARINIC ACETYLCHOLINE-RECEPTORS IN CULTURED CEREBELLAR GRANULE CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE MUSCARINIC RECEPTOR MESSENGER RNA; DESENSITIZATION; CEREBELLAR GRANULE CELLS ID DESENSITIZATION; GLUTAMATE; RELEASE; GENES AB The regulation and expression of muscarinic acetylcholine receptor (mAChR) mRNA was studied in cultured cerebellar granule cells using Northern blot hybridization. mRNA species for m2- and m3-mAChRs but not m1- and m4-mAChRs were detected in these cells. The expression of mRNAs of both m2- and m3-mAChRs reached a maximum on the tenth day in culture but their expression patterns differed. Treatment of cerebellar granule cells after 8 days in culture with 100-mu-M carbachol led to differential down-regulation of the mRNA species of both mAChR subtypes present. Muscarinic receptor antagonists, atropine (1-mu-M) and pirenzepine (10-mu-M), prevented carbachol-induced m3-mAChR mRNA down-regulation observed at 8 h. However, exposure to either atropine or pirenzepine alone for 8 h led to a significant up-regulation of m3-mAChR mRNA. Thus, the mRNA species for both m2- and m3-mAChR subtypes are differentially expressed in culture and down-regulated by agonist stimulation. The loss of these mRNA species may play a role in the down-regulation of mAChR binding sites that occurs after desensitization. C1 NIMH,BIOL PSYCHIAT BRANCH,MOLEC NEUROBIOL,BLDG 10,ROOM 3N-212,BETHESDA,MD 20892. NR 15 TC 63 Z9 63 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD FEB PY 1991 VL 56 IS 2 BP 716 EP 719 DI 10.1111/j.1471-4159.1991.tb08210.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA ET732 UT WOS:A1991ET73200051 PM 1988565 ER PT J AU HERKENHAM, M LYNN, AB JOHNSON, MR MELVIN, LS DECOSTA, BR RICE, KC AF HERKENHAM, M LYNN, AB JOHNSON, MR MELVIN, LS DECOSTA, BR RICE, KC TI CHARACTERIZATION AND LOCALIZATION OF CANNABINOID RECEPTORS IN RAT-BRAIN - A QUANTITATIVE INVITRO AUTORADIOGRAPHIC STUDY SO JOURNAL OF NEUROSCIENCE LA English DT Article ID ADENYLATE-CYCLASE; NERVOUS-SYSTEM; ANALGESIC PROPERTIES; EVOKED-POTENTIALS; CEREBRAL-CORTEX; RHESUS-MONKEYS; DENTATE GYRUS; BINDING-SITES; SPINAL-CORD; DELTA-9-TETRAHYDROCANNABINOL AB A potent, synthetic cannabinoid was radiolabeled and used to characterize and precisely localize cannabinoid receptors in slide-mounted sections of rat brain and pituitary. Assay conditions for H-3-CP55,940 binding in Tris-HCl buffer with 5% BSA were optimized, association and dissociation rate constants determined, and the equilibrium dissociation constant (K(d)) calculated (21 nM by liquid scintillation counting, 5.2 nM by quantitative autoradiography). The results of competition studies, using several synthetic cannabinoids, add to prior data showing enantioselectivity of binding and correlation of in vitro potencies with potencies with potencies in biological assays of cannabinoid actions. Inhibition of binding by guanine nucleotides was selective and profound: Nonhydrolyzable analogs of GTP and GDP inhibited binding by > 90%, and GMP and the nonhydrolyzable ATP analog showed no inhibition. Autoradiography showed great heterogeneity of binding in patterns of labeling that closely conform to cytoarchitectural and functional domains. Very dense H-3-CP55,940 binding is localized to the basal ganglia (lateral caudate-putamen, globus pallidus, entopeduncular nucleus, substantia nigra pars reticulata), cerebellar molecular layer, innermost layers of the olfactory bulb, and portions of the hippocampal formation (CA3 and dentate gyrus molecular layer). Moderately dense binding is found throughout the remaining forebrain. Sparse binding characterizes the brain stem and spinal cord. Densitometry confirmed the quantitative heterogeneity of cannabinoid receptors (10 nM H-3-CP55,940 binding ranged in density from 6.3 pmol/mg protein in the anterior lobe of the pituitary). The results suggest that the presently characterized cannabinoid receptor mediates physiological and behavioral effects of natural and synthetic cannabinoids, because it is strongly coupled to guanine nucleotide regulatory proteins and is discretely localized to cortical, basal ganglia, and cerebellar structures involved with cognition and movement. C1 GLAXO INC,RES TRIANGLE PK,NC 27709. PFIZER INC,CENT RES,GROTON,CT 06340. NIDDKD,MED CHEM LAB,BETHESDA,MD 20892. RP HERKENHAM, M (reprint author), NIMH,FUNCT NEUROANAT SECT,BETHESDA,MD 20892, USA. OI Herkenham, Miles/0000-0003-2228-4238 NR 100 TC 1272 Z9 1297 U1 6 U2 27 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD FEB PY 1991 VL 11 IS 2 BP 563 EP 583 PG 21 WC Neurosciences SC Neurosciences & Neurology GA EW680 UT WOS:A1991EW68000025 PM 1992016 ER PT J AU NIKODIJEVIC, B GUROFF, G AF NIKODIJEVIC, B GUROFF, G TI NERVE GROWTH FACTOR-INDUCED INCREASE IN CALCIUM-UPTAKE BY PC12 CELLS SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE K-252A; SYMPATHETIC AND SENSORY NEURONS; 2ND MESSENGER ID SUPERIOR CERVICAL-GANGLIA; PHEOCHROMOCYTOMA CELLS; RAT PHEOCHROMOCYTOMA; NEURITE OUTGROWTH; CHROMAFFIN CELLS; FACTOR RECEPTORS; FIBER OUTGROWTH; LOW-AFFINITY; PHOSPHORYLATION; LINE AB Treatment of PC12 cells with nerve growth factor (NGF) produces a rapid and transient increase in calcium uptake into the cells. The increased uptake is maximal after 5 minutes of NGF treatment, but after 15 minutes of NGF treatment, no such increase can be observed. The effect of NGF is partially inhibited by blockers of L-type calcium channels. K-252a, an alkaloid-like kinase inhibitor that usually is found to inhibit the actions of NGF on PC12 cells, produces an increase in calcium uptake similar to, but smaller than, that seen with NGF. NGF had no effect on calcium release under these conditions. RP NIKODIJEVIC, B (reprint author), NICHHD,GROWTH FACTORS SECT,BLDG 6,ROOM 126,BETHESDA,MD 20892, USA. NR 35 TC 37 Z9 37 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 FEB PY 1991 VL 28 IS 2 BP 192 EP 199 DI 10.1002/jnr.490280206 PG 8 WC Neurosciences SC Neurosciences & Neurology GA FA377 UT WOS:A1991FA37700005 PM 2033648 ER PT J AU TUCK, SF ROBINSON, CH SILVERTON, JV AF TUCK, SF ROBINSON, CH SILVERTON, JV TI ASSESSMENT OF THE ACTIVE-SITE REQUIREMENTS OF LANOSTEROL 14-ALPHA-DEMETHYLASE - EVALUATION OF NOVEL SUBSTRATE-ANALOGS AS COMPETITIVE INHIBITORS SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Article ID CHOLESTEROL-BIOSYNTHESIS; PURIFIED CYTOCHROME-P-45014DM; 14-ALPHA-METHYL DEMETHYLASE; MICROSOMAL-ENZYMES; 14-ALPHA-DEMETHYLATION; YEAST; PURIFICATION; DERIVATIVES; ALCOHOLS AB Lanosterol 14-alpha-demethylase (P450(14DM)), a cytochrome P450 enzyme, is responsible for the first stage in the biosynthesis of cholesterol (1) from lanosterol (2). Inhibitors of P450(14DM) may have therapeutic use in the treatment of familial hypercholesterolemia or as antifungal agents. The specificity of P450(14DM) has been investigated by using substrate analogues modified at the C-32 carbon. The hitherto undescribed 14-alpha-ethyl and 14-alpha-propyl analogues 15 and 13 of lanost-7-en-3-beta-ol, as well as the 14-alpha-ethenyl and 14-alpha-prop-2-enyl analogues 14 and 12, have been synthesized. These all proved to be good competitive inhibitors of the enzyme. A series of 32-oxiranes and 32-thiiranes was then synthesized and evaluated as inhibitors. Oxiranes 4 and 5 were excellent stereoselective competitive inhibitors of P450(14DM). The (2'S)-32-oxirane 4 had K(i) = 0.62-mu-M, and the (2'R)-32-oxirane 5 showed K(i) = 2-mu-M. The (2'R)-32-thiiranyl and (2'S)-32-thiiranyl compounds 10 and 11 were considerably less potent inhibitors. Comparison of the K(i) values for analogues 12-15, also good competitive inhibitors of this enzyme, indicated the P450(14DM) active site to be relatively insensitive to the size and degree of unsaturation of C-14-alpha alkyl substituents up to and including propyl. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,BALTIMORE,MD 21205. NHLBI,CHEM LAB,BETHESDA,MD 20892. NR 37 TC 15 Z9 15 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3263 J9 J ORG CHEM JI J. Org. Chem. PD FEB 1 PY 1991 VL 56 IS 3 BP 1260 EP 1266 DI 10.1021/jo00003a059 PG 7 WC Chemistry, Organic SC Chemistry GA EW182 UT WOS:A1991EW18200059 ER PT J AU RAO, CT LINDBERG, B LINDBERG, J PITHA, J AF RAO, CT LINDBERG, B LINDBERG, J PITHA, J TI SUBSTITUTION IN BETA-CYCLODEXTRIN DIRECTED BY BASICITY - PREPARATION OF 2-O-[(R)-2-HYDROXYPROPYL], 6-O-[(R)-2-HYDROXYPROPYL], 2-O-[(S)-2-HYDROXYPROPYL] AND 6-O-[(S)-2-HYDROXYPROPYL] DERIVATIVES SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Note ID SEPARATION; C-3 C1 NIA,GRC,BALTIMORE,MD 21224. UNIV STOCKHOLM,ARRHENIUS LAB,DEPT ORGAN CHEM,S-10691 STOCKHOLM,SWEDEN. NR 14 TC 62 Z9 66 U1 2 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3263 J9 J ORG CHEM JI J. Org. Chem. PD FEB 1 PY 1991 VL 56 IS 3 BP 1327 EP 1329 DI 10.1021/jo00003a082 PG 3 WC Chemistry, Organic SC Chemistry GA EW182 UT WOS:A1991EW18200082 ER PT J AU HAYTHORNTHWAITE, JA HEGEL, MT KERNS, RD AF HAYTHORNTHWAITE, JA HEGEL, MT KERNS, RD TI DEVELOPMENT OF A SLEEP DIARY FOR CHRONIC PAIN PATIENTS SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT LA English DT Article DE PAIN; SLEEP; PSYCHOMETRICS AB The present study examined the psychometric properties of the Daily Sleep Diary (DSD), an instrument developed for monitoring sleep among chronic pain patients. As part of a comprehensive evaluation, 46 chronic pain patients completed the DSD each morning. Items assessed the number of hours slept, length of sleep onset, frequency of awakenings during the night that resulted in trouble falling back to sleep, early morning awakening, quality of sleep, lack of restfulness, and the previous night's sleep compared to usual sleep. Reliability coefficients were significant. The sleep diary items significantly correlated with other retrospective measures of sleep. Duration of pain complaint was related to delayed sleep onset and lower quality of sleep. Pain severity was related to fewer hours slept and delayed sleep onset. The DSD items correlated with measures of both depression and anxiety. The results emphasize the importance of including sleep in both assessment and treatment of chronic pain patients. RP HAYTHORNTHWAITE, JA (reprint author), NIA,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 0 TC 92 Z9 96 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0885-3924 J9 J PAIN SYMPTOM MANAG JI J. Pain Symptom Manage. PD FEB PY 1991 VL 6 IS 2 BP 65 EP 72 DI 10.1016/0885-3924(91)90520-E PG 8 WC Health Care Sciences & Services; Medicine, General & Internal; Clinical Neurology SC Health Care Sciences & Services; General & Internal Medicine; Neurosciences & Neurology GA FC834 UT WOS:A1991FC83400003 PM 2007794 ER PT J AU PARKE, JC SCHNEERSON, R REIMER, C BLACK, C WELFARE, S BRYLA, D LEVI, L PAVLIAKOVA, D CRAMTON, T SCHULZ, D CADOZ, M ROBBINS, JB AF PARKE, JC SCHNEERSON, R REIMER, C BLACK, C WELFARE, S BRYLA, D LEVI, L PAVLIAKOVA, D CRAMTON, T SCHULZ, D CADOZ, M ROBBINS, JB TI CLINICAL AND IMMUNOLOGICAL RESPONSES TO HAEMOPHILUS-INFLUENZAE TYPE-B-TETANUS TOXOID CONJUGATE VACCINE IN INFANTS INJECTED AT 3, 5, 7, AND 18 MONTHS OF AGE SO JOURNAL OF PEDIATRICS LA English DT Article ID CAPSULAR POLYSACCHARIDE; SERUM ANTIBODIES; IMMUNIZATION AB The safety and immunogenicity of Haemophilus influenzae type b-tetanus toxoid conjugate vaccine (Hib-TT) were evaluated in 77 healthy infants receiving injections at 3, 5, 7, and 18 months of age. No serious local or systemic reactions were noted. After the first injection the geometric mean Hib antibody