FN Thomson Reuters Web of Science™ VR 1.0 PT J AU HOLLAND, MM FISHER, DL MITCHELL, LG RODRIGUEZ, WC CANIK, JJ MERRIL, CR WEEDN, VW AF HOLLAND, MM FISHER, DL MITCHELL, LG RODRIGUEZ, WC CANIK, JJ MERRIL, CR WEEDN, VW TI MITOCHONDRIAL-DNA SEQUENCE-ANALYSIS OF HUMAN SKELETAL REMAINS - IDENTIFICATION OF REMAINS FROM THE VIETNAM-WAR SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PHYSICAL ANTHROPOLOGY; DNA TYPING; BONE DNA EXTRACTION; HUMAN IDENTIFICATION; VIETNAM WAR ID POLYMERASE CHAIN-REACTION; ENZYMATIC AMPLIFICATION; OLIGONUCLEOTIDE PROBES; EVOLUTION; BONE; FRAGMENTS AB Deoxyribonucleic acid (DNA) sequence analysis of the control region of the mitochondrial DNA (mtDNA) genome was used to identify human skeletal remains returned to the United States government by the Vietnamese government in 1984. The postmortem interval was thought to be 24 years at the time of testing, and the remains presumed to be an American service member. DNA typing methods using nuclear genomic DNA, HLA-DQ alpha [1] and the variable number of tandem repeat (VNTR) locus D1S80 [2], were unsuccessful using the polymerase chain reaction (PCR) [3]. Amplification of a portion of the mtDNA control region was performed, and the resulting PCR product subjected to DNA sequence analysis. The DNA sequence generated from the skeletal remains was identical to the maternal reference sequence, as well as the sequence generated from two siblings (sisters). The sequence was unique when compared to more than 650 DNA sequences found both in the literature and provided by personal communications. The individual sequence polymorphisms were present in only 23 of the more than 1300 nucleotide positions analyzed. These results support the observation [4] that in cases where conventional DNA typing is unavailable, mtDNA sequencing can be used for human remains identification. C1 ARMED FORCES INST PATHOL,OFF ARMED FORCES MED EXAMINER,WASHINGTON,DC 20306. NIMH,CTR NEUROSCI,BIOCHEM GENET LAB,WASHINGTON,DC 20032. RP HOLLAND, MM (reprint author), ARMED FORCES INST PATHOL,ARMED FORCES DNA IDENTIFICAT LAB,14TH ST,ALASKA ST,WASHINGTON,DC 20306, USA. NR 28 TC 170 Z9 173 U1 2 U2 12 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD MAY PY 1993 VL 38 IS 3 BP 542 EP 553 PG 12 WC Medicine, Legal SC Legal Medicine GA LD283 UT WOS:A1993LD28300008 PM 8515208 ER PT J AU ENK, AH ANGELONI, VL UDEY, MC KATZ, SI AF ENK, AH ANGELONI, VL UDEY, MC KATZ, SI TI AN ESSENTIAL ROLE FOR LANGERHANS CELL-DERIVED IL-1-BETA IN THE INITIATION OF PRIMARY IMMUNE-RESPONSES IN SKIN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTIGEN-PRESENTING CELLS; INVIVO; SENSITIZATION; INTERLEUKIN-1; GENERATION; EXPRESSION; INDUCTION AB Langerlians cells (LC) are Ag-presenting cells required for induction of primary immune responses in skin. After activation by Ag, LC express increased levels of MHC class II Ag, exhibit increased accessory cell activity, and migrate to regional lymph nodes where they stimulate T cells. One of the earliest manifestations of LC activation is the accumulation of increased amounts of IL-1 beta mRNA in LC within 15 min after exposure to contact allergens in vivo. To determine if enhanced IL-1beta production by LC could be causally linked to epicutaneous sensitization, we injected IL-1beta intradermally into the ears of BALB/c mice and extracted total epidermal RNA 4 h later. A quantitative reverse transcriptase-polymerase chain reaction technique was used to compare changes in IL-1alpha, IL-1beta, macrophage inflammatory protein 2, IL-10, TNF-alpha, and I-Aalpha chain mRNA signals caused by intradermally-injected IL-1beta to those caused by intradermal IL-1alpha or TNFalpha, or by topical application of the contact allergen trinitrochlorobenzene (3% TNCB). Intradermal injection of 25 ng IL-1beta resulted in 5-to 100-fold enhancement of mRNA signals for IL-1alpha, IL-1beta, MIP-2, IL-10, TNFalpha, and class II I-Aalpha, mimicking the changes caused by allergen. In contrast, injection of equivalent amounts of IL-1alpha or TNFalpha did not significantly alter the epidermal cytokine pattern. Simulating the effects of topically applied TNCB, intradermally-injected IL-1beta (but not IL-1alpha or TNFalpha) also caused enhancement of LC MHC class II expression. In addition, LC derived from IL-1beta-injected skin were 2 to 3 times more potent accessory cells in an anti-CD3 proliferation assay than LC from IL-1alpha or sham-injected skin. Finally, injection of hamster anti-mIL-1beta mAb into the skin prior to TNCB treatment completely prevented sensitization to this allergen, although injections of similar amounts of hamster anti-mlL-1alpha mAb or PBS were without effect. Taken together, our data indicate that dendritic cell-derived IL-1beta may be a critical molecule required for initiation of primary immune responses in skin. C1 NCI,DERMATOL BRANCH,BLDG 10,ROOM 12N 238,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,DERMATOL CLIN,WASHINGTON,DC 20307. NR 20 TC 347 Z9 352 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 MAY 1 PY 1993 VL 150 IS 9 BP 3698 EP 3704 PG 7 WC Immunology SC Immunology GA KY452 UT WOS:A1993KY45200004 PM 8473727 ER PT J AU HONG, JX WILSON, GL FOX, CH KEHRL, JH AF HONG, JX WILSON, GL FOX, CH KEHRL, JH TI ISOLATION AND CHARACTERIZATION OF A NOVEL B-CELL ACTIVATION GENE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN LYMPHOCYTES-B; MOLECULAR-CLONING; CDNA CLONES; MEMBRANE-PROTEIN; RECEPTOR; ANTIGEN; DIFFERENTIATION; SUPERFAMILY; EXPRESSION; MEMBER AB Using subtractive cDNA cloning, we have isolated a series of cDNA clones that are differentially expressed between B and T lymphocytes. Whereas some of the isolated cDNA are from known B cell-specific genes, many of them represent previously uncharacterized genes. One of these unknown genes was denoted as BL34. Northern blot analysis performed with the BL34 cDNA revealed a 1.6-kb mRNA transcript that was present at low levels in RNA extracted from resting B lymphocytes, but whose expression was markedly increased in RNA prepared from mitogen-activated B cells. Similarly, RNA prepared from several B cell lines treated with phorbol myristate acetate (PMA) contained high levels of BL34 mRNA. In contrast, RNA from purified T cells treated with phytohemagglutinin and PMA had undetectable amounts of BL34 mRNA. In addition, high levels of BL34 mRNA were detected in RNA purified from PBMC of a patient with B cell acute lymphocytic leukemia. Southern blot analysis of human DNA from various tissues and cells lines demonstrated that BL34 is a single-copy gene without evidence of rearrangement. Two full length BL34 cDNA were sequenced, and an open reading frame of 588 bp was identified that was predicted to encode for a 196 amino acid protein. Searches of several protein data bases failed to find any homologous proteins. To directly analyze the expression of BL34 mRNA in lymphoid tissues in situ, hybridization studies with human tonsil tissue sections were performed. BL34 mRNA was detected in a portion of the cells in the germinal center region and adjacent to the mantle region. Further characterization of the BL34 gene and its protein should lead to insights to its role in B cell function and the consequences of its over-expression in acute lymphocytic leukemia. C1 NIAID,IMMUNOREGULAT LAB,BLDG 10,RM 11B08,BETHESDA,MD 20892. OI Kehrl, John/0000-0002-6526-159X NR 26 TC 76 Z9 78 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 1 PY 1993 VL 150 IS 9 BP 3895 EP 3904 PG 10 WC Immunology SC Immunology GA KY452 UT WOS:A1993KY45200024 PM 8473738 ER PT J AU SHER, A OSWALD, IP HIENY, S GAZZINELLI, RT AF SHER, A OSWALD, IP HIENY, S GAZZINELLI, RT TI TOXOPLASMA-GONDII INDUCES A T-INDEPENDENT IFN-GAMMA RESPONSE IN NATURAL-KILLER-CELLS THAT REQUIRES BOTH ADHERENT ACCESSORY CELLS AND TUMOR-NECROSIS-FACTOR-ALPHA SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CYTOKINE PRODUCTION; STIMULATORY FACTOR; INTERFERON-GAMMA; TH2 RESPONSES; SCID MICE; LYMPHOCYTES; INDUCTION; INFECTION; INVITRO AB Spleen cells from scid mice produce high levels of IFN-gamma when exposed to either live tachyzoites of Toxoplasma gondii or a soluble parasite extract. Small numbers of parasites are sufficient to stimulate this response, which is also induced by cell-free supernatants of cultured tachyzoites. The parasite molecules responsible for triggering IFN-gamma production are heat-labile but resistant to freezing and thawing. Depletion of NK cells or adherent cells from the splenocyte population abolishes the response. Moreover, cultured bone marrow-derived NK cells are stimulated by Toxoplasma to produce IFN-gamma, but only when supplemented with adherent peritoneal washout or thioglycollate-induced exudate cells. Supernatants of macrophages preincubated with T. gondii extract also induce IFN-gamma synthesis by cultured NK cells. Addition of neutralizing mAb against TNF-alpha abolishes the IFN-gamma response of scid spleen cells exposed to the parasite or of NK cells incubated with supernatants of adherent cells stimulated with T. gondii extract. Moreover, splenic adherent cells produce low levels of TNF-alpha in response to the parasite. Nevertheless, TNF-alpha alone is not sufficient to trigger IFN-gamma production from purified NK cell populations. These findings provide the first example of the stimulation of T-independent IFN-gamma production by a protozoan. The ability of T gondii to trigger this pathway may underlie its induction of strong IFN-gamma-dependent nonspecific and specific cell-mediated immunity. RP SHER, A (reprint author), NIAID,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,BLDG 4,ROOM 126,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI OSWALD, Isabelle/A-8497-2013 NR 26 TC 203 Z9 208 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 1 PY 1993 VL 150 IS 9 BP 3982 EP 3989 PG 8 WC Immunology SC Immunology GA KY452 UT WOS:A1993KY45200033 PM 8473745 ER PT J AU MELILLO, G COX, GW RADZIOCH, D VARESIO, L AF MELILLO, G COX, GW RADZIOCH, D VARESIO, L TI PICOLINIC-ACID, A CATABOLITE OF L-TRYPTOPHAN, IS A COSTIMULUS FOR THE INDUCTION OF REACTIVE NITROGEN INTERMEDIATE PRODUCTION IN MURINE MACROPHAGES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; MESSENGER-RNA EXPRESSION; HUMAN-CELLS INVITRO; INTERFERON-GAMMA; EFFECTOR MECHANISM; NITRIC-OXIDE; L-ARGININE; IFN-GAMMA; ANTIMICROBIAL ACTIVITY; GENE-EXPRESSION AB In this study we investigated the effects of picolinic acid, a catabolite Of L-tryptophan, on the production Of L-arginine-derived reactive nitrogen intermediates in the murine macrophage cell line ANA-1. ANA-1 macrophages did not produce nitrite (NO2-) constitutively, but accumulated detectable levels of NO2- on exposure to IFN-gamma. Picolinic acid, although ineffective by itself, augmented IFN-gamma-induced NO2- production. The activity of picolinic acid was evident at 1 mM and reached its maximum at 4 mM. Picolinic acid also augmented the IFN-gamma-dependent expression of TNF-alpha mRNA, but did not appreciably affect the secretion of the TNF-alpha protein. Neutralizing concentrations of anti-TNF mAb completely abrogated IFN-gamma- and IFN-gamma plus rTNF-alpha-induced NO2- production in ANA-1 macrophages, but only decreased by approximately 50% the synergistic interaction between IFN-gamma and picolinic acid. Although IL-4 inhibited the expression of IFN-gamma plus picolinic acid-induced TNF-alpha mRNA and protein, it only partially suppressed picolinic acid-dependent NO2- production. Therefore, picolinic acid may affect NO2- production via both TNF-alpha-dependent and TNF-alpha-independent pathways. Overall, this study suggests that amino acid catabolites may be important for the activation and the expression of effector functions by murine macrophages, and provides the first evidence of a possible connection between tryptophan and arginine metabolism. C1 MCGILL UNIV,MONTREAL GEN HOSP,DEPT MED,MONTREAL H3G 1A4,QUEBEC,CANADA. RP MELILLO, G (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702, USA. RI varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 46 TC 50 Z9 50 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 MAY 1 PY 1993 VL 150 IS 9 BP 4031 EP 4040 PG 10 WC Immunology SC Immunology GA KY452 UT WOS:A1993KY45200038 PM 8473748 ER PT J AU HWU, P YANNELLI, J KRIEGLER, M ANDERSON, WF PEREZ, C CHIANG, Y SCHWARZ, S COWHERD, R DELGADO, C MULE, J ROSENBERG, SA AF HWU, P YANNELLI, J KRIEGLER, M ANDERSON, WF PEREZ, C CHIANG, Y SCHWARZ, S COWHERD, R DELGADO, C MULE, J ROSENBERG, SA TI FUNCTIONAL AND MOLECULAR CHARACTERIZATION OF TUMOR-INFILTRATING LYMPHOCYTES TRANSDUCED WITH TUMOR-NECROSIS-FACTOR-ALPHA CDNA FOR THE GENE-THERAPY OF CANCER IN HUMANS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID 3' UNTRANSLATED REGION; ACID BLOT ANALYZER; MESSENGER-RNA; PHASE-I; METASTATIC MELANOMA; RETROVIRUS VECTORS; RIBONUCLEIC-ACID; AUTOLOGOUS TUMOR; MURINE TUMORS; FACTOR TNF AB TNF is effective in causing the regression of selected murine tumors when administered at high concentrations. Therapeutic levels in humans cannot be obtained systemically, however, because of dose-limiting toxicity. The development of immunotherapy with IL-2 and tumor-infiltrating lymphocytes (TIL), which can accumulate at tumor sites in some patients, and of efficient retroviral techniques for gene transfer into eukaryotic cells has allowed new therapeutic approaches using TNF. We have retrovirally transduced human TIL with the gene for TNF in an attempt to deliver high concentrations of TNF to the tumor site without dose-limiting systemic toxicity. Successful gene insertion was confirmed by Southern hybridization in 16 of 16 transduced and selected TIL cultures from 15 different patients, with an estimated 28 to 93% transduced cells within each culture. Transduced selected TIL cultures produced greater amounts of TNF, compared with nontransduced controls, in 11 of 16 cultures evaluated. However, overall production of TNF was >30-fold lower, compared with a transduced and highly selected tumor cell line control (MEL-TNF). In addition, steady state levels of vector-derived transcript in nine of 10 transduced selected TIL cultures were <14% of the amount seen in the MEL-TNF control line. In an attempt to increase TNF production, TIL were tran5duced with a mutated form of TNF containing the IFN-gamma signal peptide in place of the transmembranous region, to enhance secretion into the endoplasmic reticulum. By using this vector, TNF production increased by an average of fivefold. These studies demonstrate that TIL can be genetically modified to express and secrete a protein for use in targeted cancer therapy but that partial expression blockades exist that prevent maximal cytokine production by introduced genes in TIL. C1 CHIRON CORP,EMERYVILLE,CA 94608. GENET THERAPY INC,GAITHERSBURG,MD 20878. NHLBI,BETHESDA,MD 20892. RP HWU, P (reprint author), NCI,SURG BRANCH,BLDG 10,ROOM 2B42,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 44 TC 117 Z9 120 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 MAY 1 PY 1993 VL 150 IS 9 BP 4104 EP 4115 PG 12 WC Immunology SC Immunology GA KY452 UT WOS:A1993KY45200045 PM 8473752 ER PT J AU MARINCOLA, FM BALKISSOON, J SCHWARTZENTRUBER, DJ HOM, SS CONCEPCION, R MARCUS, SG YANNELLI, J TOPALIAN, SL PARKINSON, DR ROSENBERG, SA AF MARINCOLA, FM BALKISSOON, J SCHWARTZENTRUBER, DJ HOM, SS CONCEPCION, R MARCUS, SG YANNELLI, J TOPALIAN, SL PARKINSON, DR ROSENBERG, SA TI HEMODYNAMIC-EFFECTS OF THE ADMINISTRATION OF TUMOR-INFILTRATING LYMPHOCYTES TO CANCER-PATIENTS SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE TUMOR-INFILTRATING LYMPHOCYTES; INTERLEUKIN-2; HEMODYNAMIC EFFECTS; SEPTIC SHOCK ID ACTIVATED KILLER CELLS; NECROSIS-FACTOR-ALPHA; SEPTIC SHOCK; RECOMBINANT INTERLEUKIN-2; METASTATIC MELANOMA; SERUM; IMMUNOTHERAPY; INDUCTION; SEPSIS; HUMANS AB Tumor-infiltrating lymphocytes (TILs) can mediate tumor regression in selected patients with advanced cancer. To study some of the physiological changes associated with TIL administration, hemodynamic effects were measured while 2 x 10(10) to 20 x 10(10) TILs (mean 10 +/- 1 x 10(10)) were infused into 22 patients. In 10 patients, the first bag of TILs was administered without any interleukin-2 (IL-2) in the infusion bag; subsequent bags in the same patients and all bags in the next 12 patients contained IL-2 in low concentrations (300,000 IU). Two hours following infusion (as compared with baseline), patients developed tachycardia (110 +/- 3.3 vs. 76 +/- 3.5 beats/min; p < 0.001), increased cardiac index (4.9 t 0.2 vs. 3.2 +/- 0.13 L/min/m2; p < 0.001), decreased systemic vascular resistance (677 +/- 37 vs. 1185 +/- 63 dyn/s/cm5; p < 0.001), and increased pulmonary artery diastolic pressure (15.9 +/- 1.4 vs. 10.6 +/- 1.1 mm Hg; p = 0.002). No significant changes in systemic blood pressure were noted. Analysis of data obtained in the 10 patients after infusion of the first bag of TILs (4.5 +/- 0.4 x 10(10)) without IL-2 present in the infusate revealed similar, though less severe, changes. No significant correlation was noted between in vitro production of tumor necrosis factor-alpha, interferon-gamma, and granulocyte-macrophage colony-stimulating factor by TILs and hemodynamic effects when administered to patients. These results indicate that TIL infusion can cause hemodynamic changes similar to those previously reported in patients undergoing IL-2 therapy. RP MARINCOLA, FM (reprint author), NCI,SURG BRANCH,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2B42,BETHESDA,MD 20892, USA. NR 26 TC 4 Z9 4 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 MAY PY 1993 VL 13 IS 4 BP 282 EP 288 DI 10.1097/00002371-199305000-00008 PG 7 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA LE340 UT WOS:A1993LE34000008 PM 8334112 ER PT J AU BANSAL, GP HATFIELD, JA DUNN, FE KRAMER, AA BRADY, F RIGGIN, CH COLLETT, MS YOSHIMOTO, K KAJIGAYA, S YOUNG, NS AF BANSAL, GP HATFIELD, JA DUNN, FE KRAMER, AA BRADY, F RIGGIN, CH COLLETT, MS YOSHIMOTO, K KAJIGAYA, S YOUNG, NS TI CANDIDATE RECOMBINANT VACCINE FOR HUMAN B19-PARVOVIRUS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID B19 PARVOVIRUS INFECTION; IMMUNE-RESPONSE; EMPTY CAPSIDS; BONE-MARROW; IDENTIFICATION; ANTIBODY; INVITRO; EPITOPE; ANEMIA; REGION AB Recombinant baculoviruses were used to produce human B19 parvovirus empty capsids composed of only VP2 and VP2 capsids containing 4%, 25%, 35%, or 41% VP1 protein. Immunogenicity of the purified capsids, formulated with or without adjuvant, was evaluated in mice, guinea pigs, and rabbits. Sera were analyzed for total anti-B19 parvovirus antibodies, antibodies specific to the region unique to the VP1 capsid protein, and virus neutralizing antibodies. A relationship was observed between the development of antibodies specific to sequences unique to the VP1 protein and virus neutralization. The polypeptide composition of the empty capsid immunogens appeared to be important for elicitation of potent virus neutralizing activity. VP2 capsid immunogens devoid of VP1 protein, or consisting of only 4% VP1, the composition of naturally occurring virions, were generally poor at eliciting high levels of virus neutralizing activity. Capsids consisting of greater-than-or-equal-to 25% VP1 protein efficiently and consistently provoked vigorous B19 virus neutralizing responses. Recombinant empty capsids enriched for the VP1 protein should serve as the basis for a human B19 parvovirus vaccine. C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. RP BANSAL, GP (reprint author), MEDIMMUNE INC,35 W WATKINS MILL RD,GAITHERSBURG,MD 20878, USA. NR 23 TC 90 Z9 92 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD MAY PY 1993 VL 167 IS 5 BP 1034 EP 1044 PG 11 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KZ499 UT WOS:A1993KZ49900007 PM 8486937 ER PT J AU STRAUS, SE SAVARESE, B TIGGES, M FREIFELD, AG KRAUSE, PR MARGOLIS, DM MEIER, JL PAAR, DP ADAIR, SF DINA, D DEKKER, C BURKE, RL AF STRAUS, SE SAVARESE, B TIGGES, M FREIFELD, AG KRAUSE, PR MARGOLIS, DM MEIER, JL PAAR, DP ADAIR, SF DINA, D DEKKER, C BURKE, RL TI INDUCTION AND ENHANCEMENT OF IMMUNE-RESPONSES TO HERPES-SIMPLEX VIRUS TYPE-2 IN HUMANS BY USE OF A RECOMBINATN GLYCOPROTEIN-D VACCINE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID RECURRENT GENITAL HERPES; FACTORS INFLUENCING EFFICACY; DOUBLE-BLIND TRIAL; ORAL ACYCLOVIR; MONOCLONAL-ANTIBODIES; LETHAL CHALLENGE; SUBUNIT VACCINE; INVIVO BEHAVIOR; DNA-SEQUENCE; GUINEA-PIGS AB A vaccine for a chronic or recurrent viral infection should induce immune responses that protect against primary disease or that augment preexisting defenses sufficiently to diminish the likelihood of disease recurrence or progression. Such a vaccine was sought for genital herpes, a sexually transmitted infection of epidemic proportion. Vaccine containing recombinant herpes simplex virus type 2 glycoprotein D expressed in CHO cells was given repeatedly and safely to 24 human volunteers. In previously uninfected subjects, the vaccine induced primary antigen-specific and neutralizing antibody responses nearing or exceeding those seen at entry in subjects with genital herpes. Primary cellular immune responses were also evoked. Vaccination of previously seropositive subjects boosted antibody titers to levels that remained, for greater-than-or-equal-to 1 year, severalfold above those attained in recurrent genital herpes. Either the quantity or mode of presentation of antigen permitted this vaccine to exhibit previously unachieved immunogenicity, which may prove adequate for antiviral immunoprophylaxis or treatment of genital herpes. C1 CHIRON CORP,EMERYVILLE,CA. RP STRAUS, SE (reprint author), NIAID,CLIN INVEST LAB,BLDG 10,RM 11N228,BETHESDA,MD 20892, USA. NR 58 TC 52 Z9 53 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD MAY PY 1993 VL 167 IS 5 BP 1045 EP 1052 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KZ499 UT WOS:A1993KZ49900008 PM 8387560 ER PT J AU QUINN, TC KLINE, R MOSS, MW LIVINGSTON, RA HUTTON, N AF QUINN, TC KLINE, R MOSS, MW LIVINGSTON, RA HUTTON, N TI ACID DISSOCIATION OF IMMUNE-COMPLEXES IMPROVES DIAGNOSTIC UTILITY OF P24 ANTIGEN-DETECTION IN PERINATALLY ACQUIRED HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID HIV-INFECTION; CHILDREN; DISEASE; ZIDOVUDINE; TRIAL; ASSAY AB Since acid treatment of serum is known to disrupt immune complexes, the diagnostic utility of the p24 antigen assay was examined after acid treatment of 345 serum samples from 158 children born to women infected with human immunodeficiency virus (HIV). Although the p24 antigen assay after acid treatment was negative in 9 HIV-1-infected children <1 week old, antigen was detectable at high levels in all 30 samples obtained from infected children 1-9 months old. Overall, antigen was positive in 145 (sensitivity 89.5%) of 162 samples from 47 HIV-1-infected children greater-than-or-equal-to 1 month old. In contrast, the sensitivity of the p24 antigen assay without acid dissociation was only 18% (P < .001). Among the 76 uninfected children, 132 (specificity 99.2%) of 133 specimens were p24 antigen-negative after acid dissociation. These results demonstrate that acid treatment of serum markedly improves the sensitivity and predictive value of the p24 antigen assay for diagnosis of perinatally acquired HIV-1 infection in children 1 month of age or older. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP QUINN, TC (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT MED,ROSS RES BLDG,SUITE 1159,720 RUTLAND AVE,BALTIMORE,MD 21205, USA. FU NCRR NIH HHS [RR-0052]; NIAID NIH HHS [AI-27565]; NINR NIH HHS [NR-02069] NR 15 TC 37 Z9 37 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD MAY PY 1993 VL 167 IS 5 BP 1193 EP 1196 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KZ499 UT WOS:A1993KZ49900031 PM 8486954 ER PT J AU JU, WD SCHILLER, JT KAZEMPOUR, MK LOWY, DR AF JU, WD SCHILLER, JT KAZEMPOUR, MK LOWY, DR TI TGF-ALPHA ENHANCES LOCOMOTION OF CULTURED HUMAN KERATINOCYTES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID GROWTH-FACTOR-ALPHA; PSORIATIC EPIDERMIS; CELL-SURFACE; PRECURSOR; DIFFERENTIATION; EXPRESSION; INDUCTION; MIGRATION; AUTOCRINE; RECEPTORS AB A cDNA sequence coding for the full-length human transforming growth factor alpha (TGFalpha) precursor protein was introduced into and transcribed in cultured human keratinocytes, using a high-titer, high-expression, murine amphotropic retrovirus. Keratinocytes were shown capable of post-translationally modifying the TGFalpha primary translation product, with the subsequent formation of several cell-associated and secreted forms of TGFalpha, at least five of which, including the 50 amino acid mature species, can potentially bind and activate the epidermal growth factor receptor. Cells overexpressing the TGFalpha gene assumed a spindled morphology with long, bipolar filamentous processes and displayed increased locomotion. The soluble, mature form of TGFalpha alone also could induce the observed changes in cell shape and motility when added to keratinocyte cultures exogenously. The effects were dose dependent, and up to fourfold increases in locomotion were caused by TGFalpha in the absence of bovine pituitary extract (BPE). The addition of BPE to high concentrations of TGFalpha further enhanced keratinocyte motility to eightfold over baseline, suggesting a synergistic interaction between the two factors. These experiments demonstrate that keratinocytes can synthesize several forms of TGFalpha and that TGFalpha, besides being mitogenic, may have other important regulatory functions in keratinocytes. C1 US FDA,DIV BIOMETR,ROCKVILLE,MD 20857. NCI,CELLULAR ONCOL LAB,ROCKVILLE,MD. NR 42 TC 19 Z9 19 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD MAY PY 1993 VL 100 IS 5 BP 628 EP 632 PG 5 WC Dermatology SC Dermatology GA LA730 UT WOS:A1993LA73000004 PM 8491985 ER PT J AU PAMUKCU, R SPIEGEL, AM CHANG, EB AF PAMUKCU, R SPIEGEL, AM CHANG, EB TI BIOCHEMICAL AND IMMUNOCHEMICAL LOCALIZATION OF GTP-BINDING PROTEINS IN THE RAT ILEAL ENTEROCYTE SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Article ID INTESTINAL EPITHELIAL-CELL; PERTUSSIS TOXIN SUBSTRATE; ISLET-ACTIVATING PROTEIN; ADENYLATE-CYCLASE; GUANINE-NUCLEOTIDE; CHOLERA-TOXIN; SURFACE-MEMBRANE; ALPHA-SUBUNITS; FAMILY; IDENTIFICATION AB This study characterizes the distribution of various guanosine triphosphate-binding proteins (G proteins) in rat intestinal epithelial membranes. Enriched basolateral membranes were prepared from isolated enterocytes through differential density centrifugation; apical membranes were prepared with a chaotropic agent. Enrichment and purity of the membrane fractions were assessed by various biochemical markers. G proteins were identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis after adenosine diphosphate ribosylation in the presence of pertussis or cholera toxins. Western blotting was performed with the use of highly specific antibodies against the following subunits: alphaG(s), alphaG1(1 or 2), alphaG1(3), alphaG(o), alphaG(z), and beta subunits. Adenosine diphosphate ribosylation catalyzed by cholera toxins revealed two major substrates of molecular weights 47 and 43 kd in only the crude and basolateral fractions. The reaction catalyzed by pertussis toxin revealed a 41 kd substrate in the crude and basolateral fractions and a 40 kd substrate in the apical traction. Immunoblotting confirmed the presence of alphaG(s), alphaG1(1 or 2), and alphaG1(3) but failed to identify alphaG(o) or alphaG(z) subunits in the basolateral fraction; none of these subunits were identified in the apical fraction. Beta subunits were identified in both apical and basolateral fractions. These findings suggest selective sorting of the G proteins to regional domains in the plasma membrane of intestinal epithelial cells. The presence of previously unidentified G proteins is also suggested. C1 NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD. UNIV CHICAGO,DEPT MED,DIV DIGEST DIS,CHICAGO,IL 60637. RP PAMUKCU, R (reprint author), UNIV CINCINNATI,COLL MED,DEPT MED,DIV DIGEST DIS,231 BETHESDA AVE,ML 595,CINCINNATI,OH 45267, USA. NR 43 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-2143 J9 J LAB CLIN MED JI J. Lab. Clin. Med. PD MAY PY 1993 VL 121 IS 5 BP 689 EP 696 PG 8 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA LA302 UT WOS:A1993LA30200012 PM 8478596 ER PT J AU MOATS, LC LYON, GR AF MOATS, LC LYON, GR TI LEARNING-DISABILITIES IN THE UNITED-STATES - ADVOCACY, SCIENCE, AND THE FUTURE OF THE FIELD SO JOURNAL OF LEARNING DISABILITIES LA English DT Article ID EDUCATION DEPARTMENTS; SHARED RESPONSIBILITY; READING-DISABILITY; DEFINITION; IRRELEVANT; CHILDREN; CRITERIA; IQ AB This overview offers a perspective on the distinguishing characteristics, past and present, of the LD field in the United States. The discussion focuses on the complex relationships that exist among the social and political forces that have molded the field, advocacy, and research and teaching practices. It emphasizes the compelling need to establish clinical and scientific validation of LD, to preserve the hard-won achievements of advocacy. C1 DARTMOUTH COLL,HANOVER,NH 03755. ST MICHAELS COLL,WINOOSKI,VT 05404. NICHHD,HUMAN LEARNING & BEH BRANCH,LEARNING DISABIL RES PROGRAM,BETHESDA,MD 20892. NR 93 TC 41 Z9 42 U1 3 U2 5 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 SN 0022-2194 J9 J LEARN DISABIL JI J. Learn. Disabil. PD MAY PY 1993 VL 26 IS 5 BP 282 EP 294 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA KZ717 UT WOS:A1993KZ71700001 PM 8492047 ER PT J AU BROONER, RK HERBST, JH SCHMIDT, CW BIGELOW, GE COSTA, PT AF BROONER, RK HERBST, JH SCHMIDT, CW BIGELOW, GE COSTA, PT TI ANTISOCIAL PERSONALITY-DISORDER AMONG DRUG-ABUSERS - RELATIONS TO OTHER PERSONALITY DIAGNOSES AND THE 5-FACTOR MODEL OF PERSONALITY SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID ADDICTS AB Antisocial personality disorder among drug abusers has been associated with poor drug abuse treatment outcome and greater human immunodeficiency virus infection risk compared with drug abusers without the disorder. Despite this, less is known about the personality trait dimensions of antisocial drug abusers, or about the prevalence of axis II comorbidity among this group. Similarly, little is known about the personality trait dimensions of antisocial drug abusers compared with those with axis II diagnoses other than antisocial or those with no personality diagnosis. The present study compared the personality traits of 203 outpatient opioid drug abusers categorized into either a pure antisocial group (i.e., antisocial diagnosis only), mixed antisocial group (i.e., antisocial plus another axis II diagnosis), other axis II group (i.e., axis II diagnosis other than antisocial), or a non-axis II group. Psychiatric diagnoses were made using a structured interview and personality traits of the four groups were compared using a self-report measure of the five-factor model of personality. As predicted, the mixed group was significantly more prone to neuroticism compared with the pure group, with higher scores on the vulnerability to stress and hostility facets. The mixed group also had a greater score on the neuroticism domain compared with the non-axis II group, with higher scores on five of the six facets. Significant differences were also found on agreeableness. The mixed group had lower scores on this domain (i.e., had higher interpersonal antagonism) compared with the non-axis II group. Somewhat surprisingly, the agreeableness score for the pure group was not significantly different from those of the remaining three groups. Also, no significant differences were found on the personality domains of extraversion, openness to experience, or conscientiousness among any of the four groups. C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. FU NIDA NIH HHS [DA05127, DA05569] NR 21 TC 59 Z9 59 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD MAY PY 1993 VL 181 IS 5 BP 313 EP 319 DI 10.1097/00005053-199305000-00007 PG 7 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LC601 UT WOS:A1993LC60100007 PM 8501448 ER PT J AU NEWCOMER, S AF NEWCOMER, S TI PREVENTING ADOLESCENT PREGNANCY - MILLER,BC, CARD,JJ, PAIKOFF,RL, PETERSON,JL SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Book Review RP NEWCOMER, S (reprint author), NICHHD,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD MAY PY 1993 VL 181 IS 5 BP 336 EP 336 DI 10.1097/00005053-199305000-00022 PG 1 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LC601 UT WOS:A1993LC60100022 ER PT J AU LIPP, HP WOLFER, DP QIN, WX KLEE, CB HEIZMANN, CW AF LIPP, HP WOLFER, DP QIN, WX KLEE, CB HEIZMANN, CW TI CBP-18, A CA-2+-BINDING PROTEIN IN RAT-BRAIN - TISSUE DISTRIBUTION AND LOCALIZATION SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE BRAIN; CALCIUM-BINDING PROTEINS; IMMUNOHISTOCHEMISTRY; PARVALBUMIN; CBP-18; CALBINDIN ID CALCIUM-BINDING PROTEINS; HIPPOCAMPUS CA1 REGION; MAIN OLFACTORY-BULB; GABAERGIC NEURONS; NERVOUS-SYSTEM; PARVALBUMIN; IMMUNOREACTIVITY; COEXISTENCE; CALRETININ; MEMBRANE AB The distribution of a novel calcium-binding protein with a molecular mass of 18 kDa (CBP-18) in the rat brain was studied by means of biochemical methods and immunohistochemistry on cryostat-sectioned tissue and compared with staining patterns of parvalbumin on adjacent sections. The biochemical analysis revealed high levels of CPB-18 in cortex and cerebellum, low levels in the lungs, and undetectable levels in all other tissues tested. Immunohistochemically, the polyclonal rabbit-derived antibody for CPB-18 showed selective affinity with periglomerular cells and dendrites in the olfactory bulb. Distinct immunostaining of scattered cells and their proximal dendrites was found in the anterior olfactory nuclei and in the perirhinal and entorhinal cortex. Strong staining of neuropil with recognizable but diffusely outlined cells was observed in the retrosplenial cortex, central amygdala, hippocampal rudiment, septum, area preoptica, hypothalamus, colliculus superior, and parabrachial nuclei. The cerebellum showed strong neuropil staining of both the molecular and the granule cell layer. Less intense neuropil staining and a few scattered cells were found in the neocortex, the remaining basal forebrain, and in the entire brainstem. Immunoreactivity was barely detectable or missing in the striatum, the hippocampus, the thalamus, and in the colliculus inferior. Thus, CPB-18 shows a unique staining pattern in the CNS, different from all other Ca2+-binding proteins studied so far. C1 UNIV ZURICH,DEPT PEDIAT,DIV CLIN CHEM,STEINWIESSTR 75,CH-8032 ZURICH,SWITZERLAND. NCI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV ZURICH,INST ANAT,DIV CLIN CHEM,CH-8032 ZURICH,SWITZERLAND. RI Wolfer, David/B-3293-2016 OI Wolfer, David/0000-0002-5957-1401 NR 29 TC 6 Z9 6 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 MAY PY 1993 VL 60 IS 5 BP 1639 EP 1649 DI 10.1111/j.1471-4159.1993.tb13386.x PG 11 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KY255 UT WOS:A1993KY25500006 PM 8473888 ER PT J AU PAYZA, K YANG, HYT AF PAYZA, K YANG, HYT TI MODULATION OF NEUROPEPTIDE-FF RECEPTORS BY GUANINE-NUCLEOTIDES AND CATIONS IN MEMBRANES OF RAT-BRAIN AND SPINAL-CORD SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE FMRFAMIDE; TOLERANCE; DEPENDENCE; ADDICTION; ANALGESIA; MORPHINE ID FMRFAMIDE RECEPTORS; BINDING; MORPHINE; INHIBITION; PROTEINS; PEPTIDE AB Using a radioligand binding assay, we examined ionic modulation and G protein coupling of neuropeptide FF (NPFF) receptors in membranes of rat brain and spinal cord. We found that NaCl (but not KCl or LiCl) and MgCl2 increased specific I-125-YLFQPQRFamide (I-125-Y8Fa) binding to NPFF receptors in both tissues in a dose-dependent manner, with optimal conditions being 60 mM NaCl and 1 mM MgCl2. Guanine nucleotides dose-dependently inhibited specific I-125-Y8Fa binding to rat brain and spinal cord membranes with maximal effects of 64 +/- 6 and 71 +/- 2%, respectively. The order of potency was nonhydrolyzable GTP analogues > GTP greater-than-or-equal-to GDP much greater than GMP, ATP. The guanine nucleotide inhibition was observed in the absence and presence of NaCl and MgCl2. The mechanism of inhibition in spinal cord membranes appeared to be a reduction in the number of NPFF receptors; in one experiment, control K(D) and B(max) values were 0.068 nM and 7.2 fmol/mg of protein, respectively, and with 0.1 muM guanylylimidodiphosphate the respective values were 0.081 nM and 4.9 fmol/mg, a 32% reduction in receptor number. Similar results were obtained with guanosine 5'-O-(3-thiotriphosphate). Our data suggest that I-125-Y8Fa binding sites in rat CNS are G protein-coupled NPFF receptors regulated by GTP and cations. RP PAYZA, K (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,BIOCHEM GENET LAB,WASHINGTON,DC 20032, USA. NR 25 TC 32 Z9 32 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 MAY PY 1993 VL 60 IS 5 BP 1894 EP 1899 DI 10.1111/j.1471-4159.1993.tb13417.x PG 6 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KY255 UT WOS:A1993KY25500037 PM 8386227 ER PT J AU STOLL, J WADHWANI, KC SMITH, QR AF STOLL, J WADHWANI, KC SMITH, QR TI IDENTIFICATION OF THE CATIONIC AMINO-ACID TRANSPORTER (SYSTEM Y(+)) OF THE RAT-BLOOD BRAIN BARRIER SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE BLOOD BRAIN BARRIER; AMINO ACID TRANSPORT; LYSINE; ARGININE; ORNITHINE; CAPILLARIES; CHOROID PLEXUS ID ECOTROPIC RETROVIRUS RECEPTOR; CEREBROVASCULAR TRANSPORT; PERFUSION TECHNIQUE; MEMBRANE; KINETICS; PROTEIN; CELLS AB Cationic amino acids are transported from blood into brain by a saturable carrier at the blood-brain barrier (BBB). The transport properties of this carrier were examined in the rat using an in situ brain perfusion technique. Influx into brain via this system was found to be sodium independent and followed Michaelis-Menten kinetics with half-saturation constants (K(m)) of 50-100 muM and maximal transport rates of 22-26 nmol/min/g for L-lysine, L-arginine, and L-ornithine. The kinetic properties matched that of System y+, the sodium-independent cationic amino acid transporter, the cDNA for which has been cloned from the mouse. To determine if the cloned receptor is expressed at the BBB, we assayed RNA from rat cerebral microvessels and choroid plexus for the presence of the cloned transporter mRNA by RNase protection. The mRNA was present in both cerebral microvessels and choroid plexus and was enriched in microvessels 38-fold as compared with whole brain. The results indicate that System y+ is present at the BBB and that its mRNA is more densely expressed at cerebral microvessels than in whole brain. RP STOLL, J (reprint author), NIA,NEUROSCI LAB,BLDG 10,RM 6C-103,BETHESDA,MD 20892, USA. NR 18 TC 82 Z9 84 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD MAY PY 1993 VL 60 IS 5 BP 1956 EP 1959 DI 10.1111/j.1471-4159.1993.tb13428.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KY255 UT WOS:A1993KY25500048 PM 8473910 ER PT J AU FINIELSMARLIER, F MARINI, AM WILLIAMS, P PAUL, SM AF FINIELSMARLIER, F MARINI, AM WILLIAMS, P PAUL, SM TI THE N-METHYL-D-ASPARTATE ANTAGONIST MK-801 FAILS TO PROTECT DOPAMINERGIC-NEURONS FROM 1-METHYL-4-PHENYLPYRIDINIUM TOXICITY INVITRO SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE 1-METHYL-4-PHENYLPYRIDINIUM; MESENCEPHALIC CULTURES; DOPAMINERGIC NEURONS; N-METHYL-D-ASPARTATE RECEPTOR; MK-801 ID MONOAMINE-OXIDASE; RAT MESENCEPHALON; SUBSTANTIA-NIGRA; METABOLISM; BRAIN; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; GLUTAMATE; CULTURES AB Recent reports suggest that NMDA receptor antagonists when administered in vivo can protect dopaminergic neurons from the toxic actions of MPP+. In the present study the possible neuroprotective effects against MPP+ toxicity of the noncompetitive NMDA receptor antagonist MK-801 was studied in primary cultures of fetal rat mesencephalic dopamine neurons. MK-801 failed to protect dopaminergic neurons from MPP+ toxicity at concentrations that completely block NMDA-induced toxicity of these same neurons. In contrast to work carried out in cerebellar granule cells, MPP+ toxicity of mesencephalic dopamine neurons was unaffected by preexposure to subtoxic concentrations of either NMDA or cycloheximide. Our findings suggest that the toxic effects of MPP+ on dopaminergic neurons are not mediated through a direct interaction with the NMDA subtype of glutamate receptor. C1 NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL BRANCH,BLDG 10,ROOM 4N224,BETHESDA,MD 20892. NR 18 TC 26 Z9 27 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 MAY PY 1993 VL 60 IS 5 BP 1968 EP 1971 DI 10.1111/j.1471-4159.1993.tb13431.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KY255 UT WOS:A1993KY25500051 PM 8473912 ER PT J AU GOLDMUNTZ, EA WILDER, RL GOLDFARB, Y CASH, JM ZHA, HB CROFFORD, LJ MATHERN, P HANSEN, CT REMMERS, EF AF GOLDMUNTZ, EA WILDER, RL GOLDFARB, Y CASH, JM ZHA, HB CROFFORD, LJ MATHERN, P HANSEN, CT REMMERS, EF TI THE ORIGIN OF THE AUTOIMMUNE DISEASE-RESISTANT LER RAT - AN OUTCROSS BETWEEN THE BUFFALO AND AUTOIMMUNE DISEASE-PRONE LEWIS INBRED RAT STRAINS SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Note DE LEWIS RAT; LEWIS RESISTANT RAT; BUFFALO RAT; AUTOIMMUNITY; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; GENETIC-RESISTANCE; INDUCED ARTHRITIS; R RATS; SUSCEPTIBILITY; POLYARTHRITIS; UVEITIS; EAE AB The Lewis (LEW) rat strain is highly susceptible to a large number of experimentally induced inflammatory and autoimmune diseases. The Lewis resistant (LER) rat strain, which reportedly arose as a spontaneous mutation in a closed colony of LEW rats, is resistant to many of these disorders. The mechanism of resistance is not yet clear. We report the analysis of 19 simple dinucleotide repeat polymorphisms in 13 rat strains including the LEW/N and LER/N rat strains. The LEW/N and LER/N alleles were the same in only 42% of cases. For all of the other polymorphisms, the LER/N and Buffalo (BUF/N) rat strain alleles were identical. These data provide evidence that the LER strain did not arise as a spontaneous mutation in the LEW strain but is the result of an outcross between the LEW and BUF rat strains. The LER rat strain is now a recombinant inbred rat strain. This information should facilitate the genetic analysis of the loci responsible for resistance to experimental autoimmune disease in the LER rat. C1 NIH,VET RESOURCES BRANCH,GENET RESOURCE SECT,BETHESDA,MD 20892. RP GOLDMUNTZ, EA (reprint author), NIAMSD,ARTHRITIS & RHEUMATISM BRANCH,BLDG 10,RM 9N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Crofford, Leslie/J-8010-2013 NR 22 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD MAY PY 1993 VL 44 IS 2 BP 215 EP 219 DI 10.1016/0165-5728(93)90046-2 PG 5 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA LF090 UT WOS:A1993LF09000013 PM 8505411 ER PT J AU KAMBOURIS, M SANGAMESWARAN, L TRIARHOU, LC KOZAK, CA DLOUHY, SR GHETTI, B HODES, ME AF KAMBOURIS, M SANGAMESWARAN, L TRIARHOU, LC KOZAK, CA DLOUHY, SR GHETTI, B HODES, ME TI MOLECULAR CHARACTERIZATION OF 2 NOVEL CDNAS OBTAINED BY ANTIBODY SCREENING OF A MOUSE CEREBELLAR CDNA EXPRESSION LIBRARY SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 INDIANA UNIV,MED CTR,INDIANAPOLIS,IN 46204. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1993 VL 52 IS 3 BP 287 EP 287 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA LB785 UT WOS:A1993LB78500105 ER PT J AU PETERSEN, RB GOLDFARB, L TABATON, M BROWN, P LEBLANC, A MONTAGNA, P CORTELLI, P MONARI, L AUTILIOGAMBETTI, L GAJDUSEK, DC LUGARESI, E GAMBETTI, P AF PETERSEN, RB GOLDFARB, L TABATON, M BROWN, P LEBLANC, A MONTAGNA, P CORTELLI, P MONARI, L AUTILIOGAMBETTI, L GAJDUSEK, DC LUGARESI, E GAMBETTI, P TI EFFECT OF A POLYMORPHISM ON THE PATHOGENIC 178ASN MUTATION IN THE PRION PROTEIN GENE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 CASE WESTERN RESERVE UNIV,INST PATHOL,CLEVELAND,OH 44106. NIH,BETHESDA,MD 20892. UNIV BOLOGNA,INST NEUROL,I-40126 BOLOGNA,ITALY. RI Petersen, Robert/B-5075-2011 OI Petersen, Robert/0000-0002-3154-0072 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1993 VL 52 IS 3 BP 293 EP 293 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA LB785 UT WOS:A1993LB78500130 ER PT J AU SMITH, MA KALARIA, RN JACOBOWITZ, DM PERRY, G AF SMITH, MA KALARIA, RN JACOBOWITZ, DM PERRY, G TI ALPHA(1)-CHYMOTRYPSIN AND ALPHA(1)-TRYPSIN IMMUNOLOCALIZE WITH NEUROFIBRILLARY TANGLES AND SENILE PLAQUES OF ALZHEIMER-DISEASE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. NIMH,BETHESDA,MD 20892. RI Smith, Mark/A-9053-2009; Perry, George/A-8611-2009 OI Perry, George/0000-0002-6547-0172 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1993 VL 52 IS 3 BP 303 EP 303 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA LB785 UT WOS:A1993LB78500172 ER PT J AU ACHIM, CL MASLIAH, E GE, N HEYES, MP WANG, R MINERS, D WILEY, CA AF ACHIM, CL MASLIAH, E GE, N HEYES, MP WANG, R MINERS, D WILEY, CA TI IMMUNE ACTIVATION AND NEUROLOGIC DAMAGE IN HIV ENCEPHALITIS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. NIMH,BETHESDA,MD 20892. NR 0 TC 5 Z9 5 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1993 VL 52 IS 3 BP 315 EP 315 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA LB785 UT WOS:A1993LB78500217 ER PT J AU LIU, X YAO, DL BONDY, CA BRENNER, MB ZHOU, J WEBSTER, HD AF LIU, X YAO, DL BONDY, CA BRENNER, MB ZHOU, J WEBSTER, HD TI REACTIVE ASTROCYTES PRODUCE IGF-I DURING EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS (EAE) SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 NINCDS,BETHESDA,MD 20892. NICHHD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1993 VL 52 IS 3 BP 330 EP 330 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA LB785 UT WOS:A1993LB78500279 ER PT J AU SAVORY, J HERMAN, MM WILLS, MR AF SAVORY, J HERMAN, MM WILLS, MR TI REVERSAL OF ALUMINUM-INDUCED NEURODEGENERATION BY DESFERRIOXAMINE IN ADULT MALE RABBITS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 UNIV VIRGINIA,HLTH SCI CTR,CHARLOTTESVILLE,VA 22903. NIMH,ST ELIZABETHS,CTR NEUROSCI,WASHINGTON,DC 20032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1993 VL 52 IS 3 BP 333 EP 333 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA LB785 UT WOS:A1993LB78500288 ER PT J AU HUNTER, C PETRALIA, RS VU, T WENTHOLD, RJ AF HUNTER, C PETRALIA, RS VU, T WENTHOLD, RJ TI EXPRESSION OF AMPA-SELECTIVE GLUTAMATE RECEPTOR SUBUNITS IN MORPHOLOGICALLY DEFINED NEURONS OF THE MAMMALIAN COCHLEAR NUCLEUS SO JOURNAL OF NEUROSCIENCE LA English DT Article DE GLUTAMATE RECEPTOR; INSITU HYBRIDIZATION; COCHLEAR NUCLEUS; RAT; AUDITORY SYSTEM; CELL-SPECIFIC MESSENGER RNA ID D-ASPARTATE RECEPTORS; GRANULE CELLS; GUINEA-PIG; HORSERADISH-PEROXIDASE; FUNCTIONAL EXPRESSION; SYNAPTIC TRANSMISSION; ANTERIOR DIVISION; CA2+ PERMEABILITY; KAINATE RECEPTOR; SPIRAL GANGLION AB Glutamate and related amino acids mediate fast excitatory neurotransmission in the vertebrate CNS via ligand-gated cationic channels in the neuronal membrane. These channels are composed of different subunits that assemble into a functional receptor/channel complex. Although studies have shown that these subunits are differentially expressed in neurons, few studies have quantitatively addressed the cell-specific expression of glutamate subunits in relation to known glutamatergic pathways. In the vertebrate auditory system, glutamate is the proposed neurotransmitter of the auditory nerve and parallel fiber pathways. In situ hybridization histochemistry was used to localize AMPA-selective glutamate receptor subunit mRNAs in seven cell types of the rat cochlear nucleus. GluR1-GluR4 AMPA-selective subunits were all expressed in cochlear nucleus neurons; however, the subunits expressed in identified cells varied with the cell type. Granule cells, previously not known to receive glutamatergic input, expressed GluR2 and GluR4 subunits. Cartwheel and stellate interneurons in the dorsal cochlear nucleus, which receive parallel fiber input, expressed all four subunits. Neurons receiving synaptic input from the auditory nerve, including globular, round, spherical, and fusiform cells, expressed GluR2, GluR3, and GluR4 subunits. Furthermore, a subpopulation of round cells in the ventral cochlear nucleus, and fusiform cells in the dorsal cochlear nucleus, expressed the GluR3 subunit at greatly reduced levels compared to neighboring cells. The results confirm the auditory nerve and parallel fiber pathways as glutamatergic and identify a third synaptic population, projecting to granule cells, which is likely glutamatergic. The data suggest that the composition of GluR1-GluR4 subunits on neurons in the cochlear nucleus may be related to presynaptic input; moreover, heterogeneous patterns of expression of the GluR3 subunit, in addition, suggest that variability in mRNA levels within one population of morphologically defined cells is present. RP HUNTER, C (reprint author), NIDCD,NEUROCHEM LAB,NEUROTRANSMITTER RECEPTOR BIOL SECT,BLDG 36,ROOM 5008,BETHESDA,MD 20892, USA. NR 85 TC 86 Z9 86 U1 0 U2 0 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD MAY PY 1993 VL 13 IS 5 BP 1932 EP 1946 PG 15 WC Neurosciences SC Neurosciences & Neurology GA KZ087 UT WOS:A1993KZ08700011 PM 7683046 ER PT J AU POLTORAK, M HERRANZ, AS WILLIAMS, J LAURETTI, L FREED, WJ AF POLTORAK, M HERRANZ, AS WILLIAMS, J LAURETTI, L FREED, WJ TI EFFECTS OF FRONTAL CORTICAL-LESIONS ON MOUSE STRIATUM - REORGANIZATION OF CELL RECOGNITION MOLECULE, GLIAL FIBER, AND SYNAPTIC PROTEIN EXPRESSION IN THE DORSOMEDIAL STRIATUM SO JOURNAL OF NEUROSCIENCE LA English DT Article DE CELL ADHESION MOLECULE; CELL RECOGNITION MOLECULE; CORTEX LESION; REGENERATION; REAFFERENTATION; SYNAPTIC REORGANIZATION; GLIOSIS; STRIATUM ID NEURONAL PROCESS OUTGROWTH; MESENCEPHALIC DOPAMINERGIC-NEURONS; NEURITE OUTGROWTH; SUBSTANTIA-NIGRA; PARKINSONS-DISEASE; NERVOUS-SYSTEM; ADHESION MOLECULE; ADRENAL-MEDULLA; N-CADHERIN; POTENT SUBSTRATE AB Brain injury induces trophic effects within adjacent tissue through an unknown molecular mechanism. One model of this lesion effect involves the enhanced outgrowth of neuronal processes from transplanted substantia nigra in animals with cerebral cortex lesions. Since cell recognition molecules are involved in the molecular mechanisms of contact between cells and surrounding extracellular matrix components, and are important in plasticity of the nervous system, we investigated changes in L1, N-CAM, and tenascin, as well as synapse-associated proteins and gliosis, in the striatum of mice with cortical lesions. The removal of somatosensory and motor cortex would be expected to produce changes predominantly in the dorsal striatum. Lesioned mice, however, showed a significant enhancement of both L1 and N-CAM immunostaining intensity only within the most medial-periventricular and dorsomedial parts of the striatum, as compared to the nonlesioned side. Tenascin expression was significantly decreased, but only in the most medial part of the striatum. The changes in intensity of immunostaining with L1, N-CAM, and tenascin did not diminish with time after lesioning. These changes in cell recognition molecule expression indicate a possible molecular basis of lesion-induced plasticity in neuronal circuits within the dorsomedial striatum. These changes were accompanied by decreased synapsin and synaptophysin expression, but without any significant change in neurofilament expression. In contrast, glial fibrillary acidic protein and vimentin immunoreactivities were increased in almost the entire striatum on the lesioned side. Therefore, the areas of changes in cell recognition molecule expression did not simply correlate to the increased astrogliosis or neuronal fiber damage. We postulate that the periventricular dorsomedial striatum is relatively sensitive to disturbances of corticostriatonigral circuits and, simultaneously, this striatal area has a unique ability to support and promote neurite growth. RP POLTORAK, M (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032, USA. NR 78 TC 34 Z9 35 U1 0 U2 0 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD MAY PY 1993 VL 13 IS 5 BP 2217 EP 2229 PG 13 WC Neurosciences SC Neurosciences & Neurology GA KZ087 UT WOS:A1993KZ08700033 PM 7683050 ER PT J AU SAUNDERS, RC OBOYLE, VJ AF SAUNDERS, RC OBOYLE, VJ TI REPAIR OF CRANIAL DEFECTS WITH TEFLON - A METHOD OF CRANIOPLASTY IN MONKEYS SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE CRANIOPLASTY; NEUROSURGERY; OPERATIVE TECHNIQUE; (MONKEY) AB Magnetic resonance imaging demonstrated the need for cranioplasty in experimental neurobehavioral studies with non-human primates. Postoperatively temporal lobes showed substantial deformation of the neocortex due to pressure from the overlying muscle. A new method of cranioplasty using teflon to cover a cranial defect has been developed. Teflon is easily shaped and fitted into place. This method is safe, allows for the natural shape of the brain, provides protection, and is compatible with imaging techniques. Cranioplasty with teflon should be considered whenever craniotomy is necessary for accessing the brain. C1 NIMH,CTR NEUROSCI,CLIN BRAUN DISORDERS BRANCH,WASHINGTON,DC 20032. NIMH,CTR NEUROSCI,NEUROPHYSIOL LAB,WASHINGTON,DC 20032. RP SAUNDERS, RC (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI CBDB,WASHINGTON,DC 20032, USA. NR 10 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 J9 J NEUROSCI METH JI J. Neurosci. Methods PD MAY PY 1993 VL 47 IS 3 BP 163 EP 167 DI 10.1016/0165-0270(93)90078-6 PG 5 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LG999 UT WOS:A1993LG99900001 PM 8271814 ER PT J AU LIPOSITS, Z BOHN, MC AF LIPOSITS, Z BOHN, MC TI ASSOCIATION OF GLUCOCORTICOID RECEPTOR IMMUNOREACTIVITY WITH CELL-MEMBRANE AND TRANSPORT VESICLES IN HIPPOCAMPAL AND HYPOTHALAMIC NEURONS OF THE RAT SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE ADRENALECTOMY; CORTICOSTERONE; ELECTRON MICROSCOPY; IMMUNOCYTOCHEMISTRY; SILVER INTENSIFICATION ID PARAVENTRICULAR NUCLEUS; CORTICOSTEROID RECEPTOR; BRAIN; EXCITABILITY; LOCALIZATION; HORMONES; INVITRO AB The aim of the present study was to reveal at the ultrastructural level cytoplasmic loci that display glucocorticoid receptor (GR) immunoreactivity in pyramidal neurons of the CA1 sector of the hippocampus and in cells of the medial parvicellular subnucleus of the hypothalamic paraventricular nucleus (PVN). Adrenalectomized male rats were injected intraperitoneally with corticosterone (CS) (1 mg/100 g bw) and sacrificed within 4 hr. Vibratome sections of the perfusion-fixed forebrains were processed for immunocytochemical detection of type 2 GR by means of the BuGr, anti-rat liver GR monoclonal antibody and silver-gold-intensified diaminobenzidine chromogen. The corticosterone administration gradually shifted the GR immunoreactivity (IR) from the cytoplasm to the nucleus. Samples taken 20-40 min after the steroid treatment demonstrated pyramidal cells expressing GR IR in both the cytoplasmic and nuclear pools. Although the chromatin-associated appearance of GR in the nucleus was identifiable at the light microscopic level, the nature of immunoreactive intracytoplasmic loci was not. Ultrastructural analysis of the cytoplasm indicated that fine silver-gold grains marking GR-immunoreactive sites associated with the plasma membrane and coated and regular vesicles. Noted occasionally beneath the plasma membrane of the cell bodies and dendrites, the vesicles also appeared at deeper locations in dendritic processes and around the cell nuclei. These results suggest that glucocorticoid receptors participate in signal transduction at the level of the cell membrane, as well as at the level of the genome in the cell nucleus. C1 UNIV ROCHESTER,MED CTR,DEPT NEUROBIOL & ANAT,ROCHESTER,NY 14642. RP LIPOSITS, Z (reprint author), NIEHS,LMIN,FUNCT MORPHOL SECT,BLDG 101,MAIL DROP C4-07,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU NINDS NIH HHS [NS-20832] NR 29 TC 53 Z9 54 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 MAY 1 PY 1993 VL 35 IS 1 BP 14 EP 19 DI 10.1002/jnr.490350103 PG 6 WC Neurosciences SC Neurosciences & Neurology GA LA019 UT WOS:A1993LA01900002 PM 8510182 ER PT J AU NOGUCHI, K DELEON, M NAHIN, RL SENBA, E RUDA, MA AF NOGUCHI, K DELEON, M NAHIN, RL SENBA, E RUDA, MA TI QUANTIFICATION OF AXOTOMY-INDUCED ALTERATION OF NEUROPEPTIDE MESSENGER-RNAS IN DORSAL-ROOT GANGLION NEURONS WITH SPECIAL REFERENCE TO NEUROPEPTIDE-Y MESSENGER-RNA AND THE EFFECTS OF NEONATAL CAPSAICIN TREATMENT SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE NERVE INJURY; GALANIN; VASOACTIVE INTESTINAL POLYPEPTIDE; SOMATOSTATIN; CALCITONIN GENE-RELATED PEPTIDE ID PRIMARY SENSORY NEURONS; GENE-RELATED PEPTIDE; NERVE GROWTH-FACTOR; RAT SPINAL-CORD; SUBSTANCE-P; SCIATIC-NERVE; PERIPHERAL AXOTOMY; (NPY)-LIKE IMMUNOREACTIVITY; DEVELOPMENTAL ALTERATIONS; NOCICEPTIVE THRESHOLD AB Alteration in mRNA expression in dorsal root ganglia (DRG) neurons encoding 5 neuropeptides was quantitatively compared in normal rats and in those neonatally treated with capsaicin, a selective neurotoxin which destroys a subpopulation of DRG neurons with unmyelinated axons. Adult rats received a unilateral transection of the sciatic nerve and were killed 7 days later. Oligonucleotide probes specific for the genes encoding neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), galanin (GAL), somatostatin (SOM), and calcitonin gene-related peptide (CGRP) were used for in situ hybridization and RNA blot analysis. Following the nerve cut, RNA blot analysis demonstrated a dramatic induction of NPY, VIP, and GAL mRNA levels from the undetectable constitutive level of expression. Conversely, CGRP and SOM mRNAs, which are constitutively expressed, were reduced 55% and 70%, respectively, following the nerve cut. A unimodal size distribution for neurons expressing NPY mRNA was determined, with a mean cross-sectional area of 1700 mum2 representing 24.4% of DRG neurons ipsilateral to the nerve cut. Neurons expressing VIP mRNA were mainly small sized, with a cross-sectional area of approximately 700 mum2, while those expressing GAL mRNA were both small (approximately 700 mum2) and medium (approximately 1,300 mum2) sized. The percentages of neurons expressing VIP or GAL mRNA were 19.9% and 33.7%, respectively. In neonatal capsaicin-treated rats, there was a 10% reduction in neurons expressing NPY mRNA, a 37% reduction for VIP, and a 27% for GAL mRNA compared to vehicle-treated rats after nerve cut. Capsaicin-sensitive neurons comprised 37% of CGRP neurons and 83% of SOM neurons. These observations suggest that NPY is primarily induced in myelinated primary afferent neurons, while VIP and GAL mRNA induction occurs in a mixed population, a sizeable percentage of which has unmyelinated axons. Additionally, SOM mRNA expression is associated mainly with unmyelinated primary afferents. C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,9000 ROCKVILLE PIKE,BLDG 30,RM B20,BETHESDA,MD 20892. WAKAYAMA MED COLL,DEPT ANAT & NEUROBIOL,WAKAYAMA,JAPAN. RI De Leon, Marino/A-6922-2009 OI De Leon, Marino/0000-0001-6576-785X NR 54 TC 129 Z9 130 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 MAY 1 PY 1993 VL 35 IS 1 BP 54 EP 66 DI 10.1002/jnr.490350108 PG 13 WC Neurosciences SC Neurosciences & Neurology GA LA019 UT WOS:A1993LA01900007 PM 7685398 ER PT J AU ZALEWSKI, AA KADOTA, Y AZZAM, NA AZZAM, RN AF ZALEWSKI, AA KADOTA, Y AZZAM, NA AZZAM, RN TI OBSERVATIONS ON THE BLOOD AND PERINEURIAL PERMEABILITY BARRIERS OF SURVIVING NERVE ALLOGRAFTS IN IMMUNODEFICIENT AND IMMUNOSUPPRESSED RATS SO JOURNAL OF NEUROSURGERY LA English DT Article DE NERVE REPAIR; NERVE TRANSPLANTATION; IMMUNOSUPPRESSION; CYCLOSPORINE-A; AXONAL REGENERATION; NERVE ANASTOMOSIS; PERINEURIUM; RAT ID PERIPHERAL-NERVE; CYCLOSPORIN-A; WALLERIAN DEGENERATION; VASCULAR-PERMEABILITY; SCIATIC-NERVE; LONG-TERM; REJECTION; CESSATION; VESSELS AB The authors investigate whether there are any permeability changes in the endoneurial blood-nerve barrier and the perineurium-nerve barrier of surviving nerve allografts. In a normal nerve. the blood-nerve barrier regulates the passage of substances from endoneurial blood vessels into the endoneurium, whereas the perineurium-nerve barrier protects the endoneurium from agents that escape from permeable epineurial vessels and accumulate around the