level rose to 0.55-mu-g/ml, and each subsequent injection elicited a statistically significant rise in the geometric mean. The percentage of vaccinees with Hib antibody levels > 0.15-mu-g/ml serum was 75.5% after the first, 97.4% after the second, and 100% after the third Hib-TT injection. This percentage fell to 90.9% at 18 months of age but rose again to 100% after the fourth injection. Control infants (n = 10) injected with diphtheria-tetanus toxoid-pertussis vaccine only had nondetectable levels after the second injection. Hib-TT elicited increases of Hib antibody in all isotypes: IgG > IgM > IgA. Among IgG subclasses the highest increases were of IgG1. All vaccinated subjects had > 0.01 U/ml of TT antibody (estimated protective level) throughout the study. We conclude that Hib-TT, injected at 3, 5, 7, and 18 months, is safe and induces protective levels of antibodies during the age of highest incidence of meningitis caused by Hib. C1 NICHHD, BETHESDA, MD 20892 USA. CTR DIS CONTROL, ATLANTA, GA 30333 USA. PASTEUR MERIEUX SERUMS & VACCINES, LYONS, FRANCE. NR 18 TC 50 Z9 51 U1 1 U2 1 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD FEB PY 1991 VL 118 IS 2 BP 184 EP 190 DI 10.1016/S0022-3476(05)80480-9 PG 7 WC Pediatrics SC Pediatrics GA EX302 UT WOS:A1991EX30200003 PM 1993943 ER PT J AU GOMEZ, MT MALOZOWSKI, S WINTERER, J VAMVAKOPOULOS, NC CHROUSOS, GP AF GOMEZ, MT MALOZOWSKI, S WINTERER, J VAMVAKOPOULOS, NC CHROUSOS, GP TI URINARY FREE CORTISOL VALUES IN NORMAL-CHILDREN AND ADOLESCENTS SO JOURNAL OF PEDIATRICS LA English DT Article RP GOMEZ, MT (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10N262, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 14 TC 50 Z9 52 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD FEB PY 1991 VL 118 IS 2 BP 256 EP 258 DI 10.1016/S0022-3476(05)80496-2 PG 3 WC Pediatrics SC Pediatrics GA EX302 UT WOS:A1991EX30200019 PM 1993957 ER PT J AU KHANDKE, KM FAIRWELL, T BRASWELL, EH MANJULA, BN AF KHANDKE, KM FAIRWELL, T BRASWELL, EH MANJULA, BN TI THE AMINO-TERMINAL REGION OF GROUP-A STREPTOCOCCAL-M PROTEIN DETERMINES ITS MOLECULAR-STATE OF ASSEMBLY AND FUNCTION SO JOURNAL OF PROTEIN CHEMISTRY LA English DT Article DE STREPTOCOCCAL-M PROTEIN; N-TERMINAL REGION; COILED-COIL; DIMER MONOMER; MOLECULAR ASSEMBLY; MOLECULAR HINGE ID COILED-COIL STRUCTURE; PEP-M5 PROTEIN; ACID-SEQUENCE; EPITOPES; TYPE-5; LOCALIZATION; M6-PROTEIN; SEROTYPES; IMMUNOGENICITY; DESIGN AB Group A streptococcal M protein, a major virulence factor, is an alpha-helical coiled-coil dimer on the surface of the bacteria. Limited proteolysis of type 57 streptococcus with pepsin released two fragments of the M57 molecule, with apparent molecular weights of 32,000 and 27,000 on SDS-PAGE. However, on gel filtration under nondenaturing conditions, each of these proteins eluted as two distinct molecular forms. The two forms corresponded to their dimeric and monomeric state as compared to the gel filtration characteristics of known dimeric coiled-coil proteins. The results of sedimentation equilibrium measurements were consistent with this, but further indicated that the "dimeric form" consisted of a dimer in rapid equilibrium with its monomer, whereas the "monomeric form" does not dimerize. The monomeric form was the predominant species for the 27 kD species, whereas the dimeric form predominated for the 32 kD species. Sequence analysis revealed the 27 kD species to be a truncated derivative of the 32 kD PepM57 species, lacking the N-terminal nonheptad region of the M57 molecule. These data strongly suggested that the N-terminal nonheptad region of PepM57 is important in determining the molecular state of the molecule. Consistent with this, PepM49, another nephritis-associated serotype, which lacks the nonheptad N-terminal region, also eluted as a monomer on gel filtration under nondenaturing conditions. Furthermore, removal of the N-terminal nonheptad segment of the dimeric PepM6 protein converted it into a monomeric form. The dimeric molecular from of both the 32 kD PepM57 and the 27 kD PepM57 did not represent a stable state of assembly, and were susceptible to conversion to the corresponding monomeric molecular forms by simple treatments, such as lyophilization. The 27 kD PepM57 exhibited a greater propensity than the 32 kD species to exist in the monomeric form. The 32 kD species contained the opsonic epitope of the M57 molecule, whereas the 27 kD species lacked the same. This is consistent with the previous reports on the importance of the N-terminal region of M protein for its opsonic activity. Together, these results stronly suggest that, in addition to its importance for the biological function, the N-terminal region of the M protein plays a dominant role in determining the molecular state of the M molecule, as well as its stability. C1 UNIV CONNECTICUT,NATL ANALYT ULTRACENTRIFUGE FACIL,STORRS,CT 06269. NHLBI,BETHESDA,MD 20892. RP KHANDKE, KM (reprint author), ROCKEFELLER UNIV,NEW YORK,NY 10021, USA. FU NHLBI NIH HHS [HL36025] NR 40 TC 5 Z9 5 U1 0 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0277-8033 J9 J PROTEIN CHEM JI J. Protein Chem. PD FEB PY 1991 VL 10 IS 1 BP 49 EP 59 DI 10.1007/BF01024655 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG061 UT WOS:A1991FG06100006 PM 2054063 ER PT J AU SKOPOULI, FN FOX, PC GALANOPOULOU, V ATKINSON, JC JAFFE, ES MOUTSOPOULOS, HM AF SKOPOULI, FN FOX, PC GALANOPOULOU, V ATKINSON, JC JAFFE, ES MOUTSOPOULOS, HM TI T-CELL SUBPOPULATIONS IN THE LABIAL MINOR SALIVARY-GLAND HISTOPATHOLOGIC LESION OF SJOGREN SYNDROME SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE SJOGREN SYNDROME; LABIAL MINOR SALIVARY GLAND HISTOPATHOLOGY; MEMORY CELLS; UCHL-1; LFA-1; T-GAMMA-DELTA CELLS ID GAMMA-DELTA; RHEUMATOID-ARTHRITIS; HELPER-INDUCER; LYMPHOCYTES-T; RECEPTOR; SUBSET; SURFACE; EXPRESSION; ADHESION; TISSUES AB The majority of T cells constituting the focal lymphocytic infiltrates in the labial minor salivary glands of patients with Sjogren's syndrome bear the helper phenotype (CD4); activation is expressed by class II (HLA-DR) MHC products. In our immunohistologic study of snap frozen minor salivary gland biopsies from 16 patients with primary Sjorgren's syndrome, it was shown that the majority (77%) of the infiltrating T cells exhibit the memory helper/inducer phenotype (UCHL-1) and express LFA-1 molecules. In addition most of the T cells express the alpha-beta receptor while only 2.8% express the gamma-delta receptor. Our findings suggest that these T cell infiltrates in patients with primary Sjogren's syndrome may explain the intense B lymphocyte hyperreactivity observed in the exocrine glands of patients with Sjogren's syndrome. C1 NIDA,CLIN INVEST & CARE BRANCH,BETHESDA,MD. NCI,PATHOL LAB,HEMATOPATHOL SECT,BETHESDA,MD 20892. RP SKOPOULI, FN (reprint author), UNIV IOANNINA,SCH MED,DEPT INTERNAL MED,DIV RHEUMATOL,GR-45110 IOANNINA,GREECE. NR 33 TC 100 Z9 104 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD FEB PY 1991 VL 18 IS 2 BP 210 EP 214 PG 5 WC Rheumatology SC Rheumatology GA EZ831 UT WOS:A1991EZ83100013 PM 1827160 ER PT J AU FLEISCHMAJER, R FISHER, LW MACDONALD, ED JACOBS, L PERLISH, JS TERMINE, JD AF FLEISCHMAJER, R FISHER, LW MACDONALD, ED JACOBS, L PERLISH, JS TERMINE, JD TI DECORIN INTERACTS WITH FIBRILLAR COLLAGEN OF EMBRYONIC AND ADULT HUMAN SKIN SO JOURNAL OF STRUCTURAL BIOLOGY LA English DT Article ID DERMATAN SULFATE PROTEOGLYCANS; BOVINE ARTICULAR-CARTILAGE; EXTRACELLULAR-MATRIX; CORE PROTEIN; DS-PGII; BONE; INVITRO; GLYCOSAMINOGLYCANS; TENDON; GELS C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. RP FLEISCHMAJER, R (reprint author), CUNY MT SINAI SCH MED,DEPT DERMATOL,NEW YORK,NY 10029, USA. NR 33 TC 158 Z9 158 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1047-8477 J9 J STRUCT BIOL JI J. Struct. Biol. PD FEB PY 1991 VL 106 IS 1 BP 82 EP 90 DI 10.1016/1047-8477(91)90065-5 PG 9 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FH749 UT WOS:A1991FH74900008 PM 2059554 ER PT J AU ELZEIN, M AREAS, JL KNAPKA, J DIPETTE, D HOLLAND, B ALKARADAGHI, P PREUSS, HG AF ELZEIN, M AREAS, JL KNAPKA, J DIPETTE, D HOLLAND, B ALKARADAGHI, P PREUSS, HG TI DEVELOPMENT OF SUGAR-INDUCED BLOOD-PRESSURE ELEVATION AFTER UNINEPHRECTOMY IN A RESISTANT RAT STRAIN SO JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION LA English DT Article DE SUGAR-INDUCED HYPERTENSION; UNILATERAL NEPHRECTOMY; EFFECTS ON BP; BLOOD PRESSURE; SUGAR EFFECT ID HYPERTENSION; SODIUM; SUCROSE; PLASMA; WKY; PAH AB Certain rat strains acutely increase blood pressure (BP) when given diets high in NaCl. Prior results showed that "salt-sensitive" rat strains, at least the ones studied, also increase BP in response to sugar loading. To examine this relationship further and learn more about the pathogenesis of sucrose-induced BP elevations, we examined the effects of unilateral nephrectomy (uninephrectomy) on sucrose-induced BP changes. The rationale is based upon the findings that renal mass removal sensitizes BP response to salt loading. Over 15 weeks, augmented sugar (sucrose) consumption by Long-Evans (LE) rats did not increase BP markedly compared to rats consuming a diet relatively low in sugar unless uninephrectomy was performed. The differences in BP caused by the high sugar diet in a uninephrectomized rat could not be explained adequately by alterations in catecholamine excretion, plasma renin activity, excesses in blood volume, or the other parameters examined. However, salt-induced hypertension has been attributed to the presence of circulating substances affecting ion transport. Among the dietary groups, there was a significant correlation between the ability of plasma to depress PAH and TEA renal slice uptake and the difference in BP. This is consistent with the presence of a circulating factor affecting cell transport that has its greatest activity in the high sugar-uninephrectomy group of LE rats. We conclude that reducing renal mass potentiates sugar-induced BP elevation similar to salt-induced BP elevation in a normally resistant rat strain, and the rise of BP may be caused by a circulating factor. C1 GEORGETOWN UNIV,MED CTR,DEPT MED,153 BASIC SCI BLDG,4000 RESERVOIR RD NW,WASHINGTON,DC 20007. NIH,DIV RES SERV,BETHESDA,MD 20892. UNIV TEXAS,MED BRANCH,DEPT MED ENDOCRINOL METAB & HYPERTENS,GALVESTON,TX 77550. GEORGETOWN UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20007. FU NIA NIH HHS [AG06929] NR 31 TC 2 Z9 2 U1 0 U2 0 PU AMER COLL NUTRITION PI NEW YORK PA C/O HOSP. JOINT DIS. 301 E. 17TH ST., NEW YORK, NY 10003 SN 0731-5724 J9 J AM COLL NUTR JI J. Am. Coll. Nutr. PD FEB PY 1991 VL 10 IS 1 BP 24 EP 33 PG 10 WC Nutrition & Dietetics SC Nutrition & Dietetics GA EU868 UT WOS:A1991EU86800005 PM 2010576 ER PT J AU GLOTH, FM TOBIN, JD SHERMAN, SS HOLLIS, BW AF GLOTH, FM TOBIN, JD SHERMAN, SS HOLLIS, BW TI IS THE RECOMMENDED DAILY ALLOWANCE FOR VITAMIN-D TOO LOW FOR THE HOMEBOUND ELDERLY SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID NUTRITIONAL-STATUS; D DEFICIENCY; DIETARY; OSTEOMALACIA; SUPPLEMENTS; POPULATION AB A population of sunlight-deprived elderly was studied to determine the daily intake of vitamin D and whether dietary intake was sufficient to maintain a normal vitamin D status. Twenty-two subjects over 65 years old with serum creatinine < 180 mu-mol/L and confined indoors for more than 6 months were chosen from the community and a nursing home in Southeast Baltimore. Three-day food records were obtained along with serum levels of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2 D), and intact parathyroid hormone (PTH). The mean daily vitamin D intake was over twofold greater than the adult Recommended Daily Allowance (RDA) of 200 IU. The mean 25-OHD level was 40 nmol/L (normal 25-138 nmol/L) with seven patients less than 25 nmol/L. Of those participants with 25-OHD values less than 25 nmol/L, the mean vitamin D intake was 467 IU (range 36-1096 IU). We conclude that the current RDA seems inadequate for many older individuals who do not get sun exposure. This particular population of elderly is at risk to develop vitamin D deficiency and the associated complications. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV GERIATR MED & GERONTOL,BALTIMORE,MD 21205. FRANCIS SCOTT KEY MED CTR,BALTIMORE,MD. MED UNIV S CAROLINA,CHILDRENS HOSP,DEPT PEDIAT,CHARLESTON,SC 29425. RP GLOTH, FM (reprint author), NIH,NATL INST AGING,GERONTOL RES CTR,APPL PHYSIOL SECT,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. FU NIA NIH HHS [5 T32 AG00120-03] NR 34 TC 69 Z9 71 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD FEB PY 1991 VL 39 IS 2 BP 137 EP 141 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA EX548 UT WOS:A1991EX54800004 PM 1991945 ER PT J AU SCHNELLE, JF NEWMAN, DR FOGARTY, TE WALLSTON, K ORY, M AF SCHNELLE, JF NEWMAN, DR FOGARTY, TE WALLSTON, K ORY, M TI ASSESSMENT AND QUALITY-CONTROL OF INCONTINENCE CARE IN LONG-TERM NURSING FACILITIES SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID URINARY-INCONTINENCE; HOME PATIENTS; TRIAL AB A statistical quality-control process was used to assess how well incontinence management procedures were being implemented by indigenous nursing staff in four nursing homes. Eighty-one incontinent patients were treated with the prompted-voiding toileting procedure. Thirty-six of these patients proved responsive to the toileting procedures, and nursing home staff was instructed to maintain the toileting program for these responsive patients. The first part of the quality-control model involved setting job standards specifying how dry the patients should be if toileted on a 2-hour schedule. Second, a job-monitoring control chart was used to continuously assess how well the job standards were being met. The remaining forty-five patients, who were unresponsive to the toileting protocol, were managed with a 2-hour changing schedule. Job standards specifying how wet (volume) the patient would be if changed on a two-hour basis were set. Control-chart monitoring of these patients' urine output assessed how well the changing procedures were being implemented. Incontinence care in nursing homes is difficult to supervise because of problems in measuring how consistently nursing aides change or toilet patients. This paper describes a management system for effective incontinence care. C1 NATL INST AGING,BETHESDA,MD. MIDDLE TENNESSEE STATE UNIV,MURFREESBORO,TN 37130. VANDERBILT UNIV,SCH NURSING,NASHVILLE,TN 37240. RP SCHNELLE, JF (reprint author), UNIV CALIF LOS ANGELES,BORUN CTR GERONTOL RES,SCH MED,LOS ANGELES,CA 90024, USA. FU NIA NIH HHS [5 U01 AG05270-02] NR 13 TC 17 Z9 17 U1 1 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD FEB PY 1991 VL 39 IS 2 BP 165 EP 171 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA EX548 UT WOS:A1991EX54800009 PM 1899438 ER PT J AU RACUSEN, LC FIVUSH, BA ANDERSSON, H GAHL, WA AF RACUSEN, LC FIVUSH, BA ANDERSSON, H GAHL, WA TI CULTURE OF RENAL TUBULAR CELLS FROM THE URINE OF PATIENTS WITH NEPHROPATHIC CYSTINOSIS SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article DE LYSOSOME; STORAGE DISEASE; CYSTINE; CYSTEAMINE; KIDNEY ID TRANSPORT; CHILDREN; PHOSPHOCYSTEAMINE; LEUKOCYTES; CYSTEAMINE; FRACTIONS; DEPLETION AB Nephropathic cystinosis represents a prototype for lysosomal storage diseases and is the most common cause of renal tubular Fanconi's syndrome. Mechanisms of the tubular transport defects in this disease have not been defined, however, in part because the cells readily cultured from affected patients, leukocytes and fibroblasts, do not express epithelial transport functions. Except for a single autopsy report, renal tubular cells from these patients have not been studied in vitro. In these studies, noninvasive harvesting and culture of renal tubular cells from the urine of patients with cystinosis is described. Cultures of renal tubular cells could be established from over 50% of the isolates which contained viable cells and which remained uncontaminated in vitro. Cells had an epithelial morphology in culture, and the majority of cultured cells expressed proximal tubular brush border marker enzyme. Cultured cells also expressed the storage defect in vitro, containing cystine levels up to 100 times those of normal cells. Cultured cells could be depleted of cystine by using the thiol cysteamine. This in vitro model system should be very useful for studying the mechanisms of renal tubular transport defects in this disease. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. NICHHD,BETHESDA,MD 20892. NR 35 TC 22 Z9 23 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD FEB PY 1991 VL 1 IS 8 BP 1028 EP 1033 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA FT105 UT WOS:A1991FT10500004 PM 1912401 ER PT J AU DEPALMA, L YU, M MCINTOSH, CL SWAIN, JA DAVEY, RJ AF DEPALMA, L YU, M MCINTOSH, CL SWAIN, JA DAVEY, RJ TI CHANGES IN LYMPHOCYTE SUBPOPULATIONS AS A RESULT OF CARDIOPULMONARY BYPASS - THE EFFECT OF BLOOD-TRANSFUSION SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article ID T-CELLS; PERIPHERAL-BLOOD; HOST DISEASE; ACTIVATION; RECEPTORS; STORAGE AB Cardiopulmonary bypass is associated with postoperative humoral and cellular immune changes. Postoperative decrease in T helper (CD4), T suppressor (CD8), and B lymphocyte counts; decrease or reversal of the CD4/CD8 ratio; and poor in vitro response to mitogens have also been observed. Similar changes in lymphocyte number and function have also been noted in patients receiving transfusions. To determine whether observed changes after cardiopulmonary bypass are related to the bypass itself or to associated blood transfusions, we conducted a study of lymphocyte subsets in transfused and nontransfused patients. A flow cytometric analysis of seven lymphocyte subpopulations was conducted in 18 patients undergoing bypass, eight of whom did not receive a transfusion. The transfused group comprised recipients of both homologous (n = 8) and autologous (n = 2) blood. Total lymphocytes and lymphocytes with markers for CD3 (pan-T cells), CD4, and CD8 decreased significantly postoperatively independent of transfusion. B lymphocytes decreased postoperatively in both the autologous transfusion and no transfusion groups. However, this trend was not seen in patients receiving homologous blood, and three of these patients had evidence of T cell activation, suggestive of an immune response to homologous transfusion. Bypass produces significant changes in selected lymphocyte subsets. Furthermore, simultaneous homologous blood transfusion may specifically elicit an immune response in some patients undergoing cardiopulmonary bypass. C1 WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD. NHLBI,SURG BRANCH,BETHESDA,MD 20892. NR 15 TC 28 Z9 28 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD FEB PY 1991 VL 101 IS 2 BP 240 EP 244 PG 5 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA EX304 UT WOS:A1991EX30400008 PM 1992233 ER PT J AU STRIKER, GE AF STRIKER, GE TI KUH NOTES SO JOURNAL OF UROLOGY LA English DT Note RP STRIKER, GE (reprint author), NIDDKD,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD FEB PY 1991 VL 145 IS 2 BP 376 EP 376 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA EV985 UT WOS:A1991EV98500037 ER PT J AU LIU, S EWING, MW ANGLARD, P TRAHAN, E LAROCCA, RV MYERS, CE LINEHAN, WM AF LIU, S EWING, MW ANGLARD, P TRAHAN, E LAROCCA, RV MYERS, CE LINEHAN, WM TI THE EFFECT OF SURAMIN, TUMOR-NECROSIS-FACTOR AND INTERFERON-GAMMA ON HUMAN PROSTATE CARCINOMA SO JOURNAL OF UROLOGY LA English DT Article DE SURAMIN; PROSTATE CANCER; TUMOR NECROSIS FACTOR; INTERFERON-GAMMA ID DNA TOPOISOMERASE-II; GROWTH-FACTOR; RECOMBINANT INTERLEUKIN-2; INVIVO; COMBINATION; INVITRO; CANCER; IMMUNOTHERAPY; EFFICACY; TOXICITY AB Suramin, an antiparasitic agent which has been shown to block the stimulatory effect of growth factors on certain cancers, is currently being evaluated in clinical trials and as an antineoplastic agent in patients with advanced prostate carcinoma. Preliminary studies suggested that suramin inhibits the growth in vitro of human prostate carcinoma. The present study was performed in order to evaluate the effect of suramin, recombinant human tumor necrosis factor (TNF), interferon-gamma and the combination of suramin plus TNF or interferon-gamma on proliferation of PC-3, a human, hormone unresponsive prostate carcinoma cell line. In medium containing 2% fetal calf serum (FCS) suramin, at doses of 10-mu-M, 30-mu-M and 100-mu-M (levels readily achievable in humans) inhibited proliferation of PC-3. TNF, at a concentration of 500 units/ml., induced an approximately 50% inhibition of growth of PC-3. The combination of suramin plus TNF induced a greater inhibition of growth than did either agent alone, even at the low dose of 10-mu-M suramin. Interferon-gamma, 500 units/ml., inhibited PC-3 growth. However, the combination of interferon-gamma plus suramin (30-mu-M) induced less inhibition of proliferation than did interferon-gamma alone. These results may serve as a rationale for clinical trials employing the combination of TNF plus suramin in patients with advanced prostate carcinoma. C1 NCI,SURG BRANCH,UROL ONCOL SECT,BLDG 10,RM 2B47,BETHESDA,MD 20892. NCI,DIV CANC THERAPY,MED BRANCH,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NR 31 TC 26 Z9 26 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD FEB PY 1991 VL 145 IS 2 BP 389 EP 392 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA EV985 UT WOS:A1991EV98500041 PM 1899122 ER PT J AU LAROCCA, RV DANESI, R COOPER, MR JAMISDOW, CA EWING, MW LINEHAN, WM MYERS, CE AF LAROCCA, RV DANESI, R COOPER, MR JAMISDOW, CA EWING, MW LINEHAN, WM MYERS, CE TI EFFECT OF SURAMIN ON HUMAN PROSTATE-CANCER CELLS-INVITRO SO JOURNAL OF UROLOGY LA English DT Article DE SURAMIN; PROSTATE CANCER ID EPIDERMAL GROWTH-FACTOR; TUMOR-CELLS; SERUM-FREE; CARCINOMA; ANTIGEN; RAT; PROLACTIN; PROTEIN; MODEL; LINE AB Suramin, a polyanionic compound with known antiparasitic activity, has been shown to be adrenocorticolytic in primates and to have clinical efficacy in the treatment of patients with metastatic prostate cancer refractory to conventional hormonal manipulation. To better characterize the activity of suramin on prostate cancer biology, we studied the effect of the drug on plasma adrenal androgens of patients and on the human prostate adenocarcinoma cell lines PC-3, DU 145 and LNCaP-FGC. Five cancer patients treated with suramin had an approximate 40% decline in circulating androstenedione, dehydroepiandrosterone and dehydroepiandrosterone sulfate levels. The drug inhibited the colony formation in two of the three cell lines at concentrations clinically achievable in humans without excessive drug-related toxicity. The presence of suramin 300-mu-g./ml. partially inhibited the growth stimulatory effect of testosterone and basic fibroblast growth factor, but not that of epidermal growth factor. The cellular concentration of suramin following exposure to a single dose increases linearly over time in each of the cell