nerve. Nerves from ACI rats were transplanted into immunologically deficient nude rats or normal Fischer rats immunosuppressed with cyclosporin A. None of the nerve allografts was rejected. The blood-nerve barrier of nerve allografts at 2 and 6 weeks postoperatively was permeable to intravenously injected horseradish peroxidase, which spread into endoneurial tissue. Electron microscopy revealed that horseradish peroxidase escaped from endoneurial vessels through intercellular junctions between endothelial cells. At 24 weeks, the blood-nerve barrier of nerve allografts had recovered and the endoneurial vessels, like those in normal nerves, were impermeable to horseradish peroxidase. The perineurium-nerve barrier of nerve allografts remained impermeable to horseradish peroxidase at all times. Axons were grouped into numerous minifascicles at nerve anastomosis zones at 24 weeks. Each nerve fascicle was surrounded by an impermeable perineurium. These results demonstrate that regenerated axons in long-term surviving nerve allografts and at anastomosis zones are protected by permeability barriers. It is concluded that permeability barriers of nerve allografts are not permanently altered by a foreign environment (grafts to nude rats) even when immunosuppression with cyclosporin A is required to prevent allograft rejection (grafts to Fischer rats). RP ZALEWSKI, AA (reprint author), NINCDS,NEURAL CONTROL LAB,BLDG 36 ROOM 4A-14,BETHESDA,MD 20892, USA. NR 32 TC 8 Z9 8 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD MAY PY 1993 VL 78 IS 5 BP 794 EP 806 DI 10.3171/jns.1993.78.5.0794 PG 13 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA KY468 UT WOS:A1993KY46800016 PM 8468610 ER PT J AU BACHARACH, SL VAQUERO, JJ MOK, DY DILSIZIAN, V AF BACHARACH, SL VAQUERO, JJ MOK, DY DILSIZIAN, V TI MYOCARDIAL THICKNESS BY GATED PET AND SPECT - VARIABILITY AND BIAS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Vaquero, Juan Jose/D-3033-2009 OI Vaquero, Juan Jose/0000-0001-9200-361X NR 0 TC 4 Z9 4 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P178 EP P178 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800715 ER PT J AU BARKER, WC SAFFER, JR BACHARACH, SL AF BARKER, WC SAFFER, JR BACHARACH, SL TI PLANAR ATTENUATION CORRECTION OF GEOMETRIC MEAN IMAGES - ACCURACY OF QUANTITATION SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P61 EP P61 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800237 ER PT J AU CAMERA, L KINUYA, S GARMESTANI, K BRECHBIEL, MW PAI, LH GANSOW, OA PASTAN, I PAIK, CH CARRASQUILLO, JA AF CAMERA, L KINUYA, S GARMESTANI, K BRECHBIEL, MW PAI, LH GANSOW, OA PASTAN, I PAIK, CH CARRASQUILLO, JA TI NEW BIFUNCTIONAL CHELATES FOR Y-90 LABELING OF MONOCLONAL-ANTIBODIES - COMPARATIVE BIODISTRIBUTION IN NONTUMOR BEARING NUDE-MICE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NCI,DEPT NUCL MED,C C RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. RI Carrasquillo, Jorge/E-7120-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P241 EP P241 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800980 ER PT J AU DAUBEWITHERSPOON, ME BACHARACH, SL GREEN, MV SEIDEL, J AF DAUBEWITHERSPOON, ME BACHARACH, SL GREEN, MV SEIDEL, J TI SPATIAL DEPENDENCE OF SCATTER ENERGY-SPECTRUM SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P177 EP P177 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800710 ER PT J AU DIVGI, CR SCOTT, AM MCDERMOTT, K FALLONE, PS CARMICHAEL, N HILTON, S SILER, K FINN, RD DAGHIGHIAN, F COHEN, AM SCHLOM, J LARSON, SM AF DIVGI, CR SCOTT, AM MCDERMOTT, K FALLONE, PS CARMICHAEL, N HILTON, S SILER, K FINN, RD DAGHIGHIAN, F COHEN, AM SCHLOM, J LARSON, SM TI CLINICAL COMPARISON OF RADIOLOCALIZATION OF 2 ANTI-TAG-72 MONOCLONAL-ANTIBODIES (MABS) SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P214 EP P214 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800868 ER PT J AU ESPOSITO, G VANHORN, JD WEINBERGER, DR BERMAN, KF AF ESPOSITO, G VANHORN, JD WEINBERGER, DR BERMAN, KF TI GENDER DIFFERENCES IN CEREBRAL BLOOD-FLOW WITH PET - IS THERE AN EFFECT OF COGNITIVE STATE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIMH,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P67 EP P68 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800264 ER PT J AU FALEN, SW MCAFEE, JG MINEAR, GS KEAST, RK TRENKLER, I PAIK, C SOOD, VK AF FALEN, SW MCAFEE, JG MINEAR, GS KEAST, RK TRENKLER, I PAIK, C SOOD, VK TI RADIOLABELED LYSOZYME AS A POTENTIAL IMAGING AGENT IN ACUTE TUBULAR-NECROSIS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P48 EP P49 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800187 ER PT J AU FANG, QW JEONG, JM LEE, JT SAGA, T LE, N PARK, SG SOOD, VK CARRASQUILLO, JA NEUMANN, RD REYNOLDS, JC REBA, RC PAIK, CH AF FANG, QW JEONG, JM LEE, JT SAGA, T LE, N PARK, SG SOOD, VK CARRASQUILLO, JA NEUMANN, RD REYNOLDS, JC REBA, RC PAIK, CH TI USE OF POLYLYSINE AS LINKER FOR TC-99M CHELATE AND BIOTIN SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. RI Sood, Vinay/B-7109-2008; Carrasquillo, Jorge/E-7120-2010; Jeong, Jae Min/E-2102-2012 OI Jeong, Jae Min/0000-0003-2611-6020 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P233 EP P233 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800946 ER PT J AU FLESHER, J SCHEFFEL, U LONDON, ED FROST, JJ AF FLESHER, J SCHEFFEL, U LONDON, ED FROST, JJ TI INVIVO LABELING OF NICOTINIC CHOLINERGIC RECEPTORS IN BRAIN USING [H-3] CYTISINE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIDA,ADDICT RES CTR,DEPT NEUROSCI,BALTIMORE,MD. NIDA,JOHNS HOPKINS MED INST,DEPT RADIOL,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P199 EP P199 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800805 ER PT J AU GREEN, MV SEIDEL, J STEIN, S KERTZMAN, C ZEFFIRO, T KEMPNER, KM AF GREEN, MV SEIDEL, J STEIN, S KERTZMAN, C ZEFFIRO, T KEMPNER, KM TI A CORRECTION STRATEGY FOR HEAD MOVEMENT DURING BRAIN IMAGING SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P70 EP P70 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800276 ER PT J AU HERSCOVITCH, P CARSON, RE STABIN, M STUBBS, JB AF HERSCOVITCH, P CARSON, RE STABIN, M STUBBS, JB TI A NEW KINETIC APPROACH TO ESTIMATE THE RADIATION-DOSIMETRY OF FLOW-BASED RADIOTRACERS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. OAK RIDGE ASSOCIATED UNIV,OAK RIDGE,TN 37830. RI Carson, Richard/H-3250-2011 OI Carson, Richard/0000-0002-9338-7966 NR 0 TC 4 Z9 5 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P155 EP P156 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800623 ER PT J AU KEAST, RK MCAFEE, JG AF KEAST, RK MCAFEE, JG TI CHANGES IN TC-99M-NANOCOLL MARROW LOCALIZATION AS A RESULT OF TREATMENT WITH RECOMBINANT HUMAN GRANULOCYTE-COLONY-STIMULATING FACTOR IN THE CANINE MODEL SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NIH,MED CTR,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P174 EP P174 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800699 ER PT J AU KINUYA, S JEONG, JM SAGA, T CAMERA, L CARRASQUILLO, JA NEUMANN, RD PAIK, CH AF KINUYA, S JEONG, JM SAGA, T CAMERA, L CARRASQUILLO, JA NEUMANN, RD PAIK, CH TI EFFECT OF DEGREE OF DTPA CONJUGATION PER MOAB ON METABOLISM AND CLEARANCE OF ITS IN-111 CHELATE IN MICE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Carrasquillo, Jorge/E-7120-2010; Jeong, Jae Min/E-2102-2012 OI Jeong, Jae Min/0000-0003-2611-6020 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P58 EP P59 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800228 ER PT J AU LEE, KS COPPOLA, R SAUNDERS, R GOREY, J HE, XS DECOSTA, BR BOWEN, WD SASSAMAN, MB RICE, KC WEINBERGER, DR AF LEE, KS COPPOLA, R SAUNDERS, R GOREY, J HE, XS DECOSTA, BR BOWEN, WD SASSAMAN, MB RICE, KC WEINBERGER, DR TI SPECT IMAGING OF SIGMA-RECEPTORS INVIVO IN PRIMATES SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIMH,CBDB,WASHINGTON,DC 20032. NIDDKD,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P235 EP P235 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800955 ER PT J AU LINE, BR GREEN, MV SCHAIBLE, T AF LINE, BR GREEN, MV SCHAIBLE, T TI REMOVAL OF EARLY NONSPECIFIC BLOOD POOL ACTIVITY FROM ANTIFIBRIN IMAGES - APPLICATION TO RAT MODEL OF PULMONARY-EMBOLISM SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 ALBANY MED CTR,ALBANY,NY. NIH,BETHESDA,MD 20892. CENTOCOR INC,MALVERN,PA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P178 EP P178 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800714 ER PT J AU MATTAY, VS BERMAN, KF OSTREM, JL VANHORN, JD BIGELOW, LB GOLDBERG, TE WEINBERGER, DR AF MATTAY, VS BERMAN, KF OSTREM, JL VANHORN, JD BIGELOW, LB GOLDBERG, TE WEINBERGER, DR TI THE EFFECT OF AMPHETAMINE ON REGIONAL CEREBRAL BLOOD-FLOW DURING COGNITIVE ACTIVATION - A PET STUDY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIMH,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P228 EP P228 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800925 ER PT J AU NGUYEN, T BACHARACH, SL BACHARACH, SL BARKER, WC SAFFER, JR CARRASQUILLO, JA AF NGUYEN, T BACHARACH, SL BACHARACH, SL BARKER, WC SAFFER, JR CARRASQUILLO, JA TI ALIGNMENT OF CT DATA WITH PLANAR NUCLEAR-MEDICINE IMAGES SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Carrasquillo, Jorge/E-7120-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P124 EP P125 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800498 ER PT J AU PHILLIPS, RL CHEN, C WONG, DF STAPLETON, JM LONDON, ED AF PHILLIPS, RL CHEN, C WONG, DF STAPLETON, JM LONDON, ED TI MODELING THE PLASMA ACTIVITY CURVE FOR PET MEASUREMENT OF REGIONAL CEREBRAL METABOLIC-RATE FOR GLUCOSE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NIDA,BALTIMORE,MD. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P40 EP P40 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800152 ER PT J AU PRICE, JC BACHARACH, SL FREEDMAN, N CARSON, RE AF PRICE, JC BACHARACH, SL FREEDMAN, N CARSON, RE TI NOISE-REDUCTION IN PET ATTENUATION CORRECTION BY MAXIMUM-LIKELIHOOD (ML) HISTOGRAM SHARPENING OF ATTENUATION IMAGES SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Carson, Richard/H-3250-2011 OI Carson, Richard/0000-0002-9338-7966 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P27 EP P27 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800101 ER PT J AU SAFFER, JR BARKER, WC BACHARACH, SL AF SAFFER, JR BARKER, WC BACHARACH, SL TI PLANAR ACTIVITY QUANTITATION USING LOW-RESOLUTION MEASURED ATTENUATION SCANS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P178 EP P178 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800717 ER PT J AU SAGA, T JEONG, JM WEINSTEIN, JN HEYA, T CASCIARI, J LEE, JT OWENS, E LE, N PAIK, CH NEUMANN, RD AF SAGA, T JEONG, JM WEINSTEIN, JN HEYA, T CASCIARI, J LEE, JT OWENS, E LE, N PAIK, CH NEUMANN, RD TI 2-STEP TARGETING OF EXPERIMENTAL LUNG METASTASES WITH BIOTINYLATED ANTIBODY AND RADIOLABELED STREPTAVIDIN SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NCI,DIV CANC TREATMENT,BETHESDA,MD 20892. NCI,DEPT NUCL MED,BETHESDA,MD 20892. RI Jeong, Jae Min/E-2102-2012 OI Jeong, Jae Min/0000-0003-2611-6020 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P215 EP P215 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800870 ER PT J AU SCOTT, AM SGOUROS, G DIVGI, CR ZHANG, JJ PENTLOW, K DAGHIGIAN, F WHEATLEY, J MACAPINLAC, H GRAHAM, MC KALAIGIAN, H SCHLOM, J LARSON, SM AF SCOTT, AM SGOUROS, G DIVGI, CR ZHANG, JJ PENTLOW, K DAGHIGIAN, F WHEATLEY, J MACAPINLAC, H GRAHAM, MC KALAIGIAN, H SCHLOM, J LARSON, SM TI CLINICAL IMPLEMENTATION OF COMBINED 3-D AND MIRD-BASED DOSIMETRY FOR RADIOIMMUNOTHERAPY WITH I-13I CC49 MONOCLONAL-ANTIBODY (MAB) SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. NCI,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P127 EP P127 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800508 ER PT J AU SEIDEL, J GREEN, MV BACHARACH, SL GANDLER, WR DAUBEWITHERSPOON, ME AF SEIDEL, J GREEN, MV BACHARACH, SL GANDLER, WR DAUBEWITHERSPOON, ME TI CORRECTION FOR COMPTON SCATTER BY CURVE FITTING THE PHOTOPEAK REGION OF ENERGY-SPECTRA ACQUIRED AT EVERY IMAGE POINT SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P60 EP P60 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800235 ER PT J AU YUNG, BCK DANNALS, RF KUHAR, MJ SHAYA, EK RAVERT, HT CHEN, C CHAN, B SCHEFFEL, U RICAURTE, G FOLIO, T WAGNER, HN NEUMEYER, M WONG, DF AF YUNG, BCK DANNALS, RF KUHAR, MJ SHAYA, EK RAVERT, HT CHEN, C CHAN, B SCHEFFEL, U RICAURTE, G FOLIO, T WAGNER, HN NEUMEYER, M WONG, DF TI INVIVO DOPAMINE TRANSPORTER SITES IMAGING IN HUMAN USING [C-11] WIN 35,428 POSITRON EMISSION TOMOGRAPHY (PET) SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,NIDA,ARC,SCH MED,BALTIMORE,MD 21218. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P197 EP P197 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800797 ER PT J AU EMMERSON, KS PHANG, JM AF EMMERSON, KS PHANG, JM TI HYDROLYSIS OF PROLINE DIPEPTIDES COMPLETELY FULFILLS THE PROLINE REQUIREMENT IN A PROLINE-AUXOTROPHIC CHINESE-HAMSTER OVARY CELL-LINE SO JOURNAL OF NUTRITION LA English DT Article DE CHINESE HAMSTER OVARY CELLS; PROLIDASE; PROLINE AUXOTROPH; IMIDODIPEPTIDES; AMINO ACIDS ID GLYCYL-L-PROLINE; PROLIDASE DEFICIENCY; INTESTINAL TRANSPORT; ACID; PLASMA; PYRROLINE-5-CARBOXYLATE; BIOSYNTHESIS; NUTRITION; MUCOSAL AB Proline- and hydroxyproline-containing oligopeptides may be important in protein nutrition because intestinal hydrolases are incapable of recognizing their imido bonds. Peripheral tissues have a cytosolic enzyme prolidase that cleaves dipeptides containing C-terminal proline (X-Pro) or hydroxyproline. The role of dipeptides in intracellular metabolism is uncertain. This study examined the ability of X-Pro to provide proline to the proline-auxotrophic cell line, CHO-K1. The action of prolidase on exogenously supplied Gly-Pro, the most abundant dipeptide product of digestion, provided adequate proline to support normal cell growth of CHO-K1 cells in a dose-dependent manner. The growth curve generated by addition of Gly-Pro to CHO-K1 cells was similar to that due to proline. Two other structurally unrelated X-Pro also supported growth indistinguishably from Gly-Pro. Gly-Hyp was completely ineffective for growth. The ability of X-Pro to sustain cultures of a proline-auxotrophic cell line may be important in elucidating intracellular nutritional and physiological functions for those dipeptides. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC PREVENT & CONTROL,NUTR & MOLEC REGULAT LAB,FREDERICK,MD 21702. NR 30 TC 51 Z9 51 U1 3 U2 3 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD MAY PY 1993 VL 123 IS 5 BP 909 EP 914 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA LB236 UT WOS:A1993LB23600017 PM 8487102 ER PT J AU ATKINSON, JC SCHIODT, M ROBATAILLE, S GREENSPAN, D GREENSPAN, JS FOX, PC AF ATKINSON, JC SCHIODT, M ROBATAILLE, S GREENSPAN, D GREENSPAN, JS FOX, PC TI SALIVARY AUTOANTIBODIES IN HIV-ASSOCIATED SALIVARY-GLAND DISEASE SO JOURNAL OF ORAL PATHOLOGY & MEDICINE LA English DT Article DE HIV-1; SALIVA; SJOGRENS SYNDROME; SS-A (RO); SS-B (LA) ID ACQUIRED IMMUNODEFICIENCY SYNDROME; SJOGRENS SYNDROME; RHEUMATOID FACTORS; PAROTID-GLAND; AIDS; ABNORMALITIES; ACTIVATION; PROTEINS; COMPLEX; VIRUS AB A subset of HIV-positive patients develops salivary gland disease (HIV-SGD), characterized by salivary gland enlargement and/or decreased salivary flow. While clinical symptoms are similar to Sjogren's syndrome (SS), patients with HIV-SGD lack circulating anti-SS-A/Ro and anti-SS-B/La. Occasionally, SS patients lacking circulating anti-SS-A/Ro and anti-SS-B/La have these antibodies in their saliva. Salivas from 11 patients with HIV-SGD, 13 HIV+ patients without HIV-SGD, 14 HIV-negative men controls, and 11 patients with SS were screened for autoantibodies. Five HIV-SGD salivas had antibodies recognizing the cytoplasm of a salivary cell line. No HIV+ controls showed reactivity. Ten of 11 SS patients had salivary autoantibodies, and one HIV-negative control was positive for them. Salivary anti-SS-A/Ro was present in 8/11 SS patients, and 7 also contained anti-SS-B/La. No HIV-SGD salivary samples had these specific autoantibodies. These findings suggest that while glandular polyclonal expansion occurs in both HIV-SGD and SS, different autoantibodies are produced. C1 FREDERIKSBORG CENT CTY HOSP,DEPT ORAL MED & ORAL SURG,HILLEROD,DENMARK. UNIV CALIF SAN FRANCISCO,DEPT STOMATOL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,CTR ORAL AIDS,SAN FRANCISCO,CA 94143. RP ATKINSON, JC (reprint author), NIDR,CLIN INVEST SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 1N-113,BETHESDA,MD 20892, USA. FU NIDCR NIH HHS [P01-DE07946] NR 26 TC 5 Z9 7 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0904-2512 J9 J ORAL PATHOL MED JI J. Oral Pathol. Med. PD MAY PY 1993 VL 22 IS 5 BP 203 EP 206 DI 10.1111/j.1600-0714.1993.tb01057.x PG 4 WC Dentistry, Oral Surgery & Medicine; Pathology SC Dentistry, Oral Surgery & Medicine; Pathology GA LG768 UT WOS:A1993LG76800002 PM 8315599 ER PT J AU DESIERRA, TM KUMAR, ML WASSER, TE MURPHY, BR SUBBARAO, EK AF DESIERRA, TM KUMAR, ML WASSER, TE MURPHY, BR SUBBARAO, EK TI RESPIRATORY SYNCYTIAL VIRUS-SPECIFIC IMMUNOGLOBULINS IN PRETERM INFANTS SO JOURNAL OF PEDIATRICS LA English DT Article ID G-GLYCOPROTEINS; FUSION PROTEIN; MONOCLONAL-ANTIBODIES; MATERNAL ANTIBODY; SUBCLASS RESPONSE; PRIMARY INFECTION; COTTON RATS; SERUM; AGE; PURIFICATION AB Incomplete transfer of maternal antibodies specific to respiratory syncytial virus (RSV) has been suggested as an explanation for the increased risk of RSV infections in preterm infants. Antibodies directed against the two major RSV envelope glycoproteins, F and G, are protective in vitro and in vivo. Our study was conducted to measure IgG, IgG1, IgG2, and IgG3 antibody titers against the RSV F and G glycoproteins in cord sera from infants born at different gestational ages. Titers of neutralizing antibody were measured in a subset of the subjects. The mean (+/- SEM) log2 titers of IgG antibodies directed against the RSV F and G glycoproteins were significantly lower in infants born at less-than-or-equal-to 28 weeks of gestation (11.2 and 10.8 for F and G glycoproteins, respectively) than in term infants (12.6 and 12.8 for F and G, respectively) (p < 0.05). Preterm infants born at greater-than-or-equal-to 29 weeks had titers of antibodies against the F glycoprotein comparable to those of term infants. The highest titers of RSV-specific antibodies were in the IgG1 and IgG2 subclasses. Mean (+/- SEM) neutralizing antibody titers were lower in infants born at less-than-or-equal-to 28 weeks (7.7 +/- 0.4) than in term infants (10.2 +/- 0.3) (p < 0.001). We conclude that (1) RSV-specific antibody titers were lower than in term infants only in the most premature infants (less-than-or-equal-to 28 weeks) and (2) preterm infants born at greater-than-or-equal-to 29 or greater-than-or-equal-to 33 weeks of gestation had RSV-specific titers against F and G glycoproteins, respectively, that were comparable to those of term infants. Preterm infants born at less-than-or-equal-to 28 weeks could represent a target population for passive immunoprophylaxis. C1 NIAID, BETHESDA, MD 20892 USA. METROHLTH MED CTR, CLEVELAND, OH USA. CASE WESTERN RESERVE UNIV, DIV NEONATOL, CLEVELAND, OH 44106 USA. CASE WESTERN RESERVE UNIV, DIV INFECT DIS, CLEVELAND, OH 44106 USA. CASE WESTERN RESERVE UNIV, DEPT PEDIAT, CLEVELAND, OH 44106 USA. NR 19 TC 36 Z9 37 U1 2 U2 2 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 MAY PY 1993 VL 122 IS 5 BP 787 EP 791 DI 10.1016/S0022-3476(06)80027-2 PN 1 PG 5 WC Pediatrics SC Pediatrics GA LC745 UT WOS:A1993LC74500024 PM 8496762 ER PT J AU WAHL, SM COSTA, GL MIZEL, DE ALLEN, JB SKALERIC, U MANGAN, DF AF WAHL, SM COSTA, GL MIZEL, DE ALLEN, JB SKALERIC, U MANGAN, DF TI ROLE OF TRANSFORMING GROWTH-FACTOR-BETA IN THE PATHOPHYSIOLOGY OF CHRONIC INFLAMMATION SO JOURNAL OF PERIODONTOLOGY LA English DT Article; Proceedings Paper CT SYMP ON CURRENT PERSPECTIVES ON MOLECULAR MEDIATORS OF INFLAMMATION AND PERIODONTAL PATHOLOGY CY JAN 30-31, 1992 CL MARCO ISLAND, FL DE CYTOKINES; PERIODONTAL DISEASES PATHOGENESIS; GROWTH FACTORS; CHEMOTAXIS; LYMPHOCYTES; MONOCYTES; NEUTROPHILS ID TGF-BETA; SYNOVIAL INFLAMMATION; PERIODONTAL-DISEASE; BONE-RESORPTION; HUMAN-PLATELETS; PURIFICATION; RECEPTORS; IDENTIFICATION; LYMPHOCYTES; STIMULATION AB TRANSFORMING GROWTH FACTOR BETA (TGF-beta), a cytokine identified in acute and chronic inflammatory sites, mediates leukocyte recruitment and activation essential to the development of such lesions. Released by platelets upon aggregation and by leukocytes stimulated with bacterial products or inflammatory mediators, TGF-beta has potent chemotactic activity for blood neutrophils, monocytes, and lymphocytes. By augmenting integrin expression, TGF-beta facilitates leukocyte adhesion to the vessel wall and extracellular matrix at the site of inflammation. Once within the inflammatory site, mononuclear cells are stimulated by TGF-beta to release cytokines important in the network of molecules regulating the host response to microorganisms and immunologic challenge. Thus, bacteria and their products, in addition to directly recruiting and activating leukocytes at sites of infection, indirectly influence these events through the induction of cytokines such as TGF-beta. By antagonizing the activity of TGF-beta with neutralizing antibodies, a causal relationship between this cytokine, inflammation, and pathogenesis has been demonstrated. Administration of anti-TGF-beta to sites of chronic destructive inflammation not only blocked leukocyte recruitment and activation, but also inhibited the subsequent destruction of bone and cartilage characteristic of such lesions. RP WAHL, SM (reprint author), NIDR,CELLULAR IMMUNOL SECT,BETHESDA,MD 20892, USA. NR 41 TC 60 Z9 64 U1 0 U2 0 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD MAY PY 1993 VL 64 IS 5 SU S BP 450 EP 455 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA LF268 UT WOS:A1993LF26800007 PM 8315567 ER PT J AU MANGAN, DF MERGENHAGEN, SE WAHL, SM AF MANGAN, DF MERGENHAGEN, SE WAHL, SM TI APOPTOSIS IN HUMAN MONOCYTES - POSSIBLE ROLE IN CHRONIC INFLAMMATORY DISEASES SO JOURNAL OF PERIODONTOLOGY LA English DT Article; Proceedings Paper CT SYMP ON CURRENT PERSPECTIVES ON MOLECULAR MEDIATORS OF INFLAMMATION AND PERIODONTAL PATHOLOGY CY JAN 30-31, 1992 CL MARCO ISLAND, FL DE MONOCYTES; CYTOKINES; CELL DEATH; APOPTOSIS ID PROGRAMMED CELL-DEATH; TUMOR-NECROSIS-FACTOR; INTERLEUKIN-1; PHAGOCYTOSIS; MACROPHAGES; MECHANISMS; INTERFERON; INDUCTION; PROFILES; SUBSETS AB APOPTOSIS OR PROGRAMMED CELL DEATH is a physiological form of cell suicide that is profoundly influenced by the extracellular microenvironment. Apoptosis is characterized by a cascade of genetic and biochemical events that cause cell shrinkage, condensation of cytoplasmic and nuclear material, cleavage of chromosomal DNA into oligonucleosomesized (approximately 200 bp) fragments, and enhanced recognition of the dying cell by phagocytes. Apoptosis differs fundamentally from necrosis, the pathological form of cell death, in which the cell swells and lyses. The capacity to selectively induce apoptosis in leukocytes might be an important physiological mechanism for controlling accumulation of these cells in inflammatory lesions. In this paper, we review our data on apoptosis in human monocytes, cells which contribute both to the persistence and resolution of chronic inflammation. Apoptosis can be initiated when monocytes are cultured in the absence of appropriate exogenous stimulation. For example, addition of chemotactic factors is insufficient to block apoptosis. However, apoptosis in monocytes can be inhibited by adherence in the presence of serum, by microbial products such as lipopolysaccharide, or by certain pro-inflammatory cytokines, such as interleukin 1 and tumor necrosis factor-alpha. Cytokines derived from type 1 helper T cells (e.g., interferon-gamma) inhibit apoptosis whereas those derived from type 2 helper T cells (e.g., interleukin-4) enhance apoptosis in activated monocytes. Thus, cytokines derived from monocytes as well as T cells modulate apoptosis, implicating both autocrine and paracrine regulatory circuits in monocyte survival. The capacity to therapeutically regulate monocyte apoptosis promises to have tremendous value in promoting rapid healing or reducing the immunopathogenesis of chronic inflammation. RP MANGAN, DF (reprint author), NIDR,IMMUNOL LAB,CELLULAR IMMUNOL SECT,BLDG 30,ROOM 331,BETHESDA,MD 20892, USA. FU NIDCR NIH HHS [DE05576] NR 26 TC 67 Z9 70 U1 0 U2 2 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD MAY PY 1993 VL 64 IS 5 SU S BP 461 EP 466 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA LF268 UT WOS:A1993LF26800009 PM 8315569 ER PT J AU WAHL, LM CORCORAN, ML AF WAHL, LM CORCORAN, ML TI REGULATION OF MONOCYTE-MACROPHAGE METALLOPROTEINASE PRODUCTION BY CYTOKINES SO JOURNAL OF PERIODONTOLOGY LA English DT Article; Proceedings Paper CT SYMP ON CURRENT PERSPECTIVES ON MOLECULAR MEDIATORS OF INFLAMMATION AND PERIODONTAL PATHOLOGY CY JAN 30-31, 1992 CL MARCO ISLAND, FL DE MONOCYTES; INTERFERON-GAMMA; INTERLEUKIN-4; PROSTAGLANDINS; MACROPHAGES; ENZYMES, PROTEOLYTIC; EICOSANOIDS ID RECOMBINANT INTERFERON-GAMMA; HUMAN MONONUCLEAR PHAGOCYTES; ARACHIDONIC-ACID METABOLISM; STIMULATED HUMAN-MONOCYTES; HUMAN PERIPHERAL-BLOOD; NECROSIS FACTOR-ALPHA; COLLAGENASE PRODUCTION; IFN-GAMMA; ACTIVATED MACROPHAGES; RHEUMATOID-ARTHRITIS AB ACTIVATION OF HUMAN MONOCYTES/MACROPHAGES (MO) RESULTS in the production of metalloproteinases through a PGE2-cAMP-dependent pathway. Here we review our findings on the ability of IFN-gamma and IL-4 to modulate this signal transduction pathway as a result of the effect of these cytokines on eicosanoid synthesis. Preincubation for 1 hour with either IFN-gamma or IL-4 prior to stimulation with Con A caused a significant inhibition of MO PGE2 production. Both of these cytokines also inhibited the Con A-induced production of interstitial collagenase and 92-kDa type IV collagenase/gelatinase. The inhibition of MO metalloproteinase production by IFN-gamma and IL-4 was reversed by PGE2 or Bt2cAMP. Thus the suppression of eicosanoid synthesis by IFN-gamma and IL-4 is the primary mechanism by which these cytokines inhibit MO metalloproteinase production. These findings demonstrate that IFN-gamma and IL-4 may have potent anti-inflammatory effects. RP WAHL, LM (reprint author), NIDR,IMMUNOL LAB,CELLULAR IMMUNOL SECT,BETHESDA,MD 20892, USA. NR 53 TC 45 Z9 45 U1 0 U2 1 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD MAY PY 1993 VL 64 IS 5 SU S BP 467 EP 473 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA LF268 UT WOS:A1993LF26800010 PM 8391076 ER PT J AU LAH, TT BABNIK, J SCHIFFMANN, E TURK, V SKALERIC, U AF LAH, TT BABNIK, J SCHIFFMANN, E TURK, V SKALERIC, U TI CYSTEINE PROTEINASES AND INHIBITORS IN INFLAMMATION - THEIR ROLE IN PERIODONTAL-DISEASE SO JOURNAL OF PERIODONTOLOGY LA English DT Article DE CATHEPSINS; CYSTATINS; PROTEINASE INHIBITORS; PROTEINASES; STEFINS ID INFLAMED HUMAN GINGIVA; CATHEPSIN-B-LIKE; CREVICULAR FLUID; 7-AMINO-4-TRIFLUOROMETHYL COUMARIN; NEUTROPHIL ELASTASE; ALPHA-2-MACROGLOBULIN; METALLOPROTEINASES; MACROPHAGES; CYSTATINS; TISSUES AB CELLULAR AND MOLECULAR EVENTS DURING THE DEVELOPMENT of inflammatory disease are accompanied by the release of host lysosomal cysteine proteinases (CPs) affecting not only degradation of matrix proteins but possibly also antigen processing and chemotaxis of neutrophils. Activity measurements of Cat B and Cat L could not be used as an accurate indicator of disease activity in individual patients, although average values were higher in patients with more advanced periodontal inflammation. In contrast, simultaneous decrease of cystatin C and alpha2-macroglobulin (alpha2-M) in inflamed gingiva and gingival fluid, respectively, might be useful diagnostic/prognostic factors. While the total and the free form of alpha2-M in gingival fluid decreased with the progression of the disease, the complexed alpha2-M form was hardly detectable. This indicates an increased consumption of this inhibitor by various proteinases and clearance of protease: alpha2-M complexes by macrophages. Elevated serum levels of alpha2-M were found in patients with more pronounced disease, suggesting a systemic host response. In addition, high levels of stefin A and moderate levels of kininogen were observed in gingival tissue homogenates. Stefin A was also found to play a role in the inhibition of neutrophil chemotaxis. In addition, other proteinases which are released at inflammatory sites from neutrophils, macrophages, lymphocytes, and/or bacteria may degrade the cystatins, thereby further increasing CP activities. Increased CP activity may inactivate serine protease inhibitors, leading to the so-called ''proteolytic burst.'' C1 UNIV LJUBLJANA, DENT CLIN, DEPT ORAL MED & PATHOL, LJUBLJANA, SLOVENIA. NATL INST CANC RES, DEPT PATHOL, BETHESDA, MD USA. NR 57 TC 44 Z9 44 U1 0 U2 0 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 USA SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD MAY PY 1993 VL 64 IS 5 SU S BP 485 EP 491 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA LF268 UT WOS:A1993LF26800012 PM 8315571 ER PT J AU SWIETER, M HAMAWY, MM SIRAGANIAN, RP MERGENHAGEN, SE AF SWIETER, M HAMAWY, MM SIRAGANIAN, RP MERGENHAGEN, SE TI MAST-CELLS AND THEIR MICROENVIRONMENT - THE INFLUENCE OF FIBRONECTIN AND FIBROBLASTS ON THE FUNCTIONAL REPERTOIRE OF RAT BASOPHILIC LEUKEMIA-CELLS SO JOURNAL OF PERIODONTOLOGY LA English DT Article; Proceedings Paper CT SYMP ON CURRENT PERSPECTIVES ON MOLECULAR MEDIATORS OF INFLAMMATION AND PERIODONTAL PATHOLOGY CY JAN 30-31, 1992 CL MARCO ISLAND, FL DE CELLS, MAST; FIBROBLASTS; FIBRONECTIN; HISTAMINE ID HISTAMINE-RELEASE; HETEROGENEITY; RECEPTOR AB TO DETERMINE HOW THE MICROENVIRONMENT in which mast cells are located may influence their function, we explored the effects of fibronectin and fibroblasts on histamine secretion in vitro from a mast cell model, the rat basophilic leukemia (RBL-2H3) cell line. RBL-2H3 cells bound specifically to fibronectin-coated surfaces. Binding was maximal by 1 hour, was not detectable at 0-degrees-C or in the absence of Ca++, and was inhibited by preincubating the cells with a synthetic peptide containing the RGD sequence. Adherence to fibronectin stimulated RBL-2H3 cell spreading with a concomitant reorganization of the cytoskeleton and a repositioning of the cytoplasmic granules to the cell periphery. Although adherence to fibronectin did not by itself induce histamine release, when stimulated by either immunologic or non-immunologic means, fibronectin-adherent cells released dramatically more histamine than cells plated in wells coated with BSA only. Thus, RBL-2H3 cells bind specifically to fibronectin, and in so doing are stimulated to undergo changes in morphology and enhanced responsiveness to secretory stimuli. RBL-2H3 cells grown in coculture with 3T3 fibroblasts, but not RBL-2H3 cells grown alone, became responsive to the polymeric synthetic secretagogue Compound 48/80 and the neuropeptide Substance P. Maximum sensitivity to Compound 48/80 was attained by the second week in coculture. Histamine release was dose-dependent, non-cytotoxic and occurred even in the absence of extracellular Ca++. Contact between the 2 cell types appeared to be a critical factor. RBL-2H3 cells, separated from 3T3 cells by a 0.45 mum filter, failed to secrete histamine in response to Compound 48/80. Additionally, RBL-2H3 cells grown in Steel factor, a newly identified mast cell growth factor produced by fibroblasts, did not secrete histamine, suggesting that unidentified factors produced by fibroblasts may control mast cell function. The results of our studies show that the local microenvironment can have profound effects on mast cell structure and function. C1 NIDR,IMMUNOL LAB,BLDG 30,ROOM 332,BETHESDA,MD 20892. RI Wan, Daniel/F-4689-2010 NR 22 TC 9 Z9 11 U1 0 U2 3 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD MAY PY 1993 VL 64 IS 5 SU S BP 492 EP 496 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA LF268 UT WOS:A1993LF26800013 PM 7686221 ER PT J AU YURDAYDIN, C GU, ZQ NOWAK, G FROMM, C HOLT, AG BASILE, AS AF YURDAYDIN, C GU, ZQ NOWAK, G FROMM, C HOLT, AG BASILE, AS TI BENZODIAZEPINE RECEPTOR LIGANDS ARE ELEVATED IN AN ANIMAL-MODEL OF HEPATIC-ENCEPHALOPATHY - RELATIONSHIP BETWEEN BRAIN CONCENTRATION AND SEVERITY OF ENCEPHALOPATHY SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID INVERSE AGONISTS; RAT; ANTAGONIST; COMPLEX; GABA; FLUMAZENIL; EFFICACY; CGS-8216; FAILURE AB Elevated levels of benzodiazepine receptor agonists are found in both animal models of hepatic encephalopathy and in humans with this syndrome. The present study investigated the relationship between agonist levels and the severity of the encephalopathy, as well as the potential reversibility of the syndrome by benzodiazepine receptor antagonists. The concentrations of benzodiazepine receptor ligands in rat brains were measured at several intervals during the induction of liver failure with thioacetamide. Six hours after the first dose of thioacetamide, brain concentrations of benzodiazepine receptor ligands were increased and open field activity decreased compared to control rats. However, the brain concentrations of benzodiazepine receptor ligands correlated better with the stage of hepatic encephalopathy than time after initiation of thioacetamide treatment. The benzodiazepine receptor ligands Ro 15-3505, Ro 15-4513 and CGS-8216 ameliorated motor abnormalities in rats with stage 3 hepatic encephalopathy. Only Ro 15-3505 improved motor activity in rats in stage 2 encephalopathy to levels observed in rats with stage 1 encephalopathy. Furthermore, although Ro 15-4513 and CGS 8216 significantly increased motor activity in stage 4 hepatic encephalopathy, this may reflect their partial inverse agonist properties. These findings support the hypothesis that increased brain levels of benzodiazepine receptor agonists contribute to the severity of hepatic encephalopathy and suggest that high-affinity benzodiazepine receptor antagonists are efficacious in reversing this syndrome. C1 NIDDKD,NEUROSCI LAB,NEUROBIOL SECT,BLDG 8,ROOM 111,BETHESDA,MD 20892. NIDDKD,DIGEST DIS BRANCH,LIVER DIS SECT,BETHESDA,MD 20892. FU NIGMS NIH HHS [F31 GM013553, F31 GM013553-05] NR 34 TC 23 Z9 24 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD MAY PY 1993 VL 265 IS 2 BP 565 EP 571 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LD060 UT WOS:A1993LD06000012 PM 8388453 ER PT J AU BENVENISTE, M MAYER, ML AF BENVENISTE, M MAYER, ML TI MULTIPLE EFFECTS OF SPERMINE ON N-METHYL-D-ASPARTIC ACID RECEPTOR RESPONSES OF RAT CULTURED HIPPOCAMPAL-NEURONS SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Article ID POLYAMINE RECOGNITION SITE; MOUSE CENTRAL NEURONS; NMDA RECEPTOR; 5,7-DICHLOROKYNURENIC ACID; COMPETITIVE ANTAGONIST; ACTIVATED CHANNELS; KINETIC-ANALYSIS; XENOPUS OOCYTES; BINDING-SITES; GLYCINE SITE AB 1. The modulation by polyamines of responses to N-methyl-D-aspartic acid (NMDA) was studied using a rapid perfusion system and whole-cell voltage-clamp recording from rat hippocampal neurons in dissociated culture. 2. Concentration jump responses to 100 mum NMDA in the presence of 10 mum glycine revealed potentiation by 3 mM spermine at a membrane potential of + 60 mV, but depression at - 120 mV; the degree of potentiation at + 60 mV was variable from cell to cell while marked depression at - 120 mV was observed in all cells. The depression of responses to NMDA by spermine was highly voltage dependent (zdelta = 1.17) with an apparent equilibrium dissociation constant for block at 0 mV of 27 mm. 3. Analysis of spermine dose-potentiation curves for responses recorded at + 60 mV in the presence of 10 mum glycine revealed a half-maximal effect at 125 mum. Under the same conditions, but at - 60 mV, analysis of spermine-evoked depression was performed for cells with less than 5 % potentiation at + 60 mV, and revealed half-maximal inhibition at 344 mum. 4. Dose-response analysis for the glycine-sensitive activation of NMDA receptors at + 60 mV revealed a 3-5-fold increase in apparent affinity for glycine in the presence of 1 mm spermine. This increase in affinity for glycine was accompanied by a 3.3-fold decrease in the rate of development of glycine-sensitive desensitization, and a 2.4-fold decrease in the rate of dissociation of glycine from NMDA receptors, while the rate constant for dissociation of NMDA was not reduced. 5. In the presence of non-saturating concentrations of glycine, spermine-induced potentiation at + 60 mV developed with two exponential components: a slow glycine-sensitive component, the amplitude and time constant of which decreased with increasing glycine concentration (30 nm glycine, amplitude = 80.2 +/- 5.1 %, tau = 780 +/- 79 ms; 3 /mum glycine, amplitude = 22.6 +/- 7-1 %, tau = 45 +/- 13 ms), and a faster component (tau < 20 ms at all concentrations of glycine), the amplitude of which varied from cell to cell, and which became larger with increase in concentration of glycine. When responses to the application of spermine were measured in the presence 10 muM L-alanine instead of 100 nm glycine, the slow component of potentiation was absent. 6. The guanidine derivative arcaine, and the polyamines diethylenetriamine and 1,10-diaminodecane also produced voltage-dependent block of responses to NMDA, with apparent equilibrium dissociation constants at 0 mV of 0.75, 2.93 and 4.79 mm, respectively. None of these compounds appeared to act as potent antagonists at the site(s) at which spermine induced potentiation of responses to NMDA, nor did they block the effects of spermine on the rate of onset of the glycine-sensitive component of desensitization. 7. Our results suggest that spermine acts at multiple sites on NMDA receptors to produce potentiation and block. Potentiation results from both an increase in apparent affinity for glycine as well as an increase in maximum amplitude of responses to NMDA recorded in the presence of a saturating concentration of glycine; we propose that separate mechanisms underlie each effect. Variation in the degree to which these effects occur in individual neurons suggest the occurrence of subpopulations of NMDA receptors. Block is voltage dependent, and most likely due to binding of polyamines to sites within the ion channel. RP BENVENISTE, M (reprint author), NICHHD,CELLULAR & MOLEC NEUROPHYSIOL,BLDG 36,ROOM 2A21,BETHESDA,MD 20892, USA. RI Mayer, Mark/H-5500-2013 NR 47 TC 172 Z9 172 U1 0 U2 2 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0022-3751 J9 J PHYSIOL-LONDON JI J. Physiol.-London PD MAY PY 1993 VL 464 BP 131 EP 163 PG 33 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA LB641 UT WOS:A1993LB64100007 PM 8229795 ER PT J AU DONOGHUE, AM JOHNSTON, LA GOODROWE, KL OBRIEN, SJ WILDT, DE AF DONOGHUE, AM JOHNSTON, LA GOODROWE, KL OBRIEN, SJ WILDT, DE TI INFLUENCE OF DAY OF ESTRUS ON EGG VIABILITY AND COMPARATIVE EFFICIENCY OF INVITRO FERTILIZATION IN DOMESTIC CATS IN NATURAL OR GONADOTROPIN-INDUCED ESTRUS SO JOURNAL OF REPRODUCTION AND FERTILITY LA English DT Article ID CIRCULATING HORMONES; FOLLICULAR OOCYTES; EMBRYO DEVELOPMENT; OVARIAN ACTIVITY; SEXUAL-BEHAVIOR; SHEEP OOCYTES; SUPEROVULATION; ABNORMALITIES AB Thirty-six domestic cats received 100 iu hCG (i.m.) on day 1, 2 or 3 of a natural, behavioural oestrus. Twenty-two anoestrous cats were injected with 150 iu pregnant mares' serum gonadotrophin (PMSG; i.m.) followed 84 h later by 100 iu hCG. Twenty-four to 26 h after hCG, all cats were examined laparoscopically to determine the number of ovarian follicles and to recover follicular eggs. Mature eggs were cultured with conspecific spermatozoa and examined 30 h later for cleavage. Within the natural oestrus group, cats on day 1 produced fewer (P < 0.0.5) follicles and total eggs than females on day 2 or 3, and 88.9% of the day 1 eggs were degenerate or immature and unsuitable for in vitro fertilization (IVF). Although only 54.5% of the cats in the PMSG/hCG group exhibited overt oestrus, mean (+/-SEM) numbers of follicles (9.7 +/- 0.8) and oocytes recovered (8.7 +/- 0.8) were at least twofold greater (P < 0.001) than those measured in the natural oestrus group (3.7 +/- 0.6; 3.4 +/- 0.6, respectively) or subgroups on day 2 (3.7 +/- 0.4; 3.3 +/- 0.4) and day 3 (5.7 +/- 0.8; 5.3 +/- 0.8). Overall, the proportion of eggs cleaving in vitro was similar (P > 0.05) between the natural oestrus group (48.3%) and the PMSG/hCG group (50.9%), but the latter group produced more than twice the number of embryos per donor. Embryo quality was unaffected (P > 0.05) by day of hormone treatment, and more than 80% of all two-cell embryos were rated good-to-excellent quality. In summary, there is a temporal relationship between day of sexual receptivity and follicular egg viability in the domestic cat: eggs on the first day of oestrus are not optimally responsive to an LH-like stimulus. There is also no evidence that PMSG/hCG treatment compromises egg quality or subsequent fertilizability in vitro. On the contrary, use of these gonadotrophins markedly improves overall IVF efficiency by increasing the total number of high quality embryos produced. C1 SMITHSONIAN INST,NATL ZOOL PK,WASHINGTON,DC 20008. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. FU NICHD NIH HHS [HD 23583] NR 34 TC 17 Z9 19 U1 0 U2 3 PU J REPROD FERTIL INC PI CAMBRIDGE PA 22 NEWMARKET RD, CAMBRIDGE, ENGLAND CB5 8DT SN 0022-4251 J9 J REPROD FERTIL JI J. Reprod. Fertil. PD MAY PY 1993 VL 98 IS 1 BP 85 EP 90 PG 6 WC Reproductive Biology SC Reproductive Biology GA LH234 UT WOS:A1993LH23400011 PM 8345483 ER PT J AU CRAFT, NE EPLER, KS BUTLER, TA MAY, WE ZIEGLER, RG AF CRAFT, NE EPLER, KS BUTLER, TA MAY, WE ZIEGLER, RG TI EVALUATION OF SERUM VOLUME LOSSES DURING LONG-TERM STORAGE SO JOURNAL OF RESEARCH OF THE NATIONAL INSTITUTE OF STANDARDS AND TECHNOLOGY LA English DT Article DE DENSITY; LONG-TERM STORAGE; SERUM; SODIUM; SUBLIMATION; VOLUME LOSS ID CERVICAL-CANCER; UNITED-STATES; WHITE WOMEN; DIET; RISK AB Aliquots of serum collected in a large case-control study of cervical cancer were stored at -70-degrees-C for up to 4 years during implementation of the study. When 500 muL serum aliquots were thawed in preparation for carotenoid and vitamin A assays, volumes were noticeably variable and fell below 500 muL in the majority of the samples. We were concerned about evaporation/sublimation during storage of the samples because loss of water would concentrate the analytes of interest. We evaluated the use of density and sodium ion concentration measurements to confirm its occurrence. We found that serum density was an unreliable indicator of extent of volume loss since the anticipated increases in density due to evaporation were of the same magnitude as inter-individual variation in serum density. In contrast, Na+ concentration is tightly regulated and would rise if water bad been lost from the samples. In a representative sample of serum aliquots from the case-control study, 24 of 25 vials contained less than 500 muL of serum. The mean sodium ion concentration (138.1+/-3.6 mmol/L) was within the normal range for human serum of 136-145 mmol/L, and no correlation was observed between serum volume and Na+ concentration. These results strongly suggest that the observed low volumes were not due to evaporative losses. Instead, the variably low volumes of serum aliquots were probably due to pipetting errors in the initial aliquotting resulting from the use of air-displacement pipettes. C1 NATL INST STANDARDS & TECHNOL, INORGAN ANALYT RES DIV, GAITHERSBURG, MD 20899 USA. NATL INST STANDARDS & TECHNOL, CHEM SCI & TECHNOL LAB, GAITHERSBURG, MD 20899 USA. NCI, ENVIRONM & EPIDEMIOL BRANCH, DIV CANC ETIOL, BETHESDA, MD 20892 USA. RP CRAFT, NE (reprint author), NATL INST STANDARDS & TECHNOL, ORGAN ANALYT RES DIV, GAITHERSBURG, MD 20899 USA. NR 10 TC 0 Z9 0 U1 0 U2 2 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPERINTENDENT DOCUMENTS,, WASHINGTON, DC 20402-9325 USA SN 1044-677X J9 J RES NATL INST STAN JI J. Res. Natl. Inst. Stand. Technol. PD MAY-JUN PY 1993 VL 98 IS 3 BP 355 EP 359 DI 10.6028/jres.098.027 PG 5 WC Instruments & Instrumentation; Physics, Applied SC Instruments & Instrumentation; Physics GA LQ765 UT WOS:A1993LQ76500004 PM 28053478 ER PT J AU ALLEN, JP MATTSON, ME AF ALLEN, JP MATTSON, ME TI PSYCHOMETRIC INSTRUMENTS TO ASSIST IN ALCOHOLISM-TREATMENT PLANNING SO JOURNAL OF SUBSTANCE ABUSE TREATMENT LA English DT Article DE TREATMENT PLANNING; TESTING; ASSESSMENT INSTRUMENTS ID DRINKING PATTERNS; SUBSTANCE ABUSE; RELAPSE; REINFORCEMENT; EXPECTANCIES; PERSONALITY; INVENTORY AB The clinical practice of alcoholism treatment can be enhanced by the judicious use of standardized psychometric instruments to characterize clients during the course of treatment. Knowledge of key behavioral, personality, and alcohol-specific factors will increase the clinician's ability to select the most appropriate treatment option, or, even if treatment options are limited, at least to develop a treatment plant with the patient's unique needs in mind. Monitoring of progress towards treatment goals can also be facilitated by the use of selected assessment tools. Seven examples of well-validated instruments are discussed, with suggestions on how data derived from them may be applied in the treatment planning process. RP ALLEN, JP (reprint author), NIAAA,TREATMENT RES BRANCH,PARKLAWN BLDG,ROOM 14020,5600 FISHERS LANE,ROCKVILLE,MD 20852, USA. NR 39 TC 9 Z9 9 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0740-5472 J9 J SUBST ABUSE TREAT JI J. Subst. Abus. Treat. PD MAY-JUN PY 1993 VL 10 IS 3 BP 289 EP 296 DI 10.1016/0740-5472(93)90077-F PG 8 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA LE199 UT WOS:A1993LE19900007 PM 8315703 ER PT J AU SHAFFER, D SCHWABSTONE, M FISHER, P COHEN, P PIACENTINI, J DAVIES, M CONNERS, CK REGIER, D AF SHAFFER, D SCHWABSTONE, M FISHER, P COHEN, P PIACENTINI, J DAVIES, M CONNERS, CK REGIER, D TI THE DIAGNOSTIC INTERVIEW SCHEDULE FOR CHILDREN REVISED VERSION (DISC-R) .1. PREPARATION, FIELD TESTING, INTERRATER RELIABILITY, AND ACCEPTABILITY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE DISC; DIAGNOSTIC INTERVIEWS; DIAGNOSIS; ASSESSMENT ID PSYCHIATRIC INTERVIEW; SYMPTOMS; AGREEMENT; VALIDITY; PARENT; ADOLESCENTS AB Objective: To describe the history and assessment strategies used to investigate and revise the Diagnostic Interview Schedule for Children (DISC), a highly structured interview form used by lay interviewers to elicit diagnostic criteria for the common psychiatric disorders of childhood and adolescence. Method: Revision was based on clinical and community data that identified unreliable and undiscriminating items in an earlier version of the instrument (DISC-1). A field study was carried out with 74 parent-child pairs. Interrater reliability and acceptability to patients was high. Accompanying papers describe the test-retest and construct validity of the instrument. Conclusions: Taken together, the findings suggest that the DISC is an acceptable, brief, inexpensive, and convenient instrument for ascertaining a comprehensive range of child and adolescent diagnoses whose methodological properties are comparable with other child diagnostic instruments. C1 YALE UNIV,NEW HAVEN,CT 06520. COLUMBIA UNIV,SCH PUBL HLTH,NEW YORK,NY 10027. NIMH,DIV CLIN RES,ROCKVILLE,MD 20857. DUKE UNIV,MED CTR,DURHAM,NC 27710. RP SHAFFER, D (reprint author), COLUMBIA UNIV COLL PHYS & SURG,NEW YORK STATE PSYCHIAT INST,DIV CHILD PSYCHIAT,722 W 168TH ST,NEW YORK,NY 10032, USA. RI Piacentini, John/C-4645-2011 FU NIMH NIH HHS [MH278890001, MH278870002, MH36971] NR 36 TC 300 Z9 301 U1 7 U2 10 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 1993 VL 32 IS 3 BP 643 EP 650 DI 10.1097/00004583-199305000-00023 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KY441 UT WOS:A1993KY44100023 PM 8496128 ER PT J AU MAUTNER, SL LIN, FG MAUTNER, GC ROBERTS, WC AF MAUTNER, SL LIN, FG MAUTNER, GC ROBERTS, WC TI COMPARISON IN WOMEN VERSUS MEN OF COMPOSITION OF ATHEROSCLEROTIC PLAQUES IN NATIVE CORONARY-ARTERIES AND IN SAPHENOUS VEINS USED AS AORTOCORONARY CONDUITS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID BYPASS GRAFTS; MYOCARDIAL-INFARCTION; MORPHOMETRIC ANALYSIS; SURGERY; AGE; SEX AB Objectives. This study quantifies and compares the components of atherosclerotic plaques in native coronary arteries and in saphenous vein grafts used for aortocoronary bypass surgery in women versus those in men. Background. Plaque composition has been described in various manifestations of fatal coronary artery disease and after the bypass operation, but no reports have investigated this composition according to gender. Methods. A total of 979 5-mm segments of native coronary arteries and 842 5-mm segments of saphenous vein grafts were examined by computerized planimetric technique in 11 women and 11 men who were matched for survival time after the bypass operation. Results. Comparison of the plaque components revealed that atherosclerotic plaques in women, compared with those in men, contained significantly more cellular fibrous tissue, both in native coronary arteries (mean 38% vs. 4%, p < 0.001) and in saphenous vein grafts (mean 70% vs. 36%, p < 0.05). In contrast, the proportion of dense fibrous tissue was significantly less in the atherosclerotic plaques of women than in those of men, both in native coronary arteries (mean 50% vs. 85%, p < 0.001) and in saphenous vein grafts (mean 25% vs. 57%, p < 0.05). Conclusions. Cellular fibrous tissue is often found at an early stage of plaque development, whereas dense fibrous tissue is a major component in later stages. Thus, the plaque composition of the native coronary arteries and saphenous venous conduits differed in men and women, with the plaques of the women appearing younger than those of the men. RP MAUTNER, SL (reprint author), NHLBI,PATHOL BRANCH,BLDG 10,ROOM 2N258,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 23 TC 44 Z9 45 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAY PY 1993 VL 21 IS 6 BP 1312 EP 1318 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KZ707 UT WOS:A1993KZ70700002 PM 8473635 ER PT J AU GREENE, T BOURGOIGNIE, JJ HABWE, V KUSEK, J SNETSELAAR, L SOUCIE, JM YAMAMOTO, M AF GREENE, T BOURGOIGNIE, JJ HABWE, V KUSEK, J SNETSELAAR, L SOUCIE, JM YAMAMOTO, M TI BASE-LINE CHARACTERISTICS IN THE MODIFICATION OF DIET IN RENAL-DISEASE STUDY SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article DE PROTEIN; BLOOD PRESSURE; GFR; CLINICAL TRIAL; KIDNEY DISEASE ID PROTEIN RESTRICTION; FOLLOW-UP; PROGRESSION; FAILURE; INSUFFICIENCY; TRIAL AB The Modification of Diet in Renal Disease Study is a randomized, multicenter, clinical trial designed to determine the effects of three levels of dietary control of protein and phosphorus and two levels of blood pressure control on the rate of decline of kidney function among persons with chronic renal disease. Study participants were assigned to one of two studies, Study A or Study B, depending on their GFR just before randomization. Within each study, participants were randomly allocated to one of two levels of blood pressure control and to one of two dietary interventions according to separate 2 x 2 factorial designs. A total of 840 men and women aged 18 to 70 were randomized. This report summarizes the demographic, biochemical, and clinical characteristics of the randomized participants at the time of entry into the trial, overviews the protocol and purposes of the baseline period before randomization, and evaluates the balance among the treatment intervention groups within Studies A and B at the time of randomization. Major indicators of renal function were found to be well balanced among the treatment groups. Selected baseline characteristics of participants in the Modification of Diet in Renal Disease Study are compared with those of other renal clinical trials and with those of new cases of treated ESRD reported in the United States Renal Data System. C1 UNIV MIAMI,SCH MED,MIAMI,FL 33152. GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. NIH,BETHESDA,MD 20892. UNIV IOWA HOSP & CLIN,IOWA CITY,IA 52242. EMORY UNIV,ATLANTA,GA 30322. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,PITTSBURGH,PA 15260. RP GREENE, T (reprint author), CLEVELAND CLIN FDN,DEPT BIOSTAT & EPIDEMIOL,9500 EUCLID AVE,CLEVELAND,OH 44195, USA. NR 30 TC 16 Z9 16 U1 0 U2 2 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 MAY PY 1993 VL 3 IS 11 BP 1819 EP 1834 PG 16 WC Urology & Nephrology SC Urology & Nephrology GA LF381 UT WOS:A1993LF38100012 ER PT J AU DIETER, MP MATTHEWS, HB JEFFCOAT, RA MOSEMAN, RF AF DIETER, MP MATTHEWS, HB JEFFCOAT, RA MOSEMAN, RF TI COMPARISON OF LEAD BIOAVAILABILITY IN F344 RATS FED LEAD ACETATE, LEAD-OXIDE, LEAD SULFIDE, OR LEAD ORE CONCENTRATE FROM SKAGWAY, ALASKA SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH LA English DT Article ID EXPOSURE AB An animal model using rats was developed to initiate investigations on the bioavailability of different sources of environmental lead. Lead must be absorbed and transported to target organs like brain, liver, kidney, and bone, before susceptible cells can be harmed. The bioavailability and therefore the toxicity of lead are dependent upon the route of exposure, dose, chemical structure, solubility, particle size, matrix incorporation, and other physiological and physicochemical factors. In the present study male F344 rats were fed less-than-or-equal-to 38 mum size particles of lead sulfide, lead oxide, lead acetate, and a lead ore concentrate from Skagway, Alaska, mixed into the diet at doses of 0, 10, 30, and 100 ppm as lead for 30 d. No mortality or overt symptoms of lead toxicity were observed during the course of the study. Maximum blood lead concentrations attained in the 100 ppm groups were approximately 80 mug/dl in rats fed lead acetate and lead oxide, and were approximately 10 mug/dl in those fed lead sulfide and lead ore concentrate. Maximum bone lead levels in rats fed soluble lead oxide and lead acetate were much higher (approximately 200 mug/g) than those seen in rats fed the less soluble lead sulfide and lead ore (approximately 10 mug); kidney lead concentrations were also about 10-fold greater in rats fed the more soluble compared to the less soluble lead compounds. However, strong correlations between dose and tissue lead concentrations were observed in rats fed each of the four different lead compounds. Kidney lesions graded as minimal occurred in 7/10 rats fed 30 ppm and in 10/10 rats fed 100 ppm lead acetate, but not at lower doses or from other lead compounds. Similarly, urinary aminolevulinic acid excretion, a biomarker for lead toxicity, was increased in rats fed 100 ppm lead acetate or lead oxide, but was unaffected at lower doses or by the less soluble lead compounds. Although the histological and biochemical responses to lead toxicity were restricted to the more soluble lead compounds in this study, lead from Skagway lead ore concentrate and lead sulfide was also bioavailable, and accumulated in proportion to dose in vulnerable target organs such as bone and kidney Longer-term studies with different mining materials are being conducted to determine if tissue lead continues to increase, and whether the levels attained are toxic. Data from such studies can be used to compare the toxicity and bioavailability of lead from different sources in the environment. C1 RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. RADIAN CORP,RES TRIANGLE PK,NC. RP DIETER, MP (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 25 TC 50 Z9 51 U1 0 U2 13 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0098-4108 J9 J TOXICOL ENV HEALTH JI J. Toxicol. Environ. Health PD MAY PY 1993 VL 39 IS 1 BP 79 EP 93 PG 15 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LD083 UT WOS:A1993LD08300006 PM 8492331 ER PT J AU COSTABILE, RA CHOYKE, PL FRANK, JA GIRTON, ME DIGGS, R BILLUPS, KL MOONEN, C DESJARDINS, C AF COSTABILE, RA CHOYKE, PL FRANK, JA GIRTON, ME DIGGS, R BILLUPS, KL MOONEN, C DESJARDINS, C TI DYNAMIC ENHANCED MAGNETIC-RESONANCE-IMAGING OF TESTICULAR PERFUSION IN THE RAT SO JOURNAL OF UROLOGY LA English DT Article DE TESTIS; TORSION; MAGNETIC RESONANCE IMAGING; RATS ID CONTRAST AB Magnetic Resonance Imaging (MRI) has several theoretical advantages in the evaluation of spermatic cord torsion and testicular ischemia. The technique uses no ionizing radiation, has both excellent spatial and temporal resolution and, when used with an intravenous bolus of a paramagnetic contrast agent, provides a semiquantitative assessment of tissue perfusion and vascular injury. In clinical instances of testicular torsion, accurate estimates of tissue perfusion are desirable since testicular salvage is inversely related to the duration of torsion and the degree of tissue ischemia. Perfusion imaging of the rat testis was used as a model to demonstrate the potential use of MRI in the experimental and clinical analysis of disorders that affect blood flow to the testis. C1 NIH,DIAGNOST RADIOL RES PROGRAM,BETHESDA,MD 20892. UNIV VIRGINIA,HLTH SCI CTR,DEPT PHYSIOL,CHARLOTTESVILLE,VA 22908. RP COSTABILE, RA (reprint author), UNIV VIRGINIA,HLTH SCI CTR,DEPT UROL,BOX 422,CHARLOTTESVILLE,VA 22908, USA. RI Moonen, Chrit/K-4434-2016 OI Moonen, Chrit/0000-0001-5593-3121 FU NICHD NIH HHS [HD-20876]; NIDDK NIH HHS [DK-07642, DK-45179] NR 11 TC 14 Z9 15 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 MAY PY 1993 VL 149 IS 5 BP 1195 EP 1197 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA LA464 UT WOS:A1993LA46400080 PM 8483245 ER PT J AU NOVEMBRE, FJ JOHNSON, PR LEWIS, MG ANDERSON, DC KLUMPP, S MCCLURE, HM HIRSCH, VM AF NOVEMBRE, FJ JOHNSON, PR LEWIS, MG ANDERSON, DC KLUMPP, S MCCLURE, HM HIRSCH, VM TI MULTIPLE VIRAL DETERMINANTS CONTRIBUTE TO PATHOGENICITY OF THE ACUTELY LETHAL SIMIAN IMMUNODEFICIENCY VIRUS SIVSMMPBJ VARIANT SO JOURNAL OF VIROLOGY LA English DT Article ID LONG TERMINAL REPEAT; RHESUS-MONKEYS; LEUKEMIA-VIRUS; HIV-INFECTION; DISEASE; SIV; SEQUENCES; SIV/SMM; TYPE-1; CELLS AB Simian immunodeficiency virus (SIV) induces an immunodeficiency syndrome similar to human AIDS. Although the disease course of SIV-induced immunodeficiency is generally measured in months to years, a disease syndrome that results in death in 5 to 14 days has been described in pig-tailed macaques infected with the SIVsmmPBj (PBj) strain. The purpose of this study was to derive an acutely lethal PBj molecular clone in order to study viral genes involved in pathogenesis. Six infectious molecular clones were generated; acutely fatal disease was induced by experimental inoculation of pig-tailed macaques with virus stocks derived from either of two clones, PBj6.6 or PBj14.6. Molecular chimeras were constructed by exchange of regions of the genome of PBj6.6 and a nonlethal, related clone, SIVsmH4. Only a chimera expressing the PBj genome under the control of a SIVsmH4 long terminal repeat induced death soon after inoculation. These studies suggest that multiple viral genes of PBj are critical for development of acute disease. More specifically, the env gene but not the long terminal repeat PBj was required for acute disease induction; however env must act in concert with another gene(s) of the PBj genome. C1 NIAID,INFECT DIS LAB,ROCKVILLE,MD 20852. YERKES REG PRIMATE RES CTR,ATLANTA,GA 30322. HENRY M JACKSON FDN,RES LAB,ROCKVILLE,MD. EMORY UNIV,DEPT PATHOL,ATLANTA,GA 30322. RI Johnson, Philip/A-6892-2009 FU NCRR NIH HHS [RR-00165]; NIAID NIH HHS [N01-AI-772623] NR 39 TC 84 Z9 84 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 MAY PY 1993 VL 67 IS 5 BP 2466 EP 2474 PG 9 WC Virology SC Virology GA KX335 UT WOS:A1993KX33500006 PM 8474153 ER PT J AU LYNCH, WP PORTIS, JL AF LYNCH, WP PORTIS, JL TI MURINE RETROVIRUS-INDUCED SPONGIFORM ENCEPHALOPATHY - DISEASE EXPRESSION IS DEPENDENT ON POSTNATAL-DEVELOPMENT OF THE CENTRAL-NERVOUS-SYSTEM SO JOURNAL OF VIROLOGY LA English DT Article ID LEUKEMIA-VIRUS-TB; WILD MOUSE RETROVIRUS; MOTOR NEURON DISEASE; C RNA VIRUS; BRAIN-STEM; PARALYTOGENIC MUTANT; NEURODEGENERATIVE DISEASE; TEMPERATURE SENSITIVITY; NEUROTROPIC RETROVIRUS; AUDITORY NUCLEI AB In this report, we have examined the role of central nervous system (CNS) development in the pathogenesis of neurodegenerative disease induced by murine retroviruses. This was accomplished by comparing the effect of delivering viruses, with either severe or marginal neurovirulence (J. L. Portis, S. Czub, C. F. Garon, and F. J. McAtee, J. Virol. 