lines with LNCaP-FGC accumulating the highest levels of the drug; cellular levels of suramin, not androgen or growth factor sensitivity, correlated with the sensitivity to the drug. The concentrations of prostatic acid phosphatase and prostatic specific antigen released by LNCaP-FGC cells in cell culture medium declined in the presence of increasing levels of suramin in a manner which exceeded the decrease in cell number. We conclude that suramin, aside from decreasing circulating androgens through its adrenocorticolytic effect, is also capable exerting a direct inhibitory effect on cell proliferation of prostate cancer cells, and interfere at a cellular level with the growth stimulatory effects of exogenous testosterone and basic fibroblast growth factor. C1 NCI,DIV CANC TREATMENT,SURG BRANCH,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. RP LAROCCA, RV (reprint author), NCI,MED BRANCH,RM 12N-226,BLDG 10,BETHESDA,MD 20892, USA. NR 28 TC 80 Z9 81 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD FEB PY 1991 VL 145 IS 2 BP 393 EP 398 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA EV985 UT WOS:A1991EV98500042 PM 1824865 ER PT J AU NEVILLE, RF HOBSON, RW JAMIL, Z BREITBART, GB ANDERSON, RJ BARTORELLI, AL LEON, MB AF NEVILLE, RF HOBSON, RW JAMIL, Z BREITBART, GB ANDERSON, RJ BARTORELLI, AL LEON, MB TI INTRAVASCULAR ULTRASONOGRAPHY - VALIDATION STUDIES AND PRELIMINARY INTRAOPERATIVE OBSERVATIONS SO JOURNAL OF VASCULAR SURGERY LA English DT Article; Proceedings Paper CT 38TH SCIENTIFIC MEETING OF THE NORTH AMERICAN CHAPTER OF THE INTERNATIONAL SOC FOR CARDIOVASCULAR SURGERY CY JUN 04-06, 1990 CL LOS ANGELES, CA SP INT SOC CARDIOVASC SURG, N AMER CHAPTER ID DISEASE AB Intravascular ultrasonography is emerging as an important imaging modality to assess the presence, distribution, and extent of atherosclerotic vascular disease. To determine the accuracy and clinical utility of intravascular ultrasonography, a flexible catheter-based system was used to generate two-dimensional, cross-sectional vascular images. In 23 arteries of 11 sheep 206 in vivo images demonstrated an echo-free lumen surrounded by three distinct concentric acoustic transitions corresponding to intima, media, and adventitia. Ultrasound measurements of lumen diameter and area correlated significantly with those of corresponding arteriographic measurements obtained by use of digital calipers (r = 0.91, r = 0.86). To evaluate clinical feasibility, intraoperative images (n = 160) were obtained in 10 patients undergoing vascular bypass or hemodialysis access procedures. The images depicted luminal configuration and arterial wall morphologic characteristics. Measurements of lumen diameter and lumen area correlated closely with corresponding intraoperative arteriography (r = 0.81, r = 0.79). The ultrasound images demonstrated arterial stenoses, intimal hyperplasia, intraluminal thrombus, polytetra-fluoroethylene graft material, and anastomotic sites. We conclude that flexible catheterbased ultrasonography produces images that accurately demonstrate arterial wall architecture, lumen diameter, and area. Intraoperative application can produce images that provide unique information thus expanding the clinical potential of ultrasonography as a guidance system for vascular procedures. C1 UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT SURG,NEWARK,NJ 07103. NHLBI,BETHESDA,MD 20892. RP NEVILLE, RF (reprint author), UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,VASC SURG SECT,MSB G-532,185 S ORANGE AVE,NEWARK,NJ 07103, USA. NR 13 TC 6 Z9 6 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD FEB PY 1991 VL 13 IS 2 BP 274 EP 283 PG 10 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA EX035 UT WOS:A1991EX03500012 PM 1990168 ER PT J AU KAMINCHIK, J BASHAN, N ITACH, A SARVER, N GORECKI, M PANET, A AF KAMINCHIK, J BASHAN, N ITACH, A SARVER, N GORECKI, M PANET, A TI GENETIC-CHARACTERIZATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 NEF GENE-PRODUCTS TRANSLATED INVITRO AND EXPRESSED IN MAMMALIAN-CELLS SO JOURNAL OF VIROLOGY LA English DT Article ID VIRAL MESSENGER-RNA; PROTEIN; BINDING; REPLICATION; PP60V-SRC; RECEPTOR; TARGET; HIV-1 AB Expression of the human immunodeficiency virus type 1 nef gene was studied by in vitro transcription-translation and by transfection into monkey COS cells. Two Nef-related peptides, of 27 and 25 kDa, were identified by immunoprecipitation with anti-Nef antibodies. The relation between these two proteins was determined by metabolically labeling transfected COS cells and by deleting the initiator methionine of nef. We found that the 25-kDa polypeptide is not a cleavage product of 27-kDa Nef but rather is initiated from an internal ATG 57 bases downstream from the Nef initiation site. Myristoylation of the 27-kDa but not of the 25-kDa Nef was demonstrated by the contranslational modification of Nef in an in vitro reticulocyte translation system. The myristoylation pattern of the two Nef polypeptides further implies that the 25-kDa polypeptide lacks the amino terminus of 27-kDa Nef. Cellular localization of the various forms of Nef was studied in transiently transfected COS cells. Myristoylation was found to be necessary for membrane association of Nef. Myristoylation-deficient 27-kDa Nef mutant and 25-kDa Nef were confined to the soluble cytoplasmic fraction of transfected cells, whereas part of the wild-type 27-kDa Nef was membrane attached. C1 NIAID,DIV AIDS,BASIC RES & DEV PROGRAM,DEV THERAPEUT BRANCH,BETHESDA,MD 20892. RP KAMINCHIK, J (reprint author), BIOTECHNOL GEN LTD,KIRYAT WEIZMANN,IL-76326 REHOVOT,ISRAEL. FU NIAID NIH HHS [N01-AI-82696] NR 20 TC 99 Z9 99 U1 1 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD FEB PY 1991 VL 65 IS 2 BP 583 EP 588 PG 6 WC Virology SC Virology GA ET445 UT WOS:A1991ET44500004 PM 1987371 ER PT J AU KANESAKI, T MURPHY, BR COLLINS, PL OGRA, PL AF KANESAKI, T MURPHY, BR COLLINS, PL OGRA, PL TI EFFECTIVENESS OF ENTERIC IMMUNIZATION IN THE DEVELOPMENT OF SECRETORY IMMUNOGLOBULIN-A RESPONSE AND THE OUTCOME OF INFECTION WITH RESPIRATORY SYNCYTIAL VIRUS SO JOURNAL OF VIROLOGY LA English DT Article ID MONOCLONAL-ANTIBODIES PROTECT; RECOMBINANT VACCINIA VIRUS; COTTON RATS; NASAL SECRETIONS; G-GLYCOPROTEIN; SENDAI VIRUS; INFANTS; IMMUNITY; LIVE; MICE AB Cotton rats were immunized via intranasal, intradermal, or enteric routes with respiratory syncytial virus (RSV) or a live recombinant vaccinia virus expressing the RSV F glycoprotein (vaccinia F). The animals were tested for the appearance of RSV-specific antibody responses in the serum, bronchoalveolar lavage, and nasal wash after immunization and for virus replication 4 days after intranasal challenge with RSV. RSV antibody response in the serum and respiratory tract was demonstrated in all immunization groups and was significantly increased after intranasal challenge with RSV. Immunoglobulin A (IgA) antibody response in bronchoalveolar lavage fluid after intranasal or enteric immunization was two- to threefold higher than that after intradermal immunization. Nasal-wash IgA antibody response was not significantly different among three immunization groups, although mean antibody titer was the highest in intranasal immunization group. Complete resistance to replication of RSV challenge was observed in the lungs of cotton rats immunized by the intranasal or enteric routes, whereas a low level of replication was detected in the lungs of rats immunized intradermally. Enteric or intradermal immunization conferred partial protection to the upper respiratory tract, but complete protection of the upper respiratory tract was observed in the intranasal immunization group. These observations suggest that while enteric immunization is quite effective in inducing antibody responses in the respiratory tract, the magnitude of antiviral immunity induced in the respiratory tract after intranasal immunization may be superior to that observed after enteric immunization. C1 CHILDRENS HOSP, DIV INFECT DIS, BUFFALO, NY 14222 USA. CHILDRENS HOSP, MICROBIOL LABS, BUFFALO, NY 14222 USA. State Univ New York Buffalo, DEPT PEDIAT, BUFFALO, NY 14222 USA. State Univ New York Buffalo, DEPT MICROBIOL, BUFFALO, NY 14222 USA. NIAID, PEDIAT LAB, BETHESDA, MD 20892 USA. FU NIAID NIH HHS [AI 15939-11] NR 34 TC 35 Z9 35 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X EI 1098-5514 J9 J VIROL JI J. Virol. PD FEB PY 1991 VL 65 IS 2 BP 657 EP 663 PG 7 WC Virology SC Virology GA ET445 UT WOS:A1991ET44500013 PM 1987374 ER PT J AU SPALHOLZ, BA VANDEPOL, SB HOWLEY, PM AF SPALHOLZ, BA VANDEPOL, SB HOWLEY, PM TI CHARACTERIZATION OF THE CIS ELEMENTS INVOLVED IN BASAL AND E2-TRANSACTIVATED EXPRESSION OF THE BOVINE PAPILLOMAVIRUS-P2443 PROMOTER SO JOURNAL OF VIROLOGY LA English DT Article ID EARLY REGION TRANSFORMATION; CARBOXY-TERMINAL DOMAIN; LONG CONTROL REGION; OPEN READING FRAME; RNA POLYMERASE-II; E2 GENE; TRANSCRIPTIONAL ACTIVATION; FUNCTIONAL-ANALYSIS; TRANS-ACTIVATION; SIMIAN VIRUS-40 AB Transcriptional transactivation and repression by the viral E2 proteins are important regulatory mechanisms for the papillomaviruses. In the bovine papillomavirus type 1 (BPV-1), several viral promoters can be transactivated by E2 through E2-dependent enhancer elements located in the viral long control region (LCR), including promoters involved in E2 expression itself. This report demonstrates that the BPV-1 P2443 promoter is transactivated by E2-responsive elements in the LCR and that this promoter is responsible for a major part of the expression of the E2 and E5 gene products. Characterization of the cis elements involved in P2443 regulation indicated that the single E2-binding site directly upstream of P2443 is not required for either the E2 transactivation or for any E2 repression of the basal or transactivated activity of this promoter. Therefore, cooperative interactions between E2 bound at the LCR and E2 bound near P2443 do not have any role in the regulation of this promoter. Further definition of the cis regulatory elements of this promoter indicated that a binding site for the transcriptional factor Sp1 exists directly upstream of the P2443 TATA box and is critical for the basal level of transcription from this promoter. Disruption of this Sp1 site eliminated P2443 promoter activity in transient expression assays for E2 and E5 and resulted in a loss of transforming activity when introduced into the full viral genome. RP SPALHOLZ, BA (reprint author), NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892, USA. NR 63 TC 45 Z9 45 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD FEB PY 1991 VL 65 IS 2 BP 743 EP 753 PG 11 WC Virology SC Virology GA ET445 UT WOS:A1991ET44500023 PM 1846195 ER PT J AU CHEUNG, SC CHATTOPADHYAY, SK MORSE, HC PITHA, PM AF CHEUNG, SC CHATTOPADHYAY, SK MORSE, HC PITHA, PM TI EXPRESSION OF DEFECTIVE VIRUS AND CYTOKINE GENES IN MURINE AIDS SO JOURNAL OF VIROLOGY LA English DT Article ID INDUCED IMMUNODEFICIENCY SYNDROME; TUMOR NECROSIS FACTOR; IFN-BETA; LEUKEMIA-VIRUS; ANIMAL-MODELS; T-CELL; RETROVIRUS; INFECTION; MAIDS; INTERFERON AB A syndrome characterized by severe immunodeficiency and lymphoproliferation develops in susceptible strains of mice infected with a mixture of murine leukemia viruses (MuLVs) designated LP-BM5 MuLV. The etiologic agent in this mixture has been shown to be a replication-defective virus (BM5d) with a 4.8-kb genome that required replication-competent helper viruses, primarily ecotropic (BM5e), for cell-to-cell spread in the host. In the present study, we studied the expression of BM5d and BM5e in tissues of infected mice at various times after inoculation in relation to the expression of cytokine genes that may contribute to the pathogenesis of this disorder. Northern (RNA) analysis of total RNA showed that BM5d was expressed at significant levels in lymphoid tissues within 1 week of infection and that the levels of expression increased with time after inoculation. By 16 weeks postinfection, BM5d was expressed in all tissues examined. Expression of BM5e was relatively more restricted to lymphoid tissues and was detected at lower levels than expression of BM5d at early times after infection, but this virus was expressed in all tissues by 16 weeks. Infection with the virus mixture was associated with constitutive expression of tumor necrosis factor in all tissues examined and of interleukin-1 (IL-1) in lymphoid tissues within 1 week of infection, and at later times with widespread expression of these cytokines and gamma interferon. Also, the levels of interferon regulatory factor 1 mRNA were significantly increased in all infected tissues during the infection. In contrast, expression of IL-3, IL-4, IL-5, and IL-6 was not detectable by Northern analysis of the respective mRNAs in any infected tissue at early or late times postinfection. C1 JOHNS HOPKINS UNIV,SCH MED,CTR ONCOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [5T32CA09243, CA50158]; NIAID NIH HHS [AI19737] NR 34 TC 50 Z9 50 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD FEB PY 1991 VL 65 IS 2 BP 823 EP 828 PG 6 WC Virology SC Virology GA ET445 UT WOS:A1991ET44500031 PM 1702843 ER PT J AU MORI, S WOLFINBARGER, JB MIYAZAWA, M BLOOM, ME AF MORI, S WOLFINBARGER, JB MIYAZAWA, M BLOOM, ME TI REPLICATION OF ALEUTIAN MINK DISEASE PARVOVIRUS IN LYMPHOID-TISSUES OF ADULT MINK - INVOLVEMENT OF FOLLICULAR DENDRITIC CELLS AND MACROPHAGES SO JOURNAL OF VIROLOGY LA English DT Note ID HUMORAL IMMUNE-RESPONSE; HYBRIDIZATION PROBES; VIRAL REPLICATION; VIRUS-STRAINS; IDENTIFICATION; INFECTION; ANTIGEN; MAINTENANCE; ANTIBODIES AB By using strand-specific in situ hybridization and immunohistochemistry, evidence for replication of the Aleutian mink disease parvovirus was observed in cells resembling macrophages and cells resembling follicular dendritic cells at 10 days after infection but only in macrophages at 60 days. Sequenstration of the Aleutian mink disease parvovirus in larger numbers of macrophages and follicular dendritic cells was noted at both 10 and 60 days. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 25 TC 39 Z9 39 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD FEB PY 1991 VL 65 IS 2 BP 952 EP 956 PG 5 WC Virology SC Virology GA ET445 UT WOS:A1991ET44500046 PM 1846208 ER PT J AU NEARY, K CAUGHEY, B ERNST, D RACE, RE CHESEBRO, B AF NEARY, K CAUGHEY, B ERNST, D RACE, RE CHESEBRO, B TI PROTEASE SENSITIVITY AND NUCLEASE RESISTANCE OF THE SCRAPIE AGENT PROPAGATED INVITRO IN NEUROBLASTOMA-CELLS SO JOURNAL OF VIROLOGY LA English DT Note ID CREUTZFELDT-JAKOB DISEASE; NEURO-BLASTOMA CELLS; PRION-PROTEIN; FIBRIL PROTEIN; INFECTED BRAIN; INFECTIVITY; IDENTIFICATION; PURIFICATION; ANTIBODIES; COMPONENT AB The scrapie agent has been propagated in vitro in mouse neuroblastoma cells. To further characterize the tissue culture-derived scrapie agent, we studied the effects of protease and nuclease digestion on the agent derived from these cells. The scrapie agent in these cells was found to be resistant to protease digestions for short times but was inactivated by prolonged digestion at high protease concentrations. In contrast, digestion with a variety of nucleases did not alter the agent titer. These results demonstrate that the agent requires an essential protein or proteins for infectivity. If the agent also contains a nucleic acid genome, it must be more nuclease resistant than the majority of cellular DNA and RNA. These properties of the tissue culture-derived scrapie agent were identical to those of brain-derived scrapie agent and thus cannot be attributed to secondary effects of tissue pathology, since the infected cell cultures show no cytopathic effects as a result of infection. C1 NIAID,ROCKY MT LABS,PERSISTANT VIRAL DIS LAB,HAMILTON,MT 59840. NR 34 TC 26 Z9 27 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD FEB PY 1991 VL 65 IS 2 BP 1031 EP 1034 PG 4 WC Virology SC Virology GA ET445 UT WOS:A1991ET44500062 PM 1846182 ER PT J AU HUITFELDT, HS BRANDTZAEG, P POIRIER, MC AF HUITFELDT, HS BRANDTZAEG, P POIRIER, MC TI CARCINOGEN-INDUCED ALTERATIONS IN RAT-LIVER DNA ADDUCT FORMATION DETERMINED BY COMPUTERIZED FLUORESCENT IMAGE-ANALYSIS SO LABORATORY INVESTIGATION LA English DT Article DE N-2-ACETYLAMINOFLUORENE; IMMUNOHISTOCHEMISTRY; CARCINOGEN-DNA MODIFICATION; LIVER CELL PROLIFERATION; EXPERIMENTAL CARCINOGENESIS ID INDUCED HEPATOCYTE NODULES; OVAL CELLS; HYPERPLASTIC NODULES; FED 2-ACETYLAMINOFLUORENE; CHEMICAL CARCINOGENESIS; MONOCLONAL-ANTIBODIES; ALTERED FOCI; HEPATOCARCINOGENESIS; INVIVO; PROLIFERATION AB These studies employed continuous feeding of a carcinogenic level of N-2-acetylaminofluorene to male rats for 28 days. Under these conditions normal hepatocytes are known to be inhibited from proliferation, whereas xenobiotic-resistant putative preneoplastic hepatocytes with altered liver enzyme phenotypic expression appear to have a growth advantage. A novel technique using computerized fluorescent image analysis of triple-stained frozen liver sections was developed and used to visualize three different molecular markers in individual hepatic cells. Proliferating liver cells were identified by anti-5-bromodeoxyuridine immunostaining in livers of rats injected with 5-bromodeoxyuridine 1 hour before sacrifice. Anti-cytokeratin immunostaining was used to identify bile ducts and putative oval cells. Characterization of DNA adduct formation was achieved with an antiserum specific for N-(deoxyguanosine-8-yl)-2-aminofluorene, the major DNA adduct of 2-acetylaminofluorene. The image analysis demonstrated low but distinct DNA adduct concentrations in putative oval cells identified by anti-cytokeratin staining and in scattered, replicating liver cells recognized by anti-5-bromodeoxyuridine. Adducts were not detected in replicating foci consisting of 3 to 11 nuclei. It is possible that proliferating liver cells that have low N-2-acetylaminofluorene-DNA adduct levels may clonally expand to become foci protected from further adduct accumulation and preneoplastic liver lesions. Thus, the computerized fluorescent image analysis demonstrated here may provide a novel procedure for identification of carcinogen-induced liver cell alterations. C1 UNIV OSLO,RIKSHOSP,NATL HOSP,INST PATHOL,IMMUNOHISTOCHEM & IMMUNOPATHOL LAB,OSLO,NORWAY. UNIV OSLO,RIKSHOSP,NATL HOSP,DEPT ANIM RES,OSLO,NORWAY. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT,BETHESDA,MD 20892. NR 56 TC 26 Z9 26 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD FEB PY 1991 VL 64 IS 2 BP 207 EP 214 PG 8 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EY308 UT WOS:A1991EY30800008 PM 1997733 ER PT J AU ENG, J CECKLER, TL BALABAN, RS AF ENG, J CECKLER, TL BALABAN, RS TI QUANTITATIVE H-1 MAGNETIZATION TRANSFER IMAGING INVIVO SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article ID SPIN-LATTICE RELAXATION; PROTEIN SOLUTIONS; RATES; RESONANCE; EXCHANGE; TISSUES; TIMES RP ENG, J (reprint author), NHLBI,CARDIAC ENERGET LAB,BLDG 1,ROOM B3-07,BETHESDA,MD 20892, USA. RI Balaban, Robert/A-7459-2009 OI Balaban, Robert/0000-0003-4086-0948 NR 18 TC 210 Z9 211 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD FEB PY 1991 VL 17 IS 2 BP 304 EP 314 DI 10.1002/mrm.1910170203 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EW712 UT WOS:A1991EW71200002 PM 2062205 ER PT J AU SOTAK, CH ALGER, JR AF SOTAK, CH ALGER, JR TI A PITFALL ASSOCIATED WITH LACTATE DETECTION USING STIMULATED-ECHO PROTON SPECTROSCOPY SO MAGNETIC RESONANCE IN MEDICINE LA English DT Note ID NUCLEAR MAGNETIC-RESONANCE; NMR-SPECTROSCOPY; HIGH-RESOLUTION; PULSE SEQUENCE; INVIVO C1 NINCDS,MED NEUROL BRANCH,NEUROIMAGING SECT,BETHESDA,MD 20892. UNIV MASSACHUSETTS,SCH MED,DEPT RADIOL,WORCESTER,MA 01655. RP SOTAK, CH (reprint author), WORCESTER POLYTECH INST,DEPT BIOMED ENGN,WORCESTER,MA 01609, USA. FU NCRR NIH HHS [S07 RR07198] NR 14 TC 19 Z9 19 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD FEB PY 1991 VL 17 IS 2 BP 533 EP 538 DI 10.1002/mrm.1910170223 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EW712 UT WOS:A1991EW71200022 PM 2062220 ER PT J AU KOISTINAHO, J HERVONEN, A WINKING, H RAPOPORT, SI AF KOISTINAHO, J HERVONEN, A WINKING, H RAPOPORT, SI TI HISTOCHEMICALLY DEMONSTRABLE CATECHOLAMINES IN THE SYMPATHETIC NERVOUS-SYSTEM OF TRISOMIC-16 AND NORMAL FETAL MICE SO MECHANISMS OF AGEING AND DEVELOPMENT LA English DT Article DE SYMPATHETIC GANGLION; ADRENAL MEDULLA; DOWNS SYNDROME; MOUSE; TRISOMY-16; CATECHOLAMINES ID DOPAMINE-BETA-HYDROXYLASE; DOWNS-SYNDROME; HUMAN TRISOMY-21; GANGLIA AB The formaldehyde-induced fluorescence (FIF) and micro-spectrofluorometric techniques were used to study catecholamines in the sympathetic nervous system of normal and trisomy 16 fetal mice with a gestation age of 15 days, an animal model for human trisomy 21 (Down's syndrome). FIF intensity in the stellate sympathetic ganglion of trisomic embryos did not differ from that of controls, whereas in the adrenal medulla the FIF intensity was 38% less in trisomic than in control embryos. When adrenal medullary cells from embryos with a gestational age of 15 days were maintained in culture for 7-10 days, a difference in FIF intensity between groups was still evident. The rate of noradrenaline uptake in cultured adrenal medullary cells also was significantly less in trisomic than in control fetal mice. The results suggest that the development of adrenal medulla is slowed in trisomic 16 mice and that uptake of noradrenaline by trisomic adrenal medullary cells is impaired. C1 UNIV TAMPERE,DEPT PUBL HLTH,GERONTOL SECT,TAMPERE,FINLAND. MED UNIV LUBECK,INST BIOL,LUBECK,GERMANY. RP KOISTINAHO, J (reprint author), NIA,NEUROSCI LAB,BETHESDA,MD 20892, USA. NR 26 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0047-6374 J9 MECH AGEING DEV JI Mech. Ageing. Dev. PD FEB PY 1991 VL 57 IS 2 BP 101 EP 110 DI 10.1016/0047-6374(91)90027-W PG 10 WC Cell Biology; Geriatrics & Gerontology SC Cell Biology; Geriatrics & Gerontology GA EY324 UT WOS:A1991EY32400001 PM 1828847 ER PT J AU GOTTSTEIN, B MOWATT, MR AF GOTTSTEIN, B MOWATT, MR TI SEQUENCING AND CHARACTERIZATION OF AN ECHINOCOCCUS-MULTILOCULARIS DNA PROBE AND ITS USE IN THE POLYMERASE CHAIN-REACTION SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE ECHINOCOCCUS-MULTILOCULARIS; DNA PROBE; DNA SEQUENCE; POLYMERASE CHAIN REACTION ID ALVEOLAR ECHINOCOCCOSIS; GRANULOSUS; PLASMIDS; STRAIN; LIVER AB The nucleotide sequence of the cloned Echinococcus multilocularis DNA probe pAL1 was determined in order to simplify and improve the sensitivity of a diagnostic assay through the application of the polymerase chain reaction (PCR). The insert-specific oligonucleotides BG1 and BG2 define a 2.6-kb fragment in the genomic DNA of E. multilocularis, while BG1 and BG3 define a 0.3 kb fragment. A PCR study including 14 independent E. multilocularis isolates in addition to Echinococcus granulosus, Echinococcus vogeli, Taenia spp. and other cestodes revealed that the 2.6-kb fragment was amplified from genomic DNA of all E. multilocularis isolates tested (originating from Switzerland, Alaska, Canada, France, Germany and Japan), but from genomic DNA of none of the other cestode species. PCR with BG1 and BG2 furthermore uniquely resulted in the synthesis of a 0.55-kb fragment specific for Taenia saginata and a 0.6-kb fragment specific for T. taeniaeformis. In contrast to the species specificity of the 2.6-kb BG1/BG2 product, the 0.3 kb (BG1/BG3) product demonstrated genus specificity: the 0.3-kb product was amplified from genomic DNA of all E. multilocularis, E. granulosus and E. vogeli isolates tested, but from genomic DNA of none of the other cestode species. The diagnostic sensitivity of PCR using both primer sets was determined to be 50 pg parasite DNA, suggesting the practical utility of this simple assay in demonstrating parasite DNA in specimens from a variety of sources. At the basic level, the pAL1-derived oligonucleotides may also prove useful in assessing strain variation, RFLPs or other manifestations of genetic variation in E. multilocularis. C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. RP GOTTSTEIN, B (reprint author), UNIV ZURICH,INST PARASITOL,WINTERTHURERSTR 266A,CH-8057 ZURICH,SWITZERLAND. NR 16 TC 47 Z9 48 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-6851 J9 MOL BIOCHEM PARASIT JI Mol. Biochem. Parasitol. PD FEB PY 1991 VL 44 IS 2 BP 183 EP 194 DI 10.1016/0166-6851(91)90004-P PG 12 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA ET387 UT WOS:A1991ET38700004 PM 2052020 ER PT J AU YEW, N OSKARSSON, M DAAR, I BLAIR, DG VANDEWOUDE, GF AF YEW, N OSKARSSON, M DAAR, I BLAIR, DG VANDEWOUDE, GF TI MOS GENE TRANSFORMING EFFICIENCIES CORRELATE WITH OOCYTE MATURATION AND CYTOSTATIC FACTOR ACTIVITIES SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MURINE SARCOMA-VIRUS; PROTEIN-KINASE ACTIVITY; CELL-CYCLE; V-MOS; MEIOTIC MATURATION; ONCOGENE PRODUCT; XENOPUS HOMOLOG; CDC2 PROTEIN; SEQUENCE; ACTIVATION AB The mos proto-oncogenes from different vertebrate species transform mouse NIH 3T3 cells with markedly different efficiencies. v-mos, mouse (c-mos(mu)), and chicken (c-mos(ch)) mos transform NIH 3T3 cells 10- to 100-fold more efficiently than do human (c-mos(hu)) and Xenopus (c-mos(xe)) mos. The mos genes with the highest transforming activity efficiently induce maturation in Xenopus oocytes and mimic cytostatic factor (CSF) by causing mitotic cleavage arrest in embryos. Chimeric v-mos/c-mos(hu) proteins that had high transforming efficiencies in NIH 3T3 cells were also effective in the induction of oocyte maturation and CSF cleavage arrest. We measured the in vitro autophosphorylation activities of the different mos proteins and found that the levels of kinase activity of v-mos, c-mos(mu), and c-mos(ch) were much higher than that of c-mos(xe). These data indicate that mos gene transforming efficiency and the ability to induce oocyte maturation or mimic CSF activity are correlated with in vitro autophosphorylation activity and suggest that the mos protein plays a similar role in transformed cells and normal oocytes. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,MICROBIOL SECT,MOLEC ONCOL LAB,DCE INTRAMURAL RES PROGRAM,FREDERICK,MD 21702. OI Daar, Ira/0000-0003-2657-526X FU NCI NIH HHS [N01-CO-74101] NR 38 TC 43 Z9 43 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 604 EP 610 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600003 PM 1703629 ER PT J AU ALMOUZNI, G MECHALI, M WOLFFE, AP AF ALMOUZNI, G MECHALI, M WOLFFE, AP TI TRANSCRIPTION COMPLEX DISRUPTION CAUSED BY A TRANSITION IN CHROMATIN STRUCTURE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID RNA POLYMERASE-III; XENOPUS-LAEVIS OOCYTES; CELL-FREE SYSTEM; 5S RNA; GENE-TRANSCRIPTION; POSITIONED NUCLEOSOMES; MULTIPLE FACTORS; DNA-REPLICATION; 5S-RNA GENES; INVITRO AB Chromatin structure is known to influence class III gene expression in vitro. We describe the active transcription of Xenopus class III genes following replication and assembly into chromatin by using Xenopus egg extracts. Changes in the structure of this active chromatin dependent on the presence of exogenous Mg2+ ATP or on the addition of a mixture of histones H2A and H2B are shown to lead to the selective repression of Xenopus 5S RNA genes. Preexisting transcription complexes on 5S DNA are disrupted following the reorganization of a "disordered" histone-DNA complex into a structure consisting of physiologically spaced nucleosomes. Thus, we demonstrate that chromatin structural transitions can have dominant and specific effects on transcription. C1 NIDDKD,MOLEC BIOL LAB,BLDG 6,ROOM 131,BETHESDA,MD 20892. UNIV PARIS 07,INST JACQUES MONOD,CNRS,F-75251 PARIS 05,FRANCE. NR 67 TC 80 Z9 80 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 655 EP 665 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600008 PM 1990277 ER PT J AU ARCHER, TK CORDINGLEY, MG WOLFORD, RG HAGER, GL AF ARCHER, TK CORDINGLEY, MG WOLFORD, RG HAGER, GL TI TRANSCRIPTION FACTOR ACCESS IS MEDIATED BY ACCURATELY POSITIONED NUCLEOSOMES ON THE MOUSE MAMMARY-TUMOR VIRUS PROMOTER SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID GLUCOCORTICOID REGULATION; NUCLEAR EXTRACTS; GENE-REGULATION; MMTV PROMOTER; DNA; SEQUENCE; BINDING; INDUCTION; PROTEIN; RNA AB A fragment of the mouse mammary tumor virus (MMTV) promoter was reconstituted from pure histones into a dinucleosome with uniquely positioned octamer cores. Core boundaries for the in vitro-assembled dinucleosome corresponded to the observed in vivo phasing pattern for long terminal repeat nucleosomes A and B. Nuclear factor 1 (NF1), a constituent of the MMTV transcription initiation complex, was excluded from the assembled dinucleosome, whereas the glucocorticoid receptor was able to bind. During transcription of MMTV in vivo, displacement of nucleosome B was necessary to permit assembly of the initiation complex. These results indicate that the nucleoprotein structure of the promoter can provide differential access to sequence-specific DNA-binding proteins and that active chromatin remodeling can occur during transcription activation. C1 NCI,HORMONE ACT & ONCOGENESIS SECT,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 40 TC 321 Z9 323 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 688 EP 698 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600011 PM 1846670 ER PT J AU EVANS, T FELSENFELD, G AF EVANS, T FELSENFELD, G TI TRANSACTIVATION OF A GLOBIN PROMOTER IN NONERYTHROID CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID CHICKEN BETA-GLOBIN; DNA-BINDING FACTOR; RNA POLYMERASE-II; TRANSCRIPTIONAL ACTIVATION; GENE-EXPRESSION; ENHANCER; PROTEIN; TRANSFECTION; SITES; IDENTIFICATION AB We show that expression in fibroblasts of a single cDNA, encoding the erythroid DNA-binding protein Eryfl (GF-1, NF-E1), very efficiently activates transcription of a chicken alpha-globin promoter. trans-Activation in these cells occurred when Eryfl bound to a single site within a minimal globin promoter. In contrast, efficient activation in erythroid cells required multiple Eryfl binding sites. Our results indicate that mechanisms exist that are capable of modulating the trans-acting capabilities of Eryfl in a cell-specific manner, without affecting DNA binding. The response of the minimal globin promoter to Eryfl in fibroblasts was at least as great as for optimal constructions in erythroid cells. Therefore, the assay provides a very simple and sensitive system with which to study gene activation by a tissue-specific factor. C1 NIDDKD,MOLEC BIOL LAB,BLDG 2,ROOM 310,BETHESDA,MD 20892. NR 32 TC 87 Z9 87 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 843 EP 853 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600028 PM 1990287 ER PT J AU VOELKER, RA GIBSON, W GRAVES, JP STERLING, JF EISENBERG, MT AF VOELKER, RA GIBSON, W GRAVES, JP STERLING, JF EISENBERG, MT TI THE DROSOPHILA SUPPRESSOR OF SABLE GENE ENCODES A POLYPEPTIDE WITH REGIONS SIMILAR TO THOSE OF RNA-BINDING PROTEINS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HETEROGENEOUS NUCLEAR RIBONUCLEOPROTEIN; DEVELOPMENTAL EXPRESSION; RECOGNITION MOTIF; SNRNP PROTEIN; MELANOGASTER; LOCUS; VERMILION; CLONING; TRANSCRIPTION; MECHANISM AB The nucleotide sequence of the Drosophila melanogaster suppressor of sable [su(s)] gene has been determined. Comparison of genomic and cDNA sequences indicates that an approximately 7,860-nucleotide primary transcript is processed into an approximately 5-kb message, expressed during all stages of the life cycle, that contains an open reading frame capable of encoding a 1,322-amino-acid protein of approximately 150 kDa. The putative protein contains an RNA recognition motif-like region and a highly charged arginine-, lysine-, serine-, and aspartic or glutamic acid-rich region that is similar to a region contained in several RNA-processing proteins. In vitro translation of in vitro-transcribed RNA from a complete cDNA yields a product whose size agrees with the size predicted by the open reading frame. Antisera against su(s) fusion proteins recognize the in vitro-translated protein and detect a protein of identical size in the nuclear fractions from tissue culture cells and embryos. The protein is also present in smaller amounts in cytoplasmic fractions of embryos. That the su(s) protein has regions similar in structure to RNA-processing proteins is consistent with its known role in affecting the transcript levels of those alleles that it suppresses. RP VOELKER, RA (reprint author), NIEHS,GENET LAB,RES TRIANGLE PK,NC 27709, USA. NR 42 TC 42 Z9 43 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 894 EP 905 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600033 PM 1703632 ER PT J AU APP, H HAZAN, R ZILBERSTEIN, A ULLRICH, A SCHLESSINGER, J RAPP, U AF APP, H HAZAN, R ZILBERSTEIN, A ULLRICH, A SCHLESSINGER, J RAPP, U TI EPIDERMAL GROWTH-FACTOR (EGF) STIMULATES ASSOCIATION AND KINASE-ACTIVITY OF RAF-1 WITH THE EGF RECEPTOR SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID RIBOSOMAL PROTEIN-S6 KINASE; COMPLETE CODING SEQUENCE; PHOSPHOLIPASE C-II; TYROSINE PHOSPHORYLATION; MEDIATED ENDOCYTOSIS; SIGNAL TRANSDUCTION; PHORBOL ESTER; 3T3-L1 CELLS; S6 KINASE; ONCOGENE AB Raf-1 serine- and threonine-specific protein kinase is transiently activated in cells expressing the epidermal growth factor (EGF) receptor upon treatment with EGF. The stimulated EGF receptor coimmunoprecipitates with Raf-1 kinase and mediates protein kinase C-independent phosphorylation of Raf-1 on serine residues. Hyperphosphorylated Raf-1 has lower mobility on sodium dodecyl sulfate gels and has sixfold-increased activity in immunocomplex kinase assays with histone H1 or a Raf-1 sequence-derived peptide as a substrate. Raf-1 activation requires kinase-active EGF receptor; a point mutant lacking tyrosine kinase activity is inactive in Raf-1 coupling and association. It is noteworthy that tyrosine phosphorylation of c-Raf-1 induced by EGF was not detected in these cells. These observations suggest that Raf-1 kinase may act as an important downstream effector of EGF signal transduction. C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. RORER BIOTECHNOL INC,KING OF PRUSSIA,PA 19406. MAX PLANCK INST BIOCHEM,DEPT MOLEC BIOL,W-8033 MARTINSRIED,GERMANY. NYU MED CTR,DEPT PHARMACOL,NEW YORK,NY 10016. NR 49 TC 125 Z9 126 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 913 EP 919 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600035 PM 1990291 ER PT J AU PAPATHANASIOU, MA KERR, NCK ROBBINS, JH MCBRIDE, OW ALAMO, I BARRETT, SF