64:1648-1656, 1990), during the midgestational development of the mouse (gestation days 9 to 10). Midgestation inoculation of the marginally neurovirulent virus, 15-1, resulted in high level CNS infection, as determined by viral DNA and protein analysis. The high-level infection resulted in rapid, severe disease with 100% incidence and an average clinical onset on postnatal day 17 (P17). The disease onset was comparable to that observed for the highly neurovirulent virus, FrCas(E), when inoculated neonatally (onset ca. P16). To evaluate whether disease could be induced even earlier in CNS development, FrCas(E) was inoculated during midgestation. Surprisingly, neither clinical nor histological manifestations of CNS disease were accelerated but rather appeared at the same developmental time as seen for neonatally inoculated animals (onset of neuropathology at ca. P10; onset of clinical disease at ca. P15). CNS infection, on the other hand, occurred at earlier times (2-fold higher number of Bn receptors than did the radiolabeled antagonist. Binding studies using cell membranes, in contrast to cells, showed equal numbers of Bn receptors with either radiolabeled ligand. The radiolabeled agonist demonstrated high affinity binding to both rat pancreatic acinar and esophageal muscularis mucosa membranes, whereas the radiolabeled antagonist interacted with high affinity only with the gastrin-releasing peptide-preferring subtype of Bn receptors on pancreatic tissue. These results demonstrate that I-125-[D-Tyr6] Bn(6-13)ME is a high affinity radiolabeled antagonist that interacts specifically with Bn receptors. In contrast to the radiolabeled agonist, binding of the antagonist is not affected by guanine nucleotides and it is not internalized, which allows quantitation of only Bn cell surface receptors. Furthermore, the radiolabeled antagonist can distinguish Bn receptor subtypes, whereas the radiolabeled agonist does not. This ligand should prove useful for characterizing Bn receptors as well as studying their regulation. C1 NIDDKD,DIGEST DIS BRANCH,CELL BIOL SECT,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892. TULANE UNIV,MED CTR,DEPT MED,PEPTIDE RES LABS,NEW ORLEANS,LA 70112. FU NCI NIH HHS [CA-45153] NR 78 TC 36 Z9 36 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD MAY PY 1993 VL 43 IS 5 BP 762 EP 774 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LD299 UT WOS:A1993LD29900016 PM 7684815 ER PT J AU MORRISON, LD ELING, TE JOSEPHY, PD AF MORRISON, LD ELING, TE JOSEPHY, PD TI PROSTAGLANDIN-H SYNTHASE-DEPENDENT FORMATION OF THE DIRECT-ACTING MUTAGEN 2-NITRO-3-METHYLIMIDAZO[4,5-F]QUINOLINE (NITRO-IQ) FROM IQ SO MUTATION RESEARCH LA English DT Article DE 2-AMINO-3-METHYLIMIDAZO[4,5-F]QUINOLINE (IQ); ACETYL-COA; ARYLAMINE-N-ACETYLTRANSFERASE (EC 2.3.1.5); PROSTAGLANDIN-H SYNTHASE (EC 1.14.99.1); AMES TEST ID HETEROCYCLIC AROMATIC-AMINES; ACETYLTRANSFERASE LEVELS; ACTIVATION; SALMONELLA; 2-AMINO-3-METHYLIMIDAZO<4,5-F>QUINOLINE; IDENTIFICATION; NITROARENES; ARYLAMINES; MECHANISM; 2-AMINO-3,4-DIMETHYLIMIDAZO<4,5-F>QUINOLINE AB The mutagenic effects of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) following activation by ram seminal vesicle microsomes (RSVM, a source of prostaglandin H synthase, PHS) were studied in Salmonella typhimurium tester strains possessing elevated levels of acetyl-CoA : arylamine N-acetyltransferase (NAT). The metabolites formed by RSVM were extracted and fractionated by high pressure liquid chromatography (HPLC). One isolable product accounted for most of the direct-acting mutagenicity observed in the extracts. The metabolite was identified as 2-nitro-3-methylimidazo[4,5-f]quinoline (nitro-IQ). Since nitro-IQ is a potent direct-acting mutagen, its role in IQ genotoxicity warrants further study. C1 UNIV GUELPH,GUELPH WATERLOO CTR GRAD WORK CHEM,DEPT CHEM & BIOCHEM,GUELPH N1G 2W1,ONTARIO,CANADA. NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NR 32 TC 21 Z9 21 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD MAY PY 1993 VL 302 IS 1 BP 45 EP 52 DI 10.1016/0165-7992(93)90089-E PG 8 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA KZ114 UT WOS:A1993KZ11400008 PM 7683106 ER PT J AU LAPPE, M RAUSCHECKER, JP AF LAPPE, M RAUSCHECKER, JP TI A NEURAL NETWORK FOR THE PROCESSING OF OPTIC FLOW FROM EGO-MOTION IN MAN AND HIGHER MAMMALS SO NEURAL COMPUTATION LA English DT Letter ID SUPRASYLVIAN VISUAL-CORTEX; SUPERIOR TEMPORAL AREA; EXPANSION CONTRACTION; RESPONSE SELECTIVITY; CORTICAL CONNECTIONS; 3-DIMENSIONAL MOTION; ROTATION CELLS; MACAQUE MONKEY; FIELD STIMULI; MST NEURONS AB Interest in the processing of optic flow has increased recently in both the neurophysiological and the psychophysical communities. We have designed a neural network model of the visual motion pathway in higher mammals that detects the direction of heading from optic flow. The model is a neural implementation of the subspace algorithm introduced by Heeger and Jepson (1990). We have tested the network in simulations that are closely related to psychophysical and neurophysiological experiments and show that our results are consistent with recent data from both fields. The network reproduces some key properties of human ego-motion perception. At the same time, it produces neurons that are selective for different components of ego-motion flow fields, such as expansions and rotations. These properties are reminiscent of a subclass of neurons in cortical area MSTd, the triple-component neurons We propose that the output of such neurons could be used to generate a computational map of heading directions in or beyond MST. C1 MAX PLANCK INST BIOL CYBERNET,W-7400 TUBINGEN,GERMANY. RP LAPPE, M (reprint author), NIMH,NEUROPHYSIOL LAB,POOLESVILLE,MD 20837, USA. RI Rauschecker, Josef/A-4120-2013 NR 40 TC 107 Z9 107 U1 0 U2 2 PU MIT PRESS PI CAMBRIDGE PA 55 HAYWARD ST JOURNALS DEPT, CAMBRIDGE, MA 02142 SN 0899-7667 J9 NEURAL COMPUT JI Neural Comput. PD MAY PY 1993 VL 5 IS 3 BP 374 EP 391 DI 10.1162/neco.1993.5.3.374 PG 18 WC Computer Science, Artificial Intelligence SC Computer Science GA KZ513 UT WOS:A1993KZ51300006 ER PT J AU HUANG, KP HUANG, FL AF HUANG, KP HUANG, FL TI HOW IS PROTEIN-KINASE-C ACTIVATED IN CNS SO NEUROCHEMISTRY INTERNATIONAL LA English DT Review ID CALMODULIN-BINDING-PROTEIN; GROWTH-ASSOCIATED PROTEIN; PHORBOL ESTER BINDING; UNSATURATED FATTY-ACIDS; DIFFERENTIAL DOWN-REGULATION; MAJOR SPECIFIC SUBSTRATE; X-100 MIXED MICELLES; RAT-BRAIN; MOLECULAR-CLONING; BOVINE BRAIN AB Protein kinase C (PKC) enzyme family consists of the Ca2+-dependent and -independent subgroups of phospholipid/diacylglycerol (DAG)-stimulated serine/threonine protein kinases. These enzymes exhibit distinct cellular and subcellular localizations in CNS and subtle differences in their biochemical characteristics and substrate specificities. It is believed that each of these isoenzymes respond differently to different input signals. However, detailed mechanism for the functioning of these enzymes in vivo is largely unknown; this is in part due to the absence of specific activator, inhibitor, or substrate for each of these enzymes. Recent advances in biochemical, biophysical, and molecular characterizations have defined certain structural features important to confer the stimulatory responses of these enzymes to Ca2+, DAG or phorbol ester, and Zn2+ ; other features important for the binding of anionic phospholipids, Ca2+/phospholipid complexes, and cis-unsaturated fatty acids have not yet been characterized. Activation of PKC requires the increase in [Ca2+]i and DAG and/or cis-unsaturated fatty acids. Ca2+ promotes the interactions of the Ca2+-dependent subgroup of PKCs with membrane phosphatidylserine (PS) and the enzymes become partially active when simultaneously associated with phosphatidylinositol 4,5-bisphosphate or fully active when DAG is available. Free fatty acids such as arachidonic acid, generated by the activation of phospholipase A2, could synergize with DAG to activate the enzyme maximally. The Ca2+-independent subgroup of PKCs also become active when associated with PS at elevated level of DAG. Sustained activation of PKCs leads to the conversion of these enzymes into membrane-inserted and membrane protein-associated forms, which may be responsible for certain long-term neural responses. Activation of PKC results in the phosphorylation of cellular proteins; among them, several calmodulin (CaM)-binding proteins are the prominent substrates of these kinases. Phosphorylation of these proteins by PKC favors the release of CaM, which is required for the Ca2+/CaM-dependent enzymes. Thus, activation of PKCs can lead to diverse cellular responses through such amplification steps. Future studies should be directed at the elucidation of the activation of each PKC isoform in vivo to correlate with the physiological responses. C1 NICHHD, METAB REGULAT SECT, ENDOCRINOL & REPROD RES BRANCH, BETHESDA, MD 20892 USA. NR 166 TC 56 Z9 56 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0197-0186 EI 1872-9754 J9 NEUROCHEM INT JI Neurochem. Int. PD MAY PY 1993 VL 22 IS 5 BP 417 EP 433 DI 10.1016/0197-0186(93)90037-6 PG 17 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KZ315 UT WOS:A1993KZ31500001 PM 8485448 ER PT J AU AULAKH, CS HILL, JL MURPHY, DL AF AULAKH, CS HILL, JL MURPHY, DL TI DIFFERENTIAL EFFECT OF SHORT-TERM AND LONG-TERM LITHIUM TREATMENT ON M-CPP-INDUCED NEUROENDOCRINE CHANGES IN RATS SO NEUROENDOCRINOLOGY LA English DT Article DE PROLACTIN; CORTICOSTERONE; GROWTH HORMONE; LITHIUM TREATMENT; 5-HT1C RECEPTOR; 5-HT1A RECEPTOR ID MAJOR AFFECTIVE-DISORDERS; M-CHLOROPHENYLPIPERAZINE; GROWTH-HORMONE; FENFLURAMINE STIMULATION; PROLACTIN SECRETION; SERUM CORTISOL; PLASMA-LEVELS; RECEPTORS; CORTICOSTERONE; ACTIVATION AB Intravenous administration of the serotonergic agent m-chlorophenylpiperazine (m-CPP) to rats produced increases in plasma prolactin and corticosterone and a decrease in plasma growth hormone concentrations. Short-term (2-4 days) and long-term (21-23 days) lithium treatment did not affect baseline levels of prolactin, corticosterone or growth hormone. Long-term lithium treatment accentuated m-CPP's effect on plasma prolactin and corticosterone but not on growth hormone levels. On the other hand, short-term lithium treatment attenuated m-CPP's effect on plasma corticosterone but not on plasma prolactin or growth hormone levels. These findings demonstrate a differential effect of the duration of lithium treatment on m-CPP-induced neuroendocrine changes. One possible explanation for this differential effect may be that different 5-HT receptor subtypes are involved in mediating different neuroendocrine functions and, furthermore, these different 5-HT receptor subtypes may be affected differentially following lithium treatment. Alternatively, lithium-induced changes in other neurotransmitter systems may be responsible for this differential effect. RP AULAKH, CS (reprint author), NATL INST MENTAL HLTH,CLIN SCI LAB,BLDG 10,RM 3D41,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 39 TC 3 Z9 3 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD MAY PY 1993 VL 57 IS 5 BP 869 EP 874 DI 10.1159/000126447 PG 6 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA LU853 UT WOS:A1993LU85300013 PM 8413823 ER PT J AU GORELICK, PB ROMAN, GC AF GORELICK, PB ROMAN, GC TI VASCULAR DEMENTIA - A TIME TO SEIZE THE MOMENT SO NEUROEPIDEMIOLOGY LA English DT Editorial Material C1 RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT NEUROL SCI,STROKE SERV,CHICAGO,IL. RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT NEUROL SCI,NEUROEPIDEMIOL SERV,CHICAGO,IL. NIH,NEUROEPIDEMIOL BRANCH,BETHESDA,MD 20892. FU NIA NIH HHS [R01-AG10102] NR 13 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0251-5350 J9 NEUROEPIDEMIOLOGY JI Neuroepidemiology PD MAY-JUN PY 1993 VL 12 IS 3 BP 139 EP 140 DI 10.1159/000110312 PG 2 WC Public, Environmental & Occupational Health; Clinical Neurology SC Public, Environmental & Occupational Health; Neurosciences & Neurology GA MD509 UT WOS:A1993MD50900001 PM 8272173 ER PT J AU BOROWSKY, B MEZEY, E HOFFMAN, BJ AF BOROWSKY, B MEZEY, E HOFFMAN, BJ TI 2 GLYCINE TRANSPORTER VARIANTS WITH DISTINCT LOCALIZATION IN THE CNS AND PERIPHERAL-TISSUES ARE ENCODED BY A COMMON GENE SO NEURON LA English DT Article ID MESSENGER-RNAS; RAT-BRAIN; SEROTONIN TRANSPORTER; DOPAMINE TRANSPORTER; GLIAL-CELLS; EXPRESSION; CLONING; NEURONS; NEUROTRANSMITTERS; NORADRENALINE AB We have isolated a cDNA encoding a high affinity, Na+/Cl--dependent glycine transporter, GLYT-2, which is distinct from another glycine transporter, GLYT-1. While the 3' sequences of these two cDNAs are identical, the 5' noncoding regions and the N-termini are completely different. GLYT-1 is found only in the white matter of the CNS, while GLYT-2 is found in the gray matter of the CNS as well as in macrophages and mast cells in peripheral tissues. Our findings suggest that tissue-specific alternative splicing or alternative promoter usage from a single gene results in two mRNA products encoding similar but distinct glycine transporters. The anatomic distibution of GLYT-2 mRNA supports the emerging status of glycine as a supraspinal neurotransmitter and suggests that glycine may function as a chemical messenger outside the CNS. C1 NINCDS,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. RP BOROWSKY, B (reprint author), NIMH,CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 50 TC 172 Z9 175 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD MAY PY 1993 VL 10 IS 5 BP 851 EP 863 DI 10.1016/0896-6273(93)90201-2 PG 13 WC Neurosciences SC Neurosciences & Neurology GA LD322 UT WOS:A1993LD32200008 PM 8494645 ER PT J AU TSOULFAS, P SOPPET, D ESCANDON, E TESSAROLLO, L MENDOZARAMIREZ, JL ROSENTHAL, A NIKOLICS, K PARADA, LF AF TSOULFAS, P SOPPET, D ESCANDON, E TESSAROLLO, L MENDOZARAMIREZ, JL ROSENTHAL, A NIKOLICS, K PARADA, LF TI THE RAT TRKC LOCUS ENCODES MULTIPLE NEUROGENIC RECEPTORS THAT EXHIBIT DIFFERENTIAL RESPONSE TO NEUROTROPHIN-3 IN PC12-CELLS SO NEURON LA English DT Article ID NERVE GROWTH-FACTOR; FACTOR MESSENGER-RNA; LEUCINE-RICH ALPHA-2-GLYCOPROTEIN; PLATELET GLYCOPROTEIN-IB; TYROSINE KINASE-ACTIVITY; AMINO-ACID SEQUENCE; MOLECULAR-CLONING; HIGH-AFFINITY; FACTOR FAMILY; PROTOONCOGENE PRODUCT AB Members of the Trk tyrosine kinase family have recently been identified as functional receptors of the NGF family of neurotrophins. Here we show the rat trkC locus to be complex, encoding at least four distinct polypeptides. Three of the encoded polypeptides are full-length receptor tyrosine kinases that differ by novel amino acid insertions in the kinase domain. A fourth protein is a truncated receptor that lacks the catalytic domain. Tyrosine phosphorylation, cross-linking, and ligand binding assays indicate that TrkC receptors interact with NT-3 and not with the related neurotrophins NGF, BDNF, xNT-4, or hNT-5. Furthermore, high and low affinity NT-3-binding sites are associated with the TrkC receptors. Stable and transient expression of TrkC receptors in PC12 cells indicates that the neurite outgrowth response elicited by NT-3 is dramatic in receptors lacking the novel kinase insert (gp150trkC) but absent in receptors containing the 14 amino acid insert in the kinase domain (gp150trkC14). These data suggest that the trkC locus encodes receptors that may be capable of mediating different biological responses within the cell. This could have important implications in understanding the role of neurotrophins in the development of the vertebrate nervous system. C1 GENENTECH INC,S SAN FRANCISCO,CA 94080. UN AM,INST FISIOL CELULAR,MEXICO CITY 04510,DF,MEXICO. RP TSOULFAS, P (reprint author), NCI,FREDERICK CANC RES & DEV CTR,MOLEC EMBRYOL SECT,ABL BASIC RES PROGRAM,FREDERICK,MD 21702, USA. RI Parada, luis/B-9400-2014; OI Tsoulfas, Pantelis/0000-0003-1974-6366 FU NCI NIH HHS [N01-CO-74101] NR 88 TC 266 Z9 269 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD MAY PY 1993 VL 10 IS 5 BP 975 EP 990 DI 10.1016/0896-6273(93)90212-A PG 16 WC Neurosciences SC Neurosciences & Neurology GA LD322 UT WOS:A1993LD32200019 PM 8494648 ER PT J AU BROWN, VJ SCHWARZ, U BOWMAN, EM FUHR, P ROBINSON, DL HALLETT, M AF BROWN, VJ SCHWARZ, U BOWMAN, EM FUHR, P ROBINSON, DL HALLETT, M TI DOPAMINE DEPENDENT REACTION-TIME DEFICITS IN PATIENTS WITH PARKINSONS-DISEASE ARE TASK SPECIFIC SO NEUROPSYCHOLOGIA LA English DT Article ID PERFORMANCE; MOVEMENTS; INFORMATION; EXECUTION; ATTENTION; DEPLETION; RAT; SET AB This study tested the hypothesis that patients with Parkinson's disease are impaired when they must rely on internal information to generate a response. Choice reaction times of control subjects and patients with Parkinson's disease, on and off their medication, were measured in tasks in which the motor demands were constant but which varied in the degree to which the stimuli held intrinsic information about the required response. A dopaminergic deficit was observed only in the tasks which employed stimuli compatible with the response and not in a task employing stimuli arbitrarily associated with the response. The data do not support the hypothesis that patients are differentially impaired in using internalized stimulus-response relationships. C1 NINCDS,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. RP BROWN, VJ (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 9,ROOM 1E104,BETHESDA,MD 20892, USA. RI Bowman, Eric/A-3780-2010; Brown, Verity/A-5235-2011 OI Brown, Verity/0000-0001-5762-1797 NR 34 TC 33 Z9 33 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PD MAY PY 1993 VL 31 IS 5 BP 459 EP 469 DI 10.1016/0028-3932(93)90060-D PG 11 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA LC127 UT WOS:A1993LC12700003 PM 8099217 ER PT J AU GREENWOOD, PM PARASURAMAN, R HAXBY, JV AF GREENWOOD, PM PARASURAMAN, R HAXBY, JV TI CHANGES IN VISUOSPATIAL ATTENTION OVER THE ADULT LIFE-SPAN SO NEUROPSYCHOLOGIA LA English DT Article; Proceedings Paper CT 1989 ANNUAL MEETING OF THE SOC FOR NEUROSCIENCE CY NOV, 1989 CL PHOENIX, AZ SP SOC NEUROSCI ID MILD SENILE DEMENTIA; VISUAL-ATTENTION; SPATIAL ATTENTION; ALZHEIMER TYPE; ALLOCATION; DOMINANCE; NEGLECT; DISEASE; BRAIN; AGE AB Shifts of visual attention elicited by spatial cues were examined for detection and letter-discrimination tasks in 90 normal adults ranging in age over each decade from the 20s to the 70s. Spatial cues were valid, invalid, or neutral in indicating probable target location and were presented either centrally at fixation or peripherally 6.7 to the left or right of fixation. Stimulus-onset asynchrony (SOA) between cue and target was varied between 200, 500 and 2000 msec. Reaction time (RT) costs and benefits associated with spatial cueing did not vary with age for: (1) the detection task; (2) the letter-discrimination task with peripheral cues; and (3) the letter-discrimination task with central cues at a short (200 msec) SOA. RT costs and benefits increased with age only for SOAs greater than 200 msec with central cueing in the discrimination task. In general, the efficiency of cue-based shifts of visuospatial attention appears relatively resistant to the effects of adult age up to 79 years. When an age effect was found. RT costs and benefits increased steadily across all age decades, the correlation with age being 0.25 and 0.38 for the 500 and 2000 msec SOAs, respectively. The findings suggest a qualitative difference in the influence of normal adult aging and effects of dementia noted in previous studies; normal aging has only a weak influence on voluntary attention shifts, whereas dementia affects both voluntary and involuntary modes of attention shifting. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. CATHOLIC UNIV AMER,DEPT PSYCHOL,WASHINGTON,DC 20064. RP GREENWOOD, PM (reprint author), CATHOLIC UNIV AMER,COGNIT SCI LAB,WASHINGTON,DC 20064, USA. FU NIA NIH HHS [AG07569] NR 48 TC 104 Z9 105 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PD MAY PY 1993 VL 31 IS 5 BP 471 EP 485 DI 10.1016/0028-3932(93)90061-4 PG 15 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA LC127 UT WOS:A1993LC12700004 PM 8502379 ER PT J AU MITCHELL, CL BARNES, MI AF MITCHELL, CL BARNES, MI TI PROCONVULSANT ACTION OF DIETHYLDITHIOCARBAMATE IN STIMULATION OF THE PERFORANT PATH SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Article DE DIETHYLDITHIOCARBAMATE; ZINC; SEIZURES; WET DOG SHAKES; PERFORANT PATH; PROCONVULSANT; HEAVY METAL ID HIPPOCAMPAL MOSSY FIBERS; TEMPORAL-LOBE EPILEPSY; METHYL-D-ASPARTATE; KAINIC ACID; RAT HIPPOCAMPUS; INDUCED SEIZURES; ZINC; RELEASE; BRAIN; STAIN AB The ability of diethyldithiocarbamate (DEDTC) to prolong electrical afterdischarge (AD) and lower the threshold for behavioral seizures elicited by stimulation of the perforant path (PPS) was examined. DEDTC was given in doses of 25, 50, and 100 mg/kg, IP. The effects of DEDTC on the threshold for wet dog shakes (WDS) and the number of WDS elicited by PPS were inconsistent. It had no effect on the duration of AD accompanied with WDS. However, DEDTC, at both 50 and 100 mg/kg, significantly lowered the threshold for rearing accompanied with forelimb clonus. At 100 mg/kg, it also prolonged the duration of AD occurring with these seizures. The effects of DEDTC were transitory and coincided with the time course for its ability to chelate the mossy fiber intravesicular pool of zinc (i.e., that which is released by activation of dentate granule cells). It is suggested that release of zinc from the mossy fibers may serve to protect the hippocampus from paroxysmal seizure activity. RP MITCHELL, CL (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 48 TC 36 Z9 37 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0892-0362 J9 NEUROTOXICOL TERATOL JI Neurotoxicol. Teratol. PD MAY-JUN PY 1993 VL 15 IS 3 BP 165 EP 171 DI 10.1016/0892-0362(93)90012-D PG 7 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA LF163 UT WOS:A1993LF16300003 PM 8393131 ER PT J AU MAGAT, AH ALGER, LS NAGEY, DA HATCH, V LOVCHIK, JC AF MAGAT, AH ALGER, LS NAGEY, DA HATCH, V LOVCHIK, JC TI DOUBLE-BLIND RANDOMIZED STUDY COMPARING AMOXICILLIN AND ERYTHROMYCIN FOR THE TREATMENT OF CHLAMYDIA-TRACHOMATIS IN PREGNANCY SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID INFECTION; EFFICACY AB Objective: To compare the efficacy and patient tolerance of amoxicillin to that of erythromycin in the treatment of lower genital tract chlamydia infections during pregnancy. Methods: A double-blind, randomized study was conducted comparing oral amoxicillin 500 mg three times daily versus oral erythromycin 500 mg four times daily for 7 days. One hundred forty-three women with positive cervical cultures for chlamydia at less than 36 weeks' gestation were enrolled. A test-of-cure culture was obtained 4 weeks after entry into the study and side effects were assessed. Success of the regimen was defined as completing the course of medication and having a negative test-of-cure culture. Results: Thirty of the 65 women in the erythromycin group (46.1%) developed symptoms while taking the medication and 15 of them were unable to continue treatment (23.1%). In contrast, five of the 65 women (7.7%) in the amoxicillin group became symptomatic, with only one of these patients intolerant of the side effects (1.5%) (P < .001). Of the 50 patients in the erythromycin group who were able to complete their course of medication, only three had a positive test of cure (6.0%). In comparison, nine of the 64 patients (14.1%) taking amoxicillin who completed their course had positive cultures at test of cure. This difference was not statistically significant (P = .14). Forty-seven of the 65 patients (72.3%) in the erythromycin group successfully completed their regimen, compared to 55 of the 65 women (84.6%) in the amoxicillin group. This difference was not statistically significant. Conclusions: These findings suggest that amoxicillin is a reasonable alternative for the treatment of chlamydia in pregnant patients intolerant to erythromycin. The incidence of side effects and intolerance to therapy for amoxicillin are less than those for erythromycin. C1 UNIV MARYLAND,SCH MED,DEPT OBSTET & GYNECOL,DIV MATERNAL FETAL MED,22 S GREENE ST,BALTIMORE,MD 21201. NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. NR 20 TC 26 Z9 27 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD MAY PY 1993 VL 81 IS 5 BP 745 EP 749 PN 1 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KY490 UT WOS:A1993KY49000022 PM 8469466 ER PT J AU FELIX, CA STRAUSS, EA DAMICO, D TSOKOS, M WINTER, S MITSUDOMI, T NAU, MM BROWN, DL LEAHEY, AM HOROWITZ, ME POPLACK, DG COSTIN, D MINNA, JD AF FELIX, CA STRAUSS, EA DAMICO, D TSOKOS, M WINTER, S MITSUDOMI, T NAU, MM BROWN, DL LEAHEY, AM HOROWITZ, ME POPLACK, DG COSTIN, D MINNA, JD TI A NOVEL GERMLINE P53 SPLICING MUTATION IN A PEDIATRIC-PATIENT WITH A 2ND MALIGNANT NEOPLASM SO ONCOGENE LA English DT Article ID CELLULAR PROTEIN P53; BREAST-CANCER; GENE; TUMOR; RETINOBLASTOMA; IDENTIFICATION; ANTIBODIES; EXPRESSION; COMPLEX AB A novel germline p53 splicing mutation was identified in a pediatric patient with two metachronous primary cancers that are constituent tumors of the Li-Fraumeni syndrome. Genomic DNA from the second tumor showed the same mutation and loss of heterozygosity at the p53 locus. The mutant mRNA and protein were present in the tumor tissue. In contrast, in the normal tissues bearing the germline mutation in the heterozygous state, predominantly normal mRNA was expressed and the mutant p53 protein was not detectable. The functional silence and relative lack of mutant p53 mRNA expression in the normal tissues of this patient may be caused by decreased stability or decreased production. If this proves a more general pattern of expression of mutant p53 in individuals with germline mutations, these findings may explain the paucity of tumors in individuals affected with the Li-Fraumeni syndrome. C1 USN,MED ONCOL BRANCH,BETHESDA,MD 20892. UNIV TEXAS,SW MED CTR,SIMMONS COMPREHENS CANC RES CTR,DALLAS,TX 75235. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. RP FELIX, CA (reprint author), CHILDRENS HOSP,DEPT PEDIAT,DIV ONCOL,34TH ST & CIVIC CTR BLVD,ROOM 9093,PHILADELPHIA,PA 19104, USA. NR 44 TC 48 Z9 48 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAY PY 1993 VL 8 IS 5 BP 1203 EP 1210 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KY328 UT WOS:A1993KY32800011 PM 8479743 ER PT J AU COGLIATI, T DUNN, BK BARNER, M CULTRARO, CM SEGAL, S AF COGLIATI, T DUNN, BK BARNER, M CULTRARO, CM SEGAL, S TI TRANSFECTED WILD-TYPE AND MUTANT MAX REGULATE CELL-GROWTH AND DIFFERENTIATION OF MURINE ERYTHROLEUKEMIA-CELLS SO ONCOGENE LA English DT Article ID C-MYC; DNA-BINDING; ERYTHROID-DIFFERENTIATION; EXPRESSION; COMMITMENT; GENE; PROTEIN; G0/G1 AB Max protein forms specific DNA-binding dimeric complexes with itself and with proteins of the c-myc gene family. A large volume of data has accumulated on the role of the c-myc proto-oncogene in cell proliferation, differentiation and tumorigenesis. To elucidate the role of max in regulating c-myc functions and the effect of both proteins on cell proliferation and differentiation, we transfected murine erythroleukemia (MEL) cells with a full-length wild-type (wt) human max gene and a mutant containing a double point mutation in the basic region (bm), which abolishes specific DNA binding. All clones expressing wt-max grow slowly, and the process of inducer-mediated differentiation is delayed. Furthermore, cells transfected with the mutated max exhibit growth retardation, accumulation in the G0/G1 phase of the cell cycle and spontaneous differentiation. Our findings are consistent with a model in which a large excess of wt-Max in the cells enhances the formation of Max-Max growth-suppressor complexes, while elevated bm-Max deprives the cell of growth-promoting Myc-Max heterodimers in a dominant-negative manner, presumably by inactivating endogenous Myc and Max. C1 UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. NCI,MED ONCOL BRANCH,BETHESDA,MD 20889. NR 37 TC 20 Z9 20 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAY PY 1993 VL 8 IS 5 BP 1263 EP 1268 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KY328 UT WOS:A1993KY32800018 PM 8479748 ER PT J AU CHAN, AML CHEDID, M MCGOVERN, ES POPESCU, NC MIKI, T AARONSON, SA AF CHAN, AML CHEDID, M MCGOVERN, ES POPESCU, NC MIKI, T AARONSON, SA TI EXPRESSION CDNA CLONING OF A SERINE KINASE TRANSFORMING GENE SO ONCOGENE LA English DT Article ID ENDOCRINE NEOPLASIA TYPE-2A; DEPENDENT PROTEIN-KINASE; OKADAIC ACID; TUMOR PROMOTER; ONCOGENE; CELLS; CHROMOSOME-10; PHOSPHORYLATION; INTERLEUKIN-1; HYBRIDIZATION AB By ectopic expression of cDNAs derived from a Ewing sarcoma cell line in NIH3T3 celts, we isolated a transforming gene (est). Sequence analysis revealed homology to the cot oncogene, which encodes a novel serine kinase. Whereas the cot product was truncated at its carboxy-terminal end as a result of gene rearrangement during transfection, est encodes the normal cot product. Thus, this gene can be activated as an oncogene by overexpression as well as by gene rearrangement. NIH3T3 cells transfected with est formed progressively growing colonies in soft agar and were tumorigenic in nude mice. The 3.2-kb est transcript was expressed at low level in both human fibroblasts and epithelial cells. Addition of the tumor promoter, okadaic acid (OA), or cytokine, interleukin 1 (IL-1), but not serum or platelet-derived growth factor (PDGF), induced increased expression of the est transcript. Using fluorescence in situ hybridization, we localized the est gene to the short arm of human chromosome 10 at band p11.2. C1 NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,1E24,BETHESDA,MD 20892. NCI,BIOL LAB,BETHESDA,MD 20892. NR 41 TC 33 Z9 34 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAY PY 1993 VL 8 IS 5 BP 1329 EP 1333 PG 5 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KY328 UT WOS:A1993KY32800026 PM 8479752 ER PT J AU FAZIOLI, F WONG, WT ULLRICH, SJ SAKAGUCHI, K APPELLA, E DIFIORE, PP AF FAZIOLI, F WONG, WT ULLRICH, SJ SAKAGUCHI, K APPELLA, E DIFIORE, PP TI THE EZRIN-LIKE FAMILY OF TYROSINE KINASE SUBSTRATES - RECEPTOR-SPECIFIC PATTERN OF TYROSINE PHOSPHORYLATION AND RELATIONSHIP TO MALIGNANT TRANSFORMATION SO ONCOGENE LA English DT Article ID EPIDERMAL GROWTH-FACTOR; PHOSPHOLIPASE-C-GAMMA; PDGF BETA-RECEPTOR; ROUS-SARCOMA VIRUS; GTPASE-ACTIVATING PROTEIN; SIGNAL TRANSDUCTION; CDNA CLONING; MONOCLONAL-ANTIBODIES; MEMBRANE SKELETON; CELLULAR PROTEINS AB A method for the isolation of tyrosine kinases substrates was developed. The method takes advantage of immunoaffinity purification of an entire set of proteins phosphorylated by tyrosine kinases, followed by generation of antisera against the purified protein pool and immunological screening of bacterial expression libraries with these antisera. By applying this methodology to the study of the phosphorylation events triggered by activation of the epidermal growth factor receptors, we have isolated several cDNAs encoding novel putative tyrosine kinase substrates. One of these cDNAs encodes radixin, a protein belonging to the band 4.1 family of proteins and highly related to ezrin and moesin. We demonstrated that, despite a high degree of relatedness, these three proteins exhibit a distinct receptor-specific pattern of phosphorylation, raising the possibility that they might mediate receptor-specific cellular changes. In addition the generation of antibodies specific for either radixin, ezrin or moesin allowed us to show that a previously described tumor transplantation antigen is indeed ezrin, thus implicating this protein in the determination of the biological phenotype of certain tumors. C1 NCI,MOLEC & CELLULAR BIOL LAB,BLDG 37,ROOM 1D23,BETHESDA,MD 20892. NCI,CELL BIOL LAB,BETHESDA,MD 20892. RI Di Fiore, Pier Paolo/K-2130-2012 OI Di Fiore, Pier Paolo/0000-0002-2252-0950 NR 67 TC 93 Z9 94 U1 0 U2 6 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAY PY 1993 VL 8 IS 5 BP 1335 EP 1345 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KY328 UT WOS:A1993KY32800027 PM 8479753 ER PT J AU MARTIN, DF CHAN, CC DESMET, MD PALESTINE, AG DAVIS, JL WHITCUP, SM BURNIER, MN NUSSENBLATT, RB AF MARTIN, DF CHAN, CC DESMET, MD PALESTINE, AG DAVIS, JL WHITCUP, SM BURNIER, MN NUSSENBLATT, RB TI THE ROLE OF CHORIORETINAL BIOPSY IN THE MANAGEMENT OF POSTERIOR UVEITIS SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1992 ANNUAL MEETING OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY CY NOV, 1992 CL DALLAS, TX SP AMER ACAD OPHTHALMOL ID RETINAL NECROSIS SYNDROME; DISEASE; HISTOPATHOLOGY; TISSUE AB Background: The ideal management of intraocular inflammation may require a tissue diagnosis. Diagnostic vitrectomy is a well-established method for acquiring such tissue. However, in some patients, the diagnostic pathology is limited to the choroid and retina and vitrectomy may yield no useful information. In such cases, a more aggressive sugical approach to obtain tissue may be useful. Methods: The authors performed chorioretinal biopsies on seven patients with progressive chorioretinal lesions of unknown etiology. Indications for biopsy included (1) macular-threatening lesions unresponsive to therapy, (2) suspicion of malignancy, or (3) suspicion of an infectious etiology. In all cases, it was expected that the results would alter therapy or other aspects of clinical care. Preoperative visual acuity was 20/200 or worse in each eye biopsied with one or more peripheral chorioretinal lesions present. Biopsy specimens were divided into three parts and submitted for light and electron microscopy, immunohistochemistry, and tissue culture. Results: On the basis of the biopsy findings, a diagnosis of multifocal choroiditis and subretinal fibrosis was rendered in three eyes, sarcoidosis in two eyes, and viral retinitis in two eyes. Therapy was changed in five patients. Final visual acuity was unchanged or improved in five eyes. Complications included the progression of lens opacity in all eyes and the development of phthisis in one eye that was extensively diseased preoperatively. Conclusion: Chorioretinal biopsy may provide useful information for determining the diagnosis and guiding the subsequent management of patients with progressive chorioretinal lesions of unknown etiology. RP MARTIN, DF (reprint author), NEI,IMMUNOL LAB,BLDG 10 ROOM 10N202,BETHESDA,MD 20892, USA. OI de Smet, Marc/0000-0002-9217-5603 NR 27 TC 30 Z9 32 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD MAY PY 1993 VL 100 IS 5 BP 705 EP 714 PG 10 WC Ophthalmology SC Ophthalmology GA LB970 UT WOS:A1993LB97000027 PM 8493014 ER PT J AU TOMER, KB MCGOWN, SR DETERDING, LJ AF TOMER, KB MCGOWN, SR DETERDING, LJ TI HYBRID TANDEM MASS-SPECTROMETRY OF ELECTROSPRAY-PRODUCED PEPTIDE IONS SO ORGANIC MASS SPECTROMETRY LA English DT Article; Proceedings Paper CT 2ND EUROPEAN TANDEM MASS SPECTROMETRY CONF CY JUL 19-22, 1992 CL UNIV WARWICK, COVENTRY, ENGLAND HO UNIV WARWICK ID COLLISIONAL-ACTIVATION; IONIZATION; DECOMPOSITION; DISSOCIATION; INSTRUMENTS; INTERFACE AB The collision-induced decomposition spectra of electrospray-produced molecule ions were investigated on a hybrid tandem mass spectrometer. The molecular mass of the peptides investigated ranged from m/z 409 (as the singly protonated molcule ion) to 1758 (as the singly, doubly and triply protonated molecules). The effect of changing the center-of-mass collision energy by changing either the laboratory collision energy or the mass of the target gas was investigated. The spectra of all ions investigated showed a large number of sequence ions representative of the peptides' structures. RP TOMER, KB (reprint author), NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Tomer, Kenneth/E-8018-2013 NR 36 TC 2 Z9 2 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0030-493X J9 ORG MASS SPECTROM JI Org. Mass Spectrom. PD MAY PY 1993 VL 28 IS 5 BP 534 EP 541 DI 10.1002/oms.1210280511 PG 8 WC Chemistry, Organic; Spectroscopy SC Chemistry; Spectroscopy GA LD163 UT WOS:A1993LD16300010 ER PT J AU SNOW, JB NAUNTON, RF AF SNOW, JB NAUNTON, RF TI RESEARCH IN THE AUDITORY AND VESTIBULAR SYSTEMS - THE RECOMMENDATIONS OF THE NATIONAL-INSTITUTE-ON-DEAFNESS-AND-OTHER-COMMUNICATION-DISORDERS NATIONAL STRATEGIC RESEARCH PLAN SO ORL-JOURNAL FOR OTO-RHINO-LARYNGOLOGY AND ITS RELATED SPECIALTIES LA English DT Article DE HEREDITARY HEARING IMPAIRMENT; OTITIS MEDIA; MOLECULAR GENETICS; COCHLEAR IMPLANTS; HEARING AIDS AB Promising fundamental research opportunities identified by the National Strategic Research Plan of the National Institute on Deafness and Other Communication Disorders include encoding of sound and gravitational/acceleration force by the inner ear, processing complex signals in the central nervous system, the molecular and cellular mechanisms responsible for hair cell motility, mechanoelectric transduction, homeostasis and metabolism of the inner ear, synaptic transmission, hair cell regeneration, plasticity and otoacoustic emissions. Clinical research opportunities include the molecular genetics of hereditary hearing impairment, the etiology of sensorineural hearing loss, environmental ototoxicity, the elucidation of tinnitus, the development of vaccines against otitis media, pharmacotherapy, rehabilitation for hearing loss and deafness with hearing aids and cochlear implants and physical therapy rehabilitation for vestibular disorders. RP SNOW, JB (reprint author), NIDOCD,DEPT HLTH & HUMAN SERV,BLDG 31,ROOM B2C02,BETHESDA,MD 20892, USA. NR 0 TC 2 Z9 2 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-1569 J9 ORL J OTO-RHINO-LARY JI ORL-J. Oto-Rhino-Laryngol. Relat. Spec. PD MAY-JUN PY 1993 VL 55 IS 3 BP 154 EP 158 PG 5 WC Otorhinolaryngology SC Otorhinolaryngology GA LB577 UT WOS:A1993LB57700007 PM 8391676 ER PT J AU MCMANAWAY, ME MARTI, GE TOSATO, G LIU, AK ALNASSER, AA KIWANUKA, J MAGRATH, IT AF MCMANAWAY, ME MARTI, GE TOSATO, G LIU, AK ALNASSER, AA KIWANUKA, J MAGRATH, IT TI HETEROTRANSPLANTATION OF HUMAN BURKITTS-LYMPHOMA CELL-LINES IN ATHYMIC NUDE-MICE - TUMOR-HOST RELATIONSHIPS SO PATHOBIOLOGY LA English DT Article DE BURKITTS LYMPHOMA; TUMORIGENICITY; C-MYC; NUDE MICE; LYMPHOMA; GROWTH FACTORS ID C-MYC; INVITRO; GROWTH; INVIVO AB We have explored the factors which influence tumorigenicity of Burkitt's lymphoma (BL) cell lines in athymic nude mice. Four cell lines, Namalwa, CA46, JD38, and ST486 revealed tumor incidence of 63.5, 69.0, 45.5 and 10.0%, respectively, in nude mice, but there was no correlation between tumor incidence and growth rate in vivo. Thus, growth rate and tumorigenicity are dependent upon different biochemical pathways. Evidence of tumor cell heterogeneity was demonstrated in the CA46 parent cell line. Five subclones derived from CA46 revealed varying degrees of tumor incidence (but very similar growth rates) that were consistently less than the parent CA46 line. Line 5, for example, produced 5.7-fold less tumors than the parent line. None of the BL cell lines or clones produced any metastatic lesions in liver, lung, brain, bone marrow or spleen in athymic nude mice. Northern blot analysis of c-myc mRNA levels in different BL cell lines revealed a possible relationship between percent tumor takes (but not growth rates) and the level of c-myc oncogene expression. However, no correlation was observed between c-myc mRNA levels and tumor incidence or growth rates among the CA46 clones. There was no correlation between the ability of the cell lines and the subclones to either secrete growth factors or to respond to growth factors secreted by Epstein-Barr virus-induced lymphoblastoid cells or lipopolysaccharide-activated monocytes, and their growth rates or percent tumor takes in mice. Comparison of tumor incidence and growth rates in irradiated and unirradiated mice showed that host factors influenced the growth of BL in nude mice. Tumor heterotransplantation after whole-body X-irradiation of the mice resulted in an increase in tumor incidence in 4 of 5 lines injected. At 2 weeks after cell inoculation, subclone 5 (CA46) had a 100% tumor take in irradiated mice, whereas in untreated mice the incidence was 0%. The appearance of large tumors at this early time point also indicated an increase in growth rate. However, the lack of an increase in tumor incidence after irradiation in one cell line (ST486) strongly suggests that the interaction of tumor cell characteristics, probably surface characteristics, with host factors is required for BL growth in nude mice. C1 US FDA,CBER,DIV CYTOKINE BIOL,BETHESDA,MD 20014. RAINBOW BABIES & CHILDRENS HOSP,CLEVELAND,OH 44106. RP MCMANAWAY, ME (reprint author), NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, USA. NR 18 TC 4 Z9 4 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-2008 J9 PATHOBIOLOGY JI Pathobiology PD MAY-AUG PY 1993 VL 61 IS 3-4 BP 164 EP 172 DI 10.1159/000163785 PG 9 WC Cell Biology; Pathology SC Cell Biology; Pathology GA LZ085 UT WOS:A1993LZ08500006 PM 8216838 ER PT J AU FOWLER, MG SIMPSON, GA SCHOENDORF, KC AF FOWLER, MG SIMPSON, GA SCHOENDORF, KC TI FAMILIES ON THE MOVE AND CHILDRENS HEALTH-CARE SO PEDIATRICS LA English DT Article DE FAMILY MOVES; GEOGRAPHIC MOBILITY; PEDIATRIC HEALTH CARE ID MEDICAL-CARE; UNITED-STATES; SERVICES; ACCESS; POOR AB Objective. To evaluate the relationship of family moves to children's health care use. Design. Analyses of data from the 1988 National Health Interview Survey of Child Health (NHIS-CH). This survey uses a multisite probability cluster technique to achieve nationally representative estimates of health and demographic characteristics of the US civilian population. Participants. 17 110 US children and their families who took part in the 1988 NHIS-CH. Measurements. The 1988 NHIS-CH collected health and demographic data including family mobility information on 17 110 US children and their families. This study analyzed the relationship of number of family moves to reporting a regular site for preventive pediatric health care services, a regular site for pediatric sick care, and routine use of emergency departments when a child was sick. Results. Overall, 8% of US children were reported to lack a regular site for preventive care services, 7% a site for sick care, and 3% routinely used an emergency department for sick care. However, 14% of children who had moved three or more times lacked a regular site for preventive care and 10% lacked a regular site for sick care, compared to only 3% of children who had never moved. Children who had moved more than twice were three times as likely to lack a regular site for preventive or sick care and 1.6 times as likely to use an emergency department for sick care, as were children who had never moved. Conclusions. Families with increased mobility are more likely to lack a regular site for both preventive and sick care and to use emergency departments when their children become ill. C1 NATL CTR HLTH STAT,HYATTSVILLE,MD 20782. RP FOWLER, MG (reprint author), NIAID,DIV AIDS,ROOM 2A24,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 17 TC 15 Z9 15 U1 0 U2 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1993 VL 91 IS 5 BP 934 EP 940 PG 7 WC Pediatrics SC Pediatrics GA KZ792 UT WOS:A1993KZ79200013 PM 8474813 ER PT J AU SCHYDLOWER, M FULLER, PG HEYMAN, RB JACOBS, EA PRUITT, AW SUTTON, JM TENENBEIN, M BAILEY, GW BOYD, GM CZECHOWICZ, D STACKPOLE, JW CRAIN, LS JONES, KL SEASHORE, MR PERRIN, J ERENBERG, G KAMINER, RK LACAMERA, R NACKASHI, JA PONCHER, JR RANDALL, V WACHTEL, RC ZIRING, PR GARNER, C HAYS, R HOLLOWELL, JG GEWANTER, H AF SCHYDLOWER, M FULLER, PG HEYMAN, RB JACOBS, EA PRUITT, AW SUTTON, JM TENENBEIN, M BAILEY, GW BOYD, GM CZECHOWICZ, D STACKPOLE, JW CRAIN, LS JONES, KL SEASHORE, MR PERRIN, J ERENBERG, G KAMINER, RK LACAMERA, R NACKASHI, JA PONCHER, JR RANDALL, V WACHTEL, RC ZIRING, PR GARNER, C HAYS, R HOLLOWELL, JG GEWANTER, H TI FETAL ALCOHOL SYNDROME AND FETAL ALCOHOL EFFECTS SO PEDIATRICS LA English DT Article C1 NIAAA,ROCKVILLE,MD 20852. NIDA,LEXINGTON,KY 40583. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. CTR DIS CONTROL,CTR ENVIRONM HLTH & INJURY CONTROL,ATLANTA,GA 30333. NR 16 TC 29 Z9 29 U1 0 U2 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1993 VL 91 IS 5 BP 1004 EP 1006 PG 3 WC Pediatrics SC Pediatrics GA KZ792 UT WOS:A1993KZ79200029 ER PT J AU SCHYDLOWER, M FULLER, PG HEYMAN, RB JACOBS, EA PRUITT, AW SUTTON, JM TENENBEIN, M BAILEY, GW BOYD, GM CZECHOWICZ, D STACKPOLE, JW AF SCHYDLOWER, M FULLER, PG HEYMAN, RB JACOBS, EA PRUITT, AW SUTTON, JM TENENBEIN, M BAILEY, GW BOYD, GM CZECHOWICZ, D STACKPOLE, JW TI ROLE OF THE PEDIATRICIAN IN PREVENTION AND MANAGEMENT OF SUBSTANCE-ABUSE SO PEDIATRICS LA English DT Article ID ALCOHOL-USE; DRUG; RISK C1 NIAAA,ROCKVILLE,MD 20852. NIDA,LEXINGTON,KY 40583. NR 23 TC 15 Z9 15 U1 1 U2 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1993 VL 91 IS 5 BP 1010 EP 1013 PG 4 WC Pediatrics SC Pediatrics GA KZ792 UT WOS:A1993KZ79200031 ER PT J AU HALL, CB GRANOFF, DM GROMISCH, DS HALSEY, NA KOHL, S MARCUSE, EK MARKS, MI NANKERVIS, GA PICKERING, LK SCOTT, GB STEELE, RW YOGEV, R PETER, G BART, KJ BROOME, C JACOBS, RF MACDONALD, NE ORENSTEIN, WA RABINOVICH, G AF HALL, CB GRANOFF, DM GROMISCH, DS HALSEY, NA KOHL, S MARCUSE, EK MARKS, MI NANKERVIS, GA PICKERING, LK SCOTT, GB STEELE, RW YOGEV, R PETER, G BART, KJ BROOME, C JACOBS, RF MACDONALD, NE ORENSTEIN, WA RABINOVICH, G TI VITAMIN-A TREATMENT OF MEASLES SO PEDIATRICS LA English DT Article ID TRIAL; MORTALITY; CHILDREN C1 CTR DIS CONTROL,ATLANTA,GA 30333. US FDA,WASHINGTON,DC 20204. AMER THORAC SOC,NEW YORK,NY. NIH,BETHESDA,MD 20892. RI Steele, Russell/A-6075-2011 NR 18 TC 21 Z9 21 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1993 VL 91 IS 5 BP 1014 EP 1015 PG 2 WC Pediatrics SC Pediatrics GA KZ792 UT WOS:A1993KZ79200032 ER PT J AU MUELLER, BU PIZZO, PA AF MUELLER, BU PIZZO, PA TI HIV AND SMOOTH-MUSCLE TUMORS - REPLY SO PEDIATRICS LA English DT Letter RP MUELLER, BU (reprint author), NCI,INFECT DIS SECT,PEDIAT BRANCH,BETHESDA,MD 20892, USA. NR 1 TC 3 Z9 3 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1993 VL 91 IS 5 BP 1020 EP 1021 PG 2 WC Pediatrics SC Pediatrics GA KZ792 UT WOS:A1993KZ79200043 ER PT J AU HULIHANGIBLIN, BA PARK, YD PIVORUN, EB GOLDMAN, D AF HULIHANGIBLIN, BA PARK, YD PIVORUN, EB GOLDMAN, D TI REGIONAL-ANALYSIS OF 5-HT1A RECEPTORS IN 2 SPECIES OF PEROMYSCUS SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE 5-HT1A RECEPTOR; SEROTONIN; DEERMOUSE; TORPOR ID SELECTIVE AGONISTS; DAILY TORPOR; SEROTONIN; MICE; AUTORECEPTORS AB Two species of deer-mice, Peromyscus maniculatus (P. man) and Peromyscus leucopus (P. leu), were compared for differences in 5-hydroxytryptamine1A (5-HT1A) receptor number and affinity. Both species enter into torpor; however, P. man enters spontaneous torpor with a higher frequency and for a longer duration than P. leu. Further, compared to P. leu a higher percentage of P. man exhibit daily torpor. Deer mice can be induced to enter torpor by a reduction in food supply, shortened photoperiods, and decreasing ambient temperature. Under these conditions, P. man enters into torpor more frequently, for longer durations, and with a higher percentage of individuals as compared to P. leu. [H-3]8-OH-DPAT was used to label 5-HT1A brain receptors in three brain regions: the frontal cortex, brainstem, and striatum. In addition, the hypothalamus and hippocampus were examined for 5-HT1A receptor differences; however, no measurable specific binding could be determined in these regions. In the frontal cortex, the B(max) values were significantly lower in P. man compared to P. leu. There were no significant differences in the B(max) values in the striatum and brainstem between P. man and P. leu. Further, there were no significant differences in the K(d) values between the two species in any of the brain regions examined. The absence of any difference in receptor number or affinity in any of the brain regions examined, except the cortex, suggests that the 5-HT1A receptor is most likely not involved in a more efficient pathway to torpor. C1 CLEMSON UNIV,DEPT BIOL SCI,CLEMSON,SC 29634. RP HULIHANGIBLIN, BA (reprint author), NIAAA,NEUROGENET LAB,BLDG 10,ROOM 3C-216,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 16 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD MAY PY 1993 VL 45 IS 1 BP 143 EP 145 DI 10.1016/0091-3057(93)90097-D PG 3 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA KZ167 UT WOS:A1993KZ16700020 PM 8516353 ER PT J AU ELMER, GI MATHURA, CB GOLDBERG, SR AF ELMER, GI MATHURA, CB GOLDBERG, SR TI GENETIC-FACTORS IN CONDITIONED TOLERANCE TO THE ANALGESIC EFFECTS OF ETONITAZENE SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Note DE GENETICS; ANALGESIA; TOLERANCE; CONDITIONING; ETONITAZENE; CXBK/BYJ; MICE ID MORPHINE; SENSITIVITY; OPIATE; MOUSE; MICE; RAT AB Tolerance to the analgesic effects of opioids have been reported to include unconditioned (physiological) and conditioned (associative) components. The purpose of the current study was to investigate the genetic and environmental factors important in the development of tolerance by using three inbred strains of mice with varying opiate receptor concentration and acute behavioral response to opioids: C57BL/6J, CXBK/ByJ, and CXBH/ByJ mice. Each strain was divided into three groups; each group received two injections per day as part of the tolerance development procedure. One group of each strain was administered an opioid (etonitazene) specifically paired with the testing room and a second injection of saline in the home colony (paired). The second group of each strain was administered saline in the testing room and etonitazene in the home colony (unpaired). A third group of each strain was administered saline in both the testing room and home colony (control). Etonitazene and saline were administered in this manner for 4 days. On day 5, animals were tested for hot-plate analgesic response following administration of etonitazene. There was a significant effect of treatment condition (paired, unpaired, control) on etonitazene-induced analgesia. In all strains, only the paired treatment condition demonstrated tolerance to the analgesic effects of etonitazene compared to the control groups. There was no significant effect of genotype or a genotype x condition interaction. Thus, genotype significantly affects the acute analgesic effects of opioids but did not affect the development of conditioned tolerance. Consideration of both components of the drug response, genetic and environmental, will lead to a better understanding of factors associated with the development of tolerance and the importance of environmental stimuli. C1 COPPIN STATE COLL,DEPT PSYCHOL,BALTIMORE,MD 21216. RP ELMER, GI (reprint author), NIDA,ADDICT RES CTR,PRECLIN PHARMACOL LAB,BEHAV PHARMACOL & GENET SECT,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 12 TC 8 Z9 8 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD MAY PY 1993 VL 45 IS 1 BP 251 EP 253 DI 10.1016/0091-3057(93)90115-A PG 3 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA KZ167 UT WOS:A1993KZ16700038 PM 8100074 ER PT J AU KIM, H KIRSCHENBAUM, LJ ROSENTHAL, I RIESZ, P AF KIM, H KIRSCHENBAUM, LJ ROSENTHAL, I RIESZ, P TI PHOTOSENSITIZED FORMATION OF ASCORBATE RADICALS BY RIBOFLAVIN - AN ESR STUDY SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID CYTO-TOXICITY; HYDROGEN-PEROXIDE; SINGLET OXYGEN; ACID; OXIDATION; PHOTOOXYGENATION; ISOALLOXAZINES; DERIVATIVES; ANTIOXIDANT; REDUCTION AB The riboflavin-sensitized photooxidation of ascorbate ion (HA-) to ascorbate radical (A.-) was followed by electron spin resonance (ESR) spectroscopy in conjunction with oxygen depletion measurements. In air-saturated aqueous media, steady-state amounts of A.- are rapidly established upon irradiation. The ESR signal disappears within a few seconds after the light is extinguished-more slowly under constant irradiation as oxygen is depleted. No photooxidation was observed in deaerated media. Similar results were obtained with other flavins and when ascorbyl palmitate was substituted for HA . The effect of added superoxide dismutase, catalase, desferrioxamine, and singlet oxygen scavengers (NaN3 and tryptophan) was studied, as was replacement of water by D2O and saturation with O2. The results are indicative of ascorbate free radical production via direct reaction between ascorbate ion and triplet riboflavin in the presence Of O2. While the presence of superoxide ion tends to reduce the steady-state concentration of A.-, competition from the reaction of HA with singlet oxygen is less apparent in this system (at HA- greater-than-or-equal-to 1 mM) than in the previously studied aluminum phthalocyanine tetrasulfonate-photosensitized reaction. C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. UNIV RHODE ISL,DEPT CHEM,KINGSTON,RI 02881. ARO,VOLCANI CTR,DEPT FOOD SCI,IL-50250 BET DAGAN,ISRAEL. NR 57 TC 45 Z9 45 U1 0 U2 4 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD MAY PY 1993 VL 57 IS 5 BP 777 EP 784 DI 10.1111/j.1751-1097.1993.tb09210.x PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LE902 UT WOS:A1993LE90200003 PM 8393195 ER PT J AU CROWELL, MD MUSIAL, F FRENCH, AW AF CROWELL, MD MUSIAL, F FRENCH, AW TI EATING LOWERS DEFECATION THRESHOLD IN PIGS THROUGH CHOLINERGIC PATHWAYS SO PHYSIOLOGY & BEHAVIOR LA English DT Note DE DEFECATION THRESHOLD; PIGS; RECTAL BALLOON DISTENSION; FEEDING; ATROPINE ID GASTROCOLONIC RESPONSE; COLONIC RESPONSE AB The effect of atropine on defecation threshold was compared to placebo pre- and postprandially in four 20- to 30-kg pigs. Stepwise balloon distention was performed 10 cm from the anal verge with a 5-cm latex balloon. Volume was increased in steps of 10 ml up to 200 ml of air or until the balloon was defecated (defecation threshold). Dependent measures were balloon volume, rectal pressure, rectal compliance, and an index of distention-induced contractile activity. Under placebo conditions, the volume and pressure to elicit defecation were significantly lower after feeding (p < 0.05). The distention-induced contractile activity significantly increased near the defecation threshold, but pre- and postprandial conditions were not different. No differences were seen between pre- and postprandial rectal compliance curves. Atropine abolished the postprandial decrease in defecation threshold, but did not affect rectal compliance. The increase in contractile activity at defecation threshold seen with placebo was abolished by atropine. These results show that eating lowers the defecation threshold in terms of distention volume and rectal pressure, and demonstrate that these changes are mediated through cholinergic pathways. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21224. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. OI Crowell, Michael/0000-0002-1162-3831 FU NIDDK NIH HHS [R01 DK31369] NR 15 TC 6 Z9 6 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD MAY PY 1993 VL 53 IS 5 BP 1029 EP 1032 DI 10.1016/0031-9384(93)90287-P PG 4 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA LD499 UT WOS:A1993LD49900030 PM 8511197 ER PT J AU PLOUZEK, CA LESLIE, KK STEPHENS, JK CHOU, JY AF PLOUZEK, CA LESLIE, KK STEPHENS, JK CHOU, JY TI DIFFERENTIAL GENE-EXPRESSION IN THE AMNION, CHORION, AND TROPHOBLAST OF THE HUMAN PLACENTA SO PLACENTA LA English DT Article ID PREGNANCY-SPECIFIC BETA-1-GLYCOPROTEIN; CARCINOEMBRYONIC ANTIGEN; HLA-G; GONADOTROPIN; PROTEINS; ALPHA; CDNA; SP1; MALIGNANCIES; SUBUNITS C1 NICHHD,HUMAN GENET BRANCH,BLDG 10,ROOM 9S242,BETHESDA,MD 20892. UNIV COLORADO,HLTH SCI CTR,DEPT PATHOL,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT OBSTET & GYNECOL,DENVER,CO 80262. NR 31 TC 20 Z9 20 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0143-4004 J9 PLACENTA JI Placenta PD MAY-JUN PY 1993 VL 14 IS 3 BP 277 EP 285 DI 10.1016/S0143-4004(05)80427-8 PG 9 WC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology SC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology GA LK456 UT WOS:A1993LK45600002 PM 8367411 ER PT J AU CHALLIS, JRG ADAMSONS, K CATZ, CS YAFFE, SJ AF CHALLIS, JRG ADAMSONS, K CATZ, CS YAFFE, SJ TI BIOLOGICAL CONSEQUENCES OF EARLY PLACENTAL LOSS - REPORT OF THE MEETING, AND ISSUES FOR FURTHER INVESTIGATION SAN-JUAN, PUERTO-RICO 21-23 NOVEMBER 1991 SO PLACENTA LA English DT Editorial Material C1 NICHHD,CTR RES MOTHERS & CHILDREN,BETHESDA,MD 20892. UNIV PUERTO RICO,SCH MED,DEPT OBSTET & GYNECOL,SAN JUAN,PR 00936. NICHHD,PREGNANCY & PERINATOL BRANCH,BETHESDA,MD 20892. RP CHALLIS, JRG (reprint author), UNIV WESTERN ONTARIO,LAWSON RES INST,MRC,FETAL & NEONATAL HLTH & DEV GRP,LONDON N6A 3K7,ONTARIO,CANADA. RI Challis, John/E-7419-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0143-4004 J9 PLACENTA JI Placenta PD MAY-JUN PY 1993 VL 14 IS 3 BP 355 EP 360 DI 10.1016/S0143-4004(05)80433-3 PG 6 WC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology SC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology GA LK456 UT WOS:A1993LK45600008 PM 8103598 ER PT J AU GLANZ, K KRISTAL, AR SORENSEN, G PALOMBO, R HEIMENDINGER, J PROBART, C AF GLANZ, K KRISTAL, AR SORENSEN, G PALOMBO, R HEIMENDINGER, J PROBART, C TI DEVELOPMENT AND VALIDATION OF MEASURES OF PSYCHOSOCIAL FACTORS INFLUENCING FAT-RELATED AND FIBER-RELATED DIETARY BEHAVIOR SO PREVENTIVE MEDICINE LA English DT Article ID MODEL; RISK C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MASSACHUSETTS DEPT HLTH,BOSTON,MA. NCI,BETHESDA,MD 20892. UNIV FLORIDA,GAINESVILLE,FL 32611. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. RP GLANZ, K (reprint author), TEMPLE UNIV,DEPT HLTH EDUC,304 SELTZER HALL,PHILADELPHIA,PA 19122, USA. RI Kristal, Alan/A-8779-2008 FU NCI NIH HHS [U01 CA51687, U01 CA51686, U01 CA51671] NR 28 TC 93 Z9 93 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 0091-7435 J9 PREV MED JI Prev. Med. PD MAY PY 1993 VL 22 IS 3 BP 373 EP 387 DI 10.1006/pmed.1993.1031 PG 15 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA LC523 UT WOS:A1993LC52300008 PM 8392175 ER PT J AU KURUCZ, I JOST, CR GEORGE, AJT ANDREW, SM SEGAL, DM AF KURUCZ, I JOST, CR GEORGE, AJT ANDREW, SM SEGAL, DM TI A BACTERIALLY EXPRESSED SINGLE-CHAIN FV CONSTRUCT FROM THE 2B4 T-CELL RECEPTOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ANTIGEN-BINDING SITE; MONOCLONAL-ANTIBODIES; ESCHERICHIA-COLI; BETA-CHAIN; CYTOCHROME-C; I-E; GENE; RECOGNITION; PROTEIN; INVIVO AB A single-chain Fv construct of the 2B4 T-cell receptor has been made and expressed in Escherichia coli as bacterial inclusion bodies. After solubilization in 6 M guanidine hydrochloride and formation of mixed disulfides with glutathione, the protein was refolded by diluting out the denaturant and allowing intramolecular disulfide bridges to form by disulfide exchange. Approximately 65-100 mg of refolded protein was obtained from 1 liter of bacterial culture, an appreciable fraction of which was monomeric in nondenaturing solvents. This protein bound to three monoclonal antibodies specific for allotypic or idiotypic determinants on the native 2B4 variable region but did not bind several other anti-T-cell-receptor monoclonal antibodies that lacked such specificity. These experiments show that T-cell-receptor variable regions, like the V regions of antibodies, can form a well-behaved single-chain Fv molecule and provide large amounts of recombinant single-chain Fv T-cell receptor that can be used to study T-cell function. RP KURUCZ, I (reprint author), NCI, EXPTL IMMUNOL BRANCH, BLDG 10, ROOM 4B17, BETHESDA, MD 20892 USA. OI George, Andrew/0000-0002-2866-0241 NR 47 TC 46 Z9 46 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 3830 EP 3834 DI 10.1073/pnas.90.9.3830 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000013 PM 8387198 ER PT J AU LISZIEWICZ, J SUN, D METELEV, V ZAMECNIK, P GALLO, RC AGRAWAL, S AF LISZIEWICZ, J SUN, D METELEV, V ZAMECNIK, P GALLO, RC AGRAWAL, S TI LONG-TERM TREATMENT OF HUMAN IMMUNODEFICIENCY VIRUS-INFECTED CELLS WITH ANTISENSE OLIGONUCLEOTIDE PHOSPHOROTHIOATES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AIDS THERAPY ID INHIBITION; REPLICATION; EXPRESSION; OLIGODEOXYNUCLEOTIDES; GENE; RNA AB The antiviral activity of antisense oligodeoxy-nucleotide phosphorothioates complementary to the tat gene, the gag mRNA, and the rev mRNA were studied in a long-term infection model. Three antisense oligonucleotides directed to the splice-acceptor site of the tat gene failed to suppress human immunodeficiency virus type 1 replication at 1 muM concentration in long-term culture. In contrast, two oligodeoxynucleotide phosphorothioates (28-mer) complementary to the gag and the rev mRNAs inhibited viral replication for >80 days, and the antiviral activity was sequence- and length-dependent. In addition, after pretreatment of cells we could reduce the concentration of the antisense oligodeoxynucleotides by >10-fold and still maintain the inhibition of viral replication. These results suggest that chemotherapy for human immunodeficiency virus type 1 infection with antisense oligodeoxynucleotide phosphorothioates may be achieved by an initial high-dose treatment followed by a lower maintenance dose. C1 HYBRIDON INC,1 INNOVAT DR,BIOTECHNOL RES PK,WORCESTER,MA 01605. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. WORCESTER FDN EXPTL BIOL INC,SHREWSBURY,MA 01545. RI Metelev, Valeri/I-3238-2012 NR 24 TC 94 Z9 95 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 3860 EP 3864 DI 10.1073/pnas.90.9.3860 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000019 PM 8483903 ER PT J AU KRSMANOVIC, LZ STOJILKOVIC, SS MERTZ, LM TOMIC, M CATT, KJ AF KRSMANOVIC, LZ STOJILKOVIC, SS MERTZ, LM TOMIC, M CATT, KJ TI EXPRESSION OF GONADOTROPIN-RELEASING-HORMONE RECEPTORS AND AUTOCRINE REGULATION OF NEUROPEPTIDE RELEASE IN IMMORTALIZED HYPOTHALAMIC NEURONS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GONADOTROPIN-RELEASING HORMONE RECEPTOR TRANSCRIPTS; BINDING SITES; CYTOPLASMIC CALCIUM; EPISODIC SECRETION ID ULTRASHORT-LOOP FEEDBACK; RHESUS-MONKEY; MEDIOBASAL HYPOTHALAMUS; GROWTH-HORMONE; GNRH NEURONS; FEMALE RAT; SECRETION; INHIBITION; INVITRO; MODULATION AB The hypothalamic control of gonadotropin secretion is mediated by episodic basal secretion and midcycle ovulatory surges of gonadotropin-releasing hormone (GnRH), which interacts with specific plasma membrane receptors in pituitary gonadotrophs. Similar GnRH receptors and their mRNA transcripts were found to be expressed in immortalized hypothalamic neurons, which release GnRH in a pulsatile manner in vitro. Activation of these neuronal GnRH receptors elicited dose-related intracellular Ca2+ concentration responses that were dependent on calcium mobilization and entry and were inhibited by GnRH antagonists. Exposure of perifused neurons to a GnRH agonist analog caused a transient elevation of GnRH release and subsequent suppression of the basal pulsatile secretion. This was followed by dose-dependent induction of less frequent but larger GnRH pulses and ultimately by single massive episodes of GnRH release. The ability of GnRH to exert autocrine actions on its secretory neurons, and to promote episodic release and synchronized discharge of the neuropeptide, could reflect the operation of the endogenous pulse generator and the genesis of the preovulatory GnRH surge in vivo. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLDG 49,ROOM 6A-36,BETHESDA,MD 20892. RI Tomic, Melanija/C-3371-2016 NR 36 TC 129 Z9 129 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 3908 EP 3912 DI 10.1073/pnas.90.9.3908 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000029 PM 8387201 ER PT J AU KAMMORGAN, LNW SMITHGILL, SJ TAYLOR, MG ZHANG, L WILSON, AC KIRSCH, JF AF KAMMORGAN, LNW SMITHGILL, SJ TAYLOR, MG ZHANG, L WILSON, AC KIRSCH, JF TI HIGH-RESOLUTION MAPPING OF THE HYHEL-10 EPITOPE OF CHICKEN LYSOZYME BY SITE-DIRECTED MUTAGENESIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE EPITOPE MAPPING; PROTEIN PROTEIN INTERACTION ID ANTIBODY-ANTIGEN COMPLEX; AMINO-ACID SEQUENCE; EGG-WHITE LYSOZYME; STAPHYLOCOCCAL NUCLEASE; 3-DIMENSIONAL STRUCTURE; BINDING; PROTEINS; SURFACE; ENZYME AB The complex formed between hen egg white lysozyme (HEL) and the monoclonal antibody HyHEL-10 Fab fragment has an interface composed of van der Waals interactions, hydrogen bonds, and a single ion pair. The antibody overlaps part of the active site cleft. Putative critical residues within the epitope region of HEL, identified from the x-ray crystallographic structure of the complex, were replaced by site-directed mutagenesis to probe their relative importance in determining affinity of the antibody for HEL. Twenty single mutations of HEL at three contact residues (Arg-21HEL, Asp-101HEL, and Gly-102HEL) and at a partially buried residue (Asn-19HEL) in the epitope were made, and the effects on the free energies of dissociation were measured. A correlation between increased amino acid side-chain volume and reduced affinity for HELs with mutations at position 101 was observed. The D101G(HEL) mutant is bound to HyHEL-10 as tightly as wild-type enzyme, but the DELTADELTAG(dissoc) is increased by about 2.2 kcal (9.2 kJ)/mol for the larger residues in this position. HEL variants with lysine or histidine replacements for arginine at position 21 are bound 1.4-2.7 times more tightly than those with neutral or negatively charged amino acids in this position. These exhibit 1/40 the affinity for HyHEL-10 Fab compared with wild type. There is no side-chain volume correlation with DELTADELTAG(dissoc) at position 21. Although Gly-102HEL and Asn-19HEL are in the epitope, replacements at these positions have no effect on the affinity of HEL for the antibody. C1 LAWRENCE BERKELEY LAB,CTR ADV MAT,BERKELEY,CA 94720. NCI,GENET LAB,BETHESDA,MD 20892. RP KAMMORGAN, LNW (reprint author), UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,DIV BIOCHEM & MOLEC BIOL,BERKELEY,CA 94720, USA. FU NIAID NIH HHS [AI07989]; NIGMS NIH HHS [GM14514-01] NR 34 TC 59 Z9 59 U1 1 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 3958 EP 3962 DI 10.1073/pnas.90.9.3958 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000039 PM 7683415 ER PT J AU FANANAPAZIR, L DALAKAS, MC CYRAN, F COHN, G EPSTEIN, ND AF FANANAPAZIR, L DALAKAS, MC CYRAN, F COHN, G EPSTEIN, ND TI MISSENSE MUTATIONS IN THE BETA-MYOSIN HEAVY-CHAIN GENE CAUSE CENTRAL CORE DISEASE IN HYPERTROPHIC CARDIOMYOPATHY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID VENTRICULAR ALPHA-MYOSIN; MALIGNANT HYPERTHERMIA; MITOCHONDRIAL-DNA; MUSCLE; CHROMOSOME-19; EXPRESSION; MYOPATHY AB Hypertrophic cardiomyopathy (HCM) is an important cause of sudden death in apparently healthy young individuals. In less than half of kindreds with HCM, the disease is linked to the beta-myosin heavy-chain gene locus (MYH7). We have recently described two missense MYH7 gene mutations [Arg-403 to Gln (R403Q) and Leu-908 to Val (L908V)] and found that the mutant message is present in skeletal muscle (soleus) and that the mutant beta-myosin obtained from soleus muscle has abnormal in vitro motility activity. Having identified a second kindred with the R403Q mutation, and 3 other kindreds with two additional mutations (G741R and G256E), we performed histochemical analysis of soleus muscle biopsies from 25 HCM patients with one of these four mutations. Light microscopic examination of the NADH-stained biopsies revealed the presence of central core disease (CCD) of skeletal muscle, a rare autosomal dominant nonprogressive myopathy characterized by a predominance of type I ''slow'' fibers and an absence of mitochondria in the center of many type I fibers. CCD was present in 10 of 13 patients with the L908V mutation, 5 of 8 patients with the R403Q mutation, 1 of 3 patients with the G741R mutation, and 1 patient with the G256E mutation. Mild-to-moderate myopathic changes with muscle fiber hypertrophy were present in 16 patients. Notably, CCD was present in 2 adults and 3 children with the L908V mutation who did not have cardiac hypertrophy. In contrast, soleus muscle samples from 5 patients from 4 kindreds in which HCM was not linked to the MYH7 locus showed no myopathy or CCD. Soleus muscle biopsies from 5 control subjects also showed normal histology. This work demonstrates that (i) MYH7-associated HCM is often a disease of striated muscle but with predominant cardiac involvement and (ii) a subset of HCM patients with MYH7 gene missense mutations have CCD. C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NINCDS,NEUROMUSCULAR SECT,BETHESDA,MD 20892. RP FANANAPAZIR, L (reprint author), NHLBI,CARDIOL BRANCH,ROOM 7B-14,BLDG 10,BETHESDA,MD 20892, USA. NR 33 TC 150 Z9 154 U1 1 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 3993 EP 3997 DI 10.1073/pnas.90.9.3993 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000046 PM 8483915 ER PT J AU BEATTY, WL BYRNE, GI MORRISON, RP AF BEATTY, WL BYRNE, GI MORRISON, RP TI MORPHOLOGIC AND ANTIGENIC CHARACTERIZATION OF INTERFERON GAMMA-MEDIATED PERSISTENT CHLAMYDIA-TRACHOMATIS INFECTION INVITRO SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID OUTER-MEMBRANE PROTEIN; PROTECTIVE MONOCLONAL-ANTIBODIES; ULTRASTRUCTURAL ANALYSIS; CELLS; PATHOGENESIS; PSITTACI; DISEASE; GROWTH; IMMUNOPATHOLOGY; HISTOPATHOLOGY AB An in vitro cell culture system was used to study the effect of interferon gamma (IFN-gamma) on Chlamydia trachomatis growth and differentiation. The effect of IFN-gamma on chlamydiae was dose-dependent. IFN-gamma at 2 ng/ml completely inhibited chlamydial growth and differentiation; however, persistent infection was established when chlamydiae were cultured with IFN-gamma at 0.2 ng/ml. Persistent infection was characterized by the development of noninfectious atypical chlamydial forms from which infectious progeny could be recovered only when IFN-gamma was removed from the culture system. Analysis of persistently infected cells by immunofluorescent microscopy and immunoblotting with specific antibodies revealed that the atypical chlamydial forms had near-normal levels of the 60-kDa heat shock protein, an immunopathologic antigen, and a paucity of the major outer membrane protein, a protective antigen. Furthermore, steady-state levels of other outer membrane constituents, such as the 60-kDa cysteine-rich outer membrane protein and lipopolysaccharide, were greatly reduced. If IFN-gamma causes similar events to occur in vivo, then persistently infected cells could augment the pathogenesis of the chronic inflammatory sequelae that follow chlamydial infection by serving as depots of antigen capable of stimulating a sustained inflammatory response. C1 NIAID,INTRACELLULAR PARASITES LAB,ROCKY MTN LABS,HAMILTON,MT 59840. UNIV WISCONSIN,DEPT MED MICROBIOL & IMMUNOL,MADISON,WI 53706. FU NIAID NIH HHS [AI 19782, AI 31494] NR 32 TC 319 Z9 323 U1 1 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 3998 EP 4002 DI 10.1073/pnas.90.9.3998 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000047 PM 8387206 ER PT J AU WANG, LM KEEGAN, AD LI, WQ LIENHARD, GE PACINI, S GUTKIND, JS MYERS, MG SUN, XJ WHITE, MF AARONSON, SA PAUL, WE PIERCE, JH AF WANG, LM KEEGAN, AD LI, WQ LIENHARD, GE PACINI, S GUTKIND, JS MYERS, MG SUN, XJ WHITE, MF AARONSON, SA PAUL, WE PIERCE, JH TI COMMON ELEMENTS IN INTERLEUKIN-4 AND INSULIN SIGNALING PATHWAYS IN FACTOR-DEPENDENT HEMATOPOIETIC-CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE INSULIN RECEPTOR SUBSTRATE-1; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION ID STIMULATES TYROSINE PHOSPHORYLATION; INTACT-CELLS; ENDOGENOUS SUBSTRATE; JUXTAMEMBRANE REGION; MOLECULAR-CLONING; KINASE-ACTIVITY; RECEPTOR; PROTEIN; TRANSDUCTION; GROWTH AB Interleukin 4 (IL-4), insulin, and insulin-like growth factor I (IGF-I) efficiently induced DNA synthesis in the IL-3-dependent murine myeloid cell lines FDC-P1 and FDC-P2. Although these factors could not individually sustain long-term growth of these lines, a combination of IL-4 with either insulin or IGF-I did support continuous growth. The principal tyrosine-phosphorylated substrate observed in FDC cells stimulated with IL-4, previously designated 4PS, was of the same size (170 kDa) as the major substrate phosphorylated in response to insulin or IGF-I. These substrates had phosphopeptides of the same size when analyzed by digestion with Staphylococcus aureus V8 protease, and each tightly associated with the 85-kDa component of phosphatidylinositol 3-kinase after factor stimulation. IRS-1, the principal substrate phosphorylated in response to insulin or IGF-I stimulation in nonhematopoietic cells, is similar in size to 4PS. However, anti-IRS-1 antibodies failed to efficiently precipitate 4PS, and some phosphopeptides generated by V8 protease digestion of IRS-1 were distinct in size from the phosphopeptides of 4PS. Nevertheless, IL-4, insulin and IGF-I were capable of stimulating tyrosine phosphorylation of IRS-1 in FDC cells that expressed this substrate as a result of transfection. These findings indicate that (i) IL-4, insulin, and IGF-I use signal transduction pathways in FDC lines that have at least one major feature in common, the rapid tyrosine phosphorylation of 4PS, and (ii) insulin and IGF-I stimulation of hematopoietic cell lines leads to the phosphorylation of a substrate that may be related to but is not identical to IRS-1. C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. DARTMOUTH COLL SCH MED,DEPT BIOCHEM,HANOVER,NH 03755. UNIV FLORENCE,INST GEN PATHOL,I-50121 FLORENCE,ITALY. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. HARVARD UNIV,JOSLIN DIABET CTR,SCH MED,DEPT MED,BOSTON,MA 02215. RI Gutkind, J. Silvio/A-1053-2009 NR 45 TC 175 Z9 175 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 4032 EP 4036 DI 10.1073/pnas.90.9.4032 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000054 PM 7683417 ER PT J AU KERSTING, U KERSTING, D SPRING, KR AF KERSTING, U KERSTING, D SPRING, KR TI KETOCONAZOLE ACTIVATES CL- CONDUCTANCE AND BLOCKS CL- AND FLUID ABSORPTION BY CULTURED CYSTIC-FIBROSIS (CFPAC-1) CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ARACHIDONIC-ACID METABOLISM; AIRWAY EPITHELIA; LIVER-MICROSOMES; GENE-TRANSFER; FATTY-ACIDS; TRANSPORT; INVITRO; RABBIT; MECHANISMS; CHLORIDE AB The role of arachidonic acid metabolites in the regulation of apical cell membrane Cl- conductance and transepithelial transport of fluid and Cl- by cultured pancreatic cells from cystic fibrosis (CFPAC-1) and corrected (PAC-1) cell lines was evaluated by the use of inhibitors. CFPAC-1 cells did not exhibit an apical membrane Cl- conductance, absorbed Cl- and fluid, and did not respond to stimulation or inhibition of cAMP action. PAC-1 cells exhibited a cAMP-responsive apical Cl- conductance, which was blocked by indomethacin, a cyclooxygenase inhibitor. Ketoconazole, an epoxygenase inhibitor, had virtually no effects on PAC-1 cell Cl- conductance but caused CFPAC-1 cells to develop a cAMP-insensitive Cl- conductance, blocked Cl- and fluid absorption, and reduced transepithelial electrical resistance. Ketoconazole treatment effectively reversed the cystic fibrosis defect in these cultured cells. C1 NHLBI,BETHESDA,MD 20892. NR 52 TC 26 Z9 26 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 4047 EP 4051 DI 10.1073/pnas.90.9.4047 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000057 PM 7683418 ER PT J AU MUEGGE, K WEST, M DURUM, SK AF MUEGGE, K WEST, M DURUM, SK TI RECOMBINATION SEQUENCE-BINDING PROTEIN IN THYMOCYTES UNDERGOING T-CELL RECEPTOR GENE REARRANGEMENT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID V(D)J RECOMBINATION; SIGNAL SEQUENCE; IMMUNOGLOBULIN GENES; IDENTIFICATION; DEFINITION; PROMOTER; CONTAINS AB Rearrangement of T-cell antigen receptor and immunoglobulin genes occurs in immature lymphoid cells by an unknown mechanism. To identify components of the rearrangement machinery, we isolated a population of murine thymocytes enriched for rearranging pre-T cells. In the nuclear fraction of these cells, we detected a protein that specifically bound the recombination sequences that flank T-cell receptor and immunoglobulin genes and are required for their rearrangement. This protein recognized both heptamer and nonamer motifs of the recombination sequence, separated by either 12 or 23 bp. The protein complexed with the recombination sequence oligonucleotide had an apparent molecular mass of 30 kDa. The binding characteristics of the protein and its presence in rearranging thymocytes and cell lines suggest that it could serve as the recognition unit of a recombinase complex. C1 NCI,MOLEC IMMUNOREGULAT LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. RP MUEGGE, K (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 21 TC 14 Z9 14 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 4151 EP 4155 DI 10.1073/pnas.90.9.4151 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000078 PM 8483928 ER PT J AU SCHWEINFEST, CW HENDERSON, KW SUSTER, S KONDOH, N PAPAS, TS AF SCHWEINFEST, CW HENDERSON, KW SUSTER, S KONDOH, N PAPAS, TS TI IDENTIFICATION OF A COLON MUCOSA GENE THAT IS DOWN-REGULATED IN COLON ADENOMAS AND ADENOCARCINOMAS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE COLORECTAL TUMORIGENESIS; TUMOR-SUPPRESSOR GENE; CDNA SUBTRACTION ID TRANSCRIPTION FACTOR; COLORECTAL CANCERS; EXPRESSION; MUTATIONS; CARCINOMA; ONCOGENE; DNA; CHROMOSOME-5Q21; TUMORIGENESIS; SEQUENCES AB A cDNA, which we call DRA (for down-regulated in adenoma) has been isolated. Its mRNA is expressed exclusively in normal colon tissue, probably only in the mucosal epithelia. Expression of the DRA gene is significantly decreased in adenomas (polyps) and adenocarcinomas of the colon. The DRA gene appears to be a single-copy gene present on chromosome 7, a chromosome associated with colorectal tumorigenesis. The predicted DRA polypeptide is an 84,500-Da protein that contains charged clusters of amino acids, primarily at the NH2 and COOH termini. Together with potential nuclear targeting motifs, an acidic transcriptional activation domain, and a homeobox domain, these elements suggest a transcription factor or a protein that may interact with transcription factors. Such a function may be consistent with a role in tissue-specific gene expression and/or as a candidate tumor-suppressor gene. C1 PROGRAM RESOURCES INC,FREDERICK,MD 21702. MT SINAI MED CTR,DEPT PATHOL & LAB MED,MIAMI BEACH,FL 33140. UNIV MIAMI,SCH MED,MIAMI,FL 33140. RP SCHWEINFEST, CW (reprint author), NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702, USA. NR 37 TC 156 Z9 158 U1 0 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 4166 EP 4170 DI 10.1073/pnas.90.9.4166 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000081 PM 7683425 ER PT J AU DRAKE, JW AF DRAKE, JW TI RATES OF SPONTANEOUS MUTATION AMONG RNA VIRUSES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID VESICULAR STOMATITIS-VIRUS; MURINE LEUKEMIA-VIRUS; NUCLEOTIDE-SEQUENCE; REVERSE-TRANSCRIPTASE; HIGH-FREQUENCY; CLONAL POOLS; Q-BETA; POLIOVIRUS; MUTANT; BACTERIOPHAGE AB Simple methods are presented to estimate rates of spontaneous mutation from mutant frequencies and population parameters in RNA viruses. Published mutant frequencies yield a wide range of mutation rates per genome per replication, mainly because mutational targets have usually been small and, thus, poor samples of the mutability of the average base. Nevertheless, there is a clear central tendency for lytic RNA viruses (bacteriophage Qbeta, poliomyelitis, vesicular stomatitis, and influenza A) to display rates of spontaneous mutation of almost-equal-to 1 per genome per replication. This rate is some 300-fold higher than previously reported for DNA-based microbes. Lytic RNA viruses thus mutate at a rate close to the maximum value compatible with viability. Retroviruses (spleen necrosis, murine leukemia, Rous sarcoma), however, mutate at an average rate about an order of magnitude lower than lytic RNA viruses. RP DRAKE, JW (reprint author), NIEHS,MOLEC GENET LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 39 TC 410 Z9 419 U1 6 U2 20 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 4171 EP 4175 DI 10.1073/pnas.90.9.4171 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000082 PM 8387212 ER PT J AU SHAHABUDDIN, M TOYOSHIMA, T AIKAWA, M KASLOW, DC AF SHAHABUDDIN, M TOYOSHIMA, T AIKAWA, M KASLOW, DC TI TRANSMISSION-BLOCKING ACTIVITY OF A CHITINASE INHIBITOR AND ACTIVATION OF MALARIAL PARASITE CHITINASE BY MOSQUITO PROTEASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE PLASMODIUM; PERITROPHIC MATRIX; ZYMOGEN; VACCINE; ALLOSAMIDIN ID PLASMODIUM-GALLINACEUM; PERITROPHIC MEMBRANE; ALLOSAMIDIN; PENETRATION; MIDGUT AB During development in the mosquito midgut, malarial parasites must traverse a chitin-containing peritrophic matrix (PM) that forms around the food bolus. Previously Huber et al. [Huber, M., Cabib, E. & Miller, L. H. (1991) Proc. Natl. Acad. Sci. USA 88, 2807-2810] reported that the parasite secretes a protein with chitinase activity, and they suggested that parasite chitinase (EC 3.2.1.14) plays an important role in the parasite's egress from the blood meal. We found that allosamidin, a specific inhibitor of chitinase, completely blocked oocyst development in vivo and thus blocked malaria parasite transmission. Addition of exogenous chitinase to the blood meal prevented the PM from forming and reversed the transmission-blocking activity of allosamidin. Using exogenous chitinase, we also found that the PM does not limit the number of parasites that develop into oocysts, suggesting that the parasite produces sufficient quantities of chitinase to penetrate this potential barrier. In addition, we found that treatment of parasite chitinase with a diisopropyl fluorophosphate-sensitive trypsinlike protease from the mosquito midgut or endoproteinase Lys-C increased its enzymatic activity. These results suggest that malaria parasite has evolved an intricate mechanism to adapt to the PM and the protease-rich environment of the mosquito midgut. C1 NIAID,MOLEC VACCINE SECT,MALARIA RES LAB,ROOM B1-37,BLDG 4,BETHESDA,MD 20892. CASE WESTERN RESERVE UNIV,SCH MED,INST PATHOL,CLEVELAND,OH 44106. FU NIAID NIH HHS [AI-10645] NR 16 TC 201 Z9 205 U1 1 U2 10 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1993 VL 90 IS 9 BP 4266 EP 4270 DI 10.1073/pnas.90.9.4266 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LA430 UT WOS:A1993LA43000101 PM 8483942 ER PT J AU ELMALLAKH, RS SUDDATH, RL WYATT, RJ AF ELMALLAKH, RS SUDDATH, RL WYATT, RJ TI INTERLEUKIN-1-ALPHA AND INTERLEUKIN-2 IN CEREBROSPINAL-FLUID OF SCHIZOPHRENIC SUBJECTS SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE CEREBROSPINAL FLUID; INTERLEUKIN-1-ALPHA; INTERLEUKIN-2; INTERLEUKINS; SCHIZOPHRENIA ID T-CELL; LYMPHOCYTES; IMMUNITY AB 1. It has been postulated that the interrelated processes of neurodegeneration, neuroplasticity, and neuroimmunological abnormalities may play a role in the pathophysiology Of schizophrenia. Since, interleukins are produced in the central nervous system and have cytokine and growth promoting properties, they are an obvious choice to consider in these neural processes. 2. Cerebrospinal fluid obtained from schizophrenic patients, on and off medications, and from normal controls was assayed for Interleukin-1alpha (IL-1alpha) and interleukin-2 (IL-2) using a sensitive enzyme-linked immunoassay. 3. IL-1alpha concentration were below the detection limits of the assay in both controls and schizophrenics. 4. IL-2 levels were under 1 ng/ml CSF in nearly all subjects. There was no significant difference in IL-2 levels between medicated and medication-free schizophrenics or when patients were compared to controls. C1 NIMH,HOSP NEUROPSYCHIAT RES,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. NR 26 TC 39 Z9 41 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0278-5846 J9 PROG NEURO-PSYCHOPH JI Prog. Neuro-Psychopharmacol. Biol. Psychiatry PD MAY PY 1993 VL 17 IS 3 BP 383 EP 391 DI 10.1016/0278-5846(93)90072-Z PG 9 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA KW160 UT WOS:A1993KW16000005 PM 8475320 ER PT J AU LEE, B AF LEE, B TI ESTIMATION OF THE MAXIMUM CHANGE IN STABILITY OF GLOBULAR-PROTEINS UPON MUTATION OF A HYDROPHOBIC RESIDUE TO ANOTHER OF SMALLER SIZE SO PROTEIN SCIENCE LA English DT Article DE HYDROPHOBIC EFFECT; MUTATION; PROTEIN STABILITY; VOLUME CORRECTION ID AMINO-ACIDS; THERMODYNAMICS; ENERGETICS; HYDRATION; PACKING; WATER AB Although the hydrophobic effect is generally considered to be one of the most important forces in stabilizing the folded structure of a globular protein molecule, there is a lack of consensus on the precise magnitude of this effect. The magnitude of the hydrophobic effect is most directly measured by observing the change in stability of a protein molecule when an internal hydrophobic residue is mutated to another of smaller size. Results of such measurements have, however, been confusing because they vary greatly and are generally considerably larger than expected from the transfer free energies of corresponding small molecules. In this article, a thermodynamic argument is presented to show (1) that the variation is mainly due to that in the flexibility of the protein molecule at the site of mutation, (2) that the maximum destabilization occurs when the protein at the site of mutation is rigid, in which case the value of the destabilization is approximately given by the work of cavity formation in water, and (3) that the transfer free energy approximately gives the minimum of the range of variations. The best numerical agreements between the small molecule and the protein systems are obtained when the data from the small molecule system are expressed as the molarity-based standard free energies without other corrections. RP LEE, B (reprint author), NCI,MOLEC BIOL LAB,BLDG 37,ROOM 4B15,BETHESDA,MD 20892, USA. NR 29 TC 82 Z9 82 U1 1 U2 2 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0961-8368 J9 PROTEIN SCI JI Protein Sci. PD MAY PY 1993 VL 2 IS 5 BP 733 EP 738 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KY938 UT WOS:A1993KY93800005 PM 8495196 ER PT J AU BRYANT, SH LAWRENCE, CE AF BRYANT, SH LAWRENCE, CE TI AN EMPIRICAL ENERGY FUNCTION FOR THREADING PROTEIN-SEQUENCE THROUGH THE FOLDING MOTIF SO PROTEINS-STRUCTURE FUNCTION AND GENETICS LA English DT Article DE PROTEIN FOLDING; RESIDUE CONTACTS; CONFORMATIONAL ENERGY ID KNOWLEDGE-BASED PREDICTION; GLOBULAR-PROTEINS; CRYSTAL-STRUCTURE; EGLIN-C; 3-DIMENSIONAL STRUCTURE; SOLVENT ACCESSIBILITY; SUBTILISIN CARLSBERG; RESIDUE CONTACTS; FOLDED PROTEINS; MEAN FORCE AB In this paper we present a new residue contact potantial derived by statistical analysis of protein crystal structures. This gives mean hydrophobic and pairwise contact energies as a function of residue type and distance interval. To test the accuracy of this potential we generate model structures by ''threading'' different sequences through backbone folding motifs found in the structural data base. We find that conformational energies calculated by summing contact potentials show perfect specificity in matching the correct sequences with each globular folding motif in a 161-protein data set. They also identify correct models with the core folding motifs of hemerythrin and immunoglobulin McPC603 V1-domain, among millions of alternatives possible when we align subsequences with alpha-helices and beta-strands, and allow for variation in the lengths of intervening loops. We suggest that contact potentials reflect important constraints on non-bonded interaction in native proteins, and that ''threading'' may be useful for structure prediction by recognition of folding motif. C1 NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,ALBANY,NY 12201. RP BRYANT, SH (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BLDG 38A,8TH FLOOR,8600 ROCKVILLE PIKE,BETHESDA,MD 20879, USA. NR 72 TC 318 Z9 327 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-3585 J9 PROTEINS JI Proteins PD MAY PY 1993 VL 16 IS 1 BP 92 EP 112 DI 10.1002/prot.340160110 PG 21 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KZ795 UT WOS:A1993KZ79500009 PM 8497488 ER PT J AU PUTNAM, FW AF PUTNAM, FW TI SEXUAL ABUSE AND PSYCHOPATHOLOGY - COMMENTARY SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Note RP PUTNAM, FW (reprint author), NIMH,DEV PSYCHOL LAB,DISSOCIAT DISORDER UNIT,BLDG 15K,BETHESDA,MD 20892, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD MAY PY 1993 VL 56 IS 2 BP 222 EP 227 PG 6 WC Psychiatry SC Psychiatry GA LK460 UT WOS:A1993LK46000010 PM 27697015 ER PT J AU COWLEY, DS ROYBYRNE, PP GREENBLATT, DJ HOMMER, DW AF COWLEY, DS ROYBYRNE, PP GREENBLATT, DJ HOMMER, DW TI PERSONALITY AND BENZODIAZEPINE SENSITIVITY IN ANXIOUS PATIENTS AND CONTROL SUBJECTS SO PSYCHIATRY RESEARCH LA English DT Article DE TRIDIMENSIONAL PERSONALITY QUESTIONNAIRE; PANIC DISORDER; GENERALIZED ANXIETY DISORDER; SACCADIC EYE MOVEMENT VELOCITY ID SINGLE UNIT-ACTIVITY; CEREBROSPINAL-FLUID; PANIC DISORDER; SUPERIOR COLLICULUS; LOCUS COERULEUS; DIAZEPAM; ALPRAZOLAM; BEHAVIOR AB Cloninger has recently proposed a model of personality variability that is based on three independent heritable traits of harm avoidance, novelty seeking, and reward dependence, each of which is thought to be mediated by a separate neurochemical and neuroanatomic mechanism. The current study tested hypotheses generated on the basis of this theory in anxious patients and control subjects. Eighteen patients with panic disorder, 12 patients with generalized anxiety disorder, and 21 control subjects underwent both personality testing and assessment of their sensitivity to diazepam, as measured by slowing of saccadic eye movement velocity. As expected, anxious patients displayed higher harm avoidance scores than controls. Although an inverse correlation between harm avoidance and benzodiazepine sensitivity was predicted, no relationship between these variables was found in any diagnostic group. However, a significant correlation was found between novelty-seeking scores and sensitivity to diazepam. This finding, although not predicted by Cloninger's theory, is consistent with prior preclinical and human studies. C1 TUFTS UNIV NEW ENGLAND MED CTR,BOSTON,MA. NIAAA,BETHESDA,MD. UNIV WASHINGTON,DEPT PSYCHIAT & BEHAV SCI,CTR ANXIETY & DEPRESS,ANXIETY DISORDERS PROGRAM,SEATTLE,WA 98195. TUFTS UNIV,SCH MED,DEPT PHARMACOL,BOSTON,MA 02111. TUFTS UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02111. TUFTS UNIV,SCH MED,DEPT MED,BOSTON,MA 02111. NR 39 TC 37 Z9 37 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD MAY PY 1993 VL 47 IS 2 BP 151 EP 162 DI 10.1016/0165-1781(93)90045-I PG 12 WC Psychiatry SC Psychiatry GA LG163 UT WOS:A1993LG16300005 PM 8341768 ER PT J AU CALLAWAY, CW WING, LL NICHOLS, DE GEYER, MA AF CALLAWAY, CW WING, LL NICHOLS, DE GEYER, MA TI SUPPRESSION OF BEHAVIORAL ACTIVITY BY NORFENFLURAMINE AND RELATED DRUGS IN RATS IS NOT MEDIATED BY SEROTONIN RELEASE SO PSYCHOPHARMACOLOGY LA English DT Article DE SEROTONIN; FENFLURAMINE; LOCOMOTION; BEHAVIOR; RATS; P-CHLOROAMPHETAMINE ID PARA-CHLOROAMPHETAMINE; BRAIN-SEROTONIN; PARA-CHLOROPHENYLALANINE; MIDBRAIN RAPHE; FENFLURAMINE; DOPAMINE; AMPHETAMINE; 3,4-METHYLENEDIOXYMETHAMPHETAMINE; 5-HYDROXYTRYPTAMINE; LOCOMOTOR AB Fenfluramine, a phenalkylamine with serotonin (5-HT) releasing properties, decreases motor activity in rats. The following studies assessed the contribution of 5-HT release to the behavioral effects of fenfluramine and norfenfluramine using a behavioral pattern monitor that simultaneously assesses locomotor and investigatory behavior. First, both fenfluramine and its active metabolite d-norfenfluramine dose-dependently reduced locomotor and investigatory activity. The norfenfluramine-induced reduction in activity was not antagonized by pretreatment with the 5-HT uptake inhibitor fluoxetine or the 5-HT synthesis inhibitor p-chlorophenylalanine, drugs that reduce drug-induced 5-HT release. Second, the d- and l-enantiomers of norfenfluramine were nearly equipotent at reducing behavioral activity, although d-norfenfluramine is more potent as a 5-HT releasing agent. Third, p-chloroamphetamine, a drug that shares the 5-HT releasing properties of fenfluramine produced locomotor hyperactivity in the same paradigm. Previous studies indicate that other 5-HT releasing phenalkylamines have behavioral effects resembling those of p-chloroamphetamine rather than those of fenfluramine. Finally, a structurally related drug, 4-methoxy-5-methyl-aminoindan (MMAI), produced dose-dependent reductions in behavioral activity that are similar to the effects of fenfluramine. The behavioral effects of MMAI were not antagonized by fluoxetine or by the 5-HT receptor antagonist methiothepin. These data suggest that the decrease in activity induced by fenfluramine, norfenfluramine and the related drug MMAI is not related to 5-HT release. C1 UNIV CALIF SAN DIEGO,SCH MED,DEPT PSYCHIAT,9500 GILMAN DR,LA JOLLA,CA 92093. PURDUE UNIV,SCH PHARM & PHARMACAL SCI,DEPT PHARMACOL & TOXICOL,W LAFAYETTE,IN 47907. PURDUE UNIV,SCH PHARM & PHARMACAL SCI,DEPT MED CHEM & PHARMACOGNOSY,W LAFAYETTE,IN 47907. ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. FU NIDA NIH HHS [DA05438, DA04758, DA02925] NR 53 TC 21 Z9 21 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD MAY PY 1993 VL 111 IS 2 BP 169 EP 178 DI 10.1007/BF02245519 PG 10 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LA821 UT WOS:A1993LA82100007 PM 7870948 ER PT J AU SALIVE, ME SATTERFIELD, S OSTFELD, AM WALLACE, RB HAVLIK, RJ AF SALIVE, ME SATTERFIELD, S OSTFELD, AM WALLACE, RB HAVLIK, RJ TI DISABILITY AND COGNITIVE IMPAIRMENT ARE RISK-FACTORS FOR PNEUMONIA-RELATED MORTALITY IN OLDER ADULTS SO PUBLIC HEALTH REPORTS LA English DT Article ID PNEUMOCOCCAL POLYSACCHARIDE VACCINE; INFECTIOUS-DISEASES; ELDERLY PATIENTS; SMOKING; HOSPITALIZATIONS; IMMUNIZATION; POPULATION; DEATHS; MEN AB The role of functional and cognitive limitations in the risk of pneumonia-related mortality in older adults was examined. As part of a cohort study in 3 communities (East Boston, MA; New Haven, CT; and Iowa and Washington Counties, IA), 6,234 women and 4,035 men ages 65 or older completed baseline interviews between 1981 an 1983 and were followed for up to 6 years. Sex-specific Cox proportional-hazards regression models were used to examine the association of baseline physical and cognitive functioning with report pneumonia (ICD9 480-486) as an underlying, immediate, or contributing cause of death. During followup, a total of 243 men and 160 women died with pneumonia. Adjusting for age, race, education, evidence of five chronic diseases, and smoking status, a significantly increased risk of pneumonia mortality (P < 0.05) was found for limitations in activities of daily living and cognitive impairment among both men and women. Inability to walk a half mile, climb stairs, or perform heavy housework was significantly associated with increased risk of pneumonia mortality for women but not for men in the same multivariate models. Men and women whose body-mass index was above the median had significantly lower risk of pneumonia mortality compared with those in the lowest quartile. Further elucidation of the sequence between physical and cognitive impairment and risk of pneumonia will be important in reducing pneumonia-associated morbidity and mortality. C1 NIA, DEMOG & BIOMETRY PROGRAM, BETHESDA, MD 20892 USA. HARVARD UNIV, SCH MED, DEPT MED, CHANNING LAB, BOSTON, MA 02115 USA. YALE UNIV, SCH MED, DEPT EPIDEMIOL & PUBL HLTH, NEW HAVEN, CT 06510 USA. E BOSTON NEIGHBORHOOD HLTH CTR, BOSTON, MA USA. UNIV IOWA, DEPT PREVENT MED & ENVIRONM HLTH, IOWA CITY, IA 52242 USA. FU NIA NIH HHS [N01-AG-02105, N01-AG-02107, N01-AG-02106] NR 53 TC 44 Z9 44 U1 3 U2 4 PU ASSOC SCHOOLS PUBLIC HEALTH PI WASHINGTON PA 1900 M ST NW, STE 710, WASHINGTON, DC 20036 USA SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD MAY-JUN PY 1993 VL 108 IS 3 BP 314 EP 322 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LF949 UT WOS:A1993LF94900008 PM 8497569 ER PT J AU LAND, CE SHIMOSATO, Y SACCOMANNO, G TOKUOKA, S AUERBACH, O TATEISHI, R GREENBERG, SD NAMBU, S CARTER, D AKIBA, S KEEHN, R MADIGAN, P MASON, TJ TOKUNAGA, M AF LAND, CE SHIMOSATO, Y SACCOMANNO, G TOKUOKA, S AUERBACH, O TATEISHI, R GREENBERG, SD NAMBU, S CARTER, D AKIBA, S KEEHN, R MADIGAN, P MASON, TJ TOKUNAGA, M TI RADIATION-ASSOCIATED LUNG-CANCER - A COMPARISON OF THE HISTOLOGY OF LUNG CANCERS IN URANIUM MINERS AND SURVIVORS OF THE ATOMIC BOMBINGS OF HIROSHIMA AND NAGASAKI SO RADIATION RESEARCH LA English DT Article ID CIGARETTE-SMOKING; MORTALITY; EXPOSURE C1 NATL CANC RES CTR,TOKYO,JAPAN. ST MARYS HOSP,GRAND JCT,CO. HIROSHIMA UNIV,SCH MED,HIROSHIMA 730,JAPAN. RADIAT EFFECTS RES FDN,HIROSHIMA 730,JAPAN. VET ADM MED CTR,E ORANGE,NJ. CTR ADULT DIS,OSAKA 537,JAPAN. BAYLOR UNIV,SCH MED,HOUSTON,TX. RED CROSS HOSP,HIROSHIMA,JAPAN. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. NATL RES COUNCIL,BOARD RADIAT EFFECTS RES,WASHINGTON,DC 20418. KAGOSHIMA MUNICIPAL HOSP,KAGOSHIMA,JAPAN. RP LAND, CE (reprint author), NCI,BETHESDA,MD 20892, USA. NR 25 TC 31 Z9 33 U1 1 U2 2 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD MAY PY 1993 VL 134 IS 2 BP 234 EP 243 DI 10.2307/3578464 PG 10 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA LB850 UT WOS:A1993LB85000014 PM 8387679 ER PT J AU RUDOLPH, DL YEE, J PALKER, T COLIGAN, JE LAL, RB AF RUDOLPH, DL YEE, J PALKER, T COLIGAN, JE LAL, RB TI ANTIBODY-RESPONSES TO THE ENV EPITOPES OF HUMAN T-LYMPHOTROPIC VIRUS TYPE-I IN RHESUS MACAQUES NATURALLY INFECTED WITH SIMIAN T-LYMPHOTROPIC VIRUS TYPE-I SO RESEARCH IN VIROLOGY LA English DT Article DE HTLV; STLV; ENVELOPE PROTEIN; EPITOPE; IMMUNODOMINANCE; SYNTHETIC PEPTIDE; SENSITIVITY ID CELL LEUKEMIA-VIRUS; SYNTHETIC PEPTIDES; LINEAR EPITOPES; HTLV-I; SEQUENCE; GP46; GLYCOPROTEINS; PROTEINS; GP21 AB Synthetic peptides derived from the env protein of human T-lymphotropic virus type I (HTLV-I) were used to identify the immunodominant motifs in rhesus macaques naturally infected with simian T-lymphotropic virus type I (STLV-I). Of the 13 peptides derived from the env protein of HTLV-I, Env-1(191-214) and Env-5(242-257) reacted with 81 % (44/54) and 54 % (29/54) of specimens from infected monkeys, respectively. A recombinant protein (MTA-I162-209) reacted with 53 of 54 (98 %) STLV-1-infected serum specimens. While similar immune reactivities to Env-1 and MTA-1 were observed in both HTLV-I-infected human sera and STLV-I-infected monkey sera, the reactivity to Env-5 was significantly higher in HTLV-I-infected human sera. Differential reactivities may be attributed to the differences in the secondary structures of the STLV-I and HTLV-I envelope protein in the Env-5 region, since homologous peptide with STLV-I sequence did not result in enhanced sensitivity of anti-Env-5 antibody detection. C1 UNIV CALIF DAVIS,CALIF PRIMATE RES CTR,SIMIAN RETROVIRUS REF LAB,DAVIS,CA 95616. DUKE UNIV,MED CTR,DIV RHEUMATOL & IMMUNOL,DURHAM,NC 27710. NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. RP RUDOLPH, DL (reprint author), CTR DIS CONTROL,NATL CTR INFECT DIS,DIV VIRAL & RICKETTSIAL DIS,ATLANTA,GA 30333, USA. NR 21 TC 3 Z9 3 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2516 J9 RES VIROLOGY JI Res. Virol. PD MAY-JUN PY 1993 VL 144 IS 3 BP 193 EP 199 DI 10.1016/S0923-2516(06)80029-4 PG 7 WC Virology SC Virology GA LL323 UT WOS:A1993LL32300002 PM 8395074 ER PT J AU DUFOUR, MC STINSON, FS CACES, MF AF DUFOUR, MC STINSON, FS CACES, MF TI TRENDS IN CIRRHOSIS MORBIDITY AND MORTALITY - UNITED-STATES, 1979-1988 SO SEMINARS IN LIVER DISEASE LA English DT Review ID LIVER; REDUCTIONS C1 ALCOHOL EPIDEMIOL DATA SYST CYGNUS INC,WASHINGTON,DC. CSR INC,WASHINGTON,DC. RP DUFOUR, MC (reprint author), NIAAA,DBE,ROOM 14C-26,PARKLAWN BLDG,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 30 TC 37 Z9 37 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0272-8087 J9 SEMIN LIVER DIS JI Semin. Liver Dis. PD MAY PY 1993 VL 13 IS 2 BP 109 EP 125 DI 10.1055/s-2007-1007343 PG 17 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LL293 UT WOS:A1993LL29300002 PM 8337600 ER PT J AU GREGORY, PE GUTMANN, DH MITCHELL, A PARK, S BOGUSKI, M JACKS, T WOOD, DL JOVE, R COLLINS, FS AF GREGORY, PE GUTMANN, DH MITCHELL, A PARK, S BOGUSKI, M JACKS, T WOOD, DL JOVE, R COLLINS, FS TI NEUROFIBROMATOSIS TYPE-1 GENE-PRODUCT (NEUROFIBROMIN) ASSOCIATES WITH MICROTUBULES SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Article ID GTPASE-ACTIVATING PROTEIN; RAS GTPASE; SACCHAROMYCES-CEREVISIAE; TAU-PROTEIN; NF1 GENE; GAP; SEQUENCE; DOMAIN; IDENTIFICATION; MAP2 AB The neurofibromatosis type 1 (NF1) gene was recently identified by positional cloning and found to encode a protein with structural and functional homology to mammalian and yeast GTPase-activating proteins (GAPs). Using antibodies directed against the NF1 gene product, a protein of approximately 250 kDa was identified and termed neurofibromin. Double-indirect immunofluorescent labeling with anti-neurofibromin and anti-tubulin antibodies demonstrates that neurofibromin associates with cytoplasmic microtubules. Immunoblotting of microtubule-enriched cytoplasmic fractions, using antibodies generated against neurofibromin, shows that neurofibromin copurifies with microtubules. When portions of neurofibromin are expressed in Sf9 insect cells they associate with polymerized microtubules; furthermore, the critical residues for this interaction reside within the GAP-related domain of neurofibromin. The unexpected association of neurofibromin with microtubules suggests that neurofibromin is involved in microtubule-mediated intracellular signal transduction pathways. C1 UNIV MICHIGAN,MED CTR,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,DEPT NEUROL,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,DEPT MICROBIOL & IMMUNOL,ANN ARBOR,MI 48109. UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. NIH,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. RP GREGORY, PE (reprint author), UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,ANN ARBOR,MI 48109, USA. FU NINDS NIH HHS [NS23410, NINDS NS01590] NR 40 TC 106 Z9 109 U1 1 U2 6 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD MAY PY 1993 VL 19 IS 3 BP 265 EP 274 DI 10.1007/BF01233074 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA LP141 UT WOS:A1993LP14100006 PM 8332934 ER PT J AU BACCHETTI, P SEGAL, MR JEWELL, NP BROOKMEYER, R CARLIN, JB GELMAN, A GAIL, MH ROSENBERG, PS DEGRUTTOLA, V PAGANO, M KARON, JM SATTEN, GA SOLOMON, PJ WILSON, SR AF BACCHETTI, P SEGAL, MR JEWELL, NP BROOKMEYER, R CARLIN, JB GELMAN, A GAIL, MH ROSENBERG, PS DEGRUTTOLA, V PAGANO, M KARON, JM SATTEN, GA SOLOMON, PJ WILSON, SR TI BACKCALCULATION OF HIV-INFECTION RATES - COMMENT AND REJOINDER SO STATISTICAL SCIENCE LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PNEUMOCYSTIS-CARINII PNEUMONIA; VIRUS INFECTION; AIDS; PROPHYLAXIS; ZIDOVUDINE; TRIAL C1 UNIV CALIF SAN FRANCISCO,DEPT EPIDEMIOL & BIOSTAT,SAN FRANCISCO,CA 94143. UNIV CALIF BERKELEY,DEPT STAT,BERKELEY,CA 94720. UNIV CALIF BERKELEY,DEPT BIOSTAT,BERKELEY,CA 94720. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD 21218. UNIV CALIF BERKELEY,DEPT STAT,BERKELEY,CA 94720. ROYAL CHILDRENS HOSP,CLIN EPIDEMIOL & BIOSTAT UNIT,PARKVILLE,VIC 3052,AUSTRALIA. NCI,EPIDEMIOL METHODS SECT,ROCKVILLE,MD 20892. CTR DIS CONTROL,NATL CTR INFECT DIS,DIV HIV AIDS E48,ATLANTA,GA 30333. UNIV ADELAIDE,DEPT STAT,ADELAIDE,SA 5001,AUSTRALIA. AUSTRALIAN NATL UNIV,CTR MATH & ITS APPLICAT,CANBERRA,ACT 2601,AUSTRALIA. RI Carlin, John/B-3492-2012 OI Carlin, John/0000-0002-2694-9463 NR 30 TC 1 Z9 1 U1 4 U2 4 PU INST MATHEMATICAL STATISTICS PI HAYWARD PA IMS BUSINESS OFFICE-SUITE 6 3401 INVESTMENT BLVD, HAYWARD, CA 94545 SN 0883-4237 J9 STAT SCI JI Stat. Sci. PD MAY PY 1993 VL 8 IS 2 BP 102 EP 119 PG 18 WC Statistics & Probability SC Mathematics GA ME643 UT WOS:A1993ME64300002 ER PT J AU ACOSTA, CK RAO, PN KIM, HK AF ACOSTA, CK RAO, PN KIM, HK TI TETRAPROPYLAMMONIUM PERRUTHENATE AS A MILD AND EFFICIENT OXIDANT FOR SENSITIVE STEROIDAL ALCOHOLS SO STEROIDS LA English DT Article DE TETRAPROPYLAMMONIUM PERRUTHENATE; N-METHYLMORPHOLINE N-OXIDE; OXIDATION; STEROIDAL ALCOHOLS; STEROID ID OXIDATION AB Tetrapropylammonium perruthenate N-methylmorpholine N-oxide oxidation of steroidal alcohols is described. The reagent combination is mild and gave good yields of the corresponding ketones. Although the oxidation can generate ketones from 3-, 11-, 15-, 17-, and 20-hydroxy steroids, the oxidation of homoallylic alcohols proceeds in low yields. Finally, we observed that the oxidation reagents will convert 17alpha-hydroxy-20-keto steroids to 17-keto systems in excellent yield. C1 NICHHD,BETHESDA,MD 20892. RP ACOSTA, CK (reprint author), SW FDN BIOMED RES,DEPT ORGAN CHEM,POB 28147,SAN ANTONIO,TX 78228, USA. FU NICHD NIH HHS [N01-HD-6-2928] NR 17 TC 18 Z9 18 U1 0 U2 3 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0039-128X J9 STEROIDS JI Steroids PD MAY PY 1993 VL 58 IS 5 BP 205 EP 208 DI 10.1016/0039-128X(93)90019-J PG 4 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA LL621 UT WOS:A1993LL62100002 PM 8356571 ER PT J AU TOROGONZALEZ, G NAVARROROMAN, L ROMAN, GC CANTILLO, J SERRANO, B HERRERA, M VERGARA, I AF TOROGONZALEZ, G NAVARROROMAN, L ROMAN, GC CANTILLO, J SERRANO, B HERRERA, M VERGARA, I TI ACUTE ISCHEMIC STROKE FROM FIBROCARTILAGINOUS EMBOLISM TO THE MIDDLE CEREBRAL-ARTERY SO STROKE LA English DT Article DE CEREBRAL ISCHEMIA; EMBOLISM; TRAUMA ID INFARCTION AB Background and Purpose: Fibrocartilaginous embolism from the nucleus pulposus. has been reported as a rare cause of spinal cord ischemia. We were unable to find previous reports of embolism from this source to cerebral arteries. Case Description: A previously healthy 17-year-old girl fell during a basketball game. Left hemiparesis and unresponsiveness developed followed by signs of right uncal herniation and death over a 3 -day period. There was no evidence of neck, head, or spine trauma, and cardiac evaluation was normal. Neuropathological examination showed extensive ischemic infarction of the right middle cerebral artery territory, brain edema, and herniation. Complete embolic occlusion of the right middle cerebral artery by fibrocartilaginous material, consistent with nucleus pulposus, was documented. Small, terminal coronary artery branches also showed embolism by the same material and limited areas of myocardial infarction. Conclusions: Acute cerebral embolism after minor trauma in a young patient may be rarely due to fibrocartilaginous embolism from the nucleus pulposus. The pathogenesis of this problem remains poorly understood, but systemic embolism appeared to have occurred in this case. C1 UNIV NACL COLOMBIA, FAC MED, DEPT PATHOL, BOGOTA, 20892, COLOMBIA. UNIV NACL COLOMBIA, FAC MED, DEPT NEUROL, BOGOTA, 20892, COLOMBIA. NCI, BETHESDA, MD USA. NINCDS, NEUROEPIDEMIOL BRANCH, BETHESDA, MD USA. NR 11 TC 11 Z9 11 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0039-2499 EI 1524-4628 J9 STROKE JI Stroke PD MAY PY 1993 VL 24 IS 5 BP 738 EP 740 PG 3 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA KZ843 UT WOS:A1993KZ84300026 PM 8488530 ER PT J AU CADET, JL KUJIRAI, K CARLSON, E EPSTEIN, CJ AF CADET, JL KUJIRAI, K CARLSON, E EPSTEIN, CJ TI AUTORADIOGRAPHIC DISTRIBUTION OF [H-3] NEUROTENSIN RECEPTORS IN THE BRAINS OF SUPEROXIDE-DISMUTASE TRANSGENIC MICE SO SYNAPSE LA English DT Article DE QUANTITATIVE AUTORADIOGRAPHY; TRANSGENIC MICE; SUPEROXIDE DISMUTASE; FREE RADICALS; FRONTAL CORTEX; STRIATUM; NUCLEUS ACCUMBENS; SUBSTANTIA-NIGRA; NEUROTENSIN RECEPTORS; AGING ID RAT CEREBRAL-CORTEX; VENTRAL TEGMENTAL AREA; DOPAMINERGIC-NEURONS; NEUROTENSIN BINDING; SUBSTANTIA NIGRA; PARKINSONS-DISEASE; SEROTONIN UPTAKE; OXYGEN-TOXICITY; BASAL FOREBRAIN; UPTAKE SITES AB Superoxide dismutase (SOD) plays an important role in the protection of cells against the deleterious effects of free radicals by dismutating the toxic superoxide anion radical. Although oxygen-based radicals have been implicated in the process of aging and in neurodegenerative disorders such as Parkinson's disease, the contribution of these free radicals to the pathology of these entities has yet to be clarified. It is also not certain that increased levels of free radical scavenging enzymes would attenuate the molecular and cellular processes that lead to these pathological states. In order to assess the contribution of increased SOD gene dosage to the pathogenesis of Down's syndrome, transgenic mice have been constructed that overexpress the human CuZnSOD. We are also using this model to evaluate the role of free radicals in age-associated changes in brain neurotransmitters and their receptors. In the present study, transgenic mice and their nontransgenic littermates, aged 6 weeks and 21 months, were used in an autoradiographic receptor study of the distribution of brain neurotensin receptors. At 6 weeks of age, there were no significant differences between the two groups of mice in most brain regions. In addition, [H-3]NT binding sites showed parallel age-related decreases in the majority of the areas examined in both groups. However, significant age-related decreases in the septum, the diagonal band of Broca, and in some subdivisions of the caudate-putamen were observed only in SOD-Tg mice. In contrast, significant age-related decreases in the core area of the nucleus accumbens and the dorsal aspect of the dentate gyrus of the hippocampus were seen only in non-Tg mice. Interestingly, there were increases in NT binding sites in the-CA2 area of the hippocampus in both groups of mice. These results suggest that oxygen-based radicals might play a role in the biochemical changes that occur in NT receptors during the process of aging since these receptors were differentially affected in some regions of the brains of SOD-Tg mice and of their littermates, which contrast in their ability to scavenge the superoxide radical. C1 YAMAGATA UNIV,SCH MED,DEPT INTERNAL MED 3,YAMAGATA 990,JAPAN. UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT BIOCHEM,SAN FRANCISCO,CA 94143. RP CADET, JL (reprint author), NIDA,ARC,CLIN PSYCHOPHARMACOL SECT,CELLULAR & MOLEC NEUROTOXICOL UNIT,POB 5180,BALTIMORE,MD 21224, USA. FU NIA NIH HHS [AG-08958] NR 65 TC 13 Z9 13 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-4476 J9 SYNAPSE JI Synapse PD MAY PY 1993 VL 14 IS 1 BP 24 EP 33 DI 10.1002/syn.890140105 PG 10 WC Neurosciences SC Neurosciences & Neurology GA KZ846 UT WOS:A1993KZ84600004 PM 8390106 ER PT J AU ROTHMAN, RB LEWIS, B DERSCH, C XU, H RADESCA, L DECOSTA, BR RICE, KC KILBURN, RB AKUNNE, HC PERT, A AF ROTHMAN, RB LEWIS, B DERSCH, C XU, H RADESCA, L DECOSTA, BR RICE, KC KILBURN, RB AKUNNE, HC PERT, A TI IDENTIFICATION OF A GBR12935 HOMOLOG, LR1111, WHICH IS OVER 4,000-FOLD SELECTIVE FOR THE DOPAMINE TRANSPORTER, RELATIVE TO SEROTONIN AND NOREPINEPHRINE TRANSPORTERS SO SYNAPSE LA English DT Article DE GBR12909; GBR12935; COCAINE; DOPAMINE; SEROTONIN; NOREPINEPHRINE; TRANSPORTERS ID PHARMACOLOGICAL CHARACTERIZATION; UPTAKE INHIBITOR; COCAINE; GBR-12909; RAT; BEHAVIOR; BINDING; BRAIN AB The di-substituted piperazines, GBR12909 (1-[2-[bis(4-fluorophenyl)-methoxy]ethyl]-4-[3-phenylpropyl]piperazine) and GBR12935 (1-[2-(diphenyl-methoxy)-ethyl]-4-(3-phenylpropyl)piperazine), are potent and selective (20-to 100-fold) inhibitors of [H-3]dopamine reuptake, relative to [H-3]5-HT and [H-3]norepinephrine uptake. The GBR12935 analog, 1-(2-(diphenylmethoxy)ethyl)-4-(3-phenylpropyl)homopiperazine (LR1111), was synthesized as part of a systematic structure-activity study of analogs of GBR12935 and GBR12909. LR1111 differs from GBR12935 by the addition of a methylene group into the piperazine ring to yield a compound with a seven-member homopiperazine ring. The IC50 values for LR1111 at the dopamine, norepinephrine, and serotonin transporters were 7.2 nM, 34,072 nM, and greater than 20,000 nM, respectively, whereas the IC50 values of GBR12935 were 3.7 nM, 289 nM, and 1261 nM for these same transporters. This demonstrates that the addition of a single methylene group in the piperazine ring results in a compound with similar affinity but significantly higher selectivity for the dopamine transporter. LR1111 increased motoric activity in rats after intravenous administration. These indicate that LR1111 is a potent and highly selective inhibitor of the dopamine transporter. C1 NIDDK,MED CHEM LAB,BETHESDA,MD 20892. WARNER LAMBERT PARKE DAVIS,PARKE DAVIS PHARMACEUT RES,DEPT PHARMACOL,ANN ARBOR,MI 48105. NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. RP ROTHMAN, RB (reprint author), NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,BOX 5180,BALTIMORE,MD 21224, USA. NR 18 TC 73 Z9 73 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-4476 J9 SYNAPSE JI Synapse PD MAY PY 1993 VL 14 IS 1 BP 34 EP 39 DI 10.1002/syn.890140106 PG 6 WC Neurosciences SC Neurosciences & Neurology GA KZ846 UT WOS:A1993KZ84600005 PM 8511716 ER PT J AU BAUMANN, MH RALEY, TJ PARTILLA, JS ROTHMAN, RB AF BAUMANN, MH RALEY, TJ PARTILLA, JS ROTHMAN, RB TI BIOSYNTHESIS OF DOPAMINE AND SEROTONIN IN THE RAT-BRAIN AFTER REPEATED COCAINE INJECTIONS - A MICRODISSECTION MAPPING STUDY SO SYNAPSE LA English DT Article DE DOPAMINE; 3,4-DIHYDROXYPHENYLALANINE; SEROTONIN; 5-HYDROXYTRYPTOPHAN; SYNTHESIS; CHRONIC COCAINE ID VENTRAL TEGMENTAL AREA; TYROSINE-HYDROXYLASE IMMUNOREACTIVITY; MEDIAL PREFRONTAL CORTEX; NUCLEUS-ACCUMBENS; EXTRACELLULAR DOPAMINE; INVIVO MICRODIALYSIS; H-3 DOPAMINE; SYSTEM; BINDING; NEURONS AB The purpose of the present study was to examine the effects of chronic cocaine on dopamine (DA) and serotonin (5-HT) synthesis in several rat brain regions implicated in drug reinforcement. Male rats were treated twice daily with cocaine (15 mg/kg, ip) or saline for 1 week. After 42 hr of abstinence, rats were challenged with either cocaine (15 mg/kg, ip) or saline, followed by the aromatic L-amino acid decarboxylase inhibitor 3-hydroxybenzylhydrazine (NSD-1015; 100 mg/kg, ip). Animals were decapitated 30 min after NSD-1015 and discrete brain regions were microdissected from 300 mum frozen sections. Postmortem tissue levels of 3,4-dihydroxyphenylalanine (DOPA) and 5-hyroxytryptophan (5-HTP) were quantified by HPLC with electrochemical detection and used to estimate biosynthesis of DA and 5-HT, respectively. In chronic saline-treated rats, cocaine dramatically suppressed DA and 5-HT synthesis in all forebrain regions examined, including: medial prefrontal cortex, nucleus accumbens, caudate nucleus, olfactory tubercle, and basolateral amygdala. The degree of inhibition ranged from 35-65% and was more pronounced in 5-HT neurons compared to DA neurons in the same tissue sample. In general, chronic cocaine did not significantly alter basal levels of DOPA or 5-HTP; a notable exception was lateral hypothalamus, where chronic cocaine reduced basal DA synthesis to 75% of control. After repeated cocaine injections, the synthesis-inhibiting effect of a challenge injection of cocaine was attenuated in many brain areas. These data suggest that whereas acute cocaine decreases DA and 5-HT synthesis in forebrain, chronic cocaine is not neurotoxic to DA and 5-HT neurons. In addition, the mechanism(s) mediating cocaine-induced suppression of monoamine synthesis may become desensitized by chronic exposure to the drug. RP BAUMANN, MH (reprint author), NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,POB 5180,BALTIMORE,MD 21224, USA. NR 57 TC 56 Z9 56 U1 3 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-4476 J9 SYNAPSE JI Synapse PD MAY PY 1993 VL 14 IS 1 BP 40 EP 50 DI 10.1002/syn.890140107 PG 11 WC Neurosciences SC Neurosciences & Neurology GA KZ846 UT WOS:A1993KZ84600006 PM 8511717 ER PT J AU KOHN, MC LUCIER, GW CLARK, GC SEWALL, C TRITSCHER, AM PORTIER, CJ AF KOHN, MC LUCIER, GW CLARK, GC SEWALL, C TRITSCHER, AM PORTIER, CJ TI A MECHANISTIC MODEL OF EFFECTS OF DIOXIN ON GENE-EXPRESSION IN THE RAT-LIVER SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; ESTROGEN-RECEPTOR; FACTOR-ALPHA; AH-RECEPTOR; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN TCDD; 2-HYDROXYLASE ACTIVITY; TISSUE DISTRIBUTION; CELL-PROLIFERATION; CYTOCHROME P-450D; 2-STAGE MODEL RP KOHN, MC (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 56 TC 107 Z9 107 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 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD MAY PY 1993 VL 120 IS 1 BP 138 EP 154 DI 10.1006/taap.1993.1096 PG 17 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA LC603 UT WOS:A1993LC60300018 PM 8511776 ER PT J AU MELNICK, RL HUFF, J AF MELNICK, RL HUFF, J TI LIVER CARCINOGENESIS IS NOT A PREDICTED OUTCOME OF CHEMICALLY-INDUCED HEPATOCYTE PROLIFERATION SO TOXICOLOGY AND INDUSTRIAL HEALTH LA English DT Article DE ALTERED HEPATIC FOCI; APOPTOSIS; CELL PROLIFERATION; CHEMICAL CARCINOGENESIS; DNA SYNTHESIS; LIVER; NONGENOTOXIC CARCINOGENS ID <4-CHLORO-6-(2,3-XYLIDINO)-2-PYRIMIDINYLTHIO>ACETIC ACID WY-14,643; 2-ACETYLAMINOFLUORENE-INDUCED HEPATIC TUMORIGENESIS; CELL-PROLIFERATION; DNA-SYNTHESIS; PEROXISOME PROLIFERATOR; ALTERED FOCI; RAT-LIVER; B6C3F1 MICE; HEPATOCARCINOGENESIS; NAFENOPIN AB Cell proliferation has long been recognized as a basic component of multistage carcinogenesis. Based largely on the finding that certain nongenotoxic chemical carcinogens induce cell proliferation in the same organ that develops tumors after long-term exposure, some suggest that the increased rates of cell division account for the carcinogenicity of these chemicals. This paper examines relationships between chemically induced liver toxicity, cell proliferation, and liver carcinogenesis; major factors include consistency, transient vs. sustained dose-response correspondence, and scientific plausibility. For a presumed mechanism to be valid, a sustained proliferative response is critical, largely because transient increases in hepatocyte proliferation are not sufficient to induce cancer or promote liver tumor development. A consistent association between liver toxicity and carcinogenicity has not been established. Our evaluation of studies on purported relationships between chemically induced cell proliferation and liver carcinogenesis shows: 1) that inconsistencies in sex and species specificity exist, 2) that a large percentage of proliferative responses are transient, 3) that inconsistencies in response to various hepatic peroxisome proliferators are common, and 4) that dose-response and duration relationships have not been sufficiently examined. Studies of proliferative responses of putative preneoplastic cells in the liver indicate that these cells divide faster than normal hepatocytes and also have higher death rates. Chemicals that induce cell proliferation in preneoplastic foci do not always provide a persistent increase in replication rates, even with continuous exposure. A selective growth advantage to preneoplastic cells in the liver may be provided either by an enhancement of the replication rates of these cells compared to the surrounding normal hepatocytes, by inhibition of cell loss, or by inhibition of the growth rate of normal cells. More work is needed to understand how chemical carcinogens and noncarcinogens affect cell division and cell loss of normal hepatocytes and of preneoplastic cells; measurements of hepatocyte proliferation alone are not sufficient to elucidate mechanisms of liver tumor development or to predict liver carcinogenesis. Because of our limited knowledge of the complex molecular changes occurring during liver cancer, it would be inappropriate and far too premature to amend scientific risk assessment procedures for nongenotoxic chemical carcinogens based on oversimplified or incompletely tested speculations. RP MELNICK, RL (reprint author), NIEHS,ENVIRONM CARCINOGENESIS PROGRAM,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 53 TC 38 Z9 38 U1 0 U2 1 PU PRINCETON SCIENTIFIC PUBL INC PI PRINCETON PA PO BOX 2155, PRINCETON, NJ 08543 SN 0748-2337 J9 TOXICOL IND HEALTH JI Toxicol. Ind. Health PD MAY-JUN PY 1993 VL 9 IS 3 BP 415 EP 438 PG 24 WC Public, Environmental & Occupational Health; Toxicology SC Public, Environmental & Occupational Health; Toxicology GA LK173 UT WOS:A1993LK17300003 PM 8367884 ER PT J AU SUDA, BA LEITMAN, SF DAVEY, RJ AF SUDA, BA LEITMAN, SF DAVEY, RJ TI CHARACTERISTICS OF RED-CELLS IRRADIATED AND SUBSEQUENTLY FROZEN FOR LONG-TERM STORAGE SO TRANSFUSION LA English DT Article ID VERSUS-HOST DISEASE; POTASSIUM LEVELS; BLOOD-CELLS; GRAFT; TRANSFUSION; PREVENTION; GLYCEROL AB Irradiation of blood components eliminates the risk of transfusion-associated graft-versus-host disease. Freezing directed or rare red cell units that are irradiated but not transfused would facilitate inventory management and would increase the transfusion options for the involved patients. However, no studies have been performed to evaluate whether prestorage irradiation damages subsequently frozen red cells. Ten normal volunteers donated a unit of whole blood on two separate occasions. One unit was irradiated with 15 Gy (1500 rad), stored at 4-degrees-C for 6 days, and then frozen and stored at - 75-degrees-C for 56 days. The other unit (control) was similarly stored but was not irradiated. Aliquots of the units were tested on Day 0 and Day 6 and, after deglycerolization, on Day 62. Comparison of means and changes in means showed no significant differences in red cell ATP, 2,3 DPG, or supernatant hemoglobin and glucose in control and irradiated units. The difference in the change in supernatant potassium from Day 0 to Day 6 in control and irradiated units was significant (1.5 to 28.6 mmol/L vs. 1.5 to 48.5 mmol/L: p<0.0001). Irradiation did not cause significant differences in postdeglycerolization red cell recovery (control, 84.5% vs. irradiated, 81.2%) or in 24-hour posttransfusion autologous red cell survival (control. 