HICKSON, ID FORNACE, AJ AF PAPATHANASIOU, MA KERR, NCK ROBBINS, JH MCBRIDE, OW ALAMO, I BARRETT, SF HICKSON, ID FORNACE, AJ TI INDUCTION BY IONIZING-RADIATION OF THE GADD45 GENE IN CULTURED HUMAN-CELLS - LACK OF MEDIATION BY PROTEIN-KINASE-C SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DNA-DAMAGING AGENTS; CHINESE-HAMSTER CELLS; MAMMALIAN-CELLS; MESSENGER-RNA; ADAPTIVE RESPONSE; HUMAN-LYMPHOCYTES; CDNA CLONING; REGION; HYPERSENSITIVITY; LOCALIZATION AB The effect of ionizing radiation on the expression of two DNA-damage-inducible genes, designated gadd45 and gadd153, was examined in cultured human cells. These genes have previously been shown to be strongly and coordinately induced by UV radiation and alkylating agents in human and hamster cells. We found that the gadd45 but not the gadd153 gene is strongly induced by X rays in human cells. The level of gadd45 mRNA increased rapidly after X rays at doses as low as 2 Gy. After 20 Gy of X rays, gadd45 induction, as measured by increased amounts of mRNA, was similar to that produced by the most effective dose of the alkylating agent methyl methanesulfonate. No induction was seen after treatment of either human or hamster cells with 12-O-tetradecanoylphorbol-13-acetate, a known activator of protein kinase C (PKC). Therefore, gadd45 represents the only known mammalian X-ray-responsive gene whose induction is not mediated by PKC. However, induction was blocked by the protein kinase inhibitor H7, indicating that induction is mediated by some other kinase(s). Sequence analysis of human and hamster cDNA clones demonstrated that this gene has been highly conserved and encodes a novel 165-amino-acid polypeptide which is 96% identical in the two species. This gene was localized to the short arm of human chromosome 1 between p12 and p34. When induction in lymphoblast lines from four normal individuals was compared with that in lines from four patients with ataxia telangiectasia, induction by X rays of gadd45 mRNA was less in the cell lines from this cancer-prone radiosensitive disorder. Our results provide evidence for the existence of an X-ray stress response in human cells which is independent of PKC and which is abnormal in ataxia telangiectasia. C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NCI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV OXFORD,JOHN RADCLIFFE HOSP,INST MOLEC MED,IMPERIAL CANC RES FUND,OXFORD OX3 9DU,ENGLAND. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 41 TC 254 Z9 259 U1 1 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 1009 EP 1016 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600046 PM 1990262 ER PT J AU MURTAGH, JJ EDDY, R SHOWS, TB MOSS, J VAUGHAN, M AF MURTAGH, JJ EDDY, R SHOWS, TB MOSS, J VAUGHAN, M TI DIFFERENT FORMS OF GO-ALPHA MESSENGER-RNA ARISE BY ALTERNATIVE SPLICING OF TRANSCRIPTS FROM A SINGLE GENE ON HUMAN CHROMOSOME-16 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID GTP-BINDING PROTEIN; SIGNAL-TRANSDUCTION PROTEIN; POLYMERASE CHAIN-REACTION; AMINO-ACID SEQUENCE; HUMAN CDNA CLONES; ALPHA-SUBUNIT; MOLECULAR-CLONING; ADP-RIBOSYLATION; RAT-BRAIN; IMMUNOHISTOCHEMICAL LOCALIZATION AB G(o-alpha), (gene symbol GNA01), a member of the signal-transducing guanine nucleotide-binding (G) protein family, has been implicated in ion channel regulation. Some tissues contain multiple G(o-alpha) mRNAs of different sizes that differ in the 3' untranslated regions (UTRs). Using sequence-specific 48-base oligonucleotides, two complementary to the different 3' UTRs and one complementary to the coding region, we investigated the origin of the multiple G(o-alpha) transcripts, the organization of the G(o-alpha) gene, the interspecies conservation of 3' UTRs, and the chromosomal localization of G(o-alpha). Oligonucleotides labeled to high specific activity by using terminal deoxynucleotidyltransferase each hybridized with a single band of restriction enzyme-digested mouse and human DNAs. In three of four digests of human DNA, the two probes specific for the different 3' UTRs hybridized with the same restriction fragment. Thus, these nucleotide sequences are in close proximity in the human genome. The order of the UTRs in the bovine, human, and mouse genomes was confirmed directly by polymerase chain reaction (PCR) amplification and sequencing. Hybridization of bovine oligonucleotide sequences with mouse and human genomic DNA indicated a high degree of interspecies sequence conservation; conservation was confirmed by PCR amplification and sequencing. Bands detected by both UTR probes, as well as the predominant bands detected by a bovine G(o-alpha) cDNA, segregated with human chromosome 16 on Southern blot analysis of human-mouse somatic cell hybrids. We conclude that G(o-alpha) mRNAs with different 3' UTRs arise by alternative splicing of transcripts from a single gene. The UTRs, which exhibit a high degree of interspecies conservation, may play a role in regulation of G(o-alpha) expression during differentiation or in specific tissues. The use of oligonucleotide probes of the type described here represents a new strategy, potentially widely applicable for mapping and elucidating structural features of genes. C1 NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. RP MURTAGH, JJ (reprint author), NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892, USA. NR 69 TC 26 Z9 26 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 1146 EP 1155 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600062 PM 1899283 ER PT J AU HAO, QL FERRIS, DK WHITE, G HEISTERKAMP, N GROFFEN, J AF HAO, QL FERRIS, DK WHITE, G HEISTERKAMP, N GROFFEN, J TI NUCLEAR AND CYTOPLASMIC LOCATION OF THE FER TYROSINE KINASE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Note ID ABL GENE-PRODUCT; ENCODED PROTEIN; DISTINCT; IDENTIFICATION; TRANSLOCATION; EXPRESSION; INVITRO; CELLS AB The location of the FER protein within the cell was investigated by using subcellular fractionation and immunofluorescence. FER was found in the cytoplasm and in the nucleus, where it was associated with the chromatin fraction. Its ubiquitous expression and its subcellular location indicate that it may be involved in key regulatory processes. C1 CHILDRENS HOSP LOS ANGELES,DEPT PATHOL,MOLEC DIAGNOSIS SECT,4650 SUNSET BLVD,LOS ANGELES,CA 90027. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. FU NCI NIH HHS [CA 47456, N01-CO-74102] NR 19 TC 53 Z9 56 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 1180 EP 1183 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600068 PM 1990274 ER PT J AU LAD, RP SMITH, MA HILT, DC AF LAD, RP SMITH, MA HILT, DC TI MOLECULAR-CLONING AND REGIONAL DISTRIBUTION OF RAT-BRAIN CYCLOPHILIN SO MOLECULAR BRAIN RESEARCH LA English DT Article DE CYCLOPHILIN; CYCLOSPORINE-A; INSITU HYBRIDIZATION ID A-BINDING PROTEIN; CYCLOSPORIN-A; DNA; ACID AB Cyclosporine A (CsA) is a potent immunosuppressive drug that has widespread clinical uses in organ transplanation and the treatment of autoimmune disorders. However, the drug's clinical applications are on an empiric basis with a poor understanding of the basic mechanism(s) of action. CsA may exert some of its effects by binding to a cellular receptor protein - the cyclosporine receptor (also called cyclophilin). Cyclophilin (CyP) is an ubiquitous, soluble, cytoplasmic 17 kDa protein which has recently been shown to be a peptide-prolyl isomerase. CsA specifically binds to this protein and inhibits its isomerase activity. A rat cyclophilin cDNA clone was isolated from a rat brain lambda gt11 cDNA library. Northern blot analysis shows a single 1 kb messenger RNA in rat brain. In order to determine the regional distribution of the Cyp mRNA in situ hybridization was performed. The Cyp mRNA appeared to be expressed throughout the brain but there were particularly high levels in the cerebral cortex and hippocampus compared to the relatively low levels in white matter areas and tracts. At the cellular level, the Cyp mRNA is expressed at much higher levels in neurons than in glia. The high levels of Cyp in cortical (neuronal) areas may, in part, explain the global encephalopathic symtoms clinically observed in CsA neurotoxicity. C1 NIH,BIOCHEM GENET LAB,BETHESDA,MD 20892. UNIV MARYLAND,VET ADM HOSP,SCH MED,DEPT NEUROL,BALTIMORE,MD 21201. UNIV MARYLAND,VET ADM HOSP,SCH MED,DEPT BIOCHEM,BALTIMORE,MD 21201. UNIV MARYLAND,VET ADM HOSP,SCH MED,CTR MED BIOTECHNOL,BALTIMORE,MD 21201. NIH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. NR 23 TC 52 Z9 54 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD FEB PY 1991 VL 9 IS 3 BP 239 EP 244 DI 10.1016/0169-328X(91)90007-K PG 6 WC Neurosciences SC Neurosciences & Neurology GA EX053 UT WOS:A1991EX05300007 ER PT J AU SCHAEFFER, JC LIN, CL KITAYAMA, S UHL, GR AF SCHAEFFER, JC LIN, CL KITAYAMA, S UHL, GR TI LIGAND AUTORADIOGRAPHIC RECEPTOR SCREENING .2. EXPRESSION OF RECEPTOR CDNA IN TRANSFECTED COS CELLS GROWN ON POLYESTER DISKS AND ITS RECOVERY SO MOLECULAR BRAIN RESEARCH LA English DT Note DE RECEPTOR CLONING; CDNA; BETA-ADRENERGIC RECEPTOR; EXPRESSION CLONING; LIGAND AUTORADIOGRAPHIC RECEPTOR SCREENING ID BETA-ADRENERGIC-RECEPTOR; MOLECULAR-CLONING; RHODOPSIN; ANTIGEN; SYSTEM AB A receptor autoradiographic method that can detect expressed receptor cDNA in 0.002% of plasmid clones and can allow cDNA recoveries and enrichments up to 300-fold in one cycle of screening is described. C1 NIDA,ARC,MOLEC NEUROBIOL LAB,BOX 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. RI Lin, Chien-liang/E-3513-2011 NR 15 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD FEB PY 1991 VL 9 IS 3 BP 271 EP 276 DI 10.1016/0169-328X(91)90012-M PG 6 WC Neurosciences SC Neurosciences & Neurology GA EX053 UT WOS:A1991EX05300012 ER PT J AU WASHBURN, T HOCUTT, A BRAUTIGAN, DL KORACH, KS AF WASHBURN, T HOCUTT, A BRAUTIGAN, DL KORACH, KS TI UTERINE ESTROGEN-RECEPTOR INVIVO - PHOSPHORYLATION OF NUCLEAR SPECIFIC FORMS ON SERINE RESIDUES SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID PROTEIN-KINASE; GLUCOCORTICOID RECEPTORS; STRUCTURAL ORGANIZATION; PROGESTERONE-RECEPTOR; MOUSE UTERUS; BINDING; EXPRESSION; ESTRADIOL; PHOSPHOTYROSINE; TRANSFORMATION AB We have characterized further the heterogeneous nuclear-specific doublet forms of the mouse uterine estrogen receptor (ER). Estrogen treatment produced the multiple nuclear ER forms of 65 and 66.5 kDa, which were isolated and analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Soluble ER preparations exhibited only a single 65-kDa form. Isolation of the individual nuclear ER forms and reanalysis demonstrated that formation of the multiple bands was not due to artifacts of nuclear sample preparation or the presence of contaminating proteins. Analysis of individual uterine cell types (epithelial and stromal/myometrium) indicated that both ER forms were present in both cell fractions. Fractionation of nuclear components with low salt showed that both ER forms were found in the salt-resistant fraction. Extraction of nuclei with high salt (0.6 M KCl) solubilized both ER forms. Phosphorylation was studied as a protein modification to account for the multiple forms. Incorporation of P-32 into uterine protein both in vivo and in intact tissue incubation indicated P-32 labeling of uterine nuclear ER after hormone treatment. Both nuclear ER forms are labeled, although the 66.5-kDa form appears to be more heavily labeled. Phosphoamino acid analysis of the immunopurified P-32-labeled ER from intact uterine tissue indicated phosphoserine as the only