91.1% vs. irradiated, 90.9%). Red cells can be irradiated, stored at 4-degrees-C for 6 days, and subsequently frozen with no increase in detectable damage as compared to controls that were not irradiated. C1 NIH,DEPT TRANSFUS MED,LAB SERV SECT,BLDG 10,ROOM 1C-711,BETHESDA,MD 20892. NIH,DEPT TRANSFUS MED,BLOOD SERV SECT,BETHESDA,MD 20892. NR 20 TC 12 Z9 12 U1 0 U2 1 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD MAY PY 1993 VL 33 IS 5 BP 389 EP 392 DI 10.1046/j.1537-2995.1993.33593255598.x PG 4 WC Hematology SC Hematology GA LB137 UT WOS:A1993LB13700006 PM 8488541 ER PT J AU WIVEL, NA AF WIVEL, NA TI REGULATORY CONSIDERATIONS FOR GENE-THERAPY STRATEGIES AND PRODUCTS SO TRENDS IN BIOTECHNOLOGY LA English DT Article RP WIVEL, NA (reprint author), NIH,DEPT HLTH & HUMAN SERV,OFF RECOMBINANT DNA ACTIV,BETHESDA,MD 20892, USA. NR 5 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-7799 J9 TRENDS BIOTECHNOL JI Trends Biotechnol. PD MAY PY 1993 VL 11 IS 5 BP 189 EP 191 DI 10.1016/0167-7799(93)90112-M PG 3 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA LN045 UT WOS:A1993LN04500008 PM 7763809 ER PT J AU ROBERTS, AB SPORN, MB LEFER, AM AF ROBERTS, AB SPORN, MB LEFER, AM TI CARDIOPROTECTIVE ACTIONS OF TRANSFORMING GROWTH-FACTOR-BETA SO TRENDS IN CARDIOVASCULAR MEDICINE LA English DT Article ID MYOCARDIAL-ISCHEMIA; REPERFUSION INJURY; NITRIC-OXIDE; FACTOR-BETA-1; CELLS; INTERLEUKIN-1; EXPRESSION; HEART AB Transforming growth factor-beta (TGF-beta) has been shown to have protective effects in experimental models of myocardial, mesenteric, and cerebral ischemia-reperfusion injury. These effects are mediated by its ability to block adhesion of neutrophils to endothelium and to preserve endothelial function in terms of physiologic release of nitric oxide (NO). TGF-beta also maintains the rhythmicity of cultured cardiac myocytes and blocks the suppressive effects of interleukin-1 on their beating rate by antagonizing the pathologic induction of NO synthase. These data suggest that TGF-beta will be useful clinically in treatment of both reperfusion injury and inflammatory diseases of the heart. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT PHYSIOL,PHILADELPHIA,PA 19107. RP ROBERTS, AB (reprint author), NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892, USA. NR 41 TC 18 Z9 18 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1050-1738 J9 TRENDS CARDIOVAS MED JI Trends Cardiovasc. Med. PD MAY-JUN PY 1993 VL 3 IS 3 BP 77 EP 81 DI 10.1016/1050-1738(93)90027-4 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA LE306 UT WOS:A1993LE30600001 PM 21244943 ER PT J AU WALDMANN, TA AF WALDMANN, TA TI THE IL-2/IL-2 RECEPTOR SYSTEM - A TARGET FOR RATIONAL IMMUNE INTERVENTION SO TRENDS IN PHARMACOLOGICAL SCIENCES LA English DT Article ID T-CELL LEUKEMIA; CARDIAC ALLOGRAFT SURVIVAL; AFFINITY INTERLEUKIN-2 RECEPTORS; TAC MONOCLONAL-ANTIBODY; IL-2 RECEPTOR; RECOMBINANT INTERLEUKIN-2; HUMANIZED ANTIBODY; BETA-CHAIN; SIGNALING PATHWAYS; CYCLOSPORINE-A AB The expression of interleukin 2 (IL-2), induction of its multisubunit receptor and subsequent interplay of this ligand with its receptor are pivotal events in T-cell activation. Our present understanding of the normal IL-2/IL-2 receptor system, and of disorders in this network in disease, opens the possibility for more specific immune intervention. Thomas Waldmann discusses how the clinical application of IL-2, agents that inhibit IL-2 synthesis and action, and anti-IL-2 receptor-directed therapy provide a novel perspective for prevention of allograft rejection and for treatment of graft-versus-host disease, select autoimmune disorders and certain neoplastic diseases. RP WALDMANN, TA (reprint author), NCI,METAB BRANCH,BETHESDA,MD 20892, USA. NR 61 TC 17 Z9 17 U1 1 U2 2 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0165-6147 J9 TRENDS PHARMACOL SCI JI Trends Pharmacol. Sci. PD MAY PY 1993 VL 14 IS 5 BP 159 EP 164 DI 10.1016/0165-6147(93)90201-T PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LM590 UT WOS:A1993LM59000007 PM 8212311 ER PT J AU YARCHOAN, R MITSUYA, H BRODER, S AF YARCHOAN, R MITSUYA, H BRODER, S TI CHALLENGES IN THE THERAPY OF HIV-INFECTION SO TRENDS IN PHARMACOLOGICAL SCIENCES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; CD4+ T-CELLS; REVERSE-TRANSCRIPTASE; BONE-MARROW; 2'-DEOXY-3'-THIACYTIDINE BCH-189; ANTIRETROVIRAL THERAPY; SELECTIVE-INHIBITION; REPLICATION INVITRO; CRYSTAL-STRUCTURE AB Drugs that inhibit human immunodeficiency virus (HIV) replication have been shown to have clinical utility in patients with HIV infection. However, the immunological improvement induced by available anti-HIV therapies in patients with acquired immune deficiency syndrome (AIDS) is incomplete and transient. Explanations for this may include immunological barriers to complete reconstitution, low therapeutic indices of the available drugs, and the development of viral resistance. An understanding of these processes, as discussed here by Robert Yarchoan and colleagues, may provide important leads for the development of improved therapy for AIDS. C1 NCI,MED BRANCH,EXPTL RETROVIRAL SECT,BETHESDA,MD 20892. RP YARCHOAN, R (reprint author), NCI,RETROVIRAL DIS SECT,BETHESDA,MD 20892, USA. NR 60 TC 18 Z9 18 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0165-6147 J9 TRENDS PHARMACOL SCI JI Trends Pharmacol. Sci. PD MAY PY 1993 VL 14 IS 5 BP 196 EP 202 DI 10.1016/0165-6147(93)90208-2 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LM590 UT WOS:A1993LM59000014 PM 8212316 ER PT J AU GNARRA, JR GLENN, GM LATIF, F ANGLARD, P LERMAN, MI ZBAR, B LINEHAN, WM AF GNARRA, JR GLENN, GM LATIF, F ANGLARD, P LERMAN, MI ZBAR, B LINEHAN, WM TI MOLECULAR-GENETIC STUDIES OF SPORADIC AND FAMILIAL RENAL-CELL CARCINOMA SO UROLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID VONHIPPEL-LINDAU DISEASE; HUMAN CHROMOSOME-3; TUMOR-CELLS; DNA; LOCALIZATION; CANCER; TRANSLOCATION; PAPILLARY; REGION; POLYMORPHISM C1 INST CHIM BIOL,GENET MOLEC EUCARYOTES LAB,CNRS,INSERM,PARIS,FRANCE. NCI,DIV CANC TREATMENT,BETHESDA,MD 20892. NCI,DIV CANC BIOL & DIAG,BETHESDA,MD 20892. NR 44 TC 38 Z9 39 U1 0 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0094-0143 J9 UROL CLIN N AM JI Urol. Clin. N. Am. PD MAY PY 1993 VL 20 IS 2 BP 207 EP 216 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA LX628 UT WOS:A1993LX62800003 PM 8098558 ER PT J AU YOSHITOMI, K BOORMAN, GA AF YOSHITOMI, K BOORMAN, GA TI PALPEBRAL AMELANOTIC MELANOMAS IN F344 RATS SO VETERINARY PATHOLOGY LA English DT Article DE AMELANOTIC MELANOMA; EYELID; MELANOMA; RATS; SKIN ID SCHWANNOMAS; NEOPLASMS; TUMORS AB Spontaneous amelanotic melanomas in the eyelids of F344 rats were found in one of 1/926 (0.11%) male and 5/925 (0.54%) female F344 rats that were used as control and treated animals in five different carcinogenicity studies conducted by the National Toxicology Program (Research Triangle Park, NC). These melanomas were grossly recognized as single, tan or white, well-circumscribed masses of the right or left eyelid. These melanomas primarily occurred in the dermis of the skin of the eyelids and consisted of poorly differentiated spindle cells characteristically arranged in interlacing fascicles. Rarely, epithelioid tumor cells were also observed, and these tumor cells showed a negative histochemical reaction for melanin. The epidermis and dermal-epidermal junction were usually uninvolved. The diagnosis of amelanotic melanoma could only be established by electron microscopic examination. The most striking ultrastructural feature of the tumor cells was a large number of intracytoplasmic premelanosomes (stage 11 melanosomes without melanin), which nearly filled the cytoplasm of most tumor cells. Giant premelanosomes and melanophagosomes were also seen. The tumor cells did not possess the ultrastructural features characteristic of Schwann cells (thin, long cell processes and pericytoplasmic basal laminae). The histologic and ultrastructural features of these palpebral tumors were similar to those of cutaneous amelanotic melanomas of the pinna in F344 rats. C1 NIEHS,NATL TOXICOL PROGRAM,CHEM CARCINOGENESIS BRANCH,RES TRIANGLE PK,NC 27709. RP YOSHITOMI, K (reprint author), NIEHS,EXPTL PATHOL LABS,POB 12766,RES TRIANGLE PK,NC 27709, USA. NR 26 TC 7 Z9 7 U1 0 U2 0 PU AMER COLL VET PATHOLOGIST PI LAWRENCE PA 810 EAST 10TH STREET, LAWRENCE, KS 66044 SN 0300-9858 J9 VET PATHOL JI Vet. Pathol. PD MAY PY 1993 VL 30 IS 3 BP 280 EP 286 PG 7 WC Pathology; Veterinary Sciences SC Pathology; Veterinary Sciences GA LC995 UT WOS:A1993LC99500009 PM 8333109 ER PT J AU MAKHOV, AM TRUS, BL CONWAY, JF SIMON, MN ZURABISHVILI, TG MESYANZHINOV, VV STEVEN, AC AF MAKHOV, AM TRUS, BL CONWAY, JF SIMON, MN ZURABISHVILI, TG MESYANZHINOV, VV STEVEN, AC TI THE SHORT TAIL-FIBER OF BACTERIOPHAGE-T4 - MOLECULAR-STRUCTURE AND A MECHANISM FOR ITS CONFORMATIONAL TRANSITION SO VIROLOGY LA English DT Article ID ELECTRON-MICROSCOPY; SECONDARY STRUCTURE; ADENOVIRUS FIBER; PROTEIN; IMAGES; SEQUENCE; MACROMOLECULES; PREDICTION; REOVIRUS C1 NIAMSD,STRUCT BIOL LAB,BLDG 6,ROOM 114,BETHESDA,MD 20892. NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. BROOKHAVEN NATL LAB,DEPT BIOL,UPTON,NY 10973. DI IVANOVSKII INST VIROL,MOSCOW 123098,RUSSIA. RI Conway, James/A-2296-2010 OI Conway, James/0000-0002-6581-4748 NR 42 TC 46 Z9 48 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD MAY PY 1993 VL 194 IS 1 BP 117 EP 127 DI 10.1006/viro.1993.1241 PG 11 WC Virology SC Virology GA KY344 UT WOS:A1993KY34400014 PM 8480415 ER PT J AU SHIMOMURA, S WONG, S BROWN, KE KOMATSU, N KAJIGAYA, S YOUNG, NS AF SHIMOMURA, S WONG, S BROWN, KE KOMATSU, N KAJIGAYA, S YOUNG, NS TI EARLY AND LATE GENE-EXPRESSION IN UT-7 CELLS INFECTED WITH B19 PARVOVIRUS SO VIROLOGY LA English DT Article ID ADENO-ASSOCIATED VIRUS; NONSTRUCTURAL PROTEIN; DNA AMPLIFICATION; MINUTE VIRUS; TRANSCRIPTION; REPLICATION; IDENTIFICATION; ACTIVATION; PROMOTER; INVITRO C1 NHLBI,CLIN HEMATOL BRANCH,CELL BIOL SECT,10-7C103,BETHESDA,MD 20892. JICHI MED SCH,DEPT MED,DIV HEMATOL,MINAMI KAWACHI,TOCHIGI 32904,JAPAN. NR 32 TC 16 Z9 17 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 0042-6822 J9 VIROLOGY JI Virology PD MAY PY 1993 VL 194 IS 1 BP 149 EP 156 DI 10.1006/viro.1993.1244 PG 8 WC Virology SC Virology GA KY344 UT WOS:A1993KY34400017 PM 8480418 ER PT J AU OGATA, N MILLER, RH ISHAK, KG PURCELL, RH AF OGATA, N MILLER, RH ISHAK, KG PURCELL, RH TI THE COMPLETE NUCLEOTIDE-SEQUENCE OF A PRECORE MUTANT OF HEPATITIS-B VIRUS IMPLICATED IN FULMINANT-HEPATITIS AND ITS BIOLOGICAL CHARACTERIZATION IN CHIMPANZEES SO VIROLOGY LA English DT Article ID POSITIVE CARRIER MOTHERS; PRECORE-REGION DEFECTS; E-ANTIGEN; SUBTYPE-ADR; INFANTS BORN; PROMOTER REGION; T-CELLS; MUTATIONAL ANALYSIS; FETAL TRANSMISSION; ESCHERICHIA-COLI C1 NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892. USAF,INST PATHOL,DEPT HEPAT & GASTROINTESTINAL PATHOL,WASHINGTON,DC 20306. FU NIAID NIH HHS [N01-AI-72623, N01-AI-05069] NR 96 TC 103 Z9 106 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 0042-6822 J9 VIROLOGY JI Virology PD MAY PY 1993 VL 194 IS 1 BP 263 EP 276 DI 10.1006/viro.1993.1257 PG 14 WC Virology SC Virology GA KY344 UT WOS:A1993KY34400030 PM 8480422 ER PT J AU COSTA, PT MCCRAE, RR AF COSTA, PT MCCRAE, RR TI PSYCHOLOGICAL-RESEARCH IN THE BALTIMORE LONGITUDINAL-STUDY OF AGING SO ZEITSCHRIFT FUR GERONTOLOGIE LA English DT Article DE LONGITUDINAL; PERSONALITY; AGING; COGNITION ID SELF-REPORTS; AGE-CHANGES; PERSONALITY; VALIDATION; RATINGS AB The Baltimore Longitudinal Study of Aging (BLSA) is an ongoing multidisciplinary study of biomedical and psychosocial aging. Over 1000 men and women are currently active, returning to the Gerontology Research Center every 2 years for a 2.5-day visit. Longitudinal studies of cognitive functioning have shown a variety of patterns of age changes in vigilance, problem solving, divergent thinking abilities, and visual memory. Studies of personality traits have shown stability in both mean levels and individual differences. Future BLSA research will add neuroimaging studies to link personality and cognition to the structure and function of the aging brain. RP COSTA, PT (reprint author), NIA,GERONTOL RES CTR,PERSONAL & COGNIT LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. OI Costa, Paul/0000-0003-4375-1712 NR 33 TC 17 Z9 17 U1 0 U2 5 PU DR DIETRICH STEINKOPFF VERLAG PI BERLIN 33 PA C/O SPRINGER-VERLAG, HEIDELBERGER PLATZ 3, 1000 BERLIN 33, GERMANY SN 0044-281X J9 Z GERONTOL PD MAY-JUN PY 1993 VL 26 IS 3 BP 138 EP 141 PG 4 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA LL055 UT WOS:A1993LL05500008 PM 8337906 ER PT J AU LONGERICH, I TARAZ, K BUDZIKIEWICZ, H TSAI, L MEYER, JM AF LONGERICH, I TARAZ, K BUDZIKIEWICZ, H TSAI, L MEYER, JM TI BACTERIAL CONSTITUENTS .57. PSEUDOVERDIN, A COMPOUND RELATED TO THE PYOVERDIN CHROMOPHORE FROM A PSEUDOMONAS-AERUGINOSA STRAIN INCAPABLE TO PRODUCE PYOVERDINS SO ZEITSCHRIFT FUR NATURFORSCHUNG C-A JOURNAL OF BIOSCIENCES LA English DT Article ID FLUORESCENT PIGMENT AB From a genetically manipulated strain of Pseudomonas aeruginosa ATCC 15692 (PAO1 strain) a compound named pseudoverdin, 3-formylamino-6,7-dihydroxycoumarin, was obtained which is related to the typical pyoverdin chromophore and thus allows to shed some light on the biogenesis of the latter. C1 UNIV COLOGNE,INST ORGAN CHEM,GREINSTR 4,W-5000 COLOGNE 41,GERMANY. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. INST LE BEL,CNRS,INST BIOL MOLEC & CELLULAIRE,MICROBIOL LAB,F-67070 STRASBOURG,FRANCE. NR 16 TC 12 Z9 12 U1 1 U2 1 PU VERLAG Z NATURFORSCH PI TUBINGEN PA POSTFACH 2645, W-7400 TUBINGEN, GERMANY SN 0939-5075 J9 Z NATURFORSCH C JI Z.Naturforsch.(C) PD MAY-JUN PY 1993 VL 48 IS 5-6 BP 425 EP 429 PG 5 WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy GA LJ082 UT WOS:A1993LJ08200005 PM 8363709 ER PT J AU AIGNER, TG MISHKIN, M AF AIGNER, TG MISHKIN, M TI SCOPOLAMINE IMPAIRS RECALL OF ONE-TRIAL STIMULUS REWARD ASSOCIATION IN MONKEYS SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE SCOPOLAMINE; CHOLINERGIC; RECALL; MONKEY ID PRIMATE BASAL FOREBRAIN; RECOGNITION MEMORY; SUBSTANTIA INNOMINATA; DIAGONAL BAND; RESPONSES; REINFORCEMENT; CONNECTIONS; HIPPOCAMPUS; AMYGDALA; NEURONS AB Performance of three rhesus monkeys on a test of one-trial stimulus-reward association, in which recall intervals ranged from 0.5 to 6.5 min, was evaluated during nondrug-control conditions and following administration of the muscarinic-receptor blocker scopolamine. During control sessions, performance averaged 78% correct responses. Following administration of 10.0 and 17.8 mug/kg of scopolamine, performance fell significantly, to 69% and 63% correct responses, respectively. This dose-dependent impairment in recall was similar to the impairment we reported previously in recognition. Although the results thus failed to support a suggestion derived from behavioral electrophysiological findings that stimulus-reward association might be more vulnerable to scopolamine than stimulus recognition, they provide additional evidence for a cholinergic contribution to cognitive memory. RP AIGNER, TG (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 9,ROOM 1N107,BETHESDA,MD 20892, USA. NR 13 TC 17 Z9 17 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-4328 J9 BEHAV BRAIN RES JI Behav. Brain Res. PD APR 30 PY 1993 VL 54 IS 2 BP 133 EP 136 DI 10.1016/0166-4328(93)90071-W PG 4 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA LC786 UT WOS:A1993LC78600003 PM 8323711 ER PT J AU QURESHI, SA JOSEPH, CK HENDRICKSON, M SONG, JG GUPTA, R BRUDER, J RAPP, U FOSTER, DA AF QURESHI, SA JOSEPH, CK HENDRICKSON, M SONG, JG GUPTA, R BRUDER, J RAPP, U FOSTER, DA TI A DOMINANT NEGATIVE RAF-1 MUTANT PREVENTS V-SRC-INDUCED TRANSFORMATION SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PROTEIN-KINASE; CELLULAR SUBSTRATE; GROWTH; PHOSPHORYLATION; ONCOGENE C1 CUNY HUNTER COLL,INST BIOMOLEC STRUCT & FUNCT,695 PK AVE,NEW YORK,NY 10021. CUNY HUNTER COLL,DEPT BIOL SCI,NEW YORK,NY 10021. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. FU NCI NIH HHS [CA46677]; NCRR NIH HHS [RRO-3037-03] NR 16 TC 21 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 30 PY 1993 VL 192 IS 2 BP 969 EP 975 DI 10.1006/bbrc.1993.1510 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LA360 UT WOS:A1993LA36000093 PM 7683468 ER PT J AU TAN, GT WICKRAMASINGHE, A VERMA, S HUGHES, SH PEZZUTO, JM BABA, M MOHAN, P AF TAN, GT WICKRAMASINGHE, A VERMA, S HUGHES, SH PEZZUTO, JM BABA, M MOHAN, P TI SULFONIC-ACID POLYMERS ARE POTENT INHIBITORS OF HIV-1 INDUCED CYTOPATHOGENICITY AND THE REVERSE TRANSCRIPTASES OF BOTH HIV-1 AND HIV-2 SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE SULFONIC ACID POLYMER; HIV-1; HIV-2; INHIBITION; REVERSE TRANSCRIPTASE ID HUMAN-IMMUNODEFICIENCY-VIRUS; GIANT-CELL FORMATION; DEXTRAN SULFATE; SELECTIVE INHIBITORS; ESCHERICHIA-COLI; AIDS; INFECTION; SURAMIN; TYPE-2; PHARMACOKINETICS AB Four novel sulfonic acid polymers were evaluated for their in vitro HIV-1 and HIV-2 reverse transcriptase (RT) inhibitory activity and found to be equipotent against both RTs. The aromatic polymers demonstrated IC50 values that were approximately 10(3)-fold lower than those observed with the aliphatic polymers. Among the aromatic polymers, poly(4-styrenesulfonic acid) (PSS) (MW 8000; IC50 = 0.02 mug/ml) was 3-fold more potent than poly(anetholesulfonic acid) (PAS) of approximately the same molecular weight range. The activity of PSS polymers increased in proportion to the size of the polymers and, relative to suramin, activity could be enhanced over 200-fold. These polymers also inhibited the cytopathic effect of HIV-1 at concentrations that were non-toxic to MT-4 cells. The potent RT inhibitory properties of these stable sulfonic acid polymers suggest that structure-activity studies are warranted to yield agents capable of inhibiting multiple stages of the viral process. C1 UNIV ILLINOIS,COLL PHARM,DEPT MED CHEM & PHARMACOGNOSY,M-C 781,BOX 6998,CHICAGO,IL 60680. UNIV ILLINOIS,COLL MED,PROGRAM COLLABORAT RES PHARMACEUT SCI,CHICAGO,IL 60680. FUKUSHIMA MED SCH,DEPT MICROBIOL,FUKUSHIMA 960,JAPAN. NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,BETHESDA,MD 20892. UNIV ILLINOIS,COLL MED,CTR SPECIALIZED CANC,CHICAGO,IL 60680. RI Baba, Masanori/G-3867-2011 FU NCI NIH HHS [N01-CO-74101] NR 29 TC 14 Z9 14 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD APR 30 PY 1993 VL 1181 IS 2 BP 183 EP 188 DI 10.1016/0925-4439(93)90109-E PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LA492 UT WOS:A1993LA49200012 PM 7683207 ER PT J AU HUANG, Q WANG, S CHEN, SC BABCOOK, DM PARK, SS GELBOIN, HV MIRVISH, SS AF HUANG, Q WANG, S CHEN, SC BABCOOK, DM PARK, SS GELBOIN, HV MIRVISH, SS TI HYDROXYLATION AND DEALKYLATION OF METHYL-N-BUTYLNITROSAMINE AND ROLE OF CERTAIN CYTOCHROME-P-450 ISOZYMES IN THESE REACTIONS SO CANCER LETTERS LA English DT Article DE METHYLBUTYLNITROSAMINE; NITROSAMINE; ESOPHAGUS; LIVER MICROSOMES; CYTOCHROME-P-450; MONOCLONAL ANTIBODY ID NORMAL-AMYLNITROSAMINE; MONOCLONAL-ANTIBODIES; RAT ESOPHAGUS; METABOLISM; NITROSAMINES; TISSUES; LIVER; DERIVATIVES; SPECIFICITY; SERIES AB We studied the metabolism of methyl-n-butylnitrosamine (MBN), a carcinogen for the rat esophagus and liver. The 2-, 3- and 4-hydroxy derivatives were identified as new metabolites of MBN. In studies on tissue slices freshly removed from MRC-Wistar rats, MBN metabolism resembled that of the previously studied methylamylnitrosamine in the esophagus catalyzed 2- and 3- hydroxylation; liver, omega-1 hydroxylation; and lung, omega-hydroxylation of both nitrosamines. Liver microsomes from Sprague-Dawley rats catalyzed 2-, 3- and 4-hydroxylation of MBN, as well as the previously studied activating reactions of demethylation and debutylation. Phenobarbital induced all five reactions of MBN by rat liver microsomes, especially debutylation; 3-methylholanthrene induced 3-hydroxylation and debutylation and isoniazid induced demethylation and debutylation. Monoclonal antibodies that inhibit specific cytochrome P-450 isozymes were used to identify the isozymes involved in each reaction. Antibody 4-7-1 appeared more specific than the previously used antibody 2-66-3 for inhibiting P-450 2B1 and/or 2B2. For the metabolism of both MBN and methylamylnitrosamine by rat liver microsomes, the antibody results indicated that P-450 2C11 mainly catalyzed demethylation and omega-1 hydroxylation, P-450 1A1 or 1A2 catalyzed 3-hydroxylation and debutylation or depentylation, P-450 2E1 produced demethylation and P-450 2B1 or 2B2 produced omega-1 hydroxylation, demethylation and debutylation or depentylation. C1 UNIV NEBRASKA,MED CTR,EPPLEY INST RES CANC,OMAHA,NE 68198. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. FU NCI NIH HHS [R01-CA-35628, CA-36727] NR 22 TC 15 Z9 15 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD APR 30 PY 1993 VL 69 IS 2 BP 107 EP 116 DI 10.1016/0304-3835(93)90162-3 PG 10 WC Oncology SC Oncology GA LC742 UT WOS:A1993LC74200005 PM 8495399 ER PT J AU KANAI, A NONOMURA, N YOSHIMURA, M OKA, T AF KANAI, A NONOMURA, N YOSHIMURA, M OKA, T TI DNA-BINDING PROTEINS AND THEIR CIS-ACTING SITES CONTROLLING HORMONAL INDUCTION OF A MOUSE BETA-CASEIN=CAT FUSION PROTEIN IN MAMMARY EPITHELIAL-CELLS SO GENE LA English DT Article DE MILK PROTEIN; CAT REPORTER GENE; 5' REGULATORY REGION; MULTIPLE DNA ELEMENTS; MILK PROTEINS; GLAND DEVELOPMENT; FOOT PRINTING; GEL-RETARDATION ASSAY ID GENE; TRANSCRIPTION; EXPRESSION; PROLACTIN; PROMOTER; SEQUENCES; INSULIN; EXTRACT AB Transcription of the mouse beta-casein (betaCAS)-encoding gene (casB) is regulated by the synergistic actions of insulin, glucocorticoid and prolactin in the mammary gland (MG). To delineate its regulatory sequence(s), we examined the hormonal inducibility of various chimeric constructs containing the promoter sequence of casB and the cat reporter gene in primary MG epithelial cells. A DNA fragment from bp -258 to +7 of casB was sufficient for the hormonal induction. Using a series of 5'- and internal deletions of the casB promoter region, at least three DNA elements were found to be necessary for full induction. These were located at bp positions -258 to -180, -154 to -136, and -98 to -62. DNase I footprinting analysis with a partially purified extract from lactating MG cells detected at least seven protected sequences, I(-242 to -219), II(-213 to -202), III(-151 to -139), IV(-125 to -110), V(-98 to -90), VI(-79 to -70) and VII(-59 to -45). Regions I/II, III and V/VI were included in the three DNA elements required for the hormonal induction, and the IV region corresponded to the MG consensus sequences of several milk protein-encoding genes. Competition gel retardation assays using nuclear extracts of lactating mouse MG revealed the presence of specific binding proteins for regions I, II, IV and VI, as well as specific protein(s) binding to both regions III and V. The binding activities of these proteins, except that associated with region IV, were increased from the virgin to lactating periods. The activity of protein binding to region IV existed in all stages, but its pattern in gel retardation assays changed during the development of MG from the virgin to lactating periods. These results suggest that multiple DNA elements and their binding proteins are involved in the hormonal induction of mouse casB expression during MG development. C1 NIDDK,LMCB,BLDG 8,ROOM 304,BETHESDA,MD 20892. OI Kanai, Akio/0000-0002-6362-2419 NR 23 TC 26 Z9 26 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD APR 30 PY 1993 VL 126 IS 2 BP 195 EP 201 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA LB932 UT WOS:A1993LB93200005 PM 8482534 ER PT J AU GAO, B VIRMANI, M ROMM, E LAZARWESLEY, E SAKAGUCHI, K APPELLA, E KUNOS, G TAKACS, L AF GAO, B VIRMANI, M ROMM, E LAZARWESLEY, E SAKAGUCHI, K APPELLA, E KUNOS, G TAKACS, L TI SEQUENCE OF A CDNA-ENCODING BOVINE APOLIPOPROTEIN-H SO GENE LA English DT Note DE BETA(2)-GLYCOPROTEIN-I; PCR; NUCLEOTIDE SEQUENCE; MONOCLONAL ANTIBODY ID BETA-2-GLYCOPROTEIN-I AB The nucleotide sequence of the ApoH cDNA encoding the bovine apolipoprotein H (ApoH) has been determined. The deduced protein, which contains a 19-amino-acid (aa) signal peptide and the 326-aa mature ApoH, shows 89% and 86% homology with human and rat ApoH, respectively, C1 NIAAA,PHYSIOL & PHARMACOL STUDIES LAB,BETHESDA,MD 20892. NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 5 TC 10 Z9 11 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD APR 30 PY 1993 VL 126 IS 2 BP 287 EP 288 DI 10.1016/0378-1119(93)90383-E PG 2 WC Genetics & Heredity SC Genetics & Heredity GA LB932 UT WOS:A1993LB93200021 PM 8482546 ER PT J AU KUO, SC LEE, HZ JUANG, JP LIN, YT WU, TS CHANG, JJ LEDNICER, D PAULL, KD LIN, CM HAMEL, E LEE, KH AF KUO, SC LEE, HZ JUANG, JP LIN, YT WU, TS CHANG, JJ LEDNICER, D PAULL, KD LIN, CM HAMEL, E LEE, KH TI SYNTHESIS AND CYTOTOXICITY OF 1,6,7,8-SUBSTITUTED 2-(4'SUBSTITUTED PHENYL)-4-QUINOLONES AND RELATED-COMPOUNDS - IDENTIFICATION AS ANTIMITOTIC AGENTS INTERACTING WITH TUBULIN SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID TUMOR-CELL-LINES; DERIVATIVES; MECHANISM AB A series of 1,6,7,8-substituted 2-(4'-substituted phenyl)-4-quinolones and related compounds been synthesized and evaluated as cytotoxic compounds and as antimitotic agents interacting with tubulin. The 2-phenyl-4-quinolones (22-30) with substituents (e.g. F, Cl, and OCH3) at C-6, C-7, and C-8 show, in general, potent cytotoxicity against human lung carcinoma (A-549), ileocecal carcinoma (HCT-8), melanoma (RPMI-7951), and epidermoid carcinoma of the nasopharynx (KB) and two murine leukemia lines (P-388 and L1210). Introduction of alkyl groups at N-1 or C-4 oxygen led to inactive compounds (35-43 and 50). In addition, compounds 24, 26, and 27 were evaluated in the National Cancer Institute's 60 human tumor cell line in vitro screen. These compounds demonstrated the most marked effects in the screen on two colon carcinoma cell lines (COLO-205 and KM-2OL2) and on a central nervous system tumor cell line (SF-539) with compound 26 the most potent of the three agents. Compounds 24, 26, and 27 were potent inhibitors of tubulin polymerization, with activity nearly comparable to that of the potent antimitotic natural products colchicine, podophyllotoxin, and combretastatin A-4. The three agents also inhibited the binding of radiolabeled colchicine to tubulin, but this inhibition was less potent than that obtained with the natural products. C1 NATL CHENG KUNG UNIV,DEPT CHEM,TAINAN,TAIWAN. UNIV N CAROLINA,SCH PHARM,DIV MED CHEM & NAT PROD,NAT PROD LAB,CHAPEL HILL,NC 27599. UNIV N CAROLINA,SCH MED,DEPT LAB ANIM SCI,CHAPEL HILL,NC 27599. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NCI,INFORMAT TECHNOL BRANCH,DRUG SYNTHESIS & CHEM BRANCH,BETHESDA,MD 20892. RP KUO, SC (reprint author), CHINA MED COLL,GRAD INST PHARMACEUT CHEM,TAICHUNG 400,TAIWAN. FU NCI NIH HHS [CA 17625] NR 31 TC 191 Z9 192 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 30 PY 1993 VL 36 IS 9 BP 1146 EP 1156 DI 10.1021/jm00061a005 PG 11 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA LA583 UT WOS:A1993LA58300005 PM 8387598 ER PT J AU HE, XS RAYMON, LP MATTSON, MV ELDEFRAWI, ME DECOSTA, BR AF HE, XS RAYMON, LP MATTSON, MV ELDEFRAWI, ME DECOSTA, BR TI SYNTHESIS AND BIOLOGICAL EVALUATION OF 1-[1-(2-BENZO[B]THIENYL)CYCLOHEXYL]PIPERIDINE HOMOLOGS AT DOPAMINE-UPTAKE AND PHENCYCLIDINE-BINDING AND SIGMA-BINDING SITES SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID NUCLEUS ACCUMBENS; HIGH-AFFINITY; COCAINE; RECEPTORS; ANALOG; PCP; HYPERACTIVITY; CONFIGURATION; TRANSPORTERS; INHIBITION AB Piperidine and cyclohexyl ring homologues of the high-affinity dopamine (DA) uptake inhibitor 1-[1-(2-benzo[b]thienyl)cyclohexyl]piperidine (BTCP, 3) were each prepared in four steps from the appropriate cycloalkanones. These compounds were tested for their ability to displace [H-3]-BTCP and [H-3]cocaine and to inhibit [H-3]DA uptake in rat striatal homogenates. The ratios IC50([H-3]cocaine)/IC50 ([H-3]BTCP) ranged from 62 for BTCP to 1.5 for 1-[2-(benzo[b]thienyl)-cyclopentylamine (17); cocaine gave a ratio of 0.6. This indicates that BTCP is the most selective of all the compounds tested for sites labeled by [H-3]BTCP whereas cocaine is most selective for sites labeled by [H-3]cocaine. The wide differences in the relative abilities of these compounds to displace [H-3]BTCP and [H-3]cocaine suggests that these two radioligands are labeling different sites on the transporter. In general, the compounds structurally related to BTCP exhibited greater selectivity for sites labeled by [H-3]BTCP. However, several of the BTCP-related derivatives showed greater (compared with BTCP and cocaine) ability to displace [H-3]cocaine. Most notably, 1-[1-(2-benzo[b]thienyl)cyclohexyl]pyrrolidine (7) exhibited a 3.4-fold greater affinity for these sites compared with BTCP and a 9-fold greater affinity at these sites than cocaine. Most of the BTCP homologues displayed greater ability to inhibit[H-3]DA uptake in rat forebrain synaptosomes than cocaine. BTCP and 7 were the most potent of all the compounds tested in terms of their ability to inhibit uptake of [H-3]DA. IC50 ratios for [H-3]cocaine binding/[H-3]DA uptake ranged from 0.47 for 1-[1-(2-benzo[b]thienyl)cyclopentyl]homopiperidine (11) to 8.8 for 1-(2-benzo[b]-thienyl)cyclohexylamine(4). The importance of this ratio remains unclear in terms of identification of potential cocaine antagonists. As for BTCP, all of the compounds tested showed K(i) values > 10 000 nM for displacement of [H-3]TCP from rat brain homogenates. These compounds were able to displace the highly selective a receptor probe [H-3]-(+)-pentazocine from guinea pig brain homogenates with K(i) values ranging from 125 to 9170 nM. The significance of their sigma-binding activity in light of their dopaminergic properties is unclear. The diverse binding properties of these compounds at the DA-uptake site and their spectrum of inhibitory activities for [H-3]DA uptake identifies them as a useful base for the development of subtype selective probes at this site. These compounds will allow further study of the structure and function of the ''cocaine' receptor as well as the development of potential cocaine antagonists. C1 NIDDKD,MED CHEM LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DEPT PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21201. FU NIDA NIH HHS [DA036802] NR 34 TC 16 Z9 16 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 30 PY 1993 VL 36 IS 9 BP 1188 EP 1193 DI 10.1021/jm00061a009 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA LA583 UT WOS:A1993LA58300009 PM 8098066 ER PT J AU SPANAGEL, R SHIPPENBERG, TS AF SPANAGEL, R SHIPPENBERG, TS TI MODULATION OF MORPHINE-INDUCED SENSITIZATION BY ENDOGENOUS KAPPA-OPIOID SYSTEMS IN THE RAT SO NEUROSCIENCE LETTERS LA English DT Article DE MORPHINE; SENSITIZATION; NOR-BINALTORPHIMINE; MESOLIMBIC DOPAMINE SYSTEM; LOCOMOTOR ACTIVITY; INVIVO MICRODIALYSIS ID LOCOMOTOR-ACTIVITY; NUCLEUS-ACCUMBENS; DEPENDENT RATS; HYPERACTIVITY; INCREASE AB Sensitization to both the motor stimulant and mesolimbic dopamine-releasing effects of morphine were studied in animals chronically treated with morphine and those that had received the K opioid receptor antagonist, nor-binaltorphimine (nor-BNI) prior to the commencement of morphine treatment. Rats were pretreated with either nor-BNI (30 mug; i.c.v.) or its vehicle and then received injections of morphine for 10 days. Locomotor activity and microdialysis studies were then conducted 3 and 30 days after termination of the chronic morphine treatment. In chronic morphine-treated rats, sensitization developed to both the motor stimulatory effects of morphine and the mesolimbic dopamine-releasing effects of this drug. Sensitization was observed 3 and 30 days after termination of morphine treatment. In animals pretreated with nor-BNI, sensitization to both the motoric and dopamine-releasing effects of morphine was significantly greater than that of chronic morphine-treated rats. These results suggest that endogenoUS K opioid systems play an important role in morphine-induced sensitization and that manipulations of these systems can markedly influence both its behavioral and neurochemical expression. C1 NIDA,ADDICT RES CTR,BEHAV PHARMACOL & GENET SECT,PRECLIN PHARMACOL LAB,BALTIMORE,MD. RP SPANAGEL, R (reprint author), MAX PLANCK INST PSYCHIAT,INST CLIN,DEPT NEUROENDOCRINOL,KRAEPELINSTR 2,W-8000 MUNICH 40,GERMANY. NR 22 TC 74 Z9 75 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD APR 30 PY 1993 VL 153 IS 2 BP 232 EP 236 DI 10.1016/0304-3940(93)90329-J PG 5 WC Neurosciences SC Neurosciences & Neurology GA LB606 UT WOS:A1993LB60600027 PM 8392157 ER PT J AU YOKOYAMA, T COPELAND, NG JENKINS, NA MONTGOMERY, CA ELDER, FFB OVERBEEK, PA AF YOKOYAMA, T COPELAND, NG JENKINS, NA MONTGOMERY, CA ELDER, FFB OVERBEEK, PA TI REVERSAL OF LEFT-RIGHT ASYMMETRY - A SITUS-INVERSUS MUTATION SO SCIENCE LA English DT Article ID GENETIC-LINKAGE MAP; MOUSE; DNA AB A recessive mutation was identified in a family of transgenic mice that resulted in a reversal of left-right polarity (situs inversus) in 100 percent of the homozygous transgenic mice tested. Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci. During early embryonic development, the direction of postimplantation turning, one of the earliest manifestations of left-right asymmetry, was reversed in homozygous transgenic embryos. This insertional mutation identifies a gene that controls embryonic turning and visceral left-right polarity. C1 BAYLOR COLL MED, INST MOLEC GENET, DEPT CELL BIOL, HOUSTON, TX 77030 USA. NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MAMMALIAN GENET LAB, FREDERICK, MD 21702 USA. BAYLOR COLL MED, INST MOLEC GENET, DEPT CELL BIOL, HOUSTON, TX 77030 USA. BAYLOR COLL MED, CTR COMPARAT MED, HOUSTON, TX 77030 USA. BAYLOR COLL MED, HOWARD HUGHES MED INST, HOUSTON, TX 77030 USA. UNIV TEXAS, HLTH SCI CTR, DEPT PATHOL & LAB MED, HOUSTON, TX 77225 USA. FU NCI NIH HHS [N01-CO-74101]; NICHD NIH HHS [HD25340] NR 25 TC 330 Z9 334 U1 0 U2 22 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD APR 30 PY 1993 VL 260 IS 5108 BP 679 EP 682 DI 10.1126/science.8480178 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KZ641 UT WOS:A1993KZ64100034 PM 8480178 ER PT J AU LAN, KKG ZUCKER, DM AF LAN, KKG ZUCKER, DM TI SEQUENTIAL MONITORING OF CLINICAL-TRIALS - THE ROLE OF INFORMATION AND BROWNIAN-MOTION SO STATISTICS IN MEDICINE LA English DT Article ID MODELS; TESTS AB Sequential monitoring has been a topic of major interest in clincal trials methodology over the past two decades. This paper presents a unified conceptual framework for sequential monitoring that covers a wide variety of monitoring procedures in a wide variety of clinical trial settings. The central elements of this framework consist of a suitable concept of statistical information and a scheme for using this concept as a basis for summarizing the accumulating results of a trial in a standardized form, through a stochastic process that can be shown to approximate classical Brownian motion. The ideas are developed in a simple step-by-step fashion and illustrated by several practical examples. C1 NHLBI,BIOSTAT RES BRANCH,BETHESDA,MD 20892. RP LAN, KKG (reprint author), GEORGE WASHINGTON UNIV,DEPT STAT COMP & INFORMAT SYST,WASHINGTON,DC 20052, USA. FU NCI NIH HHS [CA 55098] NR 21 TC 80 Z9 82 U1 1 U2 6 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD APR 30 PY 1993 VL 12 IS 8 BP 753 EP 765 DI 10.1002/sim.4780120804 PG 13 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA LA520 UT WOS:A1993LA52000003 PM 8516592 ER PT J AU OBRAMS, GI HJORTLAND, M AF OBRAMS, GI HJORTLAND, M TI THE APPLICATION OF DEVELOPMENTS IN THEORETICAL BIOSTATISTICS TO EPIDEMIOLOGIC RESEARCH SO STATISTICS IN MEDICINE LA English DT Editorial Material RP OBRAMS, GI (reprint author), NCI,6130 EXECUT BLVD,EXECUT PLAZA N,SUITE 535,ROCKVILLE,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD APR 30 PY 1993 VL 12 IS 8 BP 789 EP 793 DI 10.1002/sim.4780120807 PG 5 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA LA520 UT WOS:A1993LA52000006 PM 8516595 ER PT J AU HODOSCEK, M KOVACEK, D MAKSIC, ZB AF HODOSCEK, M KOVACEK, D MAKSIC, ZB TI INFLUENCE OF SUBSTITUENTS ON THE MILLS-NIXON EFFECT IN SOME NAPHTHODICYCLOBUTENES AND NAPHTHODICYCLOBUTADIENES SO THEOCHEM-JOURNAL OF MOLECULAR STRUCTURE LA English DT Article ID RING ANNELATED AROMATICS; PI-BOND LOCALIZATION; MOLECULES; ENERGY; QUESTION; FIXATION; BENZENE; STRAIN AB Structural features of substituted naphthalenedicyclobutenes and naphthalenedicyclobutadienes were studied using the SCF formalism and the 3-21G basis set. It is shown that substitution of fluorine and lithium atoms at the naphthalene positions leads to structural changes which strongly depend on the electronegativity of the substituents. The deformations induced are more pronounced in naphthalenedicyclobutadienes. The dominant effect which causes variation in the structural parameters is rehybridization of the local hybrid orbitals. Additional pi-electrons of the terminal double bonds in naphthalenedicyclobutadienes substantially contribute to increased bond fixation within the aromatic moiety. C1 NIH,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892. RUDJER BOSKOVIC INST,41001 ZAGREB,CROATIA. UNIV ZAGREB,FAC SCI,41000 ZAGREB,CROATIA. NR 36 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-1280 J9 THEOCHEM-J MOL STRUC JI Theochem-J. Mol. Struct. PD APR 30 PY 1993 VL 100 IS 2-3 BP 213 EP 220 PG 8 WC Chemistry, Physical SC Chemistry GA LD842 UT WOS:A1993LD84200014 ER PT J AU MOREL, A LOLAIT, SJ BROWNSTEIN, MJ AF MOREL, A LOLAIT, SJ BROWNSTEIN, MJ TI MOLECULAR-CLONING AND EXPRESSION OF RAT V1A AND V2 ARGININE-VASOPRESSIN RECEPTORS SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT SATELLITE SYMP ON THE NEUROHYPOPHYSICAL PEPTIDE SYSTEMS, AT THE 9TH INTERNATIONAL CONGRESS OF ENDOCRINOLOGY CY SEP 06-11, 1992 CL LIEGE, BELGIUM DE NEUROHYPOPHYSEAL PEPTIDE; G-PROTEIN COUPLED RECEPTOR CLONING; XENOPUS-LAEVIS OOCYTE; CALCIUM MOBILIZATION; AEQUORIN; SEQUENCE ALIGNMENT ID OXYTOCIN; LOCALIZATION; OOCYTES; BINDING; SYSTEM; FAMILY; CDNA AB Vasopressin, one of the first characterized neuropeptides, has a wide spectrum of biological action, acting on distinct tissues. Indeed, it is involved in water retention, glucose metabolism, blood pressure and its implication in the CNS has also been described. This diversity of effects on mammalian tissues is mediated by distinct G protein-coupled receptors, acting via distinct second messenger pathways. This receptor family has been subtyped by pharmacological studies, as V1a receptor whose action is mediated by intracellular calcium mobilization, and V2 receptor which is linked to adenylyl cyclase. Since so many essential functions were ensured by vasopressin, molecular characterization of its receptors became soon a great challenge. This prompted us to isolate the cDNA of AVP V1a receptor as the first member of this family, by expression cloning. Intracellular calcium mobilization was therefore assayed after rat liver mRNA injection into Xenopus oocytes. A single clone, encoding a functional AVP receptor corresponding to the V1a subtype was finally characterized as a G protein-coupled receptor. Furthermore, we used homology cloning strategy in order to clone the AVP V2 subtype from a rat kidney cDNA library. A putative receptor clone was finally characterized as the rat V2 receptor cDNA by binding and cAMP increase experiments, on transfected cells. C1 NATL INST MENTAL HLTH,CELL BIOL LAB,BETHESDA,MD. RP MOREL, A (reprint author), CTR ETUD SACLAY,DEPT BIOL CELLULAIRE & MOLEC,SERV BIOL CELLULAIRE,BAT 520,PIECE 3,F-91191 GIF SUR YVETTE,FRANCE. RI Brownstein, Michael/B-8609-2009 NR 29 TC 23 Z9 25 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD APR 29 PY 1993 VL 45 IS 1-2 BP 53 EP 59 DI 10.1016/0167-0115(93)90182-8 PG 7 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA KZ809 UT WOS:A1993KZ80900010 PM 8511367 ER PT J AU INSEL, TR WINSLOW, JT WILLIAMS, JR HASTINGS, N SHAPIRO, LE CARTER, CS AF INSEL, TR WINSLOW, JT WILLIAMS, JR HASTINGS, N SHAPIRO, LE CARTER, CS TI THE ROLE OF NEUROHYPOPHYSEAL PEPTIDES IN THE CENTRAL MEDIATION OF COMPLEX SOCIAL PROCESSES - EVIDENCE FROM COMPARATIVE-STUDIES SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT SATELLITE SYMP ON THE NEUROHYPOPHYSICAL PEPTIDE SYSTEMS, AT THE 9TH INTERNATIONAL CONGRESS OF ENDOCRINOLOGY CY SEP 06-11, 1992 CL LIEGE, BELGIUM DE OXYTOCIN; VASOPRESSIN; VOLE; AFFILIATION; AMYGDALA ID MICROTUS-OCHROGASTER; AFFILIATIVE BEHAVIOR; PRAIRIE VOLES; OXYTOCIN; VASOPRESSIN; STIMULATION; ESTRADIOL; RECEPTORS; SYSTEM; SHEEP C1 UNIV MARYLAND,DEPT ZOOL,COLL PK,MD 20742. RP INSEL, TR (reprint author), NIHAC,NIMH,NEUROPHYSIOL LAB,POB 289,POOLESVILLE,MD 20837, USA. NR 22 TC 32 Z9 32 U1 1 U2 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD APR 29 PY 1993 VL 45 IS 1-2 BP 127 EP 131 DI 10.1016/0167-0115(93)90194-D PG 5 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA KZ809 UT WOS:A1993KZ80900022 PM 8511334 ER PT J AU FLAMION, B SPRING, KR ABRAMOW, M AF FLAMION, B SPRING, KR ABRAMOW, M TI IS THERE A PARACELLULAR WATER PATHWAY IN INNER MEDULLARY COLLECTING DUCTS (IMCD) FROM DEHYDRATED RATS SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT SATELLITE SYMP ON THE NEUROHYPOPHYSICAL PEPTIDE SYSTEMS, AT THE 9TH INTERNATIONAL CONGRESS OF ENDOCRINOLOGY CY SEP 06-11, 1992 CL LIEGE, BELGIUM DE VIDEO-MICROSCOPY; FLUORESCENCE MICROSCOPY; VASOPRESSIN; TIGHT JUNCTION ID ATRIAL-NATRIURETIC-FACTOR; TIGHT JUNCTIONS; UREA TRANSPORT; PERMEABILITY; VASOPRESSIN; TUBULES; CELLS; FLOW C1 NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892. RP FLAMION, B (reprint author), FREE UNIV BRUSSELS,PHYSIOL & PATHOPHYSIOL LAB,CAMPUS ERASME,BLDG E24-108,B-1070 BRUSSELS,BELGIUM. NR 21 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD APR 29 PY 1993 VL 45 IS 1-2 BP 197 EP 201 DI 10.1016/0167-0115(93)90206-N PG 5 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA KZ809 UT WOS:A1993KZ80900034 PM 8511344 ER PT J AU EVANS, JJ CATT, KJ DOBBS, BR MOORHOUSE, AR ROBINSON, G AF EVANS, JJ CATT, KJ DOBBS, BR MOORHOUSE, AR ROBINSON, G TI OXYTOCIN MODULATION OF GONADOTROPIN-RELEASE SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT SATELLITE SYMP ON THE NEUROHYPOPHYSICAL PEPTIDE SYSTEMS, AT THE 9TH INTERNATIONAL CONGRESS OF ENDOCRINOLOGY CY SEP 06-11, 1992 CL LIEGE, BELGIUM DE LUTEINIZING HORMONE; PITUITARY; PROESTRUS; ESTRADIOL ID NEUROHYPOPHYSEAL HORMONES; FOLLICULAR DEVELOPMENT; RATS; SECRETION; BLOOD C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD. RP EVANS, JJ (reprint author), CHRISTCHURCH SCH MED,DEPT OBSTET & GYNAECOL,CHRISTCHURCH,NEW ZEALAND. NR 15 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD APR 29 PY 1993 VL 45 IS 1-2 BP 243 EP 246 DI 10.1016/0167-0115(93)90213-R PG 4 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA KZ809 UT WOS:A1993KZ80900041 PM 8511349 ER PT J AU SAAVEDRA, JM VISWANATHAN, M SHIGEMATSU, K AF SAAVEDRA, JM VISWANATHAN, M SHIGEMATSU, K TI LOCALIZATION OF ANGIOTENSIN AT1 RECEPTORS IN THE RAT-HEART CONDUCTION SYSTEM SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note DE SINOATRIAL NODE; ATRIOVENTRICULAR NODE; ANGIOTENSIN SYSTEM; ANGIOTENSIN RECEPTORS; LOSARTAN ID SITES AB We characterized angiotensin II receptor subtypes in the conduction system of the rat heart using quantitative autoradiography. In both the sinoatrial and atrioventricular nodes, binding could be totally displaced by losartan, and was insensitive to PD 123177, indicating that angiotensin II receptors in the conduction system of the rat heart belong to the AT1 subtype. Angiotensin AT1 receptors could play a direct role in the regulation of the heart chronotropic properties. RP SAAVEDRA, JM (reprint author), NIMH,CLIN SCI LAB,PHARMACOL SECT,BLDG 10,ROOM 2D-45,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 10 TC 28 Z9 29 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 APR 28 PY 1993 VL 235 IS 2-3 BP 301 EP 303 DI 10.1016/0014-2999(93)90150-G PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LA863 UT WOS:A1993LA86300018 PM 8508909 ER PT J AU COTTON, FA KOHLI, M LUCK, RL SILVERTON, JV AF COTTON, FA KOHLI, M LUCK, RL SILVERTON, JV TI ANOTHER BOGUS ISOMER - SIC TRANSIT GREEN MO2CL4(PMEPH2)4 - THE X-RAY CRYSTAL-STRUCTURE DETERMINATION OF MOOCL3(OPMEPH2)2.C6H6 SO INORGANIC CHEMISTRY LA English DT Note ID MOLECULAR-STRUCTURES; COMPLEXES; BONDS C1 AMERICAN UNIV,DEPT CHEM,WASHINGTON,DC 20016. NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. TEXAS A&M UNIV SYST,MOLEC STRUCT & BONDING LAB,COLL STN,TX 77843. NR 15 TC 17 Z9 17 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0020-1669 J9 INORG CHEM JI Inorg. Chem. PD APR 28 PY 1993 VL 32 IS 9 BP 1868 EP 1870 DI 10.1021/ic00061a055 PG 3 WC Chemistry, Inorganic & Nuclear SC Chemistry GA KZ801 UT WOS:A1993KZ80100055 ER PT J AU FERGUSON, JH DUBINSKY, M KIRSCH, PJ AF FERGUSON, JH DUBINSKY, M KIRSCH, PJ TI COURT-ORDERED REIMBURSEMENT FOR UNPROVED MEDICAL TECHNOLOGY - CIRCUMVENTING TECHNOLOGY-ASSESSMENT SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID AMYGDALIN AB Objective.-Because we found examples where courts ot law ruled against insurance carriers that had been sued for reimbursement for unproven medical procedures, we conducted a case study to determine the reasoning behind these decisions that run counter to accepted medical science. Such actions circumvent health technology assessment and could contribute to escalating health care costs and poorer quality health care. Data Sources.-A literature search identified 17 cases between 1980 and 1989 in which an insurance company was sued to reimburse a patient who had received an unproven or questionable health technology; 14 of these suits were decided in favor of the plaintiff, and the insurance company was ordered to pay. Discussed in this article are six of these cases, two involving Laetrile (amygdalin), two involving immunoaugmentative therapy, and two involving thermography, technologies that had previously been assessed as not safe, not effective, or inadequately evaluated. Data Synthesis and Conclusions.-The circumstances determining how the courts arrive at these ''unscientific'' decisions fall into three general categories: (1) for legal reasons, the insurance contract is interpreted in favor of the insured; (2) the reluctance and/or inability, legal or otherwise, of the courts to use published scientific literature; and (3) the use of adversarial ''expert'' witnesses with potential conflicts of interest. To address this situation, we first urge the legal and insurance industries to cooperate in improving the contract language and process in a way that would be both legally and scientifically appropriate. Second, we encourage the courts to use and foster the use of published peer-reviewed scientific material as evidence whenever possible. Third, we recommend that the courts choose their own unbiased expert witnesses to interpret scientific material. C1 ADM CHILDREN & FAMILIES,WASHINGTON,DC. CUTLER & STANFIELD,WASHINGTON,DC. RP FERGUSON, JH (reprint author), NIH,OFF MED APPLICAT RES,FED BLDG,RM 618,BETHESDA,MD 20892, USA. NR 14 TC 42 Z9 42 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 APR 28 PY 1993 VL 269 IS 16 BP 2116 EP 2121 DI 10.1001/jama.269.16.2116 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA KY366 UT WOS:A1993KY36600035 PM 8468767 ER PT J AU PITT, CG WANG, J SHAH, SS SIK, R CHIGNELL, CF AF PITT, CG WANG, J SHAH, SS SIK, R CHIGNELL, CF TI ESR SPECTROSCOPY AS A PROBE OF THE MORPHOLOGY OF HYDROGELS AND POLYMER-POLYMER BLENDS SO MACROMOLECULES LA English DT Article ID BLOCK COPOLYMERS; LIQUID-CHROMATOGRAPHY; SPIN-PROBE; WATER; METHACRYLATE); COEFFICIENTS; D,L-LACTIDE; PARTITION AB The use of spin-labeled solutes to determine the morphology of polymer-water blends (hydrogels) and polymer-polymer blends was evaluated. The ESR spectra of the nitroxides 4-amino-TEMPO and 4-(N-butylamino)-TEMPO were measured in poly(2-hydroxyethyl methylacrylate) (PHEMA), poly(vinyl alcohol) (PVA), and polyacrylamide (PAA) at pH 4.45 and 10.5. The spectra in PHEMA were independent of pH and could be simulated as single species using the theory of Freed et al. developed for slow-tumbling species. Similar results were obtained with the nitroxides in poly(vinyl alcohol) and polyacrylamide. There was no evidence of either bulk or ordered water existing as phase-separated domains within the hydrogels. The ability to detect aqueous domains was verified by measurement of the spectra of the nitroxides in a porous form of PHEMA; in this case, the spectra were pH dependent and could only be simulated as the sum of the spectra in water and nonporous PHEMA. The ability of ESR spectroscopy to detect phase separation in polymer-polymer blends was tested using blends of PVA with poly(glycolic acid-co-lactic acid (PGLA) and poly(epsilon-caprolactone) (PCL). Only single nitroxide species were observed in a miscible 20:80 blend of PGLA and PVA, whereas composite spectra with pH-dependent line shapes and rotational correlation times were observed for the phase-separated 80:20 blend. The method showed that both 80:20 and 20:80 blends of PVA and PCL were miscible. Three block copolymers of poly(ethylene glycol) (PEG) and poly(lactic acid) were similarly evaluated, and in one case partial phase separation was observed. The advantages and limitations to this method of characterizing blend miscibility are discussed. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RP PITT, CG (reprint author), AMGEN INC,THOUSAND OAKS,CA 91320, USA. NR 28 TC 21 Z9 21 U1 0 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0024-9297 J9 MACROMOLECULES JI Macromolecules PD APR 26 PY 1993 VL 26 IS 9 BP 2159 EP 2164 DI 10.1021/ma00061a003 PG 6 WC Polymer Science SC Polymer Science GA KZ776 UT WOS:A1993KZ77600003 ER PT J AU BIRD, GSJ ROSSIER, MF OBIE, JF PUTNEY, JW AF BIRD, GSJ ROSSIER, MF OBIE, JF PUTNEY, JW TI SINUSOIDAL OSCILLATIONS IN INTRACELLULAR CALCIUM REQUIRING NEGATIVE FEEDBACK BY PROTEIN-KINASE-C SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID PANCREATIC ACINAR-CELLS; INOSITOL TRISPHOSPHATE; CYTOSOLIC CALCIUM; LACRIMAL CELLS; PHORBOL-ESTER; HORMONE; ACETYLCHOLINE; STIMULATION; HEPATOCYTES; TRANSIENT AB Stimulation of mouse lacrimal acinar cells with submaximal concentrations of the muscarinic agonist, methacholine, resulted in an increase in intracellular calcium ([Ca2+]i), which took the form of sinusoidal oscillations. These oscillations were relatively constant (approximately 4-5/min) regardless of the methacholine concentration, suggesting that the oscillations arise from an oscillating negative feedback in the signal transduction pathway. This negative feedback appears to involve oscillations in protein kinase C activity because the oscillations were prevented by activation, inhibition, or down-regulation of protein C. Activation of protein kinase C with phorbol esters inhibited the methacholine-induced [Ca2+]i signal and formation of the Ca2+ mobilizing messenger, inositol 1,4,5-trisphosphate. [Ca2+]i signals elicited by intracellular introduction of inositol phosphates did not oscillate and were not affected by activators or inhibitors of protein kinase C. Thus, the constant frequency [Ca2+]i oscillations appear to result from a negative feedback loop involving inhibition of inositol trisphosphate production by protein kinase C. RP BIRD, GSJ (reprint author), NIEHS,CELLULAR & MOLEC PHARMACOL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 32 TC 90 Z9 91 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 APR 25 PY 1993 VL 268 IS 12 BP 8425 EP 8428 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX811 UT WOS:A1993KX81100012 PM 8473285 ER PT J AU GAO, BC EMOTO, Y GREENE, L EISENBERG, E AF GAO, BC EMOTO, Y GREENE, L EISENBERG, E TI NUCLEOTIDE BINDING-PROPERTIES OF BOVINE BRAIN UNCOATING ATPASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HEAT-SHOCK RESPONSE; PEPTIDE BINDING; COATED VESICLES; CLATHRIN COATS; PROTEINS; HSP70; TRANSLOCATION; DISSOCIATION; SUBFAMILY; ACTIN AB Many functions of the 70-kDa heat-shock proteins (hsp70s) appear to be regulated by bound nucleotide. In this study we examined the nucleotide binding properties of purified bovine brain uncoating ATPase, one of the constitutively expressed members of the hsp70 family. We found that uncoating ATPase purified by ATP-agarose column chromatography retained one ADP molecule bound per enzyme molecule which could not be removed by extensive dialysis. Since this bound ADP exchanged rapidly with free ADP or ATP, the inability to remove the bound nucleotide was not due to slow dissociation but rather to strong binding of the nucleotide to the uncoating ATPase. In confirmation of this view, equilibrium dialysis experiments suggested that the dissociation constants for both ADP and ATP were less than 0.1 muM. Schmid et al. (Schmid, S. L., Braell, W. A., and Rothman, J. E. (1985) J. Biol. Chem 260, 10057-10062) suggested that the uncoating ATPase had two sites for bound nucleotide, one specific for ATP and one binding both ATP and ATP analogues but not ADP. In contrast, we found that enzyme with bound ADP did not bind further adenosine 5'-(beta,gamma-imino)triphosphate or dATP, nor did more than one ATP molecule bind per enzyme even in 200 muM free ATP. These results strongly suggest that the enzyme has only one binding site for nucleotide. During steady-state ATP hydrolysis, 85% of the bound nucleotide at this site was determined to be ATP and 15% ADP; this is consistent with the rate of ADP release determined in the exchange experiments noted above, where ADP release was found to be six times faster than the overall rate of ATP hydrolysis. C1 MED COLL OITA,DEPT PHYSIOL,OITA 87956,JAPAN. RP GAO, BC (reprint author), NHLBI,CELL BIOL LAB,BLDG 3,RM B1-23,BETHESDA,MD 20892, USA. NR 23 TC 49 Z9 49 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 APR 25 PY 1993 VL 268 IS 12 BP 8507 EP 8513 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX811 UT WOS:A1993KX81100023 PM 8473294 ER PT J AU NISHIMURA, H PALLARDO, FV SEIDNER, GA VANNUCCI, S SIMPSON, IA BIRNBAUM, MJ AF NISHIMURA, H PALLARDO, FV SEIDNER, GA VANNUCCI, S SIMPSON, IA BIRNBAUM, MJ TI KINETICS OF GLUT1 AND GLUT4 GLUCOSE TRANSPORTERS EXPRESSED IN XENOPUS OOCYTES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RAT ADIPOSE CELL; PLASMA-MEMBRANE; 3T3-L1 ADIPOCYTES; HEXOSE-TRANSPORT; INSULIN; TRANSLOCATION; PROTEIN; PARAMETERS; GENE; 3-O-METHYLGLUCOSE AB The predominant mechanism by which insulin activates glucose transport in muscle and adipose tissue is by affecting the redistribution of the facilitated hexose carriers, GLUT1 and GLUT4, from an intracellular site to the plasma membrane. A quantitative analysis of this process has been hampered by the lack of reliable determinations for kinetic constants catalyzed by each of these isoforms. In order to obtain such information, each transporter was expressed in Xenopus oocytes by the injection of mRNA encoding rat GLUT1 or GLUT4. Equilibrium exchange 3-O-methylglucose uptake was measured and the data fitted to a two-compartment model, yielding K(m) = 26.2 mM and V(max) = 3.5 nmol/min/cell for GLUT1 and K(m) = 4.3 mM and V(max) = 0.7 nmol/min/cell for GLUT4. Measurement of the abundance of cell surface transporters was accomplished by two independent protocols: photolabeling with the impermeant hexose analog 2-N-4-(1-azi-2,2,2-trifluoroethyl)benzoyl-1,3-bis(D-mannos-4-yloxy)-2-propylamine and subcellular fractionation of oocytes. Data obtained by either technique revealed that the ratio of plasma membrane GLUT1 to GLUT4 was about 4; this paralleled the relative maximal velocities for hexose transport, indicating that the turnover numbers for the two isoforms were the same. Moreover, measurement of the concentration of exofacially disposed transporters with 2-N-4-(1-azi-2,2,2-trifluoroethyl)benzoyl-1,3-bis(D-mannos-4-yloxy)-2-propylamine allowed calculation of the turnover number to be about 20,000 min-1. These data indicate that, at low substrate concentrations, the catalytic efficiency of GLUT4 is significantly greater than GLUT1. Extrapolation to mammalian systems suggests that GLUT4 is responsible for virtually all of the hexose uptake in insulin-responsive targets, particularly in the presence of hormone. C1 HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,25 SHATTUCK ST,BOSTON,MA 02115. NIDDKD,DIABET BRANCH,EXPTL DIABET METAB & NUTR SECT,BETHESDA,MD 20892. OI Birnbaum, Morris/0000-0001-9972-8680 FU NIDDK NIH HHS [DK39519] NR 37 TC 95 Z9 96 U1 1 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 APR 25 PY 1993 VL 268 IS 12 BP 8514 EP 8520 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX811 UT WOS:A1993KX81100024 PM 8473295 ER PT J AU BURNETTE, B YU, G FELSTED, RL AF BURNETTE, B YU, G FELSTED, RL TI PHOSPHORYLATION OF HIV-1 GAG PROTEINS BY PROTEIN-KINASE-C SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; TUMOR-NECROSIS-FACTOR; RECOMBINANT VACCINIA VIRUS; LONG TERMINAL REPEAT; SUBSTRATE-SPECIFICITY; T-CELLS; PLASMA-MEMBRANE; GENE-PRODUCTS; HTLV-III/LAV; FACTOR-ALPHA AB We have demonstrated that the 17-kDa N-terminal matrix protein (p17gag) of HIV-1 Pr55gag is a substrate for protein kinase C (PKC). Phosphorylation of p17gag and Pr55gag was studied in vivo by infecting COS-7 cells with a recombinant vaccinia virus containing the HIV-1 gag-pol gene. Basal gag protein phosphorylation was inhibited up to 75% with the PKC inhibitor, H-7, and stimulated 3-4-fold with phorbol 12-myristate 13-acetate. In experiments using MCF-7 cell lines, p17gag and Pr55gag were dramatically phosphorylated only in clones with high PKC activity. Bacterially expressed and purified non-myristoylated and N-myristoylated p17gag were efficiently phosphorylated in a Ca2+ and phosphatidylserine-dependent manner by purified PKC. The N-myristoylated p17gag exhibited an apparent K(m) = 4 muM for PKC phosphorylation. Both in vitro and in vivo phosphorylated p17gag yielded identical V8 protease digestion phosphopeptide maps, indicating identical PKC phosphorylation sites. Phosphoamino acid analysis of the in vitro phosphorylated p17gag revealed only phosphoserine. These data are consistent with the identification of a highly conserved consensus PKC phosphorylation site motif in the HIV-1 gag protein at Ser111 and suggests that PKC phosphorylation plays an important role in gag protein function. C1 NCI, DIV CANC TREATMENT, BIOL CHEM LAB, BETHESDA, MD 20892 USA. NR 60 TC 37 Z9 38 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 APR 25 PY 1993 VL 268 IS 12 BP 8698 EP 8703 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX811 UT WOS:A1993KX81100050 PM 8473314 ER PT J AU LU, ZC NAGATA, S MCPHIE, P MILES, EW AF LU, ZC