phospholabeled residue. These data suggest that phosphorylation is associated with the physiological functioning of the ER in response to hormone and produces the heterogeneous ER forms in the nucleus. C1 NIEHS,REPROD & DEV TOXICOL LAB,RECEPTOR BIOL SECT,POB 12233,RES TRIANGLE PK,NC 27709. BROWN UNIV,DIV BIOL & MED,BIOCHEM SECT,PROVIDENCE,RI 02912. OI Korach, Kenneth/0000-0002-7765-418X FU NIDDK NIH HHS [DK-31374] NR 36 TC 72 Z9 72 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD FEB PY 1991 VL 5 IS 2 BP 235 EP 242 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FA907 UT WOS:A1991FA90700010 PM 2038345 ER PT J AU KIESS, W GREENSTEIN, LA LEE, L THOMAS, C NISSLEY, SP AF KIESS, W GREENSTEIN, LA LEE, L THOMAS, C NISSLEY, SP TI BIOSYNTHESIS OF THE INSULIN-LIKE GROWTH FACTOR-II (IGF-II) MANNOSE-6-PHOSPHATE RECEPTOR IN RAT C6 GLIAL-CELLS - THE ROLE OF N-LINKED GLYCOSYLATION IN BINDING OF IGF-II TO THE RECEPTOR SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID MANNOSE 6-PHOSPHATE RECEPTOR; MULTIPLICATION-STIMULATING ACTIVITY; HUMAN-FIBROBLASTS; PURIFICATION; PROTEINS; INHIBITOR; SEQUENCE; AFFINITY; ANTIBODY; TURNOVER AB We examined the role of N-linked glycosylation of the insulin-like growth factor-II (IGF-II)/mannose 6-phosphate (Man-6-P) receptor in binding of [I-125]IGF-II to the receptor. First we studied the synthesis and posttranslational processing of this receptor in rat C6 glial cells, which have abundant IGF-II/Man-6-P receptors. Cells were pulse labeled with [S-35]methionine and lysed, and the IGF-II/Man-6-P receptor was immunoprecipitated using a specific IGF-II/Man-6-P receptor antibody (no. 3637). Analysis of the immunoprecipitate by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) with reduction of disulfide bonds showed a 235-kDa receptor precursor that was processed into the mature 245-kDa IGF-II/Man-6-P receptor within 2 h of chase. Digestion of the 235-kDa precursor with endoglycosidase-H (Endo H) produced a 220-kDa form, whereas the mature 245-kDa receptor was relatively resistant to cleavage by Endo H. When cells were cultured in the presence of 2-mu-M monensin, the 235-kDa receptor was not further processed into the mature Endo H-resistant receptor form. In addition, the presence of swainsonine in C6 glial cell cultures led to the formation of a 240-kDa receptor hybrid molecule, which was cleaved by Endo H into a 225-kDa species. When tunicamycin was present during the pulse-chase labeling experiment, a 220-kDa receptor species accumulated. This species was 205 kDa by immunoblotting when SDS-PAGE was performed under nonreducing conditions. Pure IGF-II/Man-6-P receptor was digested with N-glycosidase-F, and the digest was immunoblotted with antiserum 3637 after SDS-PAGE under nonreducing conditions. Whereas undigested receptor was a single band of 215 kDa under nonreducing conditions, digested receptor was 205 kDa. The binding affinity of IGF-II for the digested receptor was the same as the binding affinity of IGF-II for the undigested receptor. In addition, affinity cross-linking experiments showed that [I-125]IGF-II also bound to the unglycosylated receptor precursor that accumulated in the tunicamycin-treated cells, and the binding affinity of IGF-II for this species was indistinguishable from the binding affinity of IGF-II for the mature receptor. We conclude that IGF-II can bind to an IGF-II/Man-6-P receptor that lacks N-linked oligosaccharides. C1 NCI,METAB BRANCH,BLDG 10,ROOM 4N115,BETHESDA,MD 20892. UNIV MUNICH,CHILDRENS HOSP,W-8000 MUNICH 2,GERMANY. NR 46 TC 14 Z9 14 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD FEB PY 1991 VL 5 IS 2 BP 281 EP 291 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FA907 UT WOS:A1991FA90700015 PM 1645456 ER PT J AU SHIH, W MEARS, T BRADLEY, DJ PARANDOOSH, Z WEINBERGER, C AF SHIH, W MEARS, T BRADLEY, DJ PARANDOOSH, Z WEINBERGER, C TI AN ADENOVIRAL VECTOR SYSTEM FOR FUNCTIONAL IDENTIFICATION OF NUCLEAR RECEPTOR LIGANDS SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID THYROID-HORMONE RECEPTOR; HUMAN GLUCOCORTICOID RECEPTOR; V-ERB-A; RETINOIC ACID; MINERALOCORTICOID RECEPTOR; FIREFLY LUCIFERASE; COMPLEMENTARY-DNA; MAMMALIAN-CELLS; GENE; EXPRESSION AB A recombinant adenovirus system has been designed that confers glucocorticoid responsiveness upon infected cells in culture. Two mutually dependent viruses are required: a trans-activator virus containing the human glucocorticoid receptor transcription unit and a second reporter virus harboring a glucocorticoid response element linked to the firefly luciferase gene. Another reciprocal pair of viruses has been generated; one member expresses the rat thyroid hormone receptor-alpha, while the other contains the luciferase gene regulated by a thyroid hormone-responsive DNA element. Corticosteroid- or thyroid hormone-induced transcription can be efficiently and accurately quantitated from cells coinfected with the appropriate complementary virus pair 20 h after infection in 96-well microtiter plates. This coinfection assay offers a convenient way to measure transcriptional activation by nuclear receptors and has certain key advantages over the commonly used cotransfection method. Its sensitivity and precision make it a practical approach to rapidly identify substances extracted from complex biological samples activating candidate "orphan" nuclear receptor molecules. C1 Scripps Res Inst, RES INST, DEPT NEUROPHARMACOL, 10666 N TORREY PINES RD, LA JOLLA, CA 92037 USA. LIGAND PHARMACEUT INC, SAN DIEGO, CA 92121 USA. NIH, HOWARD HUGHES MED INST, BETHESDA, MD 20892 USA. FU NIAAA NIH HHS [NIAAA 06420] NR 59 TC 16 Z9 16 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD FEB PY 1991 VL 5 IS 2 BP 300 EP 309 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FA907 UT WOS:A1991FA90700017 PM 1645457 ER PT J AU KOOMEY, M BERGSTROM, S BLAKE, M SWANSON, J AF KOOMEY, M BERGSTROM, S BLAKE, M SWANSON, J TI PILIN EXPRESSION AND PROCESSING IN PILUS MUTANTS OF NEISSERIA-GONORRHOEAE - CRITICAL ROLE OF GLY-1 IN ASSEMBLY SO MOLECULAR MICROBIOLOGY LA English DT Article ID PSEUDOMONAS-AERUGINOSA PILIN; NUCLEOTIDE-SEQUENCE; GENE CONVERSION; ANTIGENIC DETERMINANTS; PILIATION CONTROL; ESCHERICHIA-COLI; STRUCTURAL GENE; OUTER-MEMBRANE; PROTEINS; VARIANTS AB Spontaneous mutants of Neisseria gonorrheae failing to express pili or having diminished levels of piliation were studied with regard to pilin expression. All mutants displayed altered pilin processing detectable as the release of soluble, truncated pilin molecules (S-pilin). Of particular interest was the finding, in one mutant, that substitution of serine for glycine at position -1 of propilin, a highly conserved residue among N-metPhe and related pilins, abolished pilus expression but not S-pilin release. The degree of S-pilin processing and the levels of membrane-associated pilin varied among the different classes of mutants, suggesting that each was blocked at a distinct step of pilus biogenesis. The data support a model in which increased S-pilin processing is a result of a decreased rate of pilus polymerization. C1 ROCKEFELLER UNIV,BACTERIOL & IMMUNOL LAB,NEW YORK,NY 10021. UMEA UNIV,DEPT MICROBIOL,S-90187 UMEA,SWEDEN. NIAID,ROCKY MT LABS,HAMILTON,MT 59840. RP KOOMEY, M (reprint author), UNIV MICHIGAN,SCH MED,DEPT MICROBIOL & IMMUNOL,ANN ARBOR,MI 48109, USA. FU NIAID NIH HHS [AI 19469, AI 27837, AI 10615] NR 40 TC 40 Z9 40 U1 0 U2 2 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0950-382X J9 MOL MICROBIOL JI Mol. Microbiol. PD FEB PY 1991 VL 5 IS 2 BP 279 EP 287 DI 10.1111/j.1365-2958.1991.tb02108.x PG 9 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA EZ838 UT WOS:A1991EZ83800006 PM 1674976 ER PT J AU JI, H SANDBERG, K CATT, KJ AF JI, H SANDBERG, K CATT, KJ TI NOVEL ANGIOTENSIN-II ANTAGONISTS DISTINGUISH AMPHIBIAN FROM MAMMALIAN ANGIOTENSIN-II RECEPTORS EXPRESSED IN XENOPUS-LAEVIS OOCYTES SO MOLECULAR PHARMACOLOGY LA English DT Article ID BRAIN MESSENGER-RNA; SUBTYPES; RAT; IDENTIFICATION; SEROTONIN; RESPONSES; KIDNEY; CELLS AB Angiotensin II (All) stimulates rapid increases in cytosolic Ca2+ concentrations in Xenopus laevis oocytes after binding to specific receptors located in the surrounding follicular cells. In follicular oocytes, the peptide All receptor antagonists saralasin (IC50 = 25 nM) and CGP 42112A (IC50 = 400 nM) were orders of magnitude more potent than the non-peptide antagonists DuP 753 and PD-123177 (IC50 > 10-mu-M) as inhibitors of All-induced Ca2+ mobilization. The relative potencies of the All antagonists at the Xenopus All receptor were completely different from their activities at the two known mammalian All receptor subtypes. These results indicate that the ligand-binding doman of the amphibian All receptor has a unique conformation that distinguishes with high specificity between peptide and non-peptide All antagonists. The amphibian All receptor is pharmacologically distinct from the AT(1) receptor subtype, which mediates phosphoinositide hydrolysis and Ca2+ mobilization in mammalian adrenal cells. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLDG 10,ROOM BIL400,BETHESDA,MD 20892. NR 27 TC 38 Z9 38 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD FEB PY 1991 VL 39 IS 2 BP 120 EP 123 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EY502 UT WOS:A1991EY50200004 PM 1996080 ER PT J AU GUSOVSKY, F GUTKIND, JS AF GUSOVSKY, F GUTKIND, JS TI SELECTIVE EFFECTS OF ACTIVATION OF PROTEIN-KINASE-C ISOZYMES ON CYCLIC-AMP ACCUMULATION SO MOLECULAR PHARMACOLOGY LA English DT Article ID ADENYLATE-CYCLASE ACTIVITY; PHORBOL ESTERS; BIOCHEMICAL-CHARACTERIZATION; NCB-20 CELLS; CROSS-TALK; INHIBITION; DESENSITIZATION; PHOSPHORYLATION; EXPRESSION; PATHWAYS AB Activation of protein kinase C (PKC) in intact cells can induce significant changes, either facilitatory or inhibitory, in cyclic AMP accumulation elicited either by receptor activation or by the activator of adenylate cyclase, forskolin. Such interaction represents an example of "cross-talk" between second messenger systems and may underlie the biochemical basis of synchronization between external stimuli and biological responses. PKC is now known to comprise a variety of subspecies. Although differences among the PKC subspecies are apparent in terms of their enzymological properties, no functional differences among them have been described. In PC12 cells, where both alpha and gamma isozymes of PKC are present, activation of PKC causes enhancement of the responses of cyclic AMP-generating systems. In NCB20 cells and NIH 3T3 cells, where only the alpha isozyme is expressed, activation of PKC causes inhibition of cyclic AMP-generating systems. In NIH 3T3 cells after transfection of gamma-PKC, activation of the enzyme was no longer inhibitory; instead, a facilitation of cyclic AMP accumulation was observed. Thus, the alpha and gamma isozymes of PKC appear to have opposite actions, facilitatory for gamma-PKC and inhibitory for alpha-PKC, on the responses of cyclic AMP-generating systems in NIH 3T3 cells. Such opposing actions represent a remarkable functional distinction between two PKC subspecies. C1 NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. RP GUSOVSKY, F (reprint author), NIDDKD,BIOORGAN CHEM LAB,BLDG 8,ROOM 1A-15,BETHESDA,MD 20892, USA. RI Gutkind, J. Silvio/A-1053-2009 NR 32 TC 74 Z9 75 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD FEB PY 1991 VL 39 IS 2 BP 124 EP 129 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EY502 UT WOS:A1991EY50200005 PM 1847491 ER EF