NAGATA, S MCPHIE, P MILES, EW TI LYSINE-87 IN THE BETA-SUBUNIT OF TRYPTOPHAN SYNTHASE THAT FORMS AN INTERNAL ALDIMINE WITH PYRIDOXAL-PHOSPHATE SERVES CRITICAL ROLES IN TRANSIMINATION, CATALYSIS, AND PRODUCT RELEASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SITE-DIRECTED MUTAGENESIS; ULTRAVIOLET VISIBLE SPECTROSCOPY; COLI ASPARTATE-AMINOTRANSFERASE; ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; LYSYL RESIDUE; L-SERINE; CIRCULAR-DICHROISM; BRONSTED ANALYSIS; EXOGENOUS AMINES AB This study provides valuable insights into the functions of the lysine residue that forms an internal aldimine with pyridoxal phosphate in the beta subunit of tryptophan synthase from Salmonella typhimurium. Our spectroscopic and kinetic studies demonstrate that a mutant alpha2beta2 complex having beta subunit lysine 87 replaced by threonine forms external aldimines with several amino acids including L-serine, beta-chloro-1-alanine, L-tryptophan, and D-tryptophan. Because the rates of aldimine formation are very slow, we conclude that one role of lysine 87 in the wild type enzyme is to facilitate formation of external aldimines by transimination. Lysine 87 is an essential catalytic residue because the mutant alpha2beta2 complex has no measurable activity in reactions catalyzed by the beta subunit and does not convert external aldimines to products. The mutant enzyme carries out two slow partial beta-elimination reactions: the conversion of beta-chloro-L-alanine and L-serine to enzyme-bound aminoacrylate. The reaction with L-serine is catalyzed by ammonia, which partially replaces the deleted epsilon-amino group. Lysine 87 is important for substrate and product release because L-serine, L-tryptophan, and aminoacrylate dissociate very slowly from the mutant alpha2beta2 complex. Our ability to prepare very stable derivatives of the mutant alpha2beta2 complex containing tightly bound aldimines with a substrate, a product, or a reaction intermediate provides valuable materials for ongoing x-ray crystallographic investigations and future kinetic analyses of the allosteric activation of the alpha subunit by beta subunit ligands. C1 NIDDKD, BIOCHEM PHARMACOL LAB, BLDG 8, RM 2A09, BETHESDA, MD 20892 USA. NR 65 TC 56 Z9 57 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD APR 25 PY 1993 VL 268 IS 12 BP 8727 EP 8734 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX811 UT WOS:A1993KX81100054 PM 8473317 ER PT J AU HAUN, RS MOSS, J VAUGHAN, M AF HAUN, RS MOSS, J VAUGHAN, M TI CHARACTERIZATION OF THE HUMAN ADP-RIBOSYLATION FACTOR-III PROMOTER - TRANSCRIPTIONAL REGULATION OF A TATA-LESS PROMOTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NUCLEOTIDE-BINDING-PROTEINS; CHOLERA-TOXIN; MAMMALIAN-CELLS; MESSENGER-RNA; PLASMID DNA; SEQUENCE; EXPRESSION; GENE; INITIATION; ACTIVATOR AB The 5'-flanking region of the human ADP-ribosylation factor 3 gene contains the features of a housekeeping gene. It lacks a TATA or CAAT box, has several GC boxes within a highly GC-rich region, and utilizes multiple transcription initiation sites. The cis-acting elements involved in regulating expression of the gene were identified by transient transfections of IMR-32 neuroblastoma cells. Reporter plasmids were modified to facilitate construction of defined promoter deletions linked to chloramphenicol acetyltransferase or luciferase using ligation-independent cloning. Transfection analyses indicated that sequences within 58 base pairs of the transcription initiation site were necessary for full expression, in particular a sequence containing the 10-base pair palindrome TCTCGCGAGA. Electrophoretic mobility shift assays performed with IMR-32 nuclear extracts demonstrated that a DNA-binding protein, termed TLTF, bound to an oligonucleotide containing this palindrome. Competition experiments showed that mutations within the core of the palindrome abolished in vitro binding and that the same protein bound to a 5'-proximal sequence. Expression of the promoter containing a mutated palindrome was reduced dramatically, consistent with the conclusion that this region functions in vivo to control expression of the ARF3 gene. RP HAUN, RS (reprint author), NHLBI,CELLULAR METAB LAB,BLDG 10,RM 5N307,BETHESDA,MD 20892, USA. NR 42 TC 26 Z9 26 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 APR 25 PY 1993 VL 268 IS 12 BP 8793 EP 8800 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX811 UT WOS:A1993KX81100063 PM 8473323 ER PT J AU MISHIMA, K TSUCHIYA, M NIGHTINGALE, MS MOSS, J VAUGHAN, M AF MISHIMA, K TSUCHIYA, M NIGHTINGALE, MS MOSS, J VAUGHAN, M TI ARD-1, A 64-KDA GUANINE NUCLEOTIDE-BINDING PROTEIN WITH A CARBOXYL-TERMINAL ADP-RIBOSYLATION FACTOR DOMAIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHOLERA-TOXIN; ADENYLATE-CYCLASE; REGULATORY COMPONENT; MESSENGER-RNA; BOVINE BRAIN; GTP; EXPRESSION; ACTIVATION; MECHANISM; ACID AB Clones referred to as ARD 1 were isolated from human and rat cDNA libraries. ARD 1 genes encode a putative 64-kDa protein that contains an 18-kDa ADP-ribosylation factor (ARF) domain at the carboxyl terminus and is much larger than the other monomeric approximately 20-kDa guanine nucleotide-binding ARF proteins thus far identified. ARD 1 mRNAs of 3.7 and 4.1 kilobases were detected in all rat tissues as well as in mouse and rabbit brain, human fibroblasts, and human neuroblastoma cells but not in HL-60 cells. Based on sequence identities, ARD 1 is highly conserved between rat and human. The ARF domain of ARD 1 contains the consensus sequences believed to be involved in guanine nucleotide binding, which are conserved in the ARFs and other GTP-binding proteins. Recombinant ARD 1 or the ARF domain of ARD 1, which lacks the 15 amino acids corresponding to the amino-terminal regions of ARFs stimulated, in a GTP-dependent manner, cholera toxin ADP-ribosyltransferase activity in the presence of 0.3% Tween 20. It had no effect in the presence of SDS, dimyristoylphosphatidylcholine/cholate, or cardiolipin. These observations are consistent with the conclusion that the amino-terminal region of ARF proteins is not required for activation of cholera toxin. In addition, the characteristic features of ARF proteins may be found as domains of larger mammalian proteins. RP MISHIMA, K (reprint author), NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892, USA. NR 46 TC 40 Z9 42 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 APR 25 PY 1993 VL 268 IS 12 BP 8801 EP 8807 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX811 UT WOS:A1993KX81100064 PM 8473324 ER PT J AU CAMERINIOTERO, RD HSIEH, P AF CAMERINIOTERO, RD HSIEH, P TI PARALLEL DNA TRIPLEXES, HOMOLOGOUS RECOMBINATION, AND OTHER HOMOLOGY-DEPENDENT DNA INTERACTIONS SO CELL LA English DT Review ID DOUBLE-STRAND BREAKS; COLI RECA PROTEIN; GENETIC-RECOMBINATION; ESCHERICHIA-COLI; SACCHAROMYCES-CEREVISIAE; 3-STRANDED DNA; ATP HYDROLYSIS; HUMAN-CELLS; EXCHANGE; SITE RP CAMERINIOTERO, RD (reprint author), NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892, USA. NR 60 TC 100 Z9 102 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD APR 23 PY 1993 VL 73 IS 2 BP 217 EP 223 DI 10.1016/0092-8674(93)90224-E PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KY505 UT WOS:A1993KY50500005 PM 8477443 ER PT J AU PETTIT, GR TAN, R GAO, F WILLIAMS, MD DOUBEK, DL BOYD, MR SCHMIDT, JM CHAPUIS, JC HAMEL, E BAI, R HOOPER, JNA TACKETT, LP AF PETTIT, GR TAN, R GAO, F WILLIAMS, MD DOUBEK, DL BOYD, MR SCHMIDT, JM CHAPUIS, JC HAMEL, E BAI, R HOOPER, JNA TACKETT, LP TI ISOLATION AND STRUCTURE OF HALISTATIN-1 FROM THE EASTERN INDIAN-OCEAN MARINE SPONGE PHAKELLIA-CARTERI SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Article ID NATURAL-PRODUCTS; DISCODERMIA-CALYX; THEONELLA SP; METABOLITES; CONGENERS; MACROLIDE AB A highly potent new polyether macrolide antimitotic agent designated halistatin 1 (5) was isolated (8.8 X 10(-7) % yield) from Phakellia carteri. The marine sponge was located in coastal areas of the Republic of the Comoros, and it was also found to contain halichondrin B (3) and homohalichondrin B (4). Structure elucidation of halistatin 1 (5) was achieved primarily by employing extensive high-field (400- and 500-MHz) 2D NMR techniques. Halistatin 1, like halichondrin B and homohalichondrin B, caused the accumulation of cells arrested in mitosis, inhibited tubulin polymerization, and inhibited the binding of radiolabeled vinblastine and GTP to tubulin. C1 ARIZONA STATE UNIV,DEPT CHEM,TEMPE,AZ 85287. NCI,FREDERICK CANC RES & DEV CTR,DCT,DTP,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. NCI,DCT,DTP,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. QUEENSLAND MUSEUM,BRISBANE,QLD 4101,AUSTRALIA. RP PETTIT, GR (reprint author), ARIZONA STATE UNIV,CANC RES INST,TEMPE,AZ 85287, USA. OI Hooper, John/0000-0003-1722-5954 NR 17 TC 97 Z9 98 U1 2 U2 9 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 APR 23 PY 1993 VL 58 IS 9 BP 2538 EP 2543 DI 10.1021/jo00061a030 PG 6 WC Chemistry, Organic SC Chemistry GA KY821 UT WOS:A1993KY82100030 ER PT J AU VOLAREVIC, S NIKLINSKA, BB BURNS, CM JUNE, CH WEISSMAN, AM ASHWELL, JD AF VOLAREVIC, S NIKLINSKA, BB BURNS, CM JUNE, CH WEISSMAN, AM ASHWELL, JD TI REGULATION OF TCR SIGNALING BY CD45 LACKING TRANSMEMBRANE AND EXTRACELLULAR DOMAINS SO SCIENCE LA English DT Article ID CELL ANTIGEN RECEPTOR; LEUKOCYTE-COMMON ANTIGEN; PROTEIN-TYROSINE PHOSPHATASES; INTERLEUKIN-2 PRODUCTION; T-CELLS; B-CELLS; ASSOCIATION; ACTIVATION; EXPRESSION; PHOSPHORYLATION AB The CD45 protein is a transmembrane tyrosine phosphatase that is required for normal T cell receptor (TCR)-mediated signaling. A chimeric complementary DNA encoding the intracellular enzymatically active portion of murine CD45 preceded by a short amino-terminal sequence from p60c-src was transfected into CD45- T cells. Expression of this chimeric protein corrected most of the TCR signaling abnormalities observed in the absence of CD45, including TCR-mediated enhancement of tyrosine kinase activity and Ca2+ flux. Thus, the enzymatically active intracellular portion of CD45 is sufficient to allow TCR transmembrane signaling. C1 NCI,IMMUNE CELL BIOL LAB,BIOL RESPONSE MODIFIERS PROGRAM,BETHESDA,MD 20892. USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20889. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 29 TC 116 Z9 116 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 23 PY 1993 VL 260 IS 5107 BP 541 EP 544 DI 10.1126/science.8475386 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KY504 UT WOS:A1993KY50400034 PM 8475386 ER PT J AU WENSBO, D ERIKSSON, A JESCHKE, T ANNBY, U GRONOWITZ, S COHEN, LA AF WENSBO, D ERIKSSON, A JESCHKE, T ANNBY, U GRONOWITZ, S COHEN, LA TI PALLADIUM-CATALYZED SYNTHESIS OF HETEROCONDENSED PYRROLES SO TETRAHEDRON LETTERS LA English DT Article ID HETEROAROMATIC-COMPOUNDS; ANTHRANILATE SYNTHETASE; NICOTIANA-TABACUM; ASSISTED REACTION; FUNCTIONALIZATION; INDOLES; ANALOGS; CELLS AB The palladium-catalysed preparation of some heterocondensed pyrroles from ortho nitrogen containing hetaryl iodides and derivatives of propargyl alcohol is described. C1 UNIV LUND,CTR CHEM,DIV ORGAN CHEM 1,POB 124,S-22100 LUND,SWEDEN. NIH,CHEM LAB,BETHESDA,MD 20205. NR 30 TC 82 Z9 82 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4039 J9 TETRAHEDRON LETT JI Tetrahedron Lett. PD APR 23 PY 1993 VL 34 IS 17 BP 2823 EP 2826 DI 10.1016/S0040-4039(00)73572-6 PG 4 WC Chemistry, Organic SC Chemistry GA KZ036 UT WOS:A1993KZ03600031 ER PT J AU OLDEN, K AF OLDEN, K TI OPPORTUNITIES IN ENVIRONMENTAL-HEALTH SCIENCE RESEARCH SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Editorial Material RP OLDEN, K (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 1 TC 4 Z9 4 U1 0 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR 22 PY 1993 VL 101 IS 1 BP 6 EP 7 DI 10.2307/3431558 PG 2 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LD794 UT WOS:A1993LD79400001 PM 8513765 ER PT J AU LUCIER, GW PORTIER, CJ GALLO, MA AF LUCIER, GW PORTIER, CJ GALLO, MA TI RECEPTOR MECHANISMS AND DOSE-RESPONSE MODELS FOR THE EFFECTS OF DIOXINS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID AH RECEPTOR; TUMOR PROMOTION; 2-STAGE MODEL; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN; CARCINOGENESIS; HEPATOCARCINOGENESIS AB There is increasing evidence that receptor-mediated events impact one or more stages responsible for tumor development in experimental animals and humans. Although many chemicals and endogenous hormones require receptor interactions as a necessary event in their carcinogenic activity, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and its structural analogs are the most visible examples of receptor-mediated carcinogens. TCDD, or dioxin as it is frequently called, interacts with the Ah receptor (AhR), which functions in a manner analogous to receptors for steroids. TCDD produces a wide spectrum of biochemical and toxic responses in in vitro and in vive systems, and the Ah receptor is generally considered necessary for most if not all of these responses. Risk assessments for dioxin made by the United States and other countries throughout the world have been based on its carcinogenecity in experimental animals. Recently, epidemiology studies have indicated that TCDD is a human carcinogen at high doses. Because TCDD appears to be acting like a potent and persistent hormone agonist, it appears reasonable to incorporate mechanistic information on receptor-mediated events in risk assessments for TCDD. This information may bc obtained from steroid receptor action and from molecular data on the Ah receptor. In this paper, we evaluate the scientific foundation on which mechanistic models for estimating dioxin's risks should be based. These models need to recognize the mechanisms possible for the diversity of biological responses that are initiated by a single receptor interacting with a single ligand. The U.S. EPA is currently reevaluating dioxin's risks by examining the possibility of developing biologically based models. This paper details the considerations that must be made in developing such models, including information on mechanisms of steroid hormone action, characteristics of the Ah receptor, diversity of receptor actions, and design issues that are crucial for the translation of biological phenomenon into valid dose-response models. C1 NIEHS,RISK METHODOL SECT,RES TRIANGLE PK,NC 27709. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,PISCATAWAY,NJ 08855. RP LUCIER, GW (reprint author), NIEHS,BIOCHEM RISK ANAL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 48 TC 63 Z9 63 U1 1 U2 3 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 APR 22 PY 1993 VL 101 IS 1 BP 36 EP 44 DI 10.2307/3431569 PG 9 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LD794 UT WOS:A1993LD79400019 PM 8390353 ER PT J AU HASEMAN, JK LOCKHART, AM AF HASEMAN, JK LOCKHART, AM TI CORRELATIONS BETWEEN CHEMICALLY RELATED SITE-SPECIFIC CARCINOGENIC EFFECTS IN LONG-TERM STUDIES IN RATS AND MICE SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE INTERSPECIES CORRELATION; LABORATORY ANIMAL STUDIES; NATIONAL TOXICOLOGY PROGRAM; RODENT CARCINOGENICITY; SITE-SPECIFIC NEOPLASMS ID NATIONAL TOXICOLOGY PROGRAM AB We examined a database of 379 long-term carcinogenicity studies in rats and mice to evaluate sex and species correlations in site-specific carcinogenic responses. Within a species, most target sites showed a strong correlation between males and females. For example, chemicals producing forestomach or liver tumors in males were likely to produce these same types of tumors in females. There was also a significant correlation between species for certain site-specific carcinogenic effects, most notably tumors of the forestomach, liver, and thyroid gland. In contrast, adrenal pheochromocytoma, preputial/clitoral gland neoplasms, and lung tumors showed no significant interspecies correlation. Many chemicals produced a syndrome of carcinogenic effects involving tumors of the skin, Zymbal gland, preputial/clitoral gland, mammary gland, and/or oral cavity. Regarding different target sites, there appeared to be a correlation between thyroid and liver tumors both within and between species. Further, all chemicals producing mesotheliomas in male rats also produced mammary gland neoplasms in female rats. In contrast, kidney and urinary bladder tumors showed no significant association with any other tumor type in rats or mice. If a chemical produced a site-specific carcinogenic effect in female rats or mice, there was approximately a 65% probability that the chemical would also bc carcinogenic at that same site in males. The interspecies correlation was somewhat lower: approximately 36% of the site-specific carcinogenic effects ob-served in one species (rats or mice) were also observed in the other species. The high correlation between males and females suggests that in some instances it may be appropriate to consider a reduced protocol such as male rats and female mice. This would result in substantial cost savings, and an examination of NCI/NTP studies suggests that while there will bc some sensitivity loss associated with this approach, the rodent carcinogens not detected by this reduced protocol are not those most likely to pose a carcinogenic threat to humans. Nevertheless, the decision of whether to use a reduced protocol is best made on a case-by-case basis. C1 COMP SCI CORP,DURHAM,NC 27713. RP HASEMAN, JK (reprint author), NIEHS,STAT & BIOMATH BRANCH,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 15 TC 45 Z9 45 U1 0 U2 0 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 APR 22 PY 1993 VL 101 IS 1 BP 50 EP 54 DI 10.2307/3431571 PG 5 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LD794 UT WOS:A1993LD79400021 PM 8513764 ER PT J AU BURKHARTSCHULTZ, K THOMAS, CB THOMPSON, CL STROUT, CL BRINSON, E JONES, IM AF BURKHARTSCHULTZ, K THOMAS, CB THOMPSON, CL STROUT, CL BRINSON, E JONES, IM TI CHARACTERIZATION OF INVIVO SOMATIC MUTATIONS AT THE HYPOXANTHINE PHOSPHORIBOSYLTRANSFERASE GENE OF A HUMAN CONTROL POPULATION SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE HYPRT; LYMPHOCYTES; MUTATION SPECTRUM; SOMATIC MUTATION ID HUMAN LYMPHOCYTES-T; LESCH-NYHAN SYNDROME; GUANINE PHOSPHORIBOSYLTRANSFERASE; SEQUENCE-ANALYSIS; MUTANT FREQUENCY; CLONING ASSAY; CELL CLONING; HPRT GENE; CDNA; DELETIONS AB The ability to recognize a change in mutation spectrum after an exposure to a toxic substance and then relate that exposure to health risk depends on the knowledge of mutations that occur in the absence of exposure. Toward this end, we have been studying both the frequency and molecular nature of mutations of the hypoxanthine phosphoribosyltransferase (hprt) gene in peripheral blood lymphocytes as surrogate reporters of genetic damage. We have analyzed mutants, one per donor to ensure independence, from a control population in which the quantitative effects of smoking and age on mutant frequency have been well defined. Analyses of cDNA and genomic DNA by polymerase chain reaction and sequencing have identified the mutations in 63 mutants, 45 from males and 18 from females, of which 34 were smokers and 29 were nonsmokers. Slightly less than half of the mutations were base substitutions (28); they were predominantly at GC base pairs (19). Different mutations at the same site indicated that there are features of the hprt polypeptide that affect the mutation spectrum. Two pairs of identical mutations indicated that there may also bc hot spots. Mutations not previously reported have been detected, indicating that the mutation spectrum is only partly defined. The remainder of the mutations were deletions (32) or insertions/duplications (3); deletions ranged from one base pair to complete loss of the locus. Despite a small average increase in mutant frequency for smokers, an increased proportion of base substitutions at AT base pairs in smokers (p = 0.2) hinted at a smoking-associated shift in the mutation spectrum. Expansion of the study to include individuals with larger, smoking-associated increases of mutant frequency will determine the significance of this observation. This background mutation study provides insight into factors that determine the mutation spectra of the hprt locus and provides data for comparison with mutation spectra of other populations. C1 LAWRENCE LIVERMORE NATL LAB,BIOL & BIOTECHNOL PROGRAM,L-452,POB 808,LIVERMORE,CA 94551. NIEHS,DIV BIOMETRY & RISK ASSESSMENT,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [N1EHS Y01-ES-80171] NR 45 TC 25 Z9 25 U1 0 U2 0 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 APR 22 PY 1993 VL 101 IS 1 BP 68 EP 74 DI 10.2307/3431574 PG 7 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LD794 UT WOS:A1993LD79400024 PM 8513767 ER PT J AU LADENHEIM, EE JENSEN, RT MANTEY, SA TAYLOR, JE COY, DH MORAN, TH AF LADENHEIM, EE JENSEN, RT MANTEY, SA TAYLOR, JE COY, DH MORAN, TH TI BOMBESIN RECEPTOR ANTAGONISTS DIFFERENTIATE RECEPTOR SUBTYPES IN RAT-BRAIN SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note DE GASTRIN-RELEASING PEPTIDE; NEUROMEDIN-B; BOMBESIN AB Previous studies have shown that various bombesin receptor antagonists can distinguish between bombesin receptor subtypes in peripheral tissues. To determine whether these antagonists would be useful in differentiating bombesin receptor subtypes in the rat central nervous system, we used in vitro receptor autoradiography to examine the binding affinities of several bombesin receptor antagonists for two brain regions we had characterized as possessing distinct bombesin receptor subtypes. Our results demonstrate that, consistent with peripheral bombesin receptors, bombesin receptor subtypes in the rat brain can be differentiated by various bombesin receptor antagonists. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. BIOMEASURE INC,MILFORD,MA 01757. TULANE UNIV,MED CTR,DEPT MED,PEPTIDE RES LABS,NEW ORLEANS,LA 70112. FU NCI NIH HHS [CA-45153]; NIDDK NIH HHS [DK-19302] NR 11 TC 15 Z9 15 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 APR 22 PY 1993 VL 235 IS 1 BP 121 EP 125 DI 10.1016/0014-2999(93)90830-B PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KZ722 UT WOS:A1993KZ72200019 PM 8390937 ER PT J AU ZHOU, HX AF ZHOU, HX TI DYNAMIC SPHERICAL MODEL FOR SOLVATION IN A DIPOLAR LATTICE SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID NONEQUILIBRIUM SOLVATION; MOLECULAR THEORY; SOLVENT; ION AB The spherical model for a dipolar lattice is extended to the dynamic regime to provide a theory for nonequilibrium solvation. In this extension the dynamic susceptibility takes the same expression as the static one in the spherical model, but the dielectric constant is replaced by the dielectric function. This leads to the same result as what is obtained from the Smoluchowski-Vlasov equation if the dielectric function takes the Debye form. Otherwise it can be derived from a generalized Smoluchowski-Vlasov equation. The solvation dynamics of an ion is found by summing the product of the dynamic polarization of the homogeneous lattice and the electric field of the ion at each lattice site (except the ionic site). This constitutes the dielectric approximation. By use of dielectric functions from previous simulations, the dynamic spherical model produces results that agree very well with simulated ionic solvation dynamics. However, the dynamic spherical model fails for dipolar solvation as a result of the inherent dielectric approximation. By using the spherical model expression for the static dipolar solvation energy and ''tending it to the dynamic regime, an expression is obtained for dipolar solvation dynamics. Its results agree moderately well with simulations. Several implications for solvation dynamics in dipolar liquids can be drawn from this study. It is suggested that the dielectric function plays an essential role in theories of solvation dynamics. It is also shown that the memory function theory of Fried and Mukamel can be derived from a generalized Smoluchowski-Vlasov equation. Lastly it is concluded that the dielectric approximation has to be improved for dipolar solvation. RP ZHOU, HX (reprint author), NIDDKD,BETHESDA,MD 20892, USA. RI Zhou, Huan-Xiang/M-5170-2016 OI Zhou, Huan-Xiang/0000-0001-9020-0302 NR 21 TC 6 Z9 6 U1 0 U2 1 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 APR 22 PY 1993 VL 97 IS 16 BP 4216 EP 4223 DI 10.1021/j100118a045 PG 8 WC Chemistry, Physical SC Chemistry GA KY466 UT WOS:A1993KY46600046 ER PT J AU MARKELLO, TC BERNARDINI, IM GAHL, WA AF MARKELLO, TC BERNARDINI, IM GAHL, WA TI IMPROVED RENAL-FUNCTION IN CHILDREN WITH CYSTINOSIS TREATED WITH CYSTEAMINE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID NEPHROPATHIC CYSTINOSIS; SERUM CREATININE; COMPLICATIONS; INSUFFICIENCY; PATIENT; AGE AB Background. The lysosomal storage disease cystinosis results in renal failure at approximately 10 years of age. Although oral cysteamine therapy is recognized to preserve kidney function, the extent of renal benefit has not been determined. Methods. Between 1960 and 1992, we determined 24-hour creatinine clearances in 76 children with cystinosis during 1081 admissions to the National Institutes of Health. Seventeen children were considered to have received adequate treatment with cysteamine, since they had depletion of cystine from leukocytes and began therapy before the age of 2 years; treatment lasted a mean of 7.1 years. Thirty-two children were considered to have received partial treatment, since they had poor compliance with therapy or began treatment after the age of 2; treatment lasted a mean of 4.5 years. Twenty-seven children were followed in the era before cysteamine therapy and thus never received cysteamine. Results. Of the 27 children who never received cysteamine, 16 were followed at the National Institutes of Health until renal failure occurred: their mean (+/-SD) creatinine clearance was 8.0+/-4.8 ml per minute per 1.73 m2 of body-surface area at a mean age of 8.3+/-1.9 years. Of the 17 children who received adequate treatment, none had renal failure; their mean creatinine clearance was 57+/-20 ml per minute per 1.73 m2 at 8.3+/-3.8 years of age. The mean creatinine clearance of the children who received partial or adequate treatment with cysteamine increased with age up to the age of five years and then declined linearly with age at a normal rate. For the children who received adequate treatment, the mean creatinine clearance was predicted to reach 0 ml per minute per 1.73 m2 at the age of 74 years, as compared with 20 years of age for the children who received partial treatment. With no therapy, the mean creatinine clearance reaches 0 ml per minute per 1.73 m2 at 10 years of age. Conclusions. Children with cystinosis who are treated early and adequately with cysteamine have renal function that increases during the first five years of life and then declines at a normal rate. Patients with poorer compliance and those who are treated at an older age do less well. C1 NICHHD,HUMAN GENET BRANCH,HUMAN BIOL CHEM & GENET SECT,BLDG 10,RM 9S-242,BETHESDA,MD 20892. NR 30 TC 158 Z9 161 U1 1 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 22 PY 1993 VL 328 IS 16 BP 1157 EP 1162 DI 10.1056/NEJM199304223281604 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA KY447 UT WOS:A1993KY44700004 PM 8455682 ER PT J AU KALINER, MA AF KALINER, MA TI ASTHMA DEATHS - A SOCIAL OR MEDICAL PROBLEM SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID CHANGING PATTERNS RP KALINER, MA (reprint author), NIAID,ALLERG DIS SECT,BLDG 10,ROOM 11C205,BETHESDA,MD 20892, USA. NR 9 TC 17 Z9 17 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 APR 21 PY 1993 VL 269 IS 15 BP 1994 EP 1995 DI 10.1001/jama.269.15.1994 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KX215 UT WOS:A1993KX21500033 PM 8464134 ER PT J AU SILVERTON, JV AF SILVERTON, JV TI ORIGIN-2.0 - SCIENTIFIC GRAPHICS AND DATA-ANALYSIS IN WINDOWS SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Software Review RP SILVERTON, JV (reprint author), NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD APR 21 PY 1993 VL 115 IS 8 BP 3396 EP 3396 PG 1 WC Chemistry, Multidisciplinary SC Chemistry GA KY506 UT WOS:A1993KY50600076 ER PT J AU ROSENBERG, SA LOTZE, MT YANG, JC TOPALIAN, SL CHANG, AE SCHWARTZENTRUBER, DJ AEBERSOLD, P LEITMAN, S LINEHAN, WM SEIPP, CA WHITE, DE STEINBERG, SM AF ROSENBERG, SA LOTZE, MT YANG, JC TOPALIAN, SL CHANG, AE SCHWARTZENTRUBER, DJ AEBERSOLD, P LEITMAN, S LINEHAN, WM SEIPP, CA WHITE, DE STEINBERG, SM TI PROSPECTIVE RANDOMIZED TRIAL OF HIGH-DOSE INTERLEUKIN-2 ALONE OR IN CONJUNCTION WITH LYMPHOKINE-ACTIVATED KILLER-CELLS FOR THE TREATMENT OF PATIENTS WITH ADVANCED CANCER SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID TUMOR-INFILTRATING LYMPHOCYTES; ESTABLISHED PULMONARY METASTASES; PURIFIED HUMAN INTERLEUKIN-2; RECOMBINANT INTERLEUKIN-2; ADOPTIVE IMMUNOTHERAPY; LAK CELLS; HEPATIC METASTASES; MURINE TUMORS; HALF-LIFE; INVIVO AB Background: Treatment using interleukin-2 (IL-2) alone or in conjunction with lymphokine-activated killer (LAK) cells has been shown to mediate disease regression in selected patients with advanced cancer. Purpose: This prospective randomized trial was designed to determine whether the administration of LAK cells in conjunction with high-dose IL-2 alters response and survival rates, compared with those for IL-2 alone, in patients with advanced cancer. Methods: The 181 patients who had metastatic cancer that had failed to respond to standard therapy or who had disease for which no effective therapy existed received treatment with high-dose IL-2 alone or with LAK cells plus IL-2. Both treatment groups were to receive the same dose of IL-2 administered according to the same schedule. IL-2 doses were omitted depending on the tolerance of the patient. Of the 181 patients, 97 had renal cell cancer and 54 had melanoma. Results: Median potential follow-up was 63.2 months. There were 10 complete responses among the 85 assessable patients who received IL-2 plus LAK cells, compared with four among the 79 who received IL-2 alone. There were 14 and 12 partial responses, respectively. Complete response continues in seven patients at 50-66 months. The 36-month actuarial survival with IL-2 plus LAK cells was 31%, compared with 17% with IL-2 alone (two-sided P value [P2] = .089). A trend toward improved survival was seen for patients with melanoma who received IL-2 plus LAK cells, compared with those who received IL-2 alone (24-month survival: 32% versus 15%; 48-month survival: 18% versus 4%; P2 = .64). None of 26 patients with melanoma who received IL-2 alone are alive; five of 28 who received IL-2 plus LAK cells are alive, and three continue in complete response. No difference in survival was seen in patients with renal cell cancer in the two treatment groups. There were six treatment-related deaths (3.3%); three were due to myocardial infarction. Other toxic effects resolved by discontinuation of IL-2. Many toxic effects were related to increased vascular permeability induced by IL-2. Conclusions: Some patients with metastatic cancer have prolonged remission when they are treated with high-dose IL-2 alone or in conjunction with LAK cells. Our results suggest a trend toward increased survival when IL-2 is given with LAK cells in patients with melanoma, but no trend was observed for patients with renal cell cancer. Implications: As these studies continue, efforts are underway to develop improved immunotherapies using tumor-infiltrating lymphocytes (TIL) and gene-modified TIL. C1 NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892. RP ROSENBERG, SA (reprint author), NCI,DIV CANC TREATMENT,SURG BRANCH,BLDG 10,RM 2B42,BETHESDA,MD 20892, USA. NR 45 TC 426 Z9 437 U1 0 U2 3 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 21 PY 1993 VL 85 IS 8 BP 622 EP 632 DI 10.1093/jnci/85.8.622 PG 11 WC Oncology SC Oncology GA KX940 UT WOS:A1993KX94000011 PM 8468720 ER PT J AU ZAHAREVITZ, DW GRUBB, MF HYMAN, R CHISENA, C CYSYK, RL AF ZAHAREVITZ, DW GRUBB, MF HYMAN, R CHISENA, C CYSYK, RL TI EFFECT OF HIGH-PROTEIN DIET ON PYRMIDINE SYNTHESIS AND RESPONSE TO PALA IN MOUSE-TISSUES SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID RAT-LIVER; 5-FLUOROURACIL; PHOSPHATE; N-(PHOSPHONACETYL)-L-ASPARTATE; MODULATION; TOXICITY AB Background: High-protein diets have been found to protect mice from the lethal effects of cytotoxic pyrimidine analogues and to reduce the toxicity of the antipyrimidine fluorouracil (5-FU), but the biochemical explanation for these effects is not known. PALA potentiates the chemotherapeutic efficacy of 5-FU, and each of the two agents can produce dose-limiting intestinal toxic effects. We have shown that intraperitoneal infusion of ammonium chloride stimulates intestinal de novo pyrimidine synthesis. This stimulation with excess ammonia, which can also result from high-protein intake, is dependent on the presence of carbamoyl phosphate synthetase I, an enzyme in the liver and intestine but not in most tumors. These findings suggest that a high-protein diet can stimulate pyrimidine synthesis in the liver and intestine but leave it unchanged in tumor tissue. Purpose: The purpose of this study was to determine whether varying dietary protein causes pharmacologically relevant and preferential changes in de novo pyrimidine synthesis. Methods: Mice were fed diets containing 18%, 35%, or 50% casein. Dietary effects on de novo pyrimidine synthesis were measured in the intestine, liver, and B16 mouse melanoma in mice treated with PALA and in untreated mice. De novo synthesis was measured by infusion of [N-15]alanine into intact animals, determination of N-15 incorporation into uracil by use of gas chromatography-mass spectrometry. and calculation of the fraction of the uracil nucleotide pool formed by de novo synthesis. Results: In mice on a 50% casein diet (high protein), de novo pyrimidine synthesis increased substantially in the liver and intestine, compared with synthesis in mice receiving 18% casein. Increase in pyrimidine synthesis in B16 tumor tissue was negligible. The high-protein diet protected the intestine and liver from depletion of uracil nucleotide pools by PALA, and toxicity in tumor-free animals was reduced, as determined by mortality after PALA treatment. Sensitivity of the B16 tumor to the biochemical and cytotoxic effects of PALA was not diminished. Conclusions: We propose that the basis for these effects of a high-protein diet is the generation of excess carbamoyl phosphate in tissues containing carbamoyl phosphate synthetase I. This carbamoyl phosphate can stimulate de novo pyrimidine synthesis and compete with drugs that interact with enzymes of the de novo pathway, thereby selectively protecting the liver and intestine. Implications: These data provide a biochemical explanation for reported effects of high-protein diet on toxicity of anti-pyrimidines like 5-FU. Studies are underway to determine if stimulation of pyrimidine synthesis by excess ammonia improves therapy with 5-FU alone or combined with PALA. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BLDG 37,RM 5E-18,BETHESDA,MD 20892. NR 17 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 APR 21 PY 1993 VL 85 IS 8 BP 662 EP 666 DI 10.1093/jnci/85.8.662 PG 5 WC Oncology SC Oncology GA KX940 UT WOS:A1993KX94000017 PM 8468725 ER PT J AU SCHMITT, JM GANDJBAKHCHE, AH BONNER, RF AF SCHMITT, JM GANDJBAKHCHE, AH BONNER, RF TI USE OF POLARIZED-LIGHT TO DISCRIMINATE SHORT-PATH PHOTONS IN A MULTIPLY SCATTERING MEDIUM (VOL 31, PG 6535, 1992) SO APPLIED OPTICS LA English DT Correction C1 NIH, DIV COMP RES & TECHNOL, PHYS SCI LAB, BETHESDA, MD 20892 USA. RP SCHMITT, JM (reprint author), NIH, NATL CTR RES RESOURCES, ROOM B2S245, BLDG 10, BETHESDA, MD 20892 USA. RI Bonner, Robert/C-6783-2015 NR 1 TC 0 Z9 0 U1 1 U2 3 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA SN 0003-6935 J9 APPL OPTICS JI Appl. Optics PD APR 20 PY 1993 VL 32 IS 12 BP 2186 EP 2186 PG 1 WC Optics SC Optics GA KX397 UT WOS:A1993KX39700032 PM 20820366 ER PT J AU ROBERTS, JD NGUYEN, D KUNKEL, TA AF ROBERTS, JD NGUYEN, D KUNKEL, TA TI FRAMESHIFT FIDELITY DURING REPLICATION OF DOUBLE-STRANDED DNA IN HELA-CELL EXTRACTS SO BIOCHEMISTRY LA English DT Article ID MUTATIONAL SPECIFICITY; BASE SUBSTITUTION; INVITRO; ERRORS; MISALIGNMENT; MUTAGENESIS; INITIATION AB The processes by which minus-one frameshifts arise during replication of double-stranded DNA by a human replication apparatus were examined. Using M13mp2 DNA containing the simian virus 40 (SV40) origin of replication and a plus-one frameshift mutation in the lacZalpha reporter gene, we performed replication reactions using a HeLa cell extract and the SV40 large T antigen. Frameshifts that restore the reading frame to give a blue-plaque phenotype include the loss of one of five consecutive A.T base pairs or any one of 36 non-reiterated base pairs. Although both types of deletions were generated at rates substantially above the background mutant frequency of unreplicated DNA, the rate was highest at the A.T run, suggesting the involvement of a misaligned replication intermediate at this homopolymeric sequence. The error rate for both types of deletions increased as the concentration of dNTPs was increased. A small increase in error rate at the run of A.T base pairs was also observed when a dNMP was added to the replication reaction. These results are consistent with the correction of frameshift intermediates during replication by exonucleolytic proofreading. To examine frameshift error rates on the leading and lagging strands, we compared reversion frequencies for two vectors containing the origin of replication close to, but on opposite sides of, the mutational target. To generate strand-specific errors, nucleotide substrate imbalances were used in replication reactions with these vectors. The results suggest that there is less than a 2-fold difference in the fidelity of leading- and lagging-strand synthesis for deletions at the run of A.T base pairs. However, site-specific differences of more than 10-fold were observed for deletion of certain non-reiterated base pairs. Furthermore, the pattern of minus-one frameshifts over the 41-base-pair target was different for the two vectors, suggesting that error specificity is different on the leading and lagging strands. This could reflect differences in nucleotide selectivity and/or proofreading during replication or a difference in the efficiency of postreplication repair of misaligned heteroduplexes on the two strands. C1 NIEHS, MOLEC GENET LAB, RES TRIANGLE PK, NC 27709 USA. NR 31 TC 38 Z9 38 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 20 PY 1993 VL 32 IS 15 BP 4083 EP 4089 DI 10.1021/bi00066a033 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KY244 UT WOS:A1993KY24400033 PM 8385995 ER PT J AU LYUBCHENKO, YL SHLYAKHTENKO, LS APPELLA, E HARRINGTON, RE AF LYUBCHENKO, YL SHLYAKHTENKO, LS APPELLA, E HARRINGTON, RE TI CA RUNS INCREASE DNA FLEXIBILITY IN THE COMPLEX OF LAMBDA-CRO PROTEIN WITH THE OR3 SITE SO BIOCHEMISTRY LA English DT Article ID SEQUENCE-SPECIFIC INTERACTIONS; CIRCULAR-DICHROISM SPECTRA; CATALYZED RING-CLOSURE; OPERATOR DNA; MONTE-CARLO; ANISOTROPIC FLEXIBILITY; TORSIONAL RIGIDITY; CRYSTAL-STRUCTURE; BASE MISMATCHES; IMINO PROTON AB The alternating pyrimidine-purine elements CA, CAC, and CACA are anisotropically flexible, as deduced from gel circularization assays on point mutations and single-base mismatches in the O(R)3 site of lambda phage alone and in the specific complex with the Cro protein. These sequences evidently promote DNA bending in the specific binding region of the complex and may also facilitate overwinding in the central nonbinding region. Effects for CACA are exceptionally large and suggest that an alternative DNA structure may occur in this element. C1 UNIV NEVADA,DEPT BIOCHEM,RENO,NV 89557. ARIZONA STATE UNIV,DEPT MICROBIOL,TEMPE,AZ 85287. ARIZONA STATE UNIV,DEPT PHYS,TEMPE,AZ 85287. NCI,CELL BIOL LAB,BETHESDA,MD 20892. RUSSIAN ACAD SCI,INST MOLEC GENET,MOSCOW,RUSSIA. FU NIGMS NIH HHS [GM 33435] NR 55 TC 70 Z9 70 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 20 PY 1993 VL 32 IS 15 BP 4121 EP 4127 DI 10.1021/bi00066a038 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KY244 UT WOS:A1993KY24400038 PM 8471619 ER PT J AU ANN, DK TU, ZJ LAZOWSKI, KW WU, G KOUSVELARI, E AF ANN, DK TU, ZJ LAZOWSKI, KW WU, G KOUSVELARI, E TI MULTIFACTORIAL REGULATION OF SALIVARY GLAND-SPECIFIC PROLINE-RICH PROTEIN GENE-EXPRESSION IN TRANSGENIC MOUSE SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV MINNESOTA,SCH MED,DEPT PHARMACOL,MINNEAPOLIS,MN 55455. NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1222 EP A1222 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801069 ER PT J AU ATTAASAFOADJEI, E PHILPOT, RM AF ATTAASAFOADJEI, E PHILPOT, RM TI SITE-DIRECTED MUTAGENESIS OF RABBIT LUNG FLAVIN-CONTAINING MONOOXYGENASE (FMO1B1) - EVIDENCE THAT RESIDUES K492 AND Q493 ARE IMPORTANT IN ACTIVATION BY IMPRAMINE AND ANIONIC DETERGENT SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1204 EP A1204 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800960 ER PT J AU BAILER, SM STARR, CM BLUMENTHAL, R HANOVER, JA AF BAILER, SM STARR, CM BLUMENTHAL, R HANOVER, JA TI EXPRESSION OF NUCLEAR-PORE PROTEIN-P62 USING BACULOVIRUS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1251 EP A1251 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801234 ER PT J AU BALASUNDARAM, D TABOR, CW TABOR, H AF BALASUNDARAM, D TABOR, CW TABOR, H TI OXYGEN-TOXICITY IN A POLYAMINE-DEPLETED SACCHAROMYCES-CEREVISIAE NULL MUTANT SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1155 EP A1155 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800675 ER PT J AU BECERRA, SP NOTARIO, V CHADER, GJ AF BECERRA, SP NOTARIO, V CHADER, GJ TI STRUCTURE-FUNCTION STUDIES OF PIGMENT-EPITHELIUM DERIVED FACTOR (PEDF) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. GEORGETOWN UNIV,WASHINGTON,DC 20007. NR 0 TC 0 Z9 0 U1 0 U2 2 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 APR 20 PY 1993 VL 7 IS 7 BP A1085 EP A1085 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800272 ER PT J AU BIFULCO, M LAEZZA, C GARBI, C WOLFF, J ALOJ, SM AF BIFULCO, M LAEZZA, C GARBI, C WOLFF, J ALOJ, SM TI PROTEIN PRENYLATION IS REQUIRED FOR CYTOSKELETON ORGANIZATION AND STABILITY SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CATANZARO,DIPARTIMENTO MED SPER CLIN,CATANZARO,ITALY. NIH,BETHESDA,MD 20892. UNIV NAPLES,CEOS,CNR,I-80138 NAPLES,ITALY. UNIV NAPLES,DBPCM,I-80138 NAPLES,ITALY. NR 0 TC 1 Z9 1 U1 0 U2 2 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 APR 20 PY 1993 VL 7 IS 7 BP A1039 EP A1039 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800003 ER PT J AU BODINE, DM NIENHUIS, AW WILLIAMS, DA AF BODINE, DM NIENHUIS, AW WILLIAMS, DA TI RETROVIRUS MEDIATED GENE-TRANSFER TO THE HEMATOPOIETIC STEM-CELL SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1262 EP A1262 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801298 ER PT J AU BOYLE, T AVIS, I MULSHINE, JL GEMSKI, P FINE, RL JETT, M AF BOYLE, T AVIS, I MULSHINE, JL GEMSKI, P FINE, RL JETT, M TI STIMULATION OF LIPOXYGENASE METABOLITES IN NCI-H209 LUNG-CELLS REFLECTS TOXIC VS NONTOXIC RESPONSES - CYCLOOXYGENASE INHIBITOR INCREASED PRODUCTION OF LEUKOTRIENES FOR BOTH AGONISTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 WALTER REED ARMY INST RES,DIV PATHOL,WASHINGTON,DC 20307. NIH,DCPC,BPRB,BETHESDA,MD 20892. VET ADM MED CTR,DURHAM,NC 27705. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1309 EP A1309 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801576 ER PT J AU BRADY, JP PIATIGORSKY, J AF BRADY, JP PIATIGORSKY, J TI CHARACTERIZATION OF THE GENE ENCODING ALPHA-A-CRYBP1 - A TRANSCRIPTIONAL REGULATOR OF THE MOUSE ALPHA-A-CRYSTALLIN GENE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI,MOL & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 20 PY 1993 VL 7 IS 7 BP A1219 EP A1219 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801050 ER PT J AU BURROUGHS, SE HORROCKS, WD KLEE, CB AF BURROUGHS, SE HORROCKS, WD KLEE, CB TI CHARACTERIZATION OF CALCINEURIN USING EU3+ LUMINESCENCE SPECTROSCOPY SO FASEB JOURNAL LA English DT Meeting Abstract C1 PENN STATE UNIV,DEPT CHEM,UNIV PK,PA 16802. NCI,DEPT BIOCHEM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1158 EP A1158 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800693 ER PT J AU CAROTHERS, A YUAN, W GRUNBERGER, D SNYDERWINE, E AF CAROTHERS, A YUAN, W GRUNBERGER, D SNYDERWINE, E TI 2-AMINO-1-METHYL-6-PHENYLIMIDAZO[4,5-B]PYRIDINE (PHIP)-INDUCED MUTATIONS IN THE HAMSTER DHFR GENE SO FASEB JOURNAL LA English DT Meeting Abstract C1 COLUMBIA UNIV,NEW YORK,NY 10032. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1067 EP A1067 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800166 ER PT J AU CHAE, HZ STADTMAN, ER RHEE, SG AF CHAE, HZ STADTMAN, ER RHEE, SG TI ENHANCED SENSITIVITY TO OXIDATIVE PRESSURE OF A YEAST MUTANT LACKING THIOL-SPECIFIC ANTIOXIDANT SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1178 EP A1178 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800812 ER PT J AU CHAO, TSO FOSTER, DA RAPP, U ROSNER, MR AF CHAO, TSO FOSTER, DA RAPP, U ROSNER, MR TI ALTERNATIVE SIGNALING PATHWAYS LEADING TO ACTIVATION OF MITOGEN-ACTIVATED PROTEIN-KINASE BY DIFFERENT GROWTH-FACTORS AND TUMOR PROMOTERS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CHICAGO,BEN MAY INST,CHICAGO,IL 60637. UNIV CHICAGO,DEPT PHARM & PHYS,CHICAGO,IL 60637. CUNY HUNTER COLL,DEPT BIOL SCI,NEW YORK,NY 10021. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1125 EP A1125 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800503 ER PT J AU CHIANG, PK BROWN, N BUTLER, D NAUSS, J XIAO, W CARTER, JM AF CHIANG, PK BROWN, N BUTLER, D NAUSS, J XIAO, W CARTER, JM TI CHARACTERIZATION OF SOLUTION STRUCTURES AND BIOLOGICAL EFFECTS OF A SERIES OF THYMOPENTIN ANALOGS SO FASEB JOURNAL LA English DT Meeting Abstract C1 WALTER REED ARMY INST RES,DIV BIOCHEM,WASHINGTON,DC 20307. WALTER REED ARMY INST RES,DIV MED,WASHINGTON,DC 20307. NIDDK,BETHESDA,MD 20810. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1236 EP A1236 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801148 ER PT J AU CHIN, J ROUAULT, T KLAUSNER, R AF CHIN, J ROUAULT, T KLAUSNER, R TI EXPRESSION OF THE IRON RESPONSIVE ELEMENT-BINDING PROTEIN IN BACTERIA AND CULTURED-CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1233 EP A1233 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801133 ER PT J AU CHOI, OH LEE, JH KASSESSINOFF, T CUNHAMELO, JR JONES, SVP BEAVEN, MA AF CHOI, OH LEE, JH KASSESSINOFF, T CUNHAMELO, JR JONES, SVP BEAVEN, MA TI CARBACHOL AND ANTIGEN MOBILIZE CA2+ BY SIMILAR MECHANISMS IN TRANSFECTED RBL-2H3 (M1) CELLS THAT EXPRESS M1 MUSCARINIC RECEPTORS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. NINCDS,BIOPHYS LAB,BETHESDA,MD 20892. UFMG,FM,DEPT SURG,BELO HORIZON,MG,BRAZIL. RI Cunha-Melo, Jose Renan/C-6262-2013 NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1246 EP A1246 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801209 ER PT J AU CIOLINO, HP LEVINE, RL AF CIOLINO, HP LEVINE, RL TI IRON IS REQUIRED FOR HYDROGEN PEROXIDE-INDUCED PROTEIN OXIDATION AND CYTOTOXICITY OF ENDOTHELIAL-CELLS INVITRO SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RI Levine, Rodney/D-9885-2011 NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1188 EP A1188 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800869 ER PT J AU CIOTTI, M RITTER, J YEATMAN, M KAISER, C OWENS, I AF CIOTTI, M RITTER, J YEATMAN, M KAISER, C OWENS, I TI BILIRUBIN UDP-GLUCURONOSYLTRANSFERASE-SPECIFIC MUTATIONS IN THE UGT1 GENE-COMPLEX SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1228 EP A1228 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801103 ER PT J AU DECLUE, JE JOHNSON, MR CEN, H ZHANG, K LOWY, DR AF DECLUE, JE JOHNSON, MR CEN, H ZHANG, K LOWY, DR TI POSITIVE AND NEGATIVE REGULATION OF MAMMALIAN RAS PROTEINS SO FASEB JOURNAL LA English DT Meeting Abstract C1 AMGEN CORP,THOUSAND OAKS,CA 91320. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1125 EP A1125 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800501 ER PT J AU DEMORAIS, SMF SCHWEIKL, H BLAISDELL, J GOLDSTEIN, JA AF DEMORAIS, SMF SCHWEIKL, H BLAISDELL, J GOLDSTEIN, JA TI GENE STRUCTURE AND REGULATORY UPSTREAM REGIONS OF 2 HUMAN CYTOCHROMES-P4502C (2C9 AND 2C18) ASSOCIATED WITH S-MEPHENYTOIN HYDROXYLATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. RI Schweikl, Helmut/C-2998-2013 NR 1 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1167 EP A1167 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800751 ER PT J AU DETTORRE, C LEVINE, RL AF DETTORRE, C LEVINE, RL TI REACTIVITY OF THE SURFACE-EXPOSED CYSTEINE RESIDUE OF HIV-1 PROTEASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RI Levine, Rodney/D-9885-2011 NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1181 EP A1181 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800830 ER PT J AU DRISCOLL, WJ STROTT, CA AF DRISCOLL, WJ STROTT, CA TI DISTINCT STEROID SULFOTRANSFERASES FROM THE GUINEA-PIG ADRENAL DEMONSTRATE ALPHA-BETA STEREOSPECIFICITY FOR THE ORIENTATION OF THE 3-HYDROXYL GROUP SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,ADRENOL CELL BIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1147 EP A1147 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800630 ER PT J AU EFIOK, B CHIORINI, J SAFER, B AF EFIOK, B CHIORINI, J SAFER, B TI THE TRANSCRIPTION FACTOR ALPHA-PAL - A POTENTIAL LINK BETWEEN TRANSLATION, REPLICATION, ENERGY TRANSDUCTION AND GROWTH SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1136 EP A1136 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800565 ER PT J AU ENGLANDER, EW WOLFFE, AP HOWARD, BH AF ENGLANDER, EW WOLFFE, AP HOWARD, BH TI NUCLEOSOME INTERACTIONS WITH A HUMAN ALU ELEMENT SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,CMGR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1093 EP A1093 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800320 ER PT J AU ERPS, LT RITTER, JK HERSH, JH MARTIN, NC OWENS, IS AF ERPS, LT RITTER, JK HERSH, JH MARTIN, NC OWENS, IS TI IDENTIFICATION OF 2 SINGLE BASE SUBSTITUTIONS IN THE HUMAN GENE CODING FOR BILIRUBIN UDP-GLUCURONOSYLTRANSFERASE (UDPGT) THAT ABOLISH ENZYME-ACTIVITY SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV LOUISVILLE,SCH MED,LOUISVILLE,KY 40292. NICHHD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1073 EP A1073 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800198 ER PT J AU FISHBEIN, WN KIRSCH, IR AF FISHBEIN, WN KIRSCH, IR TI A TECHNIQUE FOR MASS-SCREENING OF PERIPHERAL-BLOOD FOR A MARKER OF GENOMIC INSTABILITY SO FASEB JOURNAL LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NCI,NNMC,BETHESDA,MD 20892. NR 2 TC 1 Z9 1 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 APR 20 PY 1993 VL 7 IS 7 BP A1130 EP A1130 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800529 ER PT J AU FRIGUET, B SZWEDA, LI STADTMAN, ER AF FRIGUET, B SZWEDA, LI STADTMAN, ER TI STRUCTURAL STABILITY AND PROTEOLYTIC SUSCEPTIBILITY OF GLUCOSE-6-PHOSPHATE-DEHYDROGENASE MODIFIED BY 4-HYDROXYNONENAL AND METAL-CATALYZED OXIDATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1178 EP A1178 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800809 ER PT J AU GONG, Q DEAN, A AF GONG, Q DEAN, A TI TRANSCRIPTION FACTORS INVOLVED IN MEDIATING ENHANCER DEPENDENT EXPRESSION OF THE HUMAN EPSILON-GLOBIN GENE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,CELLULAR & DEV BIOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1219 EP A1219 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801046 ER PT J AU GOTTESMAN, MM GERMANN, UA AKSENTIJEVICH, I PASTAN, I AF GOTTESMAN, MM GERMANN, UA AKSENTIJEVICH, I PASTAN, I TI MULTIDRUG RESISTANCE AS A SELECTABLE MARKER IN GENE-THERAPY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1261 EP A1261 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801297 ER PT J AU GOTTESMAN, S SLEDJESKI, D AF GOTTESMAN, S SLEDJESKI, D TI REGULATION OF TRANSCRIPTION OF AN UNSTABLE REGULATORY PROTEIN, RCSA, BY A SMALL RNA SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1215 EP A1215 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801028 ER PT J AU GROGAN, J SHOU, M ZHOU, D CHEN, S GELBOIN, H KORZEKWA, KR AF GROGAN, J SHOU, M ZHOU, D CHEN, S GELBOIN, H KORZEKWA, KR TI ELECTRON FLUX BETWEEN NADPH-CYTOCHROME-P450 REDUCTASE AND AROMATASE (CYP19) CONTROLS MINOR METABOLITE FORMATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. BECKMAN RES INST,DUARTE,CA 91010. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1167 EP A1167 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800746 ER PT J AU HARRISON, EH ROJAS, CJ KEMPNER, ES AF HARRISON, EH ROJAS, CJ KEMPNER, ES TI RADIATION TARGET ANALYSIS OF MICROSOMAL ACID AND NEUTRAL CHOLESTERYL ESTER HYDROLASES (CEH) IN RAT-LIVER SO FASEB JOURNAL LA English DT Meeting Abstract C1 MED COLL PENN,PHILADELPHIA,PA 19129. NIAMS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1266 EP A1266 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801324 ER PT J AU HAUN, RS MOSS, J VAUGHAN, M AF HAUN, RS MOSS, J VAUGHAN, M TI CHARACTERIZATION OF THE HUMAN ADP-RIBOSYLATION FACTOR 3 PROMOTER - TRANSCRIPTIONAL REGULATION OF A TATA-LESS PROMOTER SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1220 EP A1220 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801055 ER PT J AU HEMPSTEAD, BL DONOVAN, MJ TSOULFAS, P PARADA, LP KRAEMER, R HAJJAR, DP AF HEMPSTEAD, BL DONOVAN, MJ TSOULFAS, P PARADA, LP KRAEMER, R HAJJAR, DP TI EXPRESSION OF THE NEUROTROPHIN RECEPTOR, TRK-C, IN THE VASCULAR SYSTEM SO FASEB JOURNAL LA English DT Meeting Abstract C1 CORNELL UNIV,MED CTR,COLL MED,NEW YORK,NY 10021. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. NCI,FREDERICK,MD 21710. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1245 EP A1245 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801201 ER PT J AU HERMIDA, L YANG, DCH CURRAN, T CHOCK, PB AF HERMIDA, L YANG, DCH CURRAN, T CHOCK, PB TI PROTEIN UBIQUITINATION OF HUMAN C-JUN SO FASEB JOURNAL LA English DT Meeting Abstract C1 GEORGETOWN UNIV,DEPT CHEM,WASHINGTON,DC 20007. ROCHE INST MOLEC BIOL,NUTLEY,NJ 07110. NHLBI,BETHESDA,MD 20892. RI Curran, Tom/C-1164-2008; Curran, Tom/D-7515-2011 OI Curran, Tom/0000-0003-1444-7551; NR 0 TC 1 Z9 1 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 APR 20 PY 1993 VL 7 IS 7 BP A1187 EP A1187 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800866 ER PT J AU HONG, S RYU, JH SONG, BJ HUH, JW AF HONG, S RYU, JH SONG, BJ HUH, JW TI INHIBITION OF BOVINE ALPHA-KETOGLUTARATE DEHYDROGENASE COMPLEX BY [1,1'-BI(4-ANILINE)NAPHTHALENE-5,5'-DISULFONIC ACID](BIS-ANS) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,CLIN STUDIES LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1278 EP A1278 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801397 ER PT J AU HUANG, FL OSADA, K NAKABAYASHI, H AF HUANG, FL OSADA, K NAKABAYASHI, H TI PURIFICATION AND CHARACTERIZATION OF MULTIPLE FORMS OF PROTEIN KINASE-C-EPSILON FROM RAT-BRAIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1118 EP A1118 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800464 ER PT J AU HUANG, KP HUANG, FL CHEN, HC AF HUANG, KP HUANG, FL CHEN, HC TI CHARACTERIZATION OF RAT-BRAIN 7.5-KDA CALMODULIN-BINDING PROTEIN-KINASE-C SUBSTRATE (RC3 PROTEIN, NEUROGRANIN) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1118 EP A1118 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800463 ER PT J AU IBEANU, G SCHWEIKL, H DEMORAIS, SMF GOLDSTEIN, JA AF IBEANU, G SCHWEIKL, H DEMORAIS, SMF GOLDSTEIN, JA TI PROMOTOR ACTIVITY OF THE UPSTREAM REGULATORY REGIONS OF THE HUMAN 2C9 AND 2C18 GENES IN HEPG2 CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. RI Schweikl, Helmut/C-2998-2013 NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1167 EP A1167 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800750 ER PT J AU ILAGAN, J SAX, CM PIATIGORSKY, J AF ILAGAN, J SAX, CM PIATIGORSKY, J TI ANALYSIS OF THE ALPHA-A-CRYSTALLIN PROMOTER IN TRANSGENIC MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI,LMDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1222 EP A1222 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801065 ER PT J AU JONES, TLZ SPIEGEL, AM MACKAY, VL AF JONES, TLZ SPIEGEL, AM MACKAY, VL TI OVEREXPRESSION OF THE MYRISTOYLATED G-PROTEIN ALPHA-I1 SUBUNIT IN HAPLOID YEAST CAUSES CONSTITUTIVE ACTIVATION OF THE MATING RESPONSE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDKD,MPB,BETHESDA,MD 20892. ZYMOGENET,SEATTLE,WA 98105. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1045 EP A1045 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800039 ER PT J AU KIM, IY VERES, Z STADTMAN, TC AF KIM, IY VERES, Z STADTMAN, TC TI THE PROPERTIES OF MUTANT ESCHERICHIA-COLI SELENOPHOSPHATE SYNTHETASES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1195 EP A1195 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800908 ER PT J AU KIM, SJ LEE, YM KIM, YS AF KIM, SJ LEE, YM KIM, YS TI IDENTIFICATION OF CIS-ACTING DNA ELEMENTS RESPONSIBLE FOR THE EXPRESSION OF THE DROSOPHILA NK1 HOMEOBOX GENE IN TRANSFECTED CELL-LINES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1100 EP A1100 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800362 ER PT J AU KIM, SMF BAK, CI PAOLETTI, F SONG, BJ AF KIM, SMF BAK, CI PAOLETTI, F SONG, BJ TI CHARACTERIZATION OF A CDNA CLONE FOR RAT TRANSKETOLASE AND ITS ACTIVATION IN NEONATAL RAT-LIVER SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,CLIN STUDIES LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1136 EP A1136 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800564 ER PT J AU KINCAID, RL MURAMATSU, T UEKI, K AF KINCAID, RL MURAMATSU, T UEKI, K TI FUNCTIONAL EQUIVALENCE OF MAMMALIAN CALCINEURIN AND NEUROSPORA-CRASSA CATALYTIC SUBUNITS IN IMMUNOSUPPRESSANT-SENSITIVE REGULATION OF TRANSCRIPTIONAL ELEMENTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,IMMUNOL SECT,ROCKVILLE,MD 20852. NR 2 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1053 EP A1053 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800086 ER PT J AU KINCAID, RL MARIETTA, CA MOOS, MC AF KINCAID, RL MARIETTA, CA MOOS, MC TI CHARACTERIZATION OF A 36 KDA PROTEIN FROM BOVINE BRAIN WITH STRUCTURAL HOMOLOGY TO THE TRYPANOSOMA-BRUCEI GLYCOSYL-PHOSPHATIDYL INOSITOL-PHOSPHOLIPASE-C SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,IMMUNOL SECT,ROCKVILLE,MD 20852. NIH,FDA,MOLEC PHARMACOL LAB,BETHESDA,MD 20814. RI Moos, Malcolm/F-3673-2011 OI Moos, Malcolm/0000-0002-9575-9938 NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1045 EP A1045 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800037 ER PT J AU KITAREEWAN, S OLSON, J SCHWEIKL, H PETRELLI, N RODRIGUEZ, MA LUCIER, GW GOLDSTEIN, JA AF KITAREEWAN, S OLSON, J SCHWEIKL, H PETRELLI, N RODRIGUEZ, MA LUCIER, GW GOLDSTEIN, JA TI INTERINDIVIDUAL VARIABILITY OF CYP1A1 AND CYP1A2 IN HUMAN LIVERS AND INDUCTION BY 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (TCDD) INVITRO SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. SUNY BUFFALO,DEPT PHARM,BUFFALO,NY 14260. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT SURG,BUFFALO,NY 14263. RI Schweikl, Helmut/C-2998-2013 NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1167 EP A1167 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800748 ER PT J AU KLAUSNER, R HAILE, D HARFORD, L ROUAULT, T AF KLAUSNER, R HAILE, D HARFORD, L ROUAULT, T TI IRON SWITCHES IN GENE-EXPRESSION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1127 EP A1127 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800516 ER PT J AU KLEINER, DE STETLERSTEVENSON, WG AF KLEINER, DE STETLERSTEVENSON, WG TI INVITRO ACTIVATION OF GELATINASE-A - KINETIC-ANALYSIS BY SPECTROFLUOROMETRIC ASSAY AND QUANTITATIVE ZYMOGRAPHY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1211 EP A1211 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801001 ER PT J AU KOMATSU, K OEDA, T STROTT, CA AF KOMATSU, K OEDA, T STROTT, CA TI 5'-FLANKING REGION OF GUINEA-PIG ESTROGEN SULFOTRANSFERASE GENE - STEROID-RESPONSE ELEMENTS AND ENHANCED PROMOTER ACTIVITY BY STEROID-HORMONES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,ADRENAL CELL BIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1147 EP A1147 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800632 ER PT J AU LAWTON, MP PHILPOT, RM AF LAWTON, MP PHILPOT, RM TI IDENTIFICATION BY DELETION MUTAGENESIS OF FLAVIN-CONTAINING MONOOXYGENASE 1B1 PEPTIDES INVOLVED IN SUBSTRATE AND MEMBRANE-BINDING SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,LCMP,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1204 EP A1204 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800962 ER PT J AU LAZARUS, LH SALVADORI, S BRYANT, SD ATTILA, M AF LAZARUS, LH SALVADORI, S BRYANT, SD ATTILA, M TI PHE(3)-SUBSTITUTED DELTORPHIN-C ANALOGS - DELTA-OPIOID RECEPTOR SELECTIVITY AND SPATIAL CONFORMATION DIFFERENTIATE SUBSITE RECOGNITION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. UNIV FERRARA,I-44100 FERRARA,ITALY. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1237 EP A1237 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801152 ER PT J AU LEE, FJS MURTAGH, JJ DEAK, P HALL, LM MONACO, L LEE, CM STEVENS, LA MOSS, J VAUGHAN, M AF LEE, FJS MURTAGH, JJ DEAK, P HALL, LM MONACO, L LEE, CM STEVENS, LA MOSS, J VAUGHAN, M TI USE OF POLYMERASE CHAIN-REACTION TO CLONE ADP-RIBOSYLATION FACTOR FROM DROSOPHILA SO FASEB JOURNAL LA English DT Meeting Abstract C1 SUNY BUFFALO,DEPT BIOCHEM,BUFFALO,NY 14260. NHLBI,BETHESDA,MD 20892. RI Monaco, Lucia/A-4031-2010 NR 1 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1302 EP A1302 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801538 ER PT J AU LI, Q BEVER, C DING, L FALKLER, W AF LI, Q BEVER, C DING, L FALKLER, W TI NEUROENDOCRINE REGULATION OF INTERFERON-GAMMA-INDUCED INCREASES IN CATHEPSIN-B IN THE MACROPHAGE-LIKE CELL-LINE, THP-1 SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV MARYLAND,BALTIMORE,MD 21201. NIDDK,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1210 EP A1210 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800998 ER PT J AU MAHONEY, CW HUANG, KP AF MAHONEY, CW HUANG, KP TI DIFFERENTIAL ACTIVATION OF PKC ISOZYMES BY DIACYLGLYCEROLS DERIVED FROM BRAIN PHOSPHOINOSITIDE AND PHOSPHATIDYLCHOLINE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 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 APR 20 PY 1993 VL 7 IS 7 BP A1118 EP A1118 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800465 ER PT J AU MCDONALD, LJ MOSS, J AF MCDONALD, LJ MOSS, J TI NITRIC OXIDE-INDEPENDENT, THIOL-ASSOCIATED ADP-RIBOSYLATION INACTIVATES ALDEHYDE DEHYDROGENASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1179 EP A1179 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800815 ER PT J AU MILLER, MW HANOVER, JA AF MILLER, MW HANOVER, JA TI CHANGES IN PHOSPHORYLATION AND GLYCOSYLATION OF O-LINKED N-ACETYLGLUCOSAMINE GLYCOPROTEINS DURING THE CELL-CYCLE INVITRO SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1250 EP A1250 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801230 ER PT J AU MISHIMA, K TSUCHIYA, M NIGHTINGALE, MS MOSS, J VAUGHAN, M AF MISHIMA, K TSUCHIYA, M NIGHTINGALE, MS MOSS, J VAUGHAN, M TI ARD-1, A 64-KDA GUANINE NUCLEOTIDE-BINDING PROTEIN WITH A CARBOXY-TERMINAL ADP-RIBOSYLATION FACTOR (ARF) DOMAIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1247 EP A1247 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801216 ER PT J AU MITAS, M KAMP, TJ CHOCK, JY MARBAN, E NIRENBERG, M AF MITAS, M KAMP, TJ CHOCK, JY MARBAN, E NIRENBERG, M TI TRINUCLEOTIDE REPEATS - PROTEIN-BINDING AND EFFECTS ON GENE-EXPRESSION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM GENET LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,DEPT MED,DIV CARDIOL,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 3 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1232 EP A1232 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801128 ER PT J AU MURAYAMA, M AF MURAYAMA, M TI RATE OF FIBRIN MONOMER POLYMERIZATION AS A FUNCTION OF PRESSURE - TRANSITION POINT BETWEEN COMPRESSION AND DECOMPRESSION AT ONE ATMOSPHERE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAMS,PHYS BIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1190 EP A1190 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800883 ER PT J AU MURTAGH, JJ LEE, OM LEE, FJS BAI, X MISHIMA, K MOSS, J VAUGHAN, M AF MURTAGH, JJ LEE, OM LEE, FJS BAI, X MISHIMA, K MOSS, J VAUGHAN, M TI ADP-RIBOSYLATION FACTORS (ARFS) IN CAENORHABDITIS-ELEGANS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. VET ADM MED CTR ATLANTA,DECATUR,GA 30033. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1299 EP A1299 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801516 ER PT J AU NAKATSUKA, M DAVILA, JC TSAI, AL KULMACZ, RJ OSAWA, Y AF NAKATSUKA, M DAVILA, JC TSAI, AL KULMACZ, RJ OSAWA, Y TI FORMATION OF PROTEIN-BOUND HEME ADDUCTS DURING THE REACTION OF PROSTAGLANDIN-H SYNTHASE WITH H2O2 SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT INTERNAL MED,HOUSTON,TX 77030. NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. NR 2 TC 2 Z9 2 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 APR 20 PY 1993 VL 7 IS 7 BP A1074 EP A1074 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800207 ER PT J AU NIKBAKHT, KN CARVER, G PHILPOT, RM LAWTON, MP AF NIKBAKHT, KN CARVER, G PHILPOT, RM LAWTON, MP TI ISOLATION AND STRUCTURAL CHARACTERIZATION OF THE GENE ENCODING RABBIT FLAVIN-CONTAINING MONOOXYGENASE-(FMO)-1A1 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,LCMP,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1204 EP A1204 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800963 ER PT J AU NONOMURA, N KANAI, A OKA, T AF NONOMURA, N KANAI, A OKA, T TI IMPORTANCE OF MILK PROTEIN GENE CONSENSUS SEQUENCE AND ITS BINDING-PROTEINS FOR HORMONAL INDUCTION OF MOUSE BETA-CASEIN GENE-TRANSCRIPTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,MOLEC & CELLULAR BIOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1134 EP A1134 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800554 ER PT J AU OKAZAKI, IJ ZOLKIEWSKA, A MOSS, J AF OKAZAKI, IJ ZOLKIEWSKA, A MOSS, J TI EXPRESSION OF ADP-RIBOSYLTRANSFERASE CDNA FROM RABBIT SKELETAL-MUSCLE REVEALS A GLYCOSYLPHOSPHATIDYLINOSITOL-ANCHORED PROTEIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 0 TC 6 Z9 6 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1042 EP A1042 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800024 ER PT J AU PACHECORODRIGUEZ, G MOSS, J ALVAREZGONZALEZ, R AF PACHECORODRIGUEZ, G MOSS, J ALVAREZGONZALEZ, R TI ADP-RIBOSE ELONGATION OF MONO(ADP-RIBOSYL)-ARGININE METHYL-ESTER BY POLY(ADP-RIBOSE)POLYMERASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNT TCOM,DEPT MICROBIOL & IMMUNOL,FT WORTH,TX 76107. UNT TCOM,DEPT BIOCHEM & MOL BIOL,FT WORTH,TX 76107. NHLBI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 20 PY 1993 VL 7 IS 7 BP A1196 EP A1196 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800916 ER PT J AU PARK, JM CHOI, IS HATFIELD, D LEE, BJ AF PARK, JM CHOI, IS HATFIELD, D LEE, BJ TI THE PROMOTER ELEMENTS AND TRANSCRIPTION FACTORS REQUIRED FOR SELENOCYSTEINE TRNA([SER]SEC) GENE-TRANSCRIPTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 SEOUL NATL UNIV,INST MOLEC BIOL,DEPT MICROBIOL,SEOUL 151,SOUTH KOREA. NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1218 EP A1218 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801044 ER PT J AU POSTON, JM AF POSTON, JM TI FREE AMINO-ACID CONTENT OF FILTERED RAT SERUM FROM ANIMALS OF VARIOUS AGES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1305 EP A1305 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801554 ER PT J AU PRASAD, GL FULDNER, RA COOPER, HL AF PRASAD, GL FULDNER, RA COOPER, HL TI STUDIES ON UTILIZATION OF TROPOMYOSIN IN NORMAL AND TRANSFORMED FIBROBLASTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1080 EP A1080 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800240 ER PT J AU REMETA, DP GINSBURG, A BLUMENTHAL, R KRUMBIEGEL, M AF REMETA, DP GINSBURG, A BLUMENTHAL, R KRUMBIEGEL, M TI CALORIMETRIC STUDIES ON THE THERMALLY INDUCED UNFOLDING OF THE INFLUENZA-VIRUS HEMAGGLUTININ SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1287 EP A1287 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801448 ER PT J AU RIBEIRO, P WANG, Y CITRON, B KAUFMAN, S AF RIBEIRO, P WANG, Y CITRON, B KAUFMAN, S TI STUDIES ON THE FUNCTIONAL-ORGANIZATION OF TYROSINE-HYDROXYLASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIMH,NEUROCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1085 EP A1085 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800273 ER PT J AU RITTER, J PILON, A DRAGNEV, K LUBET, R OWENS, I AF RITTER, J PILON, A DRAGNEV, K LUBET, R OWENS, I TI IS HUMAN PHENOL UDP-GLUCURONOSYLTRANSFERASE GENE-EXPRESSION REGULATED BY POLYCYCLIC AROMATIC-HYDROCARBONS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1231 EP A1231 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801118 ER PT J AU RIZZO, P TINELLO, C SHAH, M TANIUCHI, H AF RIZZO, P TINELLO, C SHAH, M TANIUCHI, H TI MODELING OF THE VARIABLE DOMAINS OF MONOCLONAL-ANTIBODIES TO YEAST ISO-1-CYTOCHROME-C SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 6 TC 1 Z9 1 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1308 EP A1308 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801574 ER PT J AU SANTINI, F YAMADA, K OZAWA, K BEAVEN, MA AF SANTINI, F YAMADA, K OZAWA, K BEAVEN, MA TI ACTIVATION OF PHOSPHOLIPASE-C THROUGH TYROSINE KINASE(S) AND A G-PROTEIN (G(ALPHA-S)) IN ANTIGEN-STIMULATED RBL-2H3 CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1138 EP A1138 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800577 ER PT J AU SIDHU, JS NIMS, RW REILLY, MT KAVANAGH, TJ OMIECINSKI, CJ AF SIDHU, JS NIMS, RW REILLY, MT KAVANAGH, TJ OMIECINSKI, CJ TI INDUCTION OF CYP2B1, 2B2 AND 3A1 GENES BY 5-ETHYL-5-PHENYLHYDANTOIN IN PRIMARY RAT HEPATOCYTE CULTURES DERIVED FROM SPRAGUE-DAWLEY, FISCHER F344 AND MARSHALL M520 STRAINS - ABSENCE OF STEREOSPECIFICITY SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV WASHINGTON,DEPT ENVIRONM HLTH,SEATTLE,WA 98195. NCI,FCRDC,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1168 EP A1168 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800752 ER PT J AU SITKOVSKY, M REDEGELD, F SMITH, P AF SITKOVSKY, M REDEGELD, F SMITH, P TI PP1 CLASS OF ECTO-PROTEINPHOSPHATASES ON THE T-CELLS SURFACE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. RI Redegeld, Frank/O-6534-2016 OI Redegeld, Frank/0000-0001-8830-7960 NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1157 EP A1157 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800691 ER PT J AU SZWEDA, LI STADTMAN, ER AF SZWEDA, LI STADTMAN, ER TI AGE-RELATED INCREASE OF RETINYL PALMITATE IN RAT-LIVER SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1256 EP A1256 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801269 ER PT J AU TAKADA, T IIDA, K MOSS, J AF TAKADA, T IIDA, K MOSS, J TI CLONING AND SITE-DIRECTED MUTAGENESIS OF HUMAN BRAIN ADP-RIBOSYLARGININE HYDROLASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1066 EP A1066 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800157 ER PT J AU THOMPSON, MW MAURIZI, MR AF THOMPSON, MW MAURIZI, MR TI ACTIVITY AND SPECIFICITY OF ATP-DEPENDENT CLP PROTEASE IN CLEAVING MODEL PEPTIDE-SUBSTRATES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1184 EP A1184 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800848 ER PT J AU TSAI, L SOKOLOSKI, E STADTMAN, ER AF TSAI, L SOKOLOSKI, E STADTMAN, ER TI PROTEIN MODIFICATION - REACTION OF 4-HYDROXY-2-NONENAL AND N-ALPHA-ACETYLHISTIDINE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1177 EP A1177 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800806 ER PT J AU TSAI, SC ADAMIK, R HAUN, RS MOSS, J VAUGHAN, M AF TSAI, SC ADAMIK, R HAUN, RS MOSS, J VAUGHAN, M TI ASSOCIATION OF MYRISTOYLATED ADP-RIBOSYLATION FACTORS WITH GOLGI SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1248 EP A1248 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801217 ER PT J AU TSAIMORRIS, CH XIE, XZ BUCZKO, E DUFAU, ML AF TSAIMORRIS, CH XIE, XZ BUCZKO, E DUFAU, ML TI TRANSCRIPTIONAL DOMAINS OF THE RAT LUTEINIZING-HORMONE RECEPTOR GENE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,MOLEC ENDOCRINOL SECT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 20 PY 1993 VL 7 IS 7 BP A1113 EP A1113 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800435 ER PT J AU UCHIDA, K SZWEDA, LI CHAE, HZ STADTMAN, ER AF UCHIDA, K SZWEDA, LI CHAE, HZ STADTMAN, ER TI IMMUNOCHEMICAL DETECTION OF 4-HYDROXY-2-NONENAL MODIFIED PROTEIN IN OXIDIZED RAT HEPATOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 20 PY 1993 VL 7 IS 7 BP A1177 EP A1177 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800808 ER PT J AU UEKI, K MURAMATSU, T KINCAID, RL AF UEKI, K MURAMATSU, T KINCAID, RL TI IDENTIFICATION OF THE CALCINEURIN-B-BINDING DOMAIN - A DIMERIC ENZYME STRUCTURE IS REQUIRED FOR IMMUNOPHILIN INTERACTIONS AND TRANSCRIPTIONAL ACTIVATION INVIVO SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,IMMUNOL SECT,ROCKVILLE,MD 20852. NR 0 TC 3 Z9 3 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 APR 20 PY 1993 VL 7 IS 7 BP A1158 EP A1158 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800696 ER PT J AU UHLINHANSEN, L YANAGISHITA, M AF UHLINHANSEN, L YANAGISHITA, M TI DIFFERENTIAL EFFECT OF BREFELDIN-A ON THE BIOSYNTHESIS OF HEPARAN-SULFATE AND CHONDROITIN SULFATE PROTEOGLYCANS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1260 EP A1260 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801290 ER PT J AU VERES, Z STADTMAN, TC AF VERES, Z STADTMAN, TC TI PRODUCT OF SELENOPHOSPHATE SYNTHETASE SERVES AS A SELENIUM DONOR FOR SELENATION OF TRANSFER-RNAS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1195 EP A1195 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800911 ER PT J AU WANG, LH CHMELIK, B NIRENBERG, M AF WANG, LH CHMELIK, B NIRENBERG, M TI SEQUENCE-SPECIFIC DNA-BINDING BY THE NK-2 HOMEODOMAIN OF DROSOPHILA SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1221 EP A1221 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801062 ER PT J AU WANG, LH KOMAS, N TAIRA, M MANGANIELLO, VC AF WANG, LH KOMAS, N TAIRA, M MANGANIELLO, VC TI EXPRESSION OF HUMAN CARDIAC CGMP-INHIBITED (TYPE-III) CYCLIC-NUCLEOTIDE PHOSPHODIESTERASE (CGI PDE) IN SF9 INSECT CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1152 EP A1152 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84800658 ER PT J AU ZOLKIEWSKI, M REDOWICZ, MJ KORN, ED GINSBURG, A AF ZOLKIEWSKI, M REDOWICZ, MJ KORN, ED GINSBURG, A TI NUCLEOTIDE EFFECTS ON THERMAL TRANSITIONS OF MYOSIN-II FROM ACANTHAMOEBA-CASTELLANII SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. RI Redowicz, Maria Jolanta/R-4083-2016 NR 0 TC 0 Z9 0 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 APR 20 PY 1993 VL 7 IS 7 BP A1281 EP A1281 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY848 UT WOS:A1993KY84801413 ER PT J AU ROSENBERG, SA AF ROSENBERG, SA TI THE DEVELOPMENT OF IMMUNOTHERAPY FOR CANCER - A CITATION-CLASSIC COMMENTARY ON OBSERVATIONS ON THE SYSTEMIC ADMINISTRATION OF AUTOLOGOUS LYMPHOKINE-ACTIVATED KILLER-CELLS AND RECOMBINANT INTERLEUKIN-2 TO PATIENTS WITH METASTATIC CANCER BY ROSENBERG,S.A., LOTZE,M.T., MUUL,,L.M., LEITMAN,S., CHANG,A.E., ETTINGHAUSEN,S.E., MATORY,Y.L., SKIBBER,J.M., SHILONI,E., VETTO,J.T., SEIPP,C.A., SIMPSON,C. AND REICHERT,C.M. SO CURRENT CONTENTS/CLINICAL MEDICINE LA English DT Article ID ESTABLISHED PULMONARY METASTASES; ADOPTIVE IMMUNOTHERAPY; INVITRO GROWTH; LYMPHOCYTES; TUMORS RP ROSENBERG, SA (reprint author), NCI,BETHESDA,MD 20892, USA. NR 9 TC 0 Z9 0 U1 0 U2 3 PU INST SCI INFORM INC PI PHILADELPHIA PA 3501 MARKET ST, PHILADELPHIA, PA 19104 SN 0891-3358 J9 CC/CLIN MED PD APR 19 PY 1993 IS 16 BP 8 EP 8 PG 1 WC Multidisciplinary Sciences; Social Sciences, Interdisciplinary SC Science & Technology - Other Topics; Social Sciences - Other Topics GA KV057 UT WOS:A1993KV05700001 ER PT J AU BOAL, TR CHIORINI, JA COHEN, RB MIYAMOTO, S FREDERICKSON, RM SONENBERG, N SAFER, B AF BOAL, TR CHIORINI, JA COHEN, RB MIYAMOTO, S FREDERICKSON, RM SONENBERG, N SAFER, B TI REGULATION OF EUKARYOTIC TRANSLATION INITIATION-FACTOR EXPRESSION DURING T-CELL ACTIVATION SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE T-CELL; TRANSLATION; PHOSPHORYLATION; MITOGEN; EIF-2-ALPHA; EIF-4-ALPHA ID PROTEIN-SYNTHESIS-INITIATION; CAP-BINDING PROTEINS; ASCITES TUMOR-CELLS; MESSENGER-RNA; LYMPHOCYTES-T; HELA-CELLS; PHOSPHORYLATION; STIMULATION; ELONGATION; COMPLEX AB Primary T-cells are metabolically quiescent, with little DNA, RNA or protein synthesis. Upon mitogenic stimulation the rate of protein synthesis increases 10-fold. We have studied the role of eIF-2 and eIF-4alpha (eIF-4E) expression in the mechanism of translational activation. During this period, the levels of eIF-2alpha and eIF-4alpha mRNA increase some 50-fold. Similar to the increase in ribosomes and mRNA, the number of eIF-2alpha, eIF-2beta, and eIF-4alpha molecules per cell also increase 2-3-fold. This suggests that in addition to an increase in the pool size of translational components, an additional mechanism exists which results in an increased efficiency of factor utilization. We have looked at initiation factor phosphorylation. We find that eIF-2alpha does not undergo significant changes in its phosphorylation state nor is there a change in the efficiency of eIF-2 utilization. However, there is a rapid increase in the phosphorylation state of eIF-4alpha which correlates with the rapid increase in translational activity. It thus appears there are 2 distinct components responsible for the translational activation of quiescent T-cells during mitogenic stimulation. The first is the phosphorylation of eIF-4alpha, with a concomitant increase in the efficiency of eIF-4alpha utilization. The second is an increase in the pool sizes of eIF-2 and eIF-4alpha. C1 NHLBI,MOLEC HEMATOL BRANCH,PROT & RNA BIOSYNTH SECT,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,PROGRAM GENET,WASHINGTON,DC 20052. MCGILL UNIV,DEPT BIOCHEM,MONTREAL H3A 2T5,QUEBEC,CANADA. NR 47 TC 32 Z9 32 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD APR 16 PY 1993 VL 1176 IS 3 BP 257 EP 264 DI 10.1016/0167-4889(93)90053-R PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KY385 UT WOS:A1993KY38500009 PM 8471627 ER PT J AU OLAH, Z LEHEL, C ANDERSON, WB AF OLAH, Z LEHEL, C ANDERSON, WB TI DIFFERENTIAL-EFFECTS OF ACTIVATION OF PROTEIN-KINASE-C AND CYCLIC-AMP-DEPENDENT PROTEIN-KINASE ON SODIUM-DEPENDENT PHOSPHATE-UPTAKE IN NIH-3T3 CELLS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE PHOSPHATE TRANSPORT; PROTEIN KINASE-C; CYCLIC-AMP-DEPENDENT PROTEIN KINASE; PHORBOL ESTER; FORSKOLIN; (NIH-3T3 CELL) ID OK CELLS; LLC-PK1 CELLS; TRANSPORT; COTRANSPORT; STIMULATION; INHIBITION AB Activation of protein kinase C (PKC) by phorbol ester (PMA), or by diacylglycerol analogue (OAG) treatment of NIH 3T3 cells resulted in the rapid (within 2-5 min) stimulation (approx. 2-fold) of sodium-dependent phosphate (P(i)) transport. Conversely, preincubation of these cells with forskolin and cholera toxin, or incubation with 8-bromo-cAMP, to activate cAMP-dependent protein kinase (PKA), resulted in a decrease in Na+/P(i) transport. Activation of either PKC or PKA did not change the V(max) of P(i) uptake. However, activation of PKC did result in an increase, white activation of PKA caused a decrease, in the affinity for P(i). These results indicate that there is differential regulation of Na+/P(i) uptake in NIH 3T3 cells by activators of PKC (stimulated) and PKA (inhibited) as a consequence of changes in the affinity of the transporter for P(i). RP OLAH, Z (reprint author), NCI, CELLULAR ONCOL LAB, BLDG 36, RM 1D22, BETHESDA, MD 20892 USA. NR 22 TC 10 Z9 10 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 JI Biochim. Biophys. Acta PD APR 16 PY 1993 VL 1176 IS 3 BP 333 EP 338 DI 10.1016/0167-4889(93)90063-U PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KY385 UT WOS:A1993KY38500019 PM 8471634 ER PT J AU BEHAR, T SCHAFFNER, A LAING, P HUDSON, L KOMOLY, S BARKER, J AF BEHAR, T SCHAFFNER, A LAING, P HUDSON, L KOMOLY, S BARKER, J TI MANY SPINAL-CORD CELLS TRANSIENTLY EXPRESS LOW-MOLECULAR-WEIGHT FORMS OF GLUTAMIC-ACID DECARBOXYLASE DURING EMBRYONIC-DEVELOPMENT SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE GAMMA-AMINOBUTYRIC ACID; DIFFERENTIATION; IMMUNOCYTOCHEMISTRY; INSITU HYBRIDIZATION; RAT; SPINAL CORD ID GAMMA-AMINOBUTYRIC-ACID; RAT-BRAIN; REGULATORY PROPERTIES; PROTEINS; GABA; SEQUENCE; TRACT; GENE; GAD AB At early developmental stages in the rat spinal cord (embryonic day 13), when neuronal progenitors are still proliferating, most differentiating neurons express truncated forms of glutamic acid decarboxylase (GAD) (approximately 25 kDa) which are the products of alternative splicing of the GAD67 gene. These truncated proteins do not appear to synthesize gamma-aminobutyric acid (GABA). The amino acid is detected in cells only after alternative splicing of the GAD67 gene generates a full-length, 67 kDa enzymatically active form of GAD. Both the 67 kDa GAD and GABA colocalize and appear diffusely distributed in the cytoplasm of embryonic neurons. GABA does not appear associated with synaptic vesicles until after birth, when its intracellular distribution becomes punctate and it colocalizes with synaptophysin. At this time, it also colocalizes with an immunologically distinct 65 kDa GAD protein encoded by a second GAD gene (GAD65). Expression of different GAD-related proteins with distinct intracellular distributions during development suggests that GABA, the product of these enzymes, may have trophic or metabolic roles during spinal cord differentiation. C1 NINCDS,MOLEC & VIRAL PATHOGENESIS LAB,BETHESDA,MD 20898. NINCDS,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20898. NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BETHESDA,MD 20898. NR 39 TC 47 Z9 47 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD APR 16 PY 1993 VL 72 IS 2 BP 203 EP 218 DI 10.1016/0165-3806(93)90185-D PG 16 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA KW770 UT WOS:A1993KW77000006 PM 8485844 ER PT J AU GU, ZQ WONG, G DOMINGUEZ, C DECOSTA, BR RICE, KC SKOLNICK, P AF GU, ZQ WONG, G DOMINGUEZ, C DECOSTA, BR RICE, KC SKOLNICK, P TI SYNTHESIS AND EVALUATION OF IMIDAZO[1,5-A][1,4]BENZODIAZEPINE ESTERS WITH HIGH AFFINITIES AND SELECTIVITIES AT DIAZEPAM-INSENSITIVE BENZODIAZEPINE RECEPTORS SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID ALCOHOL SENSITIVITY; RO 15-4513; BINDING; ANTAGONIST; ETHANOL AB A series of imidazo[1,5-a][1,4]benzodiazepine esters have been synthesized with varying ester side chains and 8-position substituents. The affinities of these compounds were evaluated at both ''diazepam-insensitive'' (DI) and diazepam-sensitive (DS) subtypes of the benzodiazepine receptor (BZR). A profound steric effect of the 3-position ester side chain moiety was observed on ligand affinity at DI. In contrast, ester size had a less robust effect on ligand affinity at DS. The tertbutyl ester compound 8 displayed the highest affinity (K(i) = 1.7 nM) for DI within a series of 8-chloro esters. Furthermore, halogens at the 8-position resulted in an enhancement of both ligand affinity and selectivity at DI among the series of tert-butyl esters examined. The 8-nitro derivative 23 and 8-isothiocyanato congener 25 had high affinities for both DI and DS but exhibited little subtype selectivity (10.8 and 2.7 nM at DI versus 14 and 3.7 nM at DS, respectively). The 8-azido tert-butyl ester 29 exhibited a significantly higher affinity (K(i) = 0.43 nM) and selectivity (DI/DS ratio of 0.2) than the corresponding ethyl ester, the prototypic DI ligand 1 (Ro 15-4513). Among the compounds synthesized, 29 is the highest affinity ligand for DI described to date while its 8-bromo analog 18 is the most selective ligand (DI/DS ratio of 0.17) for this novel BZR subtype. C1 NIDDKD,MED CHEM LAB,BETHESDA,MD 20892. NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892. NR 22 TC 64 Z9 64 U1 0 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 16 PY 1993 VL 36 IS 8 BP 1001 EP 1006 DI 10.1021/jm00060a007 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA KY382 UT WOS:A1993KY38200007 PM 8386769 ER PT J AU TAUB, DD CONLON, K LLOYD, AR OPPENHEIM, JJ KELVIN, DJ AF TAUB, DD CONLON, K LLOYD, AR OPPENHEIM, JJ KELVIN, DJ TI PREFERENTIAL MIGRATION OF ACTIVATED CD4+ AND CD8+ T-CELLS IN RESPONSE TO MIP-1-ALPHA AND MIP-1-BETA SO SCIENCE LA English DT Article ID LANGERHANS CELLS; FLUORESCEIN ISOTHIOCYANATE; ADHESION RECEPTORS; CYTOKINE FAMILY; DENDRITIC CELLS; LYMPHOCYTES-T; ANTIGEN; INHIBITION; CHEMOTAXIS; SKIN AB Recombinant human macrophage inflammatory protein-1alpha (rhMIP-1alpha) and rhMIP-1beta were potent chemoattractants of human T lymphocytes. These rhMIP-1 cytokines attracted only T cells activated by monoclonal antibody to CD3 and did not attract unstimulated lymphocytes. Phenotypic analysis revealed that CD4+ T cells were capable of migrating in response to rhMIP-1beta, whereas rhMIP-1alpha induced chemotaxis of predominantly CD8+ T lymphocytes. Activated naive and memory T cells also migrated in response to rhMIP-1 cytokines. Furthermore, these cytokines enhanced the ability of T cells to bind to an endothelial cell monolayer. These results suggest that rhMIP-1 cytokines preferentially recruit specific T cell subsets during the evolution of the immune response. C1 NCI,FCRDC,BIOL RESPONSE MODIFIER PROGRAM,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. RP TAUB, DD (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIER PROGRAM,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702, USA. FU PHS HHS [N01-C0-74102] NR 28 TC 698 Z9 701 U1 1 U2 6 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 16 PY 1993 VL 260 IS 5106 BP 355 EP 358 DI 10.1126/science.7682337 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX800 UT WOS:A1993KX80000039 PM 7682337 ER PT J AU MAUTNER, SL KLUES, HG MAUTNER, GC PROSCHAN, MA ROBERTS, WC MARON, BJ AF MAUTNER, SL KLUES, HG MAUTNER, GC PROSCHAN, MA ROBERTS, WC MARON, BJ TI COMPARISON OF MITRAL-VALVE DIMENSIONS IN ADULTS WITH VALVULAR AORTIC-STENOSIS, PURE AORTIC REGURGITATION AND HYPERTROPHIC CARDIOMYOPATHY SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article AB To assess the effect of left ventricular dilatation on mitral valve size, this study compared the dimensions of the mitral valve in patients with aortic valve disease and hypertrophic cardiomyopathy (HC). A total of 216 valves, removed at operation or necropsy, was analyzed by quantitative morphometric methods from: (1) 2 patient groups with dilated left ventricular cavities (i.e., 17 patients with dilated valvular aortic stenosis [AS] and 31 with pure aortic regurgitation), (2) 2 patient groups without dilated left ventricular cavities (i.e., 29 patients with nondilated AS and 94 with HC), and (3) 45 control subjects without heart disease. Mean mitral leaflet areas in patients with AS with dilated left ventricular cavities (13.1 +/- 3.0 cm2) and aortic regurgitation (12.0 +/-3.6 cm2) were significantly greater than in control subjects (8.7 +/- 2.0 cm2; p < 0.001). Mean mitral leaflet areas in patients with AS without dilated left ventricular cavities (9.8 +/- 2.0 cm2) were similar to those of normal valves (p = NS). However, mean mitral leaflet area in patients with HC, in whom left ventricular cavities were also nondilated, was significantly greater (12.8 +/- 3.7 cm2) than in those with nondilated AS and in normal subjects (p < 0.001). Therefore, increased mitral leaflet area: (1) is often present in patients with aortic valve disease with dilated left ventricles in whom it appears to be secondary to left ventricular chamber dilatation; and (2) cannot be attributed to left ventricular cavity dilatation in patients with HC, since their cavities were of normal or small size. Thus, increased mitral leaflet area in HC, which is considered to be a primary myocardial and not valvular disease, may be due to a primary effect on the mitral valve. C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NHLBI,BIOSTAT RES BRANCH,BETHESDA,MD 20892. RP MAUTNER, SL (reprint author), NHLBI,PATHOL BRANCH,BLDG 10,ROOM 2N258,BETHESDA,MD 20892, USA. NR 14 TC 10 Z9 10 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 APR 15 PY 1993 VL 71 IS 11 BP 949 EP 953 DI 10.1016/0002-9149(93)90912-V PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KX265 UT WOS:A1993KX26500012 PM 8465787 ER PT J AU GURALNIK, JM LACROIX, AZ ABBOTT, RD BERKMAN, LF SATTERFIELD, S EVANS, DA WALLACE, RB AF GURALNIK, JM LACROIX, AZ ABBOTT, RD BERKMAN, LF SATTERFIELD, S EVANS, DA WALLACE, RB TI MAINTAINING MOBILITY IN LATE-LIFE .1. DEMOGRAPHIC CHARACTERISTICS AND CHRONIC CONDITIONS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ACTIVITIES OF DAILY LIVING; AGED; CHRONIC DISEASE; DEMOGRAPHY; EDUCATION; INCOME; PROSPECTIVE STUDIES ID CORONARY HEART-DISEASE; PHYSICAL-DISABILITY; HIP FRACTURE; RISK-FACTORS; PREDICTORS; COMMUNITY; RECOVERY; IMPACT; ELDERS; STROKE AB To assess the role of demographic tactors and chronic conditions in maintaining mobility in older persons, this study utilized longitudinal data collected as part of the Established Populations for Epidemiologic Studies of the Elderly between 1981 and 1987 on 6,981 men and women aged 65 years and older in East Boston, Massachusetts; Iowa and Washington counties, Iowa; and New Haven, Connecticut. Results are presented for those who at baseline reported intact mobility, defined as the ability to climb stairs and walk a half mile without help, and who were followed annually for up to 4 years for changes in mobility status. Age, income, education, and chronic conditions present at baseline and occurring during follow-up were evaluated for their association with loss of mobility. Over the follow-up period, 55.1% of subjects maintained mobility, 36.2% lost mobility, and 8.7% died without evidence of mobility loss prior to death. In both men and women, increasing age and lower income levels were associated with increased risk of losing mobility, even after controlling for the presence of chronic conditions at baseline. After adjustment for age, income, and chronic conditions, lower education levels were a significant risk factor for mobility loss in men, but not in women. Baseline reports of previous heart attack, stroke, high blood pressure, diabetes, dyspnea, and exertional leg pain were associated with small but significant risks for mobility loss. There was a stepwise increase in the risk of mobility loss according to the number of chronic conditions present at baseline that was very consistent between men and women. The occurrence during the study of a new heart attack, stroke, cancer, or hip fracture was associated with a substantially greater risk of mobility loss than was associated with the presence of these conditions at baseline. C1 UNIV VIRGINIA,MED CTR,SCH MED,DEPT MED,DIV BIOSTAT,CHARLOTTESVILLE,VA 22901. GRP HLTH COOPERAT PUGET SOUND,CTR HLTH STUDIES,SEATTLE,WA. UNIV WASHINGTON,DEPT EPIDEMIOL,SEATTLE,WA 98195. YALE UNIV,SCH MED,DEPT MICROBIOL,NEW HAVEN,CT 06510. HARVARD UNIV,SCH MED,CHANNING LAB,BOSTON,MA 02115. RUSH PRESBYTERIAN ST LUKES MED CTR,CTR HLTH & AGING,CHICAGO,IL 60612. E BOSTON NEIGHBORHOOD HLTH CTR,BOSTON,MA. UNIV IOWA,DEPT PREVENT MED & ENVIRONM HLTH,IOWA CITY,IA 52242. RP GURALNIK, JM (reprint author), NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,7201 WISCONSIN AVE,ROOM 3C-309,BETHESDA,MD 20892, USA. FU NIA NIH HHS [N01-AG-0-2105, N01-AG-0-2106, N01-AG-0-2107] NR 34 TC 363 Z9 369 U1 0 U2 10 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 15 PY 1993 VL 137 IS 8 BP 845 EP 857 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LC830 UT WOS:A1993LC83000004 PM 8484376 ER PT J AU LACROIX, AZ GURALNIK, JM BERKMAN, LF WALLACE, RB SATTERFIELD, S AF LACROIX, AZ GURALNIK, JM BERKMAN, LF WALLACE, RB SATTERFIELD, S TI MAINTAINING MOBILITY IN LATE-LIFE .2. SMOKING, ALCOHOL-CONSUMPTION, PHYSICAL-ACTIVITY, AND BODY-MASS INDEX SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ACTIVITIES OF DAILY LIVING; AGED; ALCOHOL DRINKING; BODY MASS INDEX; EXERCISE; HANDICAPPED; PROSPECTIVE STUDIES; SMOKING ID CORONARY HEART-DISEASE; ALAMEDA COUNTY; HIP FRACTURE; RISK-FACTORS; PREDICTORS; MEN; MORTALITY; HEALTH; WOMEN; DISABILITY AB While positive health behaviors have been shown to extend life, their association with extending active life has not been well investigated. In this report, several health behaviors were investigated in relation to maintaining mobility during 4 years of follow-up among 6,981 men and women aged 65 years and older with intact mobility at baseline between 1981 and 1983 who lived in one of three communities: East Boston, Massachusetts; Iowa and Washington counties, Iowa; and New Haven, Connecticut. Intact mobility, defined as the ability to climb up and down stairs and walk a half mile, was determined annually by interview, and study subjects were classified into one of three categories at the end of 4 years of follow-up: 1) maintained mobility (55.1%); 2) lost mobility (36.2%); or 3) died without evidence of having lost mobility prior to death (8.7%). After adjustment for age and all of the health behaviors, risk of losing mobility was significantly associated with current smoking, not consuming alcohol compared with small-to-moderate amounts of alcohol consumption, high (>80th percentile) compared with moderate (21-80th percentiles) body mass index, and low physical activity levels in both men and women. These findings suggest that positive health behaviors can not only extend longevity but also reduce the risk of losing mobility and independence in later life. C1 UNIV WASHINGTON,DEPT EPIDEMIOL,SEATTLE,WA 98195. YALE UNIV,SCH MED,DEPT EPIDEMIOL,NEW HAVEN,CT 06510. E BOSTON NEIGHBORHOOD HLTH CTR,BOSTON,MA. HARVARD UNIV,SCH MED,CHANNING LAB,BOSTON,MA 02115. NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892. UNIV IOWA,DEPT PREVENT MED & ENVIRONM HLTH,IOWA CITY,IA 52242. RP LACROIX, AZ (reprint author), GRP HLTH COOPERAT PUGET SOUND,CTR HLTH STUDIES,1730 MINOR AVE,SUITE 1600,SEATTLE,WA 98101, USA. FU NIA NIH HHS [N01-AG-0-2105, N01-AG-0-2106, N01-AG-0-2107] NR 42 TC 354 Z9 359 U1 3 U2 10 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 15 PY 1993 VL 137 IS 8 BP 858 EP 869 PG 12 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LC830 UT WOS:A1993LC83000005 PM 8484377 ER PT J AU URSIN, G ZIEGLER, RG SUBAR, AF GRAUBARD, BI HAILE, RW HOOVER, R AF URSIN, G ZIEGLER, RG SUBAR, AF GRAUBARD, BI HAILE, RW HOOVER, R TI DIETARY PATTERNS ASSOCIATED WITH A LOW-FAT DIET IN THE NATIONAL-HEALTH EXAMINATION FOLLOW-UP-STUDY - IDENTIFICATION OF POTENTIAL CONFOUNDERS FOR EPIDEMIOLOGIC ANALYSES SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE CONFOUNDING FACTORS (EPIDEMIOLOGY); DIETARY FATS; FOOD HABITS ID TOTAL ENERGY-INTAKE; NHANES-II SURVEY; BREAST-CANCER; QUANTITATIVE DATA; NUTRIENT SOURCES; AMERICAN DIET; RISK; FOOD; SUPPLEMENTATION; INTERVENTION AB To identify systematically the nutrient and food group intakes associated with a low-fat diet, the authors used the detailed dietary information collected from 10,306 individuals aged 32-86 years in the 1982-1984 National Health Epidemiologic Follow-up Study. Intakes of vitamin C and percentages of calories from carbohydrates, dietary fiber, poultry, low-fat dairy products, fruits, vegetables, cereals, and whole grains were markedly higher, while intakes of protein, total fat, saturated fat, oleic and linoleic acids, cholesterol, sodium, all red meats, high-fat dairy products, eggs, nuts, white bread, fried potatoes, desserts, fats, and oils were much lower in the quartile with the lowest percentage of calories from fat. These dietary patterns associated with a low-fat diet were essentially constant across strata of age, sex, race, and socioeconomic status. This study suggests that individuals on a low-fat diet substitute certain carbohydrate-rich foods such as fruits and vegetables for fat. Given these associations between low-fat diets and other dietary factors independently associated with certain cancers, these dietary factors should be considered potential confounders in studies of dietary fat and these cancers. C1 NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,DEPT EPIDEMIOL,LOS ANGELES,CA 90024. NCI,COLL CANC CAUSE & PREVENT,SURVEILLANCE PROGRAM,APPL RES,BETHESDA,MD 20892. NCI,COLL CANC CAUSE & PREVENT,BIOMETRY BRANCH,BETHESDA,MD 20892. NR 35 TC 64 Z9 66 U1 0 U2 4 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 15 PY 1993 VL 137 IS 8 BP 916 EP 927 PG 12 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LC830 UT WOS:A1993LC83000011 PM 8484383 ER PT J AU BULPITT, KJ CLEMENTS, PJ LACHENBRUCH, PA PAULUS, HE PETER, JB AGOPIAN, MS SINGER, JZ STEEN, VD CLEGG, DO ZIMINSKI, CM ALARCON, GS LUGGEN, ME POLISSON, RP WILLKENS, RF READING, JC WILLIAMS, HJ WARD, JR AF BULPITT, KJ CLEMENTS, PJ LACHENBRUCH, PA PAULUS, HE PETER, JB AGOPIAN, MS SINGER, JZ STEEN, VD CLEGG, DO ZIMINSKI, CM ALARCON, GS LUGGEN, ME POLISSON, RP WILLKENS, RF READING, JC WILLIAMS, HJ WARD, JR TI EARLY UNDIFFERENTIATED CONNECTIVE-TISSUE DISEASE .3. OUTCOME AND PROGNOSTIC INDICATORS IN EARLY SCLERODERMA (SYSTEMIC-SCLEROSIS) SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE CONNECTIVE TISSUE DISEASES; SCLERODERMA, SYSTEMIC; CARDIOPULMONARY SYSTEM; KIDNEY DISEASES; INFLAMMATION ID SOLUBLE INTERLEUKIN-2 RECEPTORS; LIFE-TABLE ANALYSIS; DEMOGRAPHIC FACTORS; SURVIVAL; CLASSIFICATION; ANTINUCLEAR; ANTIBODIES AB Objective: To characterize the course of early scleroderma and to delineate prognostic factors present within 1 year of disease onset that might identify patients at high risk. Design: Inception cohort study. Setting: Ten university-based rheumatology clinics participating in the Cooperative Systematic Studies of Rheumatic Diseases Program. Patients: Forty-eight patients who had had scleroderma for less than 1 year. Measurements: Fifteen patients with early scleroderma who died were compared with those still living during the initial study period (1982 to 1992). Kaplan-Meier survival estimation and Cox proportional hazards analysis were used to analyze baseline variables for their ability to predict survival duration. Results: Eight of 15 deaths were due to cardiac or pulmonary system failure. The estimated 5-year survival rate was 68%. Baseline factors that were the most predictive of a poor outcome included the presence of abnormal cardiopulmonary signs and abnormal urine sediment (pyuria, hematuria). Conclusion: Evidence of early cardiopulmonary disease, renal disease, inflammation, or immune activation may identify a subset of patients with scleroderma who will experience rapidly progressive disease and early death. C1 UNIV CALIF LOS ANGELES,DIV BIOSTAT,LOS ANGELES,CA 90024. SPECIALTY LABS INC,SANTA MONICA,CA 90404. SUNY HLTH SCI CTR,BROOKLYN,NY 11203. UNIV PITTSBURGH,PITTSBURGH,PA 15261. UNIV UTAH,MED CTR,SALT LAKE CITY,UT 84132. UNIV UTAH,CTR COORDINATING COOPERAT SYSTEMAT STUDIES RHEUMAT DIS PROGRAM,SALT LAKE CITY,UT 84112. JOHNS HOPKINS UNIV,DIV RHEUMATOL,BALTIMORE,MD 21239. UNIV ALABAMA,DEPT MED,DIV RHEUMATOL,BIRMINGHAM,AL 35294. UNIV CINCINNATI,MED CTR,DIV IMMUNOL,CINCINNATI,OH 45267. DUKE UNIV,DURHAM,NC 27706. UNIV WASHINGTON,SEATTLE,WA 98195. NIH,BETHESDA,MD 20892. RP BULPITT, KJ (reprint author), UNIV CALIF LOS ANGELES,DIV RHEUMATOL,1000 VET AVE,32-47,LOS ANGELES,CA 90024, USA. FU NIADDK NIH HHS [1-AM6-2228]; NIAMS NIH HHS [AR3-6834-05] NR 37 TC 74 Z9 75 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 APR 15 PY 1993 VL 118 IS 8 BP 602 EP 609 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA KW470 UT WOS:A1993KW47000005 PM 8452326 ER PT J AU WHEAT, J HAFNER, R WULFSOHN, M SPENCER, P SQUIRES, K POWDERLY, W WONG, B RINALDI, M SAAG, M HAMILL, R MURPHY, R CONNOLLYSTRINGFIELD, P BRIGGS, N OWENS, S AF WHEAT, J HAFNER, R WULFSOHN, M SPENCER, P SQUIRES, K POWDERLY, W WONG, B RINALDI, M SAAG, M HAMILL, R MURPHY, R CONNOLLYSTRINGFIELD, P BRIGGS, N OWENS, S TI PREVENTION OF RELAPSE OF HISTOPLASMOSIS WITH ITRACONAZOLE IN PATIENTS WITH THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE ACQUIRED IMMUNODEFICIENCY SYNDROME; HISTOPLASMOSIS; ASTERISK-ITRACONAZOLE; AMPHOTERICIN-B; HUMAN IMMUNODEFICIENCY VIRUS INFECTIONS ID CAPSULATUM ANTIGEN; AMPHOTERICIN-B; AIDS; DIAGNOSIS; FLUCONAZOLE; THERAPY AB Objective: To assess the efficacy and safety of itraconazole in preventing relapse of histoplasmosis after induction therapy with amphotericin B in patients with the acquired immunodeficiency syndrome (AIDS) and disseminated histoplasmosis. Design: A prospective, multicenter, open-label clinical trial, with follow-up for at least 52 weeks. Setting: Tertiary care hospitals participating in a clinical investigation sponsored by the National Institutes of Allergy and Infectious Diseases (AIDS Clinical Trial Group and Mycoses Study Group). Patients: Forty-two patients with AIDS who had successfully completed induction therapy for disseminated histoplasmosis amphotericin B, at least 15 mg/kg body weight given over 4 to 12 weeks. Interventions: Itraconazole, 200 mg given orally twice daily. Main Outcome Measures: Response to therapy, specifically prevention of histoplasmosis relapse, was the main outcome measure. Secondary end points were survival and the effect of therapy on Histoplasma capsulatum variety capsulatum antigen levels in urine and serum. Plasma itraconazole concentrations were measured to document drug absorption and compliance with therapy. Results: The median follow-up was 109 weeks, and median survival was 98 weeks. Two relapses occurred (5%; 95% CI, 0.5% to 16%), one in a patient withdrawn from the study 18 weeks earlier and one in a patient who did not comply with the study therapy. Patients with elevated antigen levels at study entry showed clearance of antigen from urine and serum; urine specimens became negative in 43% of patients (CI, 26% to 59%), and serum specimens became negative in 75% of patients (CI, 56% to 94%). Only one patient discontinued treatment because of itraconazole toxicity (hypokalemia). Conclusions: Itraconazole, 200 mg twice daily, is safe and effective in preventing relapse of disseminated histoplasmosis in patients with AIDS. Antigen clearance from blood and urine correlates with clinical efficacy. C1 UNIV CINCINNATI,COLL MED,DEPT INTERNAL MED,CINCINNATI,OH 45221. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. RICHARD L ROUDEBUSH VET AFFAIRS HOSP,INDIANAPOLIS,IN. DEPT VET AFFAIRS MED CTR,BIRMINGHAM,AL 35233. DEPT VET AFFAIRS MED CTR,DIV INFECT DIS 111G,HOUSTON,TX 77030. FRONTIER SCI & TECH RES FDN,AMHERST,NY 14226. WASHINGTON UNIV,CLIN TRIALS UNIT,ST LOUIS,MO 63130. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. INDIANA UNIV,SCH MED,IDRC,INDIANAPOLIS,IN 46202. CORNELL UNIV,ITHACA,NY 14853. RICHARD L ROUDEBUSH VET ADM MED CTR,INDIANAPOLIS,IN 46202. NIH,DIV AIDS,BETHESDA,MD 20892. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. OI Murphy, Robert/0000-0003-3936-2052 FU NIAID NIH HHS [1-AI-15082] NR 19 TC 150 Z9 153 U1 0 U2 1 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 APR 15 PY 1993 VL 118 IS 8 BP 610 EP 616 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA KW470 UT WOS:A1993KW47000006 PM 8383934 ER PT J AU CHABNER, BA AF CHABNER, BA TI BIOLOGICAL BASIS FOR CANCER-TREATMENT SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material DE ANTINEOPLASTIC AGENTS; BIOLOGICAL THERAPY; MOLECULAR BIOLOGY; DRUG RESISTANCE; GENE THERAPY ID HAIRY-CELL LEUKEMIA; P-GLYCOPROTEIN EXPRESSION; MULTIDRUG RESISTANCE; DRUG-RESISTANCE; BREAST-CANCER; CARCINOMA; VERAPAMIL; THERAPY; TAXOL; GENE AB The new knowledge of the regulation of cell growth and the genetic and biochemical changes that lead to malignancy have created many new opportunities for cancer drug discovery. These new targets include oncogenes, growth factors and their receptors, signal transduction pathways, and cell differentiation signals. Attempts to identify new therapies based on these targets can complement traditional drug discovery efforts that rely on high-volume screening of candidate natural products and synthetic chemicals against human tumor cell lines and against defined molecular reactions. Through modern computer-based data analysis, drug screening data can be used to establish mechanisms of drug action of new agents; these analyses shed light on patterns of cross-resistance of new compounds and their interactions with defined molecular targets as well as allow selection of chemically and biologically unique agents as candidates for clinical development. RP CHABNER, BA (reprint author), NCI,DIV CANC TREATMENT,BETHESDA,MD 20892, USA. NR 53 TC 14 Z9 14 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 APR 15 PY 1993 VL 118 IS 8 BP 633 EP 637 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA KW470 UT WOS:A1993KW47000011 PM 8452330 ER PT J AU IWASAKI, M LINDBERG, RLP JUVONEN, RO NEGISHI, M AF IWASAKI, M LINDBERG, RLP JUVONEN, RO NEGISHI, M TI SITE-DIRECTED MUTAGENESIS OF MOUSE STEROID 7-ALPHA-HYDROXYLASE (CYTOCHROME-P-4507-ALPHA) - ROLE OF RESIDUE-209 IN DETERMINING STEROID CYTOCHROME-P-450 INTERACTION SO BIOCHEMICAL JOURNAL LA English DT Article ID CATALYTIC ACTIVITY; COUMARIN 7-HYDROXYLASE; SEQUENCE REQUIREMENTS; SUBSTRATE-SPECIFICITY; II P-45015-ALPHA; GENE; LIVER; 15-ALPHA-HYDROXYLASE; CYTOCHROMES-P450; HYDROXYLATION AB We have cloned a cDNA encoding mouse steroid 7alpha-hydroxylase P450(7alpha) (cytochrome P-450(7alpha) and expressed it in Saccharomyces cerevisiae. Mouse P450(7alpha) is 70 % identical in its amino acid sequence with the mouse steroid 15alpha-hydroxylase P450(15alpha) (2A4). The Leu at position 209 of P450(15alpha) is the most important residue to determine the steroid hydroxylase activity of the P450 [Lindberg and Negishi (1989) Nature (London) 339, 632-634]. The P450(7alpha) contains Asn at the position corresponding to the Leu-209 of P450(15alpha), although both P450s hydroxylate testosterone. The CO-reduced P450(7alpha) complex is unstable, so that it is quickly converted into the inactive P420, whereas the P450(15alpha) is very stable. The P450(7alpha), however, is stabilized either by addition of testosterone or by a mutation of Asn-209 to Leu. The mutant P450(7alpha) displays a 17-fold lower V(max) value than the wild-type enzyme. Unexpectedly, it also has 3-fold lower K(m) and K(d) values. Residue 209 in P450(7alpha), therefore, appears to be located at a critical site of the haem-substrate-binding pocket. Corticosterone inhibits the testosterone 7alpha-hydroxylase activity of the wild-type P450(7alpha), whereas it does not inhibit the mutant P450(7alpha). Conversely, the P450(15alpha) activity becomes inhibited by corticosterone upon the replacement of Leu-209 by Asn. In addition, this mutation increases the corticosterone 15alpha-hydroxylase activity of P450(15alpha) at least 20-fold. Whereas the inhibition by corticosterone depends on the presence of Asn at position 209, deoxycorticosterone inhibits the activities of the P450s regardless of the type of residue at 209. The results indicate, therefore, that the identity of residue 209 determines the affinity as well as specificity of steroid binding to both P450(7alpha) and P450(15alpha). C1 NIEHS,PHARMACOGENET SECT,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709. NR 30 TC 54 Z9 56 U1 0 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD APR 15 PY 1993 VL 291 BP 569 EP 573 PN 2 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KZ698 UT WOS:A1993KZ69800034 PM 8484736 ER PT J AU DEBELLIS, MD GERACIOTI, TD ALTEMUS, M KLING, MA AF DEBELLIS, MD GERACIOTI, TD ALTEMUS, M KLING, MA TI CEREBROSPINAL-FLUID MONOAMINE METABOLITES IN FLUOXETINE-TREATED PATIENTS WITH MAJOR DEPRESSION AND IN HEALTHY-VOLUNTEERS SO BIOLOGICAL PSYCHIATRY LA English DT Article DE FLUOXETINE; CEREBROSPINAL FLUID; MAJOR DEPRESSION; 5-HYDROXYINDOLEACETIC ACID; 3-METHOXY-4-HYDROPHENYLGLYCOL; HOMOVANILLIC ACID ID 5-HYDROXYINDOLEACETIC ACID; ELECTROCHEMICAL DETECTION; HOMOVANILLIC-ACID; SUICIDAL-BEHAVIOR; SEROTONIN UPTAKE; DISORDER; IMIPRAMINE; AMITRIPTYLINE; ANTIDEPRESSANTS; OUTPATIENTS AB Cerebrospinal fluid (CSF) levels of the monoamine metabolites 5-hydroxyindoleacetic acid (5-HIAA), 3-methoxy-4-hydroxyphenylglycol (MHPG), and homovanillic acid (HVA) were measured in three groups: 46 healthy volunteers; 9 medication-free patients with DSM III-R major depressive disorder, recurrent; and these same 9 patients following at least 4 weeks of fluoxetine treatment at 20 mg/day. CSF monoamine metabolite levels in medication-free patients did not differ from healthy volunteers; however, CSF 5-HIAA and MHPG decreased significantly from 95.9 +/- 24.6 (all values +/- SD) to 64.2 +/- 26.1 pmol/ml and from 46.7 +/- 14.2 to 42.6 +/- 11.6 pmol/ml, respectively, following fluoxetine treatment. Fluoxetine also significantly decreased mean Hamilton Depression Rating Scale scores from 23.2 +/- 6.5 to 17.4 +/- 5.0 and significantly increased the CSF HVA/5-HIAA ratio. C1 NIGMS,BETHESDA,MD. VANDERBILT UNIV,MED CTR,SCH MED,DEPT PSYCHIAT,NASHVILLE,TN 37232. RP DEBELLIS, MD (reprint author), NIMH,IRP,NIH CLIN CTR,CLIN NEUROENDOCRINOL BRANCH,AFFECT DISORDERS UNIT,BETHESDA,MD 20892, USA. RI Kling, Mitchel/F-4152-2010 OI Kling, Mitchel/0000-0002-2232-1409 NR 38 TC 59 Z9 59 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 1993 VL 33 IS 8-9 BP 636 EP 641 DI 10.1016/0006-3223(93)90103-K PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LJ290 UT WOS:A1993LJ29000011 PM 7687151 ER PT J AU STEIN, MB BLACK, B BROWN, TM UHDE, TW AF STEIN, MB BLACK, B BROWN, TM UHDE, TW TI LACK OF EFFICACY OF THE ADENOSINE REUPTAKE INHIBITOR DIPYRIDAMOLE IN THE TREATMENT OF ANXIETY DISORDERS SO BIOLOGICAL PSYCHIATRY LA English DT Article DE DIPYRIDAMOLE; ANXIETY; ADENOSINE; PANIC; PHARMACOTHERAPY ID RECEPTOR ANTAGONISTS; PANIC DISORDERS; CAFFEINE; ANALOGS; BRAIN; THEOPHYLLINE AB We administered dipyridamole, an adenosine reuptake inhibitor, to 12 outpatients with DSM-III-R anxiety disorders (2 patients with generalized anxiety disorder, 10 patients with panic disorder). Dipyridamole was administered at a flexible dose in a single-blinded fashion following a placebo washout phase and elimination of placebo responders. The mean duration of active treatment with dipyridamole was 46 days (range 21-88 days); the mean peak dose of dipyridamole was 202 +/- 55 mg/day (range 100-300 mg/day). Symptom ratings were completed at regular intervals by the patient and by a research nurse unaware of the treatment condition. Clinically significant improvement in anxiety symptoms was not demonstrated. The implications of these findings for an adenosinergic dysfunction model of panic disorder are discussed. C1 NIMH,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS SECT,BLDG 10,ROOM 3S239,BETHESDA,MD 20892. NR 23 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 1993 VL 33 IS 8-9 BP 647 EP 650 DI 10.1016/0006-3223(93)90105-M PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LJ290 UT WOS:A1993LJ29000013 PM 8329495 ER PT J AU CHAO, NJ SCHRIBER, JR GRIMES, K LONG, GD NEGRIN, RS RAIMONDI, CM HORNING, SJ BROWN, SL MILLER, L BLUME, KG AF CHAO, NJ SCHRIBER, JR GRIMES, K LONG, GD NEGRIN, RS RAIMONDI, CM HORNING, SJ BROWN, SL MILLER, L BLUME, KG TI GRANULOCYTE COLONY-STIMULATING FACTOR MOBILIZED PERIPHERAL-BLOOD PROGENITOR CELLS ACCELERATE GRANULOCYTE AND PLATELET RECOVERY AFTER HIGH-DOSE CHEMOTHERAPY SO BLOOD LA English DT Article ID BONE-MARROW TRANSPLANTATION; HEMATOPOIETIC STEM-CELLS; HODGKINS-DISEASE; G-CSF; RECOMBINANT; CANCER; THERAPY C1 STANFORD UNIV,SCH BUSINESS,STANFORD,CA 94305. AMGEN CO,THOUSAND OAKS,CA. NCI,CTEP,BETHESDA,MD 20892. NR 27 TC 296 Z9 298 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 APR 15 PY 1993 VL 81 IS 8 BP 2031 EP 2035 PG 5 WC Hematology SC Hematology GA KY005 UT WOS:A1993KY00500008 PM 7682454 ER PT J AU SEKHSARIA, S MALECH, HL AF SEKHSARIA, S MALECH, HL TI RECOMBINANT HUMAN STEM-CELL FACTOR ENHANCES MYELOID COLONY GROWTH FROM HUMAN PERIPHERAL-BLOOD PROGENITORS SO BLOOD LA English DT Article ID NON-LYMPHOBLASTIC LEUKEMIA; C-KIT LIGAND; STIMULATING FACTOR; AUTOLOGOUS TRANSPLANTATION; HEMATOPOIETIC PROGENITORS; GM-CSF; MARROW; PROLIFERATION; IDENTIFICATION; SUBPOPULATIONS C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 27 TC 24 Z9 24 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 APR 15 PY 1993 VL 81 IS 8 BP 2125 EP 2130 PG 6 WC Hematology SC Hematology GA KY005 UT WOS:A1993KY00500020 PM 7682456 ER PT J AU MURAKAMI, H SANDERSON, ND NAGY, P MARINO, PA MERLINO, G THORGEIRSSON, SS AF MURAKAMI, H SANDERSON, ND NAGY, P MARINO, PA MERLINO, G THORGEIRSSON, SS TI TRANSGENIC MOUSE MODEL FOR SYNERGISTIC EFFECTS OF NUCLEAR ONCOGENES AND GROWTH-FACTORS IN TUMORIGENESIS - INTERACTION OF C-MYC AND TRANSFORMING GROWTH FACTOR-ALPHA IN HEPATIC ONCOGENESIS SO CANCER RESEARCH LA English DT Note ID LIVER NEOPLASIA; RAT-LIVER; TGF-ALPHA; MICE; EXPRESSION; CELLS; HEPATOCARCINOGENESIS; ALBUMIN; OVEREXPRESSION; AMPLIFICATION AB Double transgenic mice bearing fusion genes consisting of mouse albumin enhancer/promoter-mouse c-myc complementary DNA and mouse metallothionein 1 promoter-human transforming growth factor alpha complementary DNA were generated to investigate the interaction of these genes in hepatic oncogenesis and to provide a general paradigm for characterizing the interaction of nuclear oncogenes and growth factors in tumorigenesis. Coexpression of c-myc and transforming growth factor alpha as transgenes in the mouse liver resulted in a tremendous acceleration of neoplastic development in this organ as compared to expression of either of these transgenes alone. The two distinct cellular reactions that occurred in the liver of the double transgenic mice prior to the appearance of liver tumors were dysplastic and apoptotic changes in the existing hepatocytes followed by emergence of multiple focal lesions composed of both hyperplastic and dysplastic cell populations. These observations suggest that the interaction of c-myc and transforming growth factor alpha, and possibly other combinations of nuclear oncogenes and growth factors, during development of hepatic neoplasia contributes to the selection and expansion of the preneoplastic cell populations which consequently increases the probability of malignant conversion. C1 NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 35 TC 211 Z9 213 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1993 VL 53 IS 8 BP 1719 EP 1723 PG 5 WC Oncology SC Oncology GA KY096 UT WOS:A1993KY09600001 PM 8467484 ER PT J AU AFSHARI, CA KODAMA, S BIVINS, HM WILLARD, TB FUJIKI, H BARRETT, JC AF AFSHARI, CA KODAMA, S BIVINS, HM WILLARD, TB FUJIKI, H BARRETT, JC TI INDUCTION OF NEOPLASTIC PROGRESSION IN SYRIAN-HAMSTER EMBRYO CELLS TREATED WITH PROTEIN PHOSPHATASE INHIBITORS SO CANCER RESEARCH LA English DT Article ID TUMOR-SUPPRESSOR GENE; OKADAIC ACID CLASS; MORPHOLOGICAL TRANSFORMATION; CELLULAR SENESCENCE; KARYOTYPIC CHANGES; COMMUNICATION; PROMOTERS; INVITRO; PHOSPHOTYROSINE; VANADATE AB In these studies, Syrian hamster embryo cells (SHE), which were isolated at different stages of neoplastic progression, were used to test the ability of the protein phosphatase inhibitors, okadaic acid and sodium orthovanadate (Na3VO4) to induce neoplastic progression. We observed that these chemicals can induce transition of the cells from one stage to the other at different points in the multistep process of neoplastic transformation. Three steps in this multistep process were studied: escape from cellular senescence, loss of a tumor suppressor gene function in immortal cells, and aquisition of anchorage-independent growth. Treatment of normal, primary SHE cells with okadaic acid or Na3VO4 allowed the cells to escape senescence and become immortal at a low frequency. The induction of immortality was associated with nonrandom chromosome changes. including trisomy 8 and 11 and monosomy 13 and Xq. The transition of preneoplastic cells to more advanced stages was also studied in immortal, nontumorigenic cells that either have retained (supB+) or have lost (supB-) the ability to suppress tumorigenicity of a transformed cell line in cell hybrids. SupB+ and supB- cells do not normally grow in agar, but supB- cells will grow in agar if additional growth factors are added. However, upon addition of protein phosphatase inhibitors, supB+ cells exhibited the supB- phenotype; for example, colony formation of supB+ cells was observed in agar supplemented with growth factors and protein phosphatase inhibitors. Following treatment. selection of these colonies showed that 89% of these cells heritably acquired the phenotype of cells that have lost the suppressor gene function (supB-). SupB- cells were also treated with protein phosphatase inhibitors in soft agar in the presence of additional growth factors. While the frequency of colonies in agar supplemented with growth factors in agar was not greatly enhanced, approximately 50% of the colonies acquired the ability to grow in agar autonomously without the supplemented growth factors, similar to tumorigenic cells. These studies suggest that Na3VO4 and okadaic acid induce progression of cells through various stages in this multistep system. C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,CURRICULUM TOXICOL,CHAPEL HILL,NC 27514. NATL CANC CTR,RES INST,TOKYO 104,JAPAN. NR 45 TC 24 Z9 25 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 APR 15 PY 1993 VL 53 IS 8 BP 1777 EP 1782 PG 6 WC Oncology SC Oncology GA KY096 UT WOS:A1993KY09600013 PM 8385570 ER PT J AU ROWINSKY, EK NOE, DA ETTINGER, DS CHRISTIAN, MC LUBEJKO, BG FISHMAN, EK SARTORIUS, SE BOYD, MR DONEHOWER, RC AF ROWINSKY, EK NOE, DA ETTINGER, DS CHRISTIAN, MC LUBEJKO, BG FISHMAN, EK SARTORIUS, SE BOYD, MR DONEHOWER, RC TI PHASE-I AND PHARMACOLOGICAL STUDY OF THE PULMONARY CYTOTOXIN 4-IPOMEANOL ON A SINGLE DOSE SCHEDULE IN LUNG-CANCER PATIENTS - HEPATOTOXICITY IS DOSE LIMITING IN HUMANS SO CANCER RESEARCH LA English DT Article ID POTATOES IPOMOEA-BATATAS; TARGET ORGAN ALKYLATION; METABOLIC-ACTIVATION; COVALENT BINDING; RABBIT PULMONARY; CYTO-TOXIN; TOXICITY; GLUTATHIONE; INVITRO; TISSUE AB 4-Ipomeanol (IPO), a naturally occurring pulmonary toxin, is the first cytotoxic agent to undergo clinical development based on a biochemical-biological rationale as an antineoplastic agent targeted specifically against lung cancer. This rationale is based on preclinical observations that metabolic activation and intracellular binding of IPO, as well as cytotoxicity, occurred selectively in tissues and cancers derived from tissues that are rich in specific P450 mixed function oxidase enzymes. Although tissues capable of activating IPO to cytotoxic intermediates in vitro include liver, lung, and kidney, IPO has been demonstrated in rodents and dogs to undergo in situ activation, bind covalently, and induce cytotoxicity preferentially in lung tissue at doses not similarly affecting liver or kidneys. Although the drug was devoid of antitumor activity in the conventional murine preclinical screening models, cytotoxic activity was observed in human lung cancers in vitro and in human lung cancer xenografts in vivo, adding to the rationale for clinical development. Somewhat unexpectantly, hepatocellular toxicity was the dose-limiting principal toxicity of IPO administered as a 30-min infusion every 3 weeks to patients with lung cancer. In this study, 55 patients received 254 courses at doses almost spanning 3 orders of magnitude, 6.5 to 1612 mg/m2. Transient and isolated elevations in hepatocellular enzymes, predominately alanine aminotransferase, occurred in the majority of courses of IPO at 1032 mg/m2, which is the recommended IPO dose for subsequent phase II trials. At higher doses, hepatocellular toxicity was more severe and was often associated with right upper quadrant pain and severe malaise. Toxic effects were also noted in other tissues capable of activating IPO, including possible nephrotoxicity in a patient treated with one course of IPO at 154 mg/m2 and severe, reversible pulmonary toxicity in another patient who received nine courses of IPO at doses ranging from 202 to 826 mg/m2. Although individual plasma drug disposition curves were well described by a two-compartment first order elimination model, the relationship between IPO dose and area under the disposition curve was curvilinear, suggesting saturable elimination kinetics. At the maximum tolerated dose, the mean half-lives (lambda1 and lambda2) were 6.7 and 114.5 min, respectively. Renal excretion of parent compound accounted for less than 2% of the administered dose of IPO. An unidentified metabolite was detected in the plasma of patients treated at higher doses. No objective antitumor responses were observed; however, stable disease persisted for at least eight courses in 27% of patients. The preponderance of clinical toxicity observed in liver rather than lung suggests that IPO may be preferentially activated and bound in liver rather than lung or other tissues in humans or that human lung tissue is more effective at detoxifying and/or is more tolerant to activated IPO than other species. In any event, these observations suggest further that the rationale for the clinical evaluation or ipo should be extended to include liver cancers and possibly renal cancers, as well as lung cancers. C1 JOHNS HOPKINS MED INST, DEPT RADIOL, BALTIMORE, MD 21287 USA. NCI, DIV CANC TREATMENT, DEV THERAPEUT PROGRAM, DRUG DISCOVERY RES & DEV LAB, BETHESDA, MD 20892 USA. RP ROWINSKY, EK (reprint author), JOHNS HOPKINS ONCOL CTR, DIV PHARMACOL & EXPTL THERAPEUT, 1-121, 600 N WOLFE ST, BALTIMORE, MD 21287 USA. FU NCI NIH HHS [N01-CM-57738] NR 36 TC 30 Z9 30 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 EI 1538-7445 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1993 VL 53 IS 8 BP 1794 EP 1801 PG 8 WC Oncology SC Oncology GA KY096 UT WOS:A1993KY09600016 PM 8467498 ER PT J AU VUKANOVIC, J PASSANITI, A HIRATA, T TRAYSTMAN, RJ HARTLEYASP, B ISAACS, JT AF VUKANOVIC, J PASSANITI, A HIRATA, T TRAYSTMAN, RJ HARTLEYASP, B ISAACS, JT TI ANTIANGIOGENIC EFFECTS OF THE QUINOLINE-3-CARBOXAMIDE LINOMIDE SO CANCER RESEARCH LA English DT Article ID HUMAN-ENDOTHELIAL CELLS; TUMOR ANGIOGENESIS; BASEMENT-MEMBRANE; PROSTATIC-CANCER; IMMUNOMODULATOR; LS-2616; IDENTIFICATION; METASTASIS; MELANOMA; LAMININ AB Linomide (N-phenylmethyl-1,2-dihydro-4-hydroxyl-1-methyl-2-oxoquinoline-3-carboxamide) has a reproducible in vivo antitumor effect against a series of both androgen responsive and independent Dunning R-3327 rat prostatic cancers. This antitumor effect of linomide is host mediated. One possible mechanism involving the host is that linomide has antiangiogenic activity. An indication that linomide treatment has antiangiogenic activity is the observation that prostatic cancers from linomide treated rats have more focal necrosis than sized matched tumors from untreated rats. To directly test if linomide has antiangiogenic activity, a newly developed Matrigel based quantitative in vivo angiogenic assay was used. These experiments demonstrated that linomide has dose dependent, antiangiogenic activity in vivo in the rat. Additional studies demonstrated that due to its antiangiogenic activity, linomide treatment of rats bearing prostate cancers resulted in a more than 40% decrease in tumor blood flow. Blood flow to a variety of non-tumor bearing organs was not decreased suggesting that linomide selectively inhibits angiogenesis and does not induce loss of established blood vessels. Using as a model the response of human umbilical vein endothelial cells to linomide treatment in a variety of in vitro assays, linomide was demonstrated to have cytostatic but not cytotoxic effect on human umbilical vein endothelial cells at a medium concentration of greater-than-or-equal-to 100 mug/ml. In addition, both endothelial cell chemotactic migration and invasion are steps in angiogenesis inhibited by linomide treatment. C1 JOHNS HOPKINS ONCOL CTR,422 N BOND ST,BALTIMORE,MD 21231. JOHNS HOPKINS UNIV,SCH MED,DEPT UROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205. NIA,GERONTOL RES CTR,BIOL CHEM LABS,BALTIMORE,MD 21224. KABI PHARMACIA THERAPEUT,S-22363 LUND,SWEDEN. FU NCI NIH HHS [CA50601] NR 30 TC 111 Z9 111 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 APR 15 PY 1993 VL 53 IS 8 BP 1833 EP 1837 PG 5 WC Oncology SC Oncology GA KY096 UT WOS:A1993KY09600022 PM 7682157 ER PT J AU WALTON, MI WHYSONG, D OCONNOR, PM HOCKENBERY, D KORSMEYER, SJ KOHN, KW AF WALTON, MI WHYSONG, D OCONNOR, PM HOCKENBERY, D KORSMEYER, SJ KOHN, KW TI CONSTITUTIVE EXPRESSION OF HUMAN BCL-2 MODULATES NITROGEN-MUSTARD AND CAMPTOTHECIN INDUCED APOPTOSIS SO CANCER RESEARCH LA English DT Article ID T(14-18) CHROMOSOMAL TRANSLOCATION; NON-HODGKINS LYMPHOMAS; PROGRAMMED CELL-DEATH; B-CELLS; TOPOISOMERASE-I; HEMATOPOIETIC-CELLS; MEMBRANE PROTEIN; DNA; ACTIVATION; SURVIVAL AB Bcl-2 is a novel protooncogene which prolongs cell survival and suppresses apoptosis. We examined whether constitutive expression of transfected human bcl-2 conferred resistance to two different DNA damaging drugs, nitrogen mustard (HN2) and camptothecin (CPT) in a murine, IL-3 dependent cell line (FL5.12). HN2 treatment produced 2-fold less cell death and DNA degradation in cells overexpressing bcl-2 relative to control cells transfected with a construct bearing only the neo(R) gene. DNA degradation was characterized by oligonucleosomal length fragments indicating that programmed cell death or apoptosis had occurred. Equimolar HN2 produced similar extents of interstrand cross-link formation and repair in each cell line. Cell cycle characteristics were similar for both cell lines following equimolar HN2 treatment, exhibiting a brief S phase delay followed by a longer G2 arrest. Time course studies indicated that DNA fragmentation occurred following peak G2 arrest in control cells and 12 h later in bcl-2 transfected cells. Equimolar CPT exposure also induced 2-fold less death and apoptotic DNA fragmentation in bcl-2 transfected compared to control cells. DNA single strand break formation and resealing kinetics were comparable in both cell lines following equimolar CPT treatment. CPT caused similar cell cycle perturbations in both cell lines, with a brief S phase block detectable 12 h after an equimolar drug dose. Kinetic studies showed apoptosis occurred following maximal S phase arrest in control and 12 h later in bcl-2 transfected cells. By contrast, IL-3 withdrawal produced rapid and extensive DNA degradation and apoptosis in controls 24 h postwithdrawal, and this process was inhibited 3-4-fold in bcl-2 transfectants. Cell cycle analysis showed both cell lines arrested in G0/G1 following IL-3 removal. In summary, bcl-2 transfection affords a 2-fold protection from HN2 and CPT cytotoxicity and decreases drug induced apoptosis in FL5.12 cells, despite the different mechanisms of action and cell cycle effects of each agent. Bcl-2 overexpression appears to represent a novel drug resistance mechanism of potential clinical significance. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT MED & MOLEC MICROBIOL,ST LOUIS,MO 63110. RP WALTON, MI (reprint author), INST CANC RES,DRUG DEV SECT,CLIN PHARMACOL TEAM,BLOCK E,15 COTSWOLD RD,SUTTON SM2 5NG,SURREY,ENGLAND. NR 60 TC 274 Z9 276 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1993 VL 53 IS 8 BP 1853 EP 1861 PG 9 WC Oncology SC Oncology GA KY096 UT WOS:A1993KY09600025 PM 8467505 ER PT J AU ENOMOTO, T FUJITA, M INOUE, M RICE, JM NAKAJIMA, R TANIZAWA, O NOMURA, T AF ENOMOTO, T FUJITA, M INOUE, M RICE, JM NAKAJIMA, R TANIZAWA, O NOMURA, T TI ALTERATIONS OF THE P53 TUMOR SUPPRESSOR GENE AND ITS ASSOCIATION WITH ACTIVATION OF THE C-K-RAS-2 PROTOONCOGENE IN PREMALIGNANT AND MALIGNANT LESIONS OF THE HUMAN UTERINE ENDOMETRIUM SO CANCER RESEARCH LA English DT Article ID K-RAS ACTIVATION; POLYMERASE CHAIN-REACTION; MUTATIONS; CANCERS; UTERUS; MODEL AB We previously reported (T. Enomoto et al., Cancer Res., 50: 6139-6145, 1990; T. Enomoto et al., Cancer Res., 51: 5308-5314, 1991) a significant frequency of activating point mutations in codon 12 of the c-K-ras-2 protooncogene in endometrial adenocarcinoma and its premalignant precursor lesions (series 1 and 2). To reveal the role of the p53 tumor suppressor gene in the development of endometrial adenocarcinoma and to study the association of p53 alterations with K-ras activation, an additional 28 endometrial adenocarcinomas and an additional 11 premalignant atypical uterine hyperplasias (series 3), as well as 12 cases of endometrial adenocarcinoma (10 having K- or N-ras activation) and 2 cases of atypical hyperplasia from series 1 and 2, were screened for the presence of p53 alterations. Allelic loss, recognized at the polymorphic site in codon 72 of the p53 gene, was detected in 6 of 19 (32%) informative cases of endometrial adenocarcinoma and 1 of 4 (25%) informative cases of endometrial atypical hyperplasia by restriction fragment length polymorphism analysis and by single-strand conformation polymorphism analysis of polymerase chain reaction (PCR)-amplified DNA fragments. Mutations in the highly conserved regions of the p53 gene were detected by single-strand conformation polymorphism analysis of PCR-amplified DNA fragments. Mutations were found in 9 of 40 (23%) endometrial adenocarcinomas and 1 of 13 (8%) atypical hyperplasias that were studied. Mutations in p53 were significantly more frequently found in clinical grade 3 (G3) cancers (6 of 14, 43%) than in G1-G2 cancers (3 of 26, 12%) (P = 0.033). Mutations were subsequently confirmed by direct sequencing. Single missense base substitutions were detected in 6 cases of endometrial carcinoma and in one case of atypical hyperplasia. Deletions of a single base and of 2 bases were each detected in single cases of endometrial carcinoma, and a single base insertion was found in a third case. Point mutations in K-ras were also identified in tumors of series 3 by direct sequencing of PCR-amplified DNA fragments of exons 1 and 2. Point mutations in codons 12 and 13 in K-ras were detected by direct sequencing of PCR-amplified DNA in 7 of 28 adenocarcinomas in series 3, but none were found in exon 2 (codons 59-63). The spectrum of point mutations in p53 in endometrial adenocarcinomas was almost identical to what we found in K-ras in series 1 and 2 and in series 3, suggesting the possible role of a mutagen that might be responsible for mutations in both K-ras and p53. However, there was no correlation between the presence of p53 gene mutations and K-ras activation in these tumors. It appears that inactivation of p53, as well as K-ras activation, plays a significant role in the development of endometrial adenocarcinoma. In contrast to K-ras activation, which commonly occurs as an early event, inactivation of p53 usually occurs as a later event in endometrial carcinogenesis, independently of K-ras activation. C1 OSAKA UNIV,FAC MED,DEPT OBSTET & GYNECOL,SUITA,OSAKA 565,JAPAN. NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. RP ENOMOTO, T (reprint author), OSAKA UNIV,FAC MED,DEPT RADIAT BIOL,2-2 YAMADAOKA,SUITA,OSAKA 565,JAPAN. NR 30 TC 137 Z9 141 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 APR 15 PY 1993 VL 53 IS 8 BP 1883 EP 1888 PG 6 WC Oncology SC Oncology GA KY096 UT WOS:A1993KY09600030 PM 8385572 ER PT J AU SASAKI, H NISHII, H TAKAHASHI, H TADA, A FURUSATO, M TERASHIMA, Y SIEGAL, GP PARKER, SL KOHLER, MF BERCHUCK, A BOYD, J AF SASAKI, H NISHII, H TAKAHASHI, H TADA, A FURUSATO, M TERASHIMA, Y SIEGAL, GP PARKER, SL KOHLER, MF BERCHUCK, A BOYD, J TI MUTATION OF THE KI-RAS PROTOONCOGENE IN HUMAN ENDOMETRIAL HYPERPLASIA AND CARCINOMA SO CANCER RESEARCH LA English DT Article ID ONCOGENE ACTIVATION; TUMORIGENESIS; UTERUS; MODEL; JAPAN AB Previous studies have demonstrated that some human endometrial carcinomas contain an activating point mutation in codon 12 of the Ki-ras protooncogene. To examine the hypothesis that this mutation may occur at an earlier stage of neoplastic progression in the endometrium, we analyzed 89 samples of premalignant endometrial hyperplasia and an additional 84 samples of endometrial carcinoma for point mutations of Ki-ras codon 12. Mutations were found in all three types of endometrial hyperplasia, simple, complex, and atypical, with no clear evidence of a differential distribution in any particularly. Furthermore, the overall incidence of Ki-ras mutations in the hyperplasia specimens (16%) was similar to the incidence detected in carcinomas (18%), indicating that ras mutation may represent an early event in a subset of endometrial carcinomas. When the tissue samples were segregated as to country of origin, the frequency of this mutation was approximately 2-fold higher in hyperplasia and carcinoma samples from Japan than from the United States, where the incidence, clinicopathological characteristics, and risk factors for endometrial carcinoma differ dramatically. There was no apparent correlation, however, between ras mutation and any pathological, histological, or clinical parameter examined, except survival. The presence of a ras mutation was inversely associated with death from disease, suggesting that this molecular feature may characterize a subset of endometrial carcinomas with a good prognosis. C1 NIEHS,GYNECOL PATHOBIOL SECT,MOLEC CARCINOGENESIS LAB,POB 12233,RES TRIANGLE PK,NC 27709. JIKEI UNIV SCH MED,DEPT OBSTET & GYNECOL,TOKYO 105,JAPAN. JIKEI UNIV SCH MED,DEPT PATHOL,TOKYO 105,JAPAN. UNIV ALABAMA,SCH MED,DEPT PATHOL,BIRMINGHAM,AL 35294. UNIV ALABAMA,SCH MED,DEPT CELL BIOL & SURG,BIRMINGHAM,AL 35294. DUKE UNIV,SCH MED,DEPT OBSTET & GYNECOL,DURHAM,NC 27710. RI Siegal, Gene/A-8653-2009 NR 21 TC 144 Z9 151 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 APR 15 PY 1993 VL 53 IS 8 BP 1906 EP 1910 PG 5 WC Oncology SC Oncology GA KY096 UT WOS:A1993KY09600034 PM 8467512 ER PT J AU SUNIL, S ETO, K SINGH, VK SHINOHARA, T AF SUNIL, S ETO, K SINGH, VK SHINOHARA, T TI OLIGOPEPTIDES OF 3 TO 5 RESIDUES DERIVED FROM UVEITOPATHOGENIC SITES OF RETINAL S-ANTIGEN INDUCE EXPERIMENTAL AUTOIMMUNE UVEITIS (EAU) IN LEWIS RATS SO CELLULAR IMMUNOLOGY LA English DT Article ID HISTOCOMPATIBILITY COMPLEX BINDING; LYMPHOCYTE CROSS-REACTION; T-CELL RECOGNITION; MOLECULAR MIMICRY; AMINO-ACID; ADOPTIVE TRANSFER; ALPHA-TRANSDUCIN; PEPTIDE; UVEORETINITIS; SEQUENCE C1 NEI,IMMUNOL LAB,MOLEC BIOL SECT,BETHESDA,MD 20892. SANJAY GANDHI POST GRAD INST MED SCI,DEPT IMMUNOL,LUCKNOW 226001,INDIA. NR 42 TC 4 Z9 4 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD APR 15 PY 1993 VL 148 IS 1 BP 198 EP 207 DI 10.1006/cimm.1993.1102 PG 10 WC Cell Biology; Immunology SC Cell Biology; Immunology GA LB965 UT WOS:A1993LB96500017 PM 8495487 ER PT J AU XIE, QW TABOR, CW TABOR, H AF XIE, QW TABOR, CW TABOR, H TI DELETION MUTATIONS IN THE SPEED OPERON - SPERMIDINE IS NOT ESSENTIAL FOR THE GROWTH OF ESCHERICHIA-COLI SO GENE LA English DT Note DE S-ADENOSYLMETHIONINE DECARBOXYLASE; POLYAMINES; SPERMIDINE SYNTHASE ID S-ADENOSYLMETHIONINE DECARBOXYLASE; SACCHAROMYCES-CEREVISIAE; MUTANTS; BIOSYNTHESIS; DEFICIENT; GENE AB Null mutants of Escherichia coli were constructed that cannot synthesize spermidine. because of deletions in the gene encoding S-adenosylmethionine decarboxylase. These mutants are still able to grow at near normal rates in purified media deficient in polyamines. These results in E. coli differ from recent findings that null mutants of Saccharomyces cerevisiae and of Neurospora crassa have an absolute growth requirement for spermidine. C1 NIDDKD,BIOCHEM PHARMACOL LAB,BLDG 8,ROOM 223,BETHESDA,MD 20892. NR 13 TC 18 Z9 20 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD APR 15 PY 1993 VL 126 IS 1 BP 115 EP 117 DI 10.1016/0378-1119(93)90598-W PG 3 WC Genetics & Heredity SC Genetics & Heredity GA KX623 UT WOS:A1993KX62300016 PM 8472951 ER PT J AU STOJILKOVIC, SS KUKULJAN, M TOMIC, M ROJAS, E CATT, KJ AF STOJILKOVIC, SS KUKULJAN, M TOMIC, M ROJAS, E CATT, KJ TI MECHANISM OF AGONIST-INDUCED [CA2+]I OSCILLATIONS IN PITUITARY GONADOTROPHS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PAROTID ACINAR-CELLS; CALCIUM OSCILLATIONS; INOSITOL TRISPHOSPHATE; CA-2+ OSCILLATIONS; TUMOR PROMOTER; THAPSIGARGIN; HORMONE; ACTIVATION; MOBILIZATION; METABOLISM AB Gonadotropin-releasing hormone (GnRH) activates oscillatory Ca2+ signaling in pituitary gonadotrophs at a frequency (up to 25 min-1) that is dose-dependent and is determined by the degree of receptor-mediated inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) formation. Similar dose-dependent and frequency-modulated Ca2+ oscillations were elicited by intracellular administration of Ins(1,4,5)P3 and its nonhydrolyzable analogs, consistent with models in which Ins(1,4,5)P3 levels determine the frequency of Ca2+ oscillations but do not fluctuate in synchrony with [Ca2+]i. At constant agonist concentrations, Ca2+ spiking varied in amplitude, with a number of progressively larger transients before the onset of maximal oscillations, followed by a gradual decrease in spike amplitude that was accompanied by an increase in spiking frequency. The decline in the amplitude and increase in frequency of Ca2+ transients during stimulation by GnRH were not related to a decrease in the propagation of the Ca2+ signal within the cell but were associated with gradual depletion of the agonist-sensitive Ca2+ pool. Once initiated, the pattern of Ca2+ spiking was not altered by blockade of receptor occupancy, by inhibition of phospholipase C, or by reduction of extracellular [Ca2+]. Also, the endoplasmic reticulum (Ca2+)-ATPase blocker, thapsigargin, could substitute for Ins(1,4,5)P3, in initiating the oscillatory Ca2+ response. These findings indicate that although the Ins(1,4,5)P3 concentration determines the pattern of transients at the initiation of the oscillatory Ca2+ signal, maintenance of the signal does not require a sustained rise in Ins(1,4,5)P3. Since the frequency of Ca2+ oscillations is also influenced by depletion of luminal [Ca2+], it is possible that the Ins(1,4,5)P3-sensitive channels in the endoplasmic reticulum are tonically inhibited by high intraluminal Ca2+ levels and that Ins(1,4,5)P3 surmounts such inhibition by promoting Ca2+ discharge. When a critical level of Ca2+ discharge is attained, repetitive Ca2+ transients are generated by an autocatalytic mechanism in which a sustained rise in Ins(1,4,5)P3 is not an essential requirement. C1 NIDDKD,CELL BIOL & GENET BRANCH,BETHESDA,MD 20892. RP STOJILKOVIC, SS (reprint author), NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLDG 49,RM 6A-36,BETHESDA,MD 20892, USA. RI Tomic, Melanija/C-3371-2016 NR 32 TC 58 Z9 58 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 APR 15 PY 1993 VL 268 IS 11 BP 7713 EP 7720 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW979 UT WOS:A1993KW97900022 PM 8463300 ER PT J AU GUSOVSKY, F LUEDERS, JE KOHN, EC FELDER, CC AF GUSOVSKY, F LUEDERS, JE KOHN, EC FELDER, CC TI MUSCARINIC RECEPTOR-MEDIATED TYROSINE PHOSPHORYLATION OF PHOSPHOLIPASE C-GAMMA - AN ALTERNATIVE MECHANISM FOR CHOLINERGIC-INDUCED PHOSPHOINOSITIDE BREAKDOWN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SWISS 3T3 CELLS; CALCIUM ENTRY; G-PROTEINS; VASOPRESSIN; ACTIVATION; HYDROLYSIS; ENDOTHELIN; INHIBITOR; BOMBESIN; INFLUX AB In Chinese hamster ovary cells transfected with m5 muscarinic receptors, carbachol stimulates both calcium influx and calcium release from intracellular stores. The marine toxin maitotoxin (MTX) elicits a similar response on calcium influx. Carbachol- and MTX-induced calcium influx can be inhibited by the proposed blockers of receptor-operated calcium channels (ROCC), CAI and SK&F 96365. Both carbachol and MTX induce a significant increase in total protein tyrosine phosphorylation, which is dependent on extracellular calcium and can be inhibited by CAI and SK&F 96365. Phospholipase C-gamma was identified as one of the substrates subject to calcium-dependent tyrosine phosphorylation following carbachol or MTX stimulation. Carbachol-induced [H-3]inositol trisphosphate formation was partially inhibited by an inhibitor of tyrosine kinases, by removal of extracellular calcium, and by the inhibitor of receptor-operated calcium channels CAI suggesting that phosphorylation of phospholipase C-gamma plays a role in the muscarinic activation of phosphoinositide breakdown. Such an effect of carbachol is reminiscent of effects observed with peptide growth factors and represents a novel alternative signaling pathway for a muscarinic G protein-coupled receptor. C1 NIMH,CELL BIOL LAB,BLDG 36,RM 3A-15,BETHESDA,MD 20892. NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 29 TC 88 Z9 89 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 APR 15 PY 1993 VL 268 IS 11 BP 7768 EP 7772 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW979 UT WOS:A1993KW97900031 PM 7681827 ER PT J AU LEE, NH FRASER, CM AF LEE, NH FRASER, CM TI CROSS-TALK BETWEEN M1 MUSCARINIC ACETYLCHOLINE AND BETA-2-ADRENERGIC RECEPTORS - CAMP AND THE 3RD INTRACELLULAR LOOP OF M1 MUSCARINIC RECEPTORS CONFER HETEROLOGOUS REGULATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BETA-ADRENERGIC-RECEPTOR; PROTEIN-KINASE-C; SITE-DIRECTED MUTAGENESIS; CYCLIC-AMP; ADENYLATE-CYCLASE; PHOSPHOLIPASE-C; DOWN-REGULATION; PHOSPHORYLATION; ACTIVATION; EXPRESSION AB Genes encoding the m1 muscarinic (m1 mAChR) and beta2-adrenergic receptors (beta2AR) were stably co-expressed into Chinese hamster ovary (CHO) cells to study receptor regulation and cross-talk. Persistent activation of the beta2AR/adenylate cyclase pathway by isoproterenol leads to heterologous desensitization, internalization, and down-regulation of the m1 mAChR which is comparable, but smaller in magnitude, with that seen with persistent activation of the m1 mAChR by carbachol. This heterologous effect was mimicked by dibutyryl cAMP and forskolin and antagonized by the protein kinase A (PKA) inhibitor H-8. A potential consensus sequence for phosphorylation by PKA (Lys351-Arg-Lys-Thr354) exists on the third intracellular loop of the ml mAChR, suggesting that receptor phosphorylation by PKA may be involved in heterologous regulation. The loss of ml mAChRs induced by carbachol was not reversed by H-8, indicating that homologous regulation is not dependent on PKA. Recent evidence suggests that muscarinic agonist-mediated internalization of the m1 mAChR involves the third intracellular loop (i3) (Maeda, S., Lameh, J., Mallet, W. G., Philip, M., Ramachandran, J., and Sadee, W. (1990) FEBS Lett. 269, 386-388). Three deletion mutant receptors were constructed in which the majority, or small regions, of i3 were eliminated but the membrane proximal portions of the loop were left intact. Each of the mutants was co-expressed with the beta2AR in CHO cells. A small region in i3 was identified which is crucial for carbachol- and isoproterenol-promoted internalization and down-regulation. This region contains a series of 6 serine residues within an 8-amino acid stretch. A similar domain has been identified in the carboxyl tail of the beta2AR and has been proposed to participate in receptor internalization (Hausdorff, W. P., Campbell, P. T., Ostrowski, J., Yu, S. S., Caron, M. G., and Lefkowitz, R. J. (1991) Proc. Natl. Acad. Sci. U. S. A. 88, 2979-2983). C1 NIAAA,MOLEC NEUROBIOL SECT,NEUROGENET LAB,ROCKVILLE,MD 20852. NR 51 TC 53 Z9 55 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 APR 15 PY 1993 VL 268 IS 11 BP 7949 EP 7957 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW979 UT WOS:A1993KW97900057 PM 8385129 ER PT J AU CAMA, A SIERRA, MD QUON, MJ OTTINI, L GORDEN, P TAYLOR, SI AF CAMA, A SIERRA, MD QUON, MJ OTTINI, L GORDEN, P TAYLOR, SI TI SUBSTITUTION OF GLUTAMIC-ACID FOR ALANINE-1135 IN THE PUTATIVE CATALYTIC LOOP OF THE TYROSINE KINASE DOMAIN OF THE HUMAN INSULIN-RECEPTOR - A MUTATION THAT IMPAIRS PROTEOLYTIC PROCESSING INTO SUBUNITS AND INHIBITS RECEPTOR TYROSINE KINASE-ACTIVITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DEPENDENT PROTEIN-KINASE; ACANTHOSIS NIGRICANS; CELL-SURFACE; RESISTANT PATIENT; PLASMA-MEMBRANE; MUTANT ALLELES; ALPHA-SUBUNIT; BINDING-SITE; GENE; TRANSPORT AB The intracellular domain of the insulin receptor possesses activity as a tyrosine-specific protein kinase which is stimulated by insulin binding to the extracellular domain of the receptor. We have identified a patient with a genetic form of insulin resistance who is heterozygous for a mutation substituting Glu for Ala1135 in the putative ''catalytic loop'' of the tyrosine kinase domain of the receptor. In this investigation, the Glu1135 mutant receptor was expressed by transfection of mutant cDNA into NIH-3T3 cells. Like previously described mutations in the tyrosine kinase domain, the Glu1135 mutation impairs receptor tyrosine kinase activity and inhibits the ability of insulin to stimulate thymidine incorporation and receptor endocytosis. These data support the hypothesis that the receptor tyrosine kinase activity plays a necessary role in the ability of the receptor to mediate insulin action in vitro and in vivo. However, unlike previously described mutations in the intracellular domain of the receptor, the Glu1135 mutation impairs proteolytic cleavage of the proreceptor into separate subunits and impairs the transport of the receptor to the cell surface. These latter defects provide an explanation for the decrease in the number of receptors on the cell surface observed in the patient's circulating monocytes despite the fact that the mutant receptor is resistant to endocytosis and insulin-induced down-regulation. C1 UNIV CHIETI,FAC MED & SURG,IST PATOL UMANA & MED SOCIALE,CHIETI,ITALY. RP CAMA, A (reprint author), NIDDKD,DIABET BRANCH,BETHESDA,MD 20892, USA. RI Quon, Michael/B-1970-2008; OI Quon, Michael/0000-0002-9601-9915; Quon , Michael /0000-0002-5289-3707 NR 54 TC 29 Z9 30 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 APR 15 PY 1993 VL 268 IS 11 BP 8060 EP 8069 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW979 UT WOS:A1993KW97900070 PM 8096518 ER PT J AU MADDEN, MJ MORROW, CS NAKAGAWA, M GOLDSMITH, ME FAIRCHILD, CR COWAN, KH AF MADDEN, MJ MORROW, CS NAKAGAWA, M GOLDSMITH, ME FAIRCHILD, CR COWAN, KH TI IDENTIFICATION OF 5' AND 3' SEQUENCES INVOLVED IN THE REGULATION OF TRANSCRIPTION OF THE HUMAN MDR1 GENE INVIVO SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MULTIDRUG-RESISTANCE GENE; S-TRANSFERASE-PI; CELL-LINES; DRUG-RESISTANCE; FUNCTIONAL-ANALYSIS; GLYCOPROTEIN GENE; INITIATION SITE; OVARIAN-CANCER; DNA-SEQUENCES; HUMAN-TUMORS AB The human mdr1 gene encodes a putative drug efflux pump (P-glycoprotein) whose overexpression is associated with the development of multidrug resistance (MDR). The promoter and 5'-flanking DNA of this gene were isolated from a human genomic DNA library and used to prepare a series of chloramphenicol acetyltransferase (CAT) fusion vectors under the transcriptional control of the mdr1 promoter (mdrCAT vectors). Transient transfection of these mdrCAT vectors produced CAT activities similar to those produced by transfection of CAT vectors containing viral promoters. The regulation of mdr1 expression was examined in two MDR tumor cell lines selected for resistance to doxorubicin and their corresponding parental cell lines. Although nuclear run-on analysis indicates that the expression of the mdr1 gene in these two MDR cell lines is regulated by transcriptional mechanisms, mdrCAT expression was not significantly increased in either of these lines relative to parental cells. Thus, the sequences involved in the transcriptional regulation in these cells are apparently not included in the constructs studied (-4741 to +286). Analyses of a series of deletion constructs show that the basal mdr1 promoter activity is encoded by sequences that span a region adjacent to the transcription start site (-134 to +286) and that sequences 3' to the start of mdr1 transcription are necessary for proper initiation of transcription in vivo. Structural and functional studies indicate that an initiator (Inr) sequence surrounding the major transcription start site governs accurate initiation of mdr1 transcription. C1 NCI,MED BRANCH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 69 TC 88 Z9 90 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 APR 15 PY 1993 VL 268 IS 11 BP 8290 EP 8297 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW979 UT WOS:A1993KW97900102 PM 8096520 ER PT J AU OCONNOR, PM FERRIS, DK PAGANO, M DRAETTA, G PINES, J HUNTER, T LONGO, DL KOHN, KW AF OCONNOR, PM FERRIS, DK PAGANO, M DRAETTA, G PINES, J HUNTER, T LONGO, DL KOHN, KW TI G2 DELAY INDUCED BY NITROGEN-MUSTARD IN HUMAN-CELLS AFFECTS CYCLIN A/CDK2 AND CYCLIN-B1 CDC2-KINASE COMPLEXES DIFFERENTLY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID P34CDC2 PROTEIN-KINASE; HAMSTER OVARY CELLS; DNA DAMAGE; SACCHAROMYCES-CEREVISIAE; REGULATORY PHOSPHORYLATION; ALKYLATING-AGENTS; MAMMALIAN-CELLS; HELA-CELLS; RAD9 GENE; MITOSIS AB We investigated the temporal regulation of cyclin A- and B1-dependent kinases in human lymphoma cells treated with nitrogen mustard (HN2) and pentoxifylline, to determine whether the activity of these complexes correlated with cell cycle arrest induced by DNA damage. Cells were synchronized in G1/S, treated with HN2, and then postincubated with pentoxifylline. HN2-induced a protracted delay in G2 phase. This delay correlated with suppression of cyclin B1- and cdc2-kinase activities, and stabilization of hyperphosphorylated-cdc2 in the presence of similar cyclin B1 levels to those found in mitosis. HN2 had no discernible effect on the S phase activity of cyclin A- or cdk2-immune complexes. Entry of control cells into mitosis correlated with destruction of cyclin A, disappearance of cyclin A-bound cdk2 and decreased cdk2 kinase activity. G2 delay induced by HN2 was associated with stabilization of cyclin A, increased abundance of cyclin A-bound cdk2, and increased cdk2 activity. Cyclin A was also associated with cdc2, which, contrary to complexes containing cdk2, were only activated upon entry into mitosis. Pentoxifylline abrogated cell cycle arrest induced by aphidicolin and HN2 in human lymphoma cells. Pentoxifylline also reverted the activity of cyclin A- and B1-kinases in HN2-treated cells to approximately that observed in controls. Our findings suggest that delayed entry into mitosis following DNA damage correlates with suppression of cyclin B1/cdc2 and cyclin A/cdc2 complexes, while maintaining cyclin A/cdk2 complexes in an active state. Furthermore, we found that pentoxifylline disrupts the signal transduction pathway that regulates these complexes when damaged DNA is present, resulting in abrogation of cell cycle arrest. C1 PROGRAM RESOURCES INC DYN CORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. EUROPEAN MOLEC BIOL LAB,DIFFERENTIAT PROGRAM,W-6900 HEIDELBERG,GERMANY. WELLCOME CRC INST,CAMBRIDGE CB2 1QR,ENGLAND. SALK INST,MOLEC BIOL & VIROL LAB,SAN DIEGO,CA 92186. RP OCONNOR, PM (reprint author), NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,RM 5C-19,BLDG 37,BETHESDA,MD 20892, USA. FU Wellcome Trust NR 74 TC 157 Z9 158 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 APR 15 PY 1993 VL 268 IS 11 BP 8298 EP 8308 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW979 UT WOS:A1993KW97900103 PM 8463339 ER PT J AU YURCHENCO, PD SUNG, U WARD, MD YAMADA, Y OREAR, JJ AF YURCHENCO, PD SUNG, U WARD, MD YAMADA, Y OREAR, JJ TI RECOMBINANT LAMININ-G DOMAIN MEDIATES MYOBLAST ADHESION AND HEPARIN BINDING SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BACULOVIRUS EXPRESSION SYSTEM; GLOBULAR DOMAIN; CELL-ADHESION; B-CHAINS; A-CHAIN; INTEGRIN; IDENTIFICATION; SUBUNIT; PROTEIN; POLYMERIZATION AB A recombinant mouse cDNA fragment encoding the G domain of the basement membrane laminin A chain was inserted into the eukaryotic baculovirus expression vector pVL1392 modified to produce fusion proteins carrying the rat fibronectin signal. G domain, expressed and secreted as a soluble glycoprotein (rG), was purified to near homogeneity without denaturing conditions. By electron microscopy rG possessed the same globular morphology as found in laminin. rG was cleaved with elastase into two fragments, rG70 and rG50. The latter fragment possessed the identical N terminus as laminin fragment E3 and both shared the same secondary structure by circular dichroism. rG, and rG containing a deletion (residues 2980-3028) rich in basic residues bound to heparin with similar avidity. rG also promoted mouse C2 myoblast cell adhesion and spreading, and evaluation of myoblasts on rG70 and rG50 further revealed that cell spreading was an activity confined to the more proximal sequence of rG70. Antibody specific for rG70 completely blocked cell adhesion to intact laminin in contrast to antibody specific for E3. Finally rG did not inhibit laminin polymerization. These data support the role of G domain in cell and heparin binding, but not laminin self-assembly, and the approach provides a means to further characterize these functions. C1 ROBERT WOOD JOHNSON MED SCH,DEPT MICROBIOL & MOLEC GENET,PISCATAWAY,NJ 08854. ROBERT WOOD JOHNSON MED SCH,DEPT PATHOL,PISCATAWAY,NJ 08854. NIDR,BETHESDA,MD 20892. FU NIDDK NIH HHS [DK36425, R01 DK036425] NR 38 TC 76 Z9 76 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 APR 15 PY 1993 VL 268 IS 11 BP 8356 EP 8365 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW979 UT WOS:A1993KW97900110 PM 8463343 ER PT J AU AHUJA, SS PALIOGIANNI, F YAMADA, H BALOW, JE BOUMPAS, DT AF AHUJA, SS PALIOGIANNI, F YAMADA, H BALOW, JE BOUMPAS, DT TI EFFECT OF TRANSFORMING GROWTH-FACTOR-BETA ON EARLY AND LATE ACTIVATION EVENTS IN HUMAN T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID RETINOBLASTOMA SUSCEPTIBILITY GENE; TYROSINE PHOSPHORYLATION; INTERLEUKIN-2 RECEPTOR; LYMPHOCYTES-T; TGF-BETA; EXPRESSION; PROTEIN; CYCLE; PROLIFERATION; GENERATION AB Transforming growth factors-beta (TGF-beta) modulate immune responses by inhibiting the proliferation of normal T lymphocytes. To examine the mechanism(s) of this inhibition, we studied the effect of TGF-beta1 on selected events associated with the initiation and progression of the T lymphocyte cell cycle. Human peripheral blood T cells were stimulated with anti-CD3 mAb, PHA, PMA, or ionomycin, alone or in combination. TGF-beta1 (0.5 to 10 ng/ml) partially inhibited the tyrosine phosphorylation of a 100-kDa protein, but not the calcium influx when cells were stimulated via TCR. Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2Ralpha, IL-2Rbeta, and transferrin receptor) were not affected by TGF-beta1. Total cellular RNA synthesis and cell size after T cell stimulation were also not affected by TGF-beta1. However, TGF-beta1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. This inhibition was associated with the down-regulation of IL-2-mediated tyrosine phosphorylation of proteins of 120, 100, 85, 75, and 50 kDa. TGF-beta1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. These results suggest that TGF-beta1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals. C1 USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20889. RP AHUJA, SS (reprint author), NIDDKD,KIDNEY DIS SECT,BLDG 10,ROOM 3N114,BETHESDA,MD 20892, USA. NR 39 TC 145 Z9 148 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 APR 15 PY 1993 VL 150 IS 8 BP 3109 EP 3118 PN 1 PG 10 WC Immunology SC Immunology GA KX321 UT WOS:A1993KX32100001 PM 8468460 ER PT J AU DREW, PD LONERGAN, M GOLDSTEIN, ME LAMPSON, LA OZATO, K MCFARLIN, DE AF DREW, PD LONERGAN, M GOLDSTEIN, ME LAMPSON, LA OZATO, K MCFARLIN, DE TI REGULATION OF MHC CLASS-I AND BETA-2-MICROGLOBULIN GENE-EXPRESSION IN HUMAN NEURONAL CELLS - FACTOR BINDING TO CONSERVED CIS-ACTING REGULATORY SEQUENCES CORRELATES WITH EXPRESSION OF THE GENES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; INTERFERON-INDUCED TRANSCRIPTION; TISSUE-SPECIFIC EXPRESSION; EMBRYONAL CARCINOMA-CELLS; INCREASE TRANSCRIPTION; NEGATIVE REGULATION; CONSENSUS SEQUENCE; NUCLEAR FACTOR; REL ONCOGENE AB MHC class I molecules are coexpressed with beta2-microglobulin (beta2-M) on many somatic cells. However, these proteins are normally not present on cells of the central nervous system (CNS). Cells derived from human neuroblastomas were used as a model for investigating the molecular basis for the paucity of MHC class I and beta2-M gene expression in neural cells and for the induction of these genes by two cytokines, IFN-gamma, and TNF-alpha. These cytokines independently increased MHC class I and beta2-M cell surface expression on the neuroblastoma cell lines. IFN-gamma or TNF-alpha also increased MHC class I and beta2-M steady-state RNA levels and the expression of MHC class I and beta2-M CAT reporter constructs transiently transfected into the neuroblastoma cell lines, indicating that the cytokines acted by increasing the transcription of these genes. MHC class I and beta2-M genes share two conserved regulatory elements, an NFkappaB-like site and the IFN consensus sequence, that act as a constitutive enhancer and an IFN-responsive element, respectively. Low MHC class I and beta2-M gene expression in these cells was accounted for by undetectable to low factor binding activity specific for the above regulatory elements of these genes. TNF-alpha increased factor binding activity specific for the NFkappaB-like elements and IFN-gamma increased factor binding activity specific for the IFN consensus sequence elements of the MHC class I and beta2-M genes, but not vice versa. Taken together, our results indicated that IFN-gamma and TNF-alpha increased MHC class I and beta2-M gene expression in the neuroblastoma cell lines by inducing factor binding to the regulatory elements present in both genes. C1 NINCDS,NEUROCHEM LAB,BETHESDA,MD 20892. NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. BRIGHAM & WOMENS HOSP,CTR NEUROL DIS,DEPT MED,DIV NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP DREW, PD (reprint author), NINCDS,NEUROIMMUNOL BRANCH,BLDG 10,RM 5B-16,BETHESDA,MD 20892, USA. NR 59 TC 92 Z9 93 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 APR 15 PY 1993 VL 150 IS 8 BP 3300 EP 3310 PN 1 PG 11 WC Immunology SC Immunology GA KX321 UT WOS:A1993KX32100021 PM 8468472 ER PT J AU EMOTO, M NAITO, T NAKAMURA, R YOSHIKAI, Y AF EMOTO, M NAITO, T NAKAMURA, R YOSHIKAI, Y TI DIFFERENT APPEARANCE OF GAMMA-DELTA-T-CELLS DURING SALMONELLOSIS BETWEEN ITY(R) AND ITY(S) MICE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HEAT-SHOCK PROTEINS; INNATE RESISTANCE; GENETIC-CONTROL; TYPHIMURIUM; LYMPHOCYTES; INFECTION; MACROPHAGES; EXPRESSION; PERITONEAL; ANTIGEN AB Ity gene, which is believed to be a single gene on proximal mouse chromosome 1, determines susceptibility to Salmonella infection. We have recently demonstrated that the gammadeltaT cells specific for purified protein derivative appear at the early stage after infection with Salmonella choleraesuis strain 31 N-1 (avirulent strain) in mice. In the present study, we compared the appearance of the gammadeltaT cells in Ity(r) and Ity(s) mice after infection with S. choleraesuis in an attempt to elucidate the role of the gammadeltaT cells in the in vivo effect of the Ity locus on murine salmonellosis, The numbers of gammadelta T cells in the peritoneal cavity and liver were significantly larger in DBA/2 (Ity(r)) mice than those in BALB/c (Ity(s)) mice after infection with a sublethal dose of S. choleraesuis. C.D2 Ity(r) mice, which are BALB/c mice with Ity(r) allele, also showed a significant increase in the number of the gammadelta T cells at the early stage after infection. Similar results in different appearances of the gammadelta T cells could be obtained between BALB/c and DBA/2 mice after infection with Mycobacterium bovis, bacillus Calmette-Guerin. The peritoneal adherent cells of DBA/2 mice infected with S. choleraesuis, which expressed a large amount of heat shock/stress protein (hsp) homologous to the mycobacterial 65-kDa hsp, induced significantly higher level of expansion of the peritoneal gammadelta T cells in normal mice in vivo and in vitro than did those of BALB/c mice infected with S. choleraesuis, which expressed a lesser amount of the hsp. These results suggest that the Ity locus may be closely related to the expression of hsp by macrophages after infection with Salmonella, which in turn stimulate the gammadelta T cells in the host during an early phase of salmonellosis. C1 NAGOYA UNIV,SCH MED,DIS MECH & CONTROL RES INST,GERMFREE LIFE LAB,SHOWA KU,NAGOYA,AICHI 466,JAPAN. NIH,DEPT CELLULAR IMMUNOL,BETHESDA,MD 20892. NR 37 TC 28 Z9 28 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 APR 15 PY 1993 VL 150 IS 8 BP 3411 EP 3420 PN 1 PG 10 WC Immunology SC Immunology GA KX321 UT WOS:A1993KX32100032 PM 8468480 ER PT J AU WAHL, SM COSTA, GL CORCORAN, M WAHL, LM BERGER, AE AF WAHL, SM COSTA, GL CORCORAN, M WAHL, LM BERGER, AE TI TRANSFORMING GROWTH-FACTOR-BETA MEDIATES IL-1-DEPENDENT INDUCTION OF IL-1 RECEPTOR ANTAGONIST SO JOURNAL OF IMMUNOLOGY LA English DT Article ID II INTERLEUKIN-1 RECEPTOR; SYNOVIAL INFLAMMATION; CYTOKINE PRODUCTION; TGF-BETA; EXPRESSION; INHIBITION; MODULATION; FAMILY; BINDS; ENCEPHALOMYELITIS AB Transforming growth factor-beta (TGF-beta) is a potent immunomodulatory molecule that promotes inflammation through recruitment of monocytes and induction of IL-1 and other cytokines. These proinflammatory processes may be modulated by the ability of TGF-beta to induce de novo synthesis and secretion of an IL-1 receptor antagonist (IL-1 ra) that binds to and blocks IL-1 receptors. In this study, we show that the addition of TGF-beta to human peripheral blood monocytes induced the sequential transcription of the 1.8-kb mRNA for IL-1beta and for IL-1 ra. The expression of detectable mRNA and synthesis of IL-1beta peptide routinely preceded that for IL-1 ra, suggesting possible dependency of IL-1 ra generation on IL-1beta. Antibody to IL-1 blocked TGF-beta induction of IL-1 ra mRNA expression demonstrating an unique IL-1-dependent induction of its own antagonist. Confirmatory evidence that IL-1 participates in the generation of IL-1 ra was obtained when exogenously added IL-1 induced and, IL-1 receptor antagonist blocked, IL-1 ra transcription. Thus, these data suggest that TGF-beta, after release at a site of inflammation, induces synthesis of IL-1 that participates in the initial cytokine cascade central to an inflammatory response, and then triggers the generation of its own natural inhibitor by autocrine or paracrine pathways. This TGF-beta-induced IL-1-dependent induction of IL-1 ra may provide a negative feedback loop, thereby promoting the resolution of an inflammatory response. C1 UPJOHN CO,DEPT CELL BIOL,KALAMAZOO,MI 49007. RP WAHL, SM (reprint author), NIDR,IMMUNOL LAB,BLDG 30,ROOM 331,BETHESDA,MD 20892, USA. NR 50 TC 96 Z9 96 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 APR 15 PY 1993 VL 150 IS 8 BP 3553 EP 3560 PN 1 PG 8 WC Immunology SC Immunology GA KX321 UT WOS:A1993KX32100048 PM 8468489 ER PT J AU MURPHY, WJ CONLON, KC SAYERS, TJ WILTROUT, RH BACK, TC ORTALDO, JR LONGO, DL AF MURPHY, WJ CONLON, KC SAYERS, TJ WILTROUT, RH BACK, TC ORTALDO, JR LONGO, DL TI ENGRAFTMENT AND ACTIVITY OF ANTI-CD3-ACTIVATED HUMAN PERIPHERAL-BLOOD LYMPHOCYTES TRANSFERRED INTO MICE WITH SEVERE COMBINED IMMUNE-DEFICIENCY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SEVERE COMBINED IMMUNODEFICIENCY; MOUSE AB Human PBL (huPBL) were activated with anti-CD3 mAb in vitro and then were transferred into mice with severe combined immune deficiency (SCID) to determine the effect of activation on engraftment and to determine if the engrafted human cells could provide antitumor effects in mice. Some mice were also treated with human rIL-2 after huPBL transfer. Mice were analyzed 6 to 8 wk after cell transfer and the number of human cells in the peripheral lymphoid organs was determined. Mice receiving anti-CD3-activated huPBL demonstrated a significant increase in the incidence of human T cell engraftment in the periphery as assessed by flow cytometry. Human cells were also detected in the murine thymus after anti-CD3 stimulation indicating that human T cells can migrate to the murine thymus provided that they are activated before the transfer. The transfer of anti-CD3-activated huPBL also resulted in an xenogeneic graft-vs-host reaction manifested primarily by proliferation of murine splenic hemopoietic cells. When SCID mice received the human colon carcinoma HT29, the concurrent transfer of anti-CD3-activated human cells resulted in a significant increase in survival. However, the human cells displayed low cytolytic activity toward human tumor targets when they were recovered from the lymphoid organs of the SCID recipients. Supernatants from the anti-CD3-activated cells were able to inhibit the growth of HT29 in vitro, partly because of the presence of IFN-gamma, suggesting that the human T cells are producing cytokines in vivo that have antitumor effects. Thus, the use of anti-CD3-activated huPBL in SCID mice may be of value for optimizing human cell engraftment in the human/mouse lymphoid chimeras and may be used to evaluate potential anti-neoplastic therapies that employ human effector cells. C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RP MURPHY, WJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,BLDG 567,FREDERICK,MD 21702, USA. RI Sayers, Thomas/G-4859-2015 NR 16 TC 48 Z9 48 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 APR 15 PY 1993 VL 150 IS 8 BP 3634 EP 3642 PN 1 PG 9 WC Immunology SC Immunology GA KX321 UT WOS:A1993KX32100056 PM 8468492 ER PT J AU ALEXANDER, EL PLITT, JR ANSARI, A EHRLICH, H BUGAWAN, D FRONEK, Z AF ALEXANDER, EL PLITT, JR ANSARI, A EHRLICH, H BUGAWAN, D FRONEK, Z TI MULTIPLE DQA1/DQB1 ALLELES LINKED TO HLA-DRB1 GENES ENCODING HLA-DR3, DR5, OR DRW6 - GENE DOSAGE EFFECT IN PRIMARY SJOGRENS-SYNDROME (PSS) AND PRESUMED LUPUS VARIANTS (PLVS) SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. CETUS CORP,EMERYVILLE,CA 94608. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A237 EP A237 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601367 ER PT J AU AMIN, AR SWENSON, CD XUE, B ISHIDA, Y NAIR, BG PATEL, TB CHUSED, TM THORBECKE, GJ AF AMIN, AR SWENSON, CD XUE, B ISHIDA, Y NAIR, BG PATEL, TB CHUSED, TM THORBECKE, GJ TI 2ND MESSENGER SYSTEMS IN THE UP-REGULATION OF IGD RECEPTORS ON T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NYU,SCH MED,NEW YORK,NY 10016. UNIV TENNESSEE CTR HLTH SCI,MEMPHIS,TN 38163. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A88 EP A88 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600497 ER PT J AU APASOV, SG SITKOVSKY, MV AF APASOV, SG SITKOVSKY, MV TI DEVELOPMENT AND ANTIGEN-SPECIFICITY OF CD8+ CYTOTOXIC T-LYMPHOCYTES IN BETA-2-MICROGLOBULIN NEGATIVE, MHC CLASS-I-DEFICIENT MICE IN RESPONSE TO IMMUNIZATION WITH TUMOR-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A190 EP A190 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601091 ER PT J AU BADOLATO, R WANG, JM KELVIN, D OPPENHEIM, JJ AF BADOLATO, R WANG, JM KELVIN, D OPPENHEIM, JJ TI SERUM AMYLOID-A IS A POTENT CHEMOTACTIC FACTOR FOR MONOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21701. RI Badolato, Raffaele/A-8081-2010 OI Badolato, Raffaele/0000-0001-7375-5410 NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A217 EP A217 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601248 ER PT J AU BENHAMOU, M RYBA, N NISHIKATA, H SIRAGANIAN, RP AF BENHAMOU, M RYBA, N NISHIKATA, H SIRAGANIAN, RP TI INVOLVEMENT OF P72(SYK) IN FC-EPSILON-RI SIGNALING SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A222 EP A222 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601281 ER PT J AU BERENSTEIN, E SIRAGANIAN, RP BENHAMOU, M AF BERENSTEIN, E SIRAGANIAN, RP BENHAMOU, M TI RAT FC-EPSILON-RI IS A FUNCTIONAL RECEPTOR FOR RAT IGG2A SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A223 EP A223 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601287 ER PT J AU BIRAGYN, A TURETSKAYA, RL KUPRASH, DV UDALOVA, IA NEDOSPASOV, SA AF BIRAGYN, A TURETSKAYA, RL KUPRASH, DV UDALOVA, IA NEDOSPASOV, SA TI TRANSCRIPTIONAL REGULATION OF TNF-ALPHA IN THE MURINE MACROPHAGE CELL-LINE ANA-1 SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,DCT,BRMPILMI,FREDERICK,MD 21702. ENGELHART MOLEC BIOL INST,MOSCOW 117984,RUSSIA. RI Nedospasov, Sergei/J-5936-2013; Nedospasov, Sergei/L-1990-2015; Kuprash, Dmitry/O-4899-2015; Nedospasov, Sergei/Q-7319-2016 OI Kuprash, Dmitry/0000-0002-1488-4148; NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A55 EP A55 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600311 ER PT J AU BISWAS, P POLI, G FRANZOSO, G SIEBENLIST, U FAUCI, AS AF BISWAS, P POLI, G FRANZOSO, G SIEBENLIST, U FAUCI, AS TI ENDOGENOUS TUMOR-NECROSIS-FACTOR AND NF-KAPPA-B REGULATE HUMAN-IMMUNODEFICIENCY-VIRUS REPLICATION IN PROMONOCYTIC U937 CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A297 EP A297 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601712 ER PT J AU BONOMO, A KEHN, P SHEVACH, EM AF BONOMO, A KEHN, P SHEVACH, EM TI IDENTIFICATION OF IMMATURE T-CELLS IN THE PERIPHERAL LYMPHOID-TISSUE OF NEWBORN MICE SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A9 EP A9 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600045 ER PT J AU BOULAY, JL PAUL, WE AF BOULAY, JL PAUL, WE TI THE PUTATIVE LYMPHOKINE P600 IS A MEMBER OF THE IL-4 FAMILY SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A11 EP A11 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600058 ER PT J AU BOYD, LF CORR, MP KOZLOWSKI, S RIBAUDO, R MARGULIES, DH AF BOYD, LF CORR, MP KOZLOWSKI, S RIBAUDO, R MARGULIES, DH TI COMPARISON OF VARIOUS METHODS TO EVALUATE THE BINDING OF ANTIGENIC PEPTIDES TO A CLASS-I MHC MOLECULE SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A40 EP A40 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600222 ER PT J AU CASPI, RR CHAN, CC FUJINO, Y NAJAFIAN, F GROVER, S HANSEN, CT WILDER, RL AF CASPI, RR CHAN, CC FUJINO, Y NAJAFIAN, F GROVER, S HANSEN, CT WILDER, RL TI RECRUITMENT OF NAIVE T-CELLS PLAYS A PIVOTAL ROLE IN A T-CELL-MEDIATED AUTOIMMUNE-DISEASE, EXPERIMENTAL AUTOIMMUNE UVEORETINITIS (EAU) SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. VRB,BETHESDA,MD 20892. NIAMS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A80 EP A80 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600459 ER PT J AU CHIRMULE, N OYAIZU, N SAXINGER, C GHRAYEB, J PAHWA, S AF CHIRMULE, N OYAIZU, N SAXINGER, C GHRAYEB, J PAHWA, S TI NEF PROTEIN OF HIV-1 HAS B-CELL STIMULATORY ACTIVITY SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CENTOCOR INC,MALVERN,PA. N SHORE UNIV HOSP,CORNELL UNIV MED COLL,DEPT PEDIAT,MANHASSET,NY 11030. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A242 EP A242 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601396 ER PT J AU CHRIST, M KULKARNI, A MCCARTNEYFRANCIS, N GEISER, A MACKALL, C GRESS, R HINES, K FLANDERS, K ROBERTS, A SPORN, M WARD, J WAHL, S KARLSSON, S AF CHRIST, M KULKARNI, A MCCARTNEYFRANCIS, N GEISER, A MACKALL, C GRESS, R HINES, K FLANDERS, K ROBERTS, A SPORN, M WARD, J WAHL, S KARLSSON, S TI IMMUNE DYSREGULATION IN TGF-BETA-1 KNOCKOUT MICE SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NINCDS,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A172 EP A172 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600991 ER PT J AU CHU, CC PAUL, WE MAX, EE AF CHU, CC PAUL, WE MAX, EE TI APHIDICOLIN, AN INHIBITOR OF DNA-SYNTHESIS, BLOCKS IMMUNOGLOBULIN CLASS SWITCHING SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. US FDA CBER,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A171 EP A171 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600984 ER PT J AU CLARK, DA HIRTE, H FLANDERS, KC VINCE, G STARKEY, P AF CLARK, DA HIRTE, H FLANDERS, KC VINCE, G STARKEY, P TI MURINE AND HUMAN DECIDUA-ASSOCIATED NATURAL SUPPRESSOR CELLS RELEASE A NOVEL TYPE OF TRANSFORMING GROWTH-FACTOR-BETA TYPE-2 SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 MCMASTER UNIV,HAMILTON L8N 3Z5,ONTARIO,CANADA. NIH,BETHESDA,MD 20892. UNIV OXFORD,OXFORD,ENGLAND. NR 0 TC 5 Z9 5 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 APR 15 PY 1993 VL 150 IS 8 BP A4 EP A4 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600022 ER PT J AU CLERICI, M SISON, AV BERZOFSKY, IA RAKUSAN, T BRANDT, C VENZON, DJ SEVER, JL SHEARER, GM AF CLERICI, M SISON, AV BERZOFSKY, IA RAKUSAN, T BRANDT, C VENZON, DJ SEVER, JL SHEARER, GM TI HIV-SPECIFIC T-HELPER CELL-ACTIVITY IN NEWBORNS OF HIV-INFECTED WOMEN SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20007. CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC 20010. RI Venzon, David/B-3078-2008 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A180 EP A180 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601036 ER PT J AU COLIGAN, JE WADSWORTH, SA CHANG, AC AF COLIGAN, JE WADSWORTH, SA CHANG, AC TI EXPRESSION OF MEROSIN IN THE THYMUS AND ITS INTERACTION WITH THYMOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A9 EP A9 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600048 ER PT J AU CORR, M BOYD, LF PADLAN, EA MARGULIES, DH AF CORR, M BOYD, LF PADLAN, EA MARGULIES, DH TI SELF PEPTIDES ISOLATED FROM H-2DD - 4 OF 9 PEPTIDE RESIDUES ARE THE H-2DD MOTIF SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NIDDK,BETHESDA,MD 20892. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A40 EP A40 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600224 ER PT J AU COX, GW SHEFFLER, LA WINK, DA MELILLO, G AF COX, GW SHEFFLER, LA WINK, DA MELILLO, G TI NITRIC OXIDE-RELEASING COMPOUNDS AUGMENT THE ACTIVITY OF AN ADP-RIBOSYLTRANSFERASE IN MURINE MACROPHAGES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,DCT,BRMP,MOLEC IMMUNOREGULAT,FREDERICK,MD 21702. NCI,FCROC,DCE,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A54 EP A54 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600304 ER PT J AU DASTYCH, J BIANCHINE, PJ METCALFE, DD AF DASTYCH, J BIANCHINE, PJ METCALFE, DD TI MURINE BONE-MARROW DERIVED MAST-CELLS ADHERE TO FIBRONECTIN FOLLOWING STIMULATION BY STEM-CELL FACTOR SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A146 EP A146 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600840 ER PT J AU DEBRE, P RUSCETTI, FW DALLOUL, AH OUAAZ, F BLANC, C DUJONG, R MOSSALAYI, MD AF DEBRE, P RUSCETTI, FW DALLOUL, AH OUAAZ, F BLANC, C DUJONG, R MOSSALAYI, MD TI TGF-BETA AND CD8+ THYMOCYTES DOWN-REGULATE HUMAN T-CELL DEVELOPMENT SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 HOP LA PITIE SALPETRIERE,MOLEC IMMUNOHEMATOL UNIT,PARIS,FRANCE. NCI,LEUKOCYTE BIOL LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A30 EP A30 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600166 ER PT J AU DEMAREST, JF PANTALEO, G ZOLLAPAZNER, S BANSAL, G KOENIG, S FAUCI, AS AF DEMAREST, JF PANTALEO, G ZOLLAPAZNER, S BANSAL, G KOENIG, S FAUCI, AS TI ANTI-V3 ANTIBODIES FAIL TO INHIBIT CELL-TO-CELL TRANSMISSION OF HIV-1 SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. MED IMMUNE INC,GAUTHERSBURG,MD. NYU,DEPT PATHOL,NEW YORK,NY 10003. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A317 EP A317 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601827 ER PT J AU DIBRINO, M PARKER, KC BIDDISON, W COLIGAN, JE AF DIBRINO, M PARKER, KC BIDDISON, W COLIGAN, JE TI ENDOGENOUS PEPTIDES BOUND TO CLASS-I MHC MOLECULES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NINCDS,NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A83 EP A83 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600472 ER PT J AU DING, L LINSLEY, PS HUANG, LY GERMAIN, RN SHEVACH, EM AF DING, L LINSLEY, PS HUANG, LY GERMAIN, RN SHEVACH, EM TI IL-10 INHIBITS MACROPHAGE (M0) COSTIMULATORY ACTIVITY BY SELECTIVELY INHIBITING THE UP-REGULATION OF B7 EXPRESSION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. BRISTOL MYERS SQUIBB,SEATTLE,WA 98121. NR 0 TC 4 Z9 4 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 APR 15 PY 1993 VL 150 IS 8 BP A180 EP A180 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601035 ER PT J AU DRUEY, KM DEGUCHI, Y KEHRL, JH AF DRUEY, KM DEGUCHI, Y KEHRL, JH TI EXPRESSION OF THE HUMAN HOMEOBOX GENE HLX IN BACTERIA AND DEMONSTRATION OF SPECIFIC DNA-BINDING SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A264 EP A264 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601519 ER PT J AU DURUM, S WEST, M MUEGGE, K AF DURUM, S WEST, M MUEGGE, K TI RECOMBINATION SEQUENCE-BINDING PROTEIN IN REARRANGING THYMOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21702. PRI,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A189 EP A189 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601088 ER PT J AU EISENSTEIN, EM CHUA, K STROBER, W AF EISENSTEIN, EM CHUA, K STROBER, W TI PURIFIED B-CELLS FROM PATIENTS WITH COMMON VARIABLE IMMUNODEFICIENCY CAN BE INDUCED INVITRO TO EXPRESS C-GAMMA MESSENGER-RNA SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A95 EP A95 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600539 ER PT J AU FALK, LA FREY, JL BURNS, CM MCVICAR, DW FERRIS, D LONGO, DL KENNY, JJ ORTALDO, JR AF FALK, LA FREY, JL BURNS, CM MCVICAR, DW FERRIS, D LONGO, DL KENNY, JJ ORTALDO, JR TI EXPRESSION OF A NOVEL 220,000 DALTON CD45-RELATED PROTEIN ON HUMAN NK CELLS - DIFFERENTIAL MODULATION OF NK CELL-FUNCTION VIA STIMULATION OF SPECIFIC CD45 EPITOPES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 PRI,DYNCORP,FREDERICK,MD 21702. NCI,FCRDC,BRMP,FREDERICK,MD 21702. NCI,BRMP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A303 EP A303 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601746 ER PT J AU FRANCO, A APPELLA, E KAGNOFF, M CHOWERS, Y GREY, HM SETTE, A AF FRANCO, A APPELLA, E KAGNOFF, M CHOWERS, Y GREY, HM SETTE, A TI T-CELL RESPONSE TO A-GLIADIN IN CELIAC-DISEASE - DIFFERENTIAL PRESENTATION CAPACITIES OF EBV-B-CELLS AND FIBROBLASTS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 CYTEL,SAN DIEGO,CA 92121. NCI,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. NR 0 TC 0 Z9 0 U1 1 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 APR 15 PY 1993 VL 150 IS 8 BP A175 EP A175 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601010 ER PT J AU FRANZOSO, G BOURS, V AZARENKO, V MICHIYO, SP YAMAGUCHI, T SIEBENLIST, U AF FRANZOSO, G BOURS, V AZARENKO, V MICHIYO, SP YAMAGUCHI, T SIEBENLIST, U TI BCL-3 CAN CAUSE KAPPA-B-DEPENDENT TRANSACTIVATION BY AN INDIRECT MECHANISM SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A205 EP A205 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601178 ER PT J AU GAUEN, LKT LETOURNEUR, F KONG, ANT SAMELSON, LE KLAUSNER, RD SHAW, AS AF GAUEN, LKT LETOURNEUR, F KONG, ANT SAMELSON, LE KLAUSNER, RD SHAW, AS TI THE P59(FYN) TYROSINE KINASE ASSOCIATES WITH CD3 EPSILON CYTOPLASMIC RESIDUES REQUIRED FOR T-CELL ACTIVATION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. NR 2 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A269 EP A269 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601549 ER PT J AU GAZZINELLI, RT HIENY, S WYNN, T WOLF, S SHER, A AF GAZZINELLI, RT HIENY, S WYNN, T WOLF, S SHER, A TI IL-12 IS REQUIRED FOR T-INDEPENDENT INDUCTION OF IFN-GAMMA BY TOXOPLASMA-GONDII AND MEDIATES RESISTANCE AGAINST THE PARASITE IN SCID MICE SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LPO,BETHESDA,MD 20892. GENET INST,CAMBRIDGE,MA 02140. NR 0 TC 3 Z9 3 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 APR 15 PY 1993 VL 150 IS 8 BP A86 EP A86 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600488 ER PT J AU GERMOLEC, DR YOSHIDA, T KAYAMA, F LUSTER, MI AF GERMOLEC, DR YOSHIDA, T KAYAMA, F LUSTER, MI TI CYTOKINE PRODUCTION IN CULTURED LIVER SLICES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIEHS,STB,ENVIRONM IMMUNOL GRP,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A124 EP A124 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600709 ER PT J AU HAKIM, FT GAZZINELLI, R OSWALD, IP PAYNE, SM SHER, A SHEARER, GM AF HAKIM, FT GAZZINELLI, R OSWALD, IP PAYNE, SM SHER, A SHEARER, GM TI MODULATION OF HOST DEFENSES TO PARASITIC INFECTION DURING ACUTE GRAFT-VS-HOST REACTION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,EXPT IMMUNOL BRANCH,BETHESDA,MD 20892. RI OSWALD, Isabelle/A-8497-2013 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A231 EP A231 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601335 ER PT J AU HAMAWY, MM MERGENHAGEN, SE SIRAGANIAN, RP AF HAMAWY, MM MERGENHAGEN, SE SIRAGANIAN, RP TI AGGREGATING THE HIGH-AFFINITY IGE RECEPTORS (FC-EPSILON-RI) AND ADHERENCE TO FIBRONECTIN SYNERGISTICALLY REGULATE TYROSINE PHOSPHORYLATION OF PP125(FAK) IN RAT BASOPHILIC LEUKEMIA (RBL-2H3) CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A250 EP A250 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601440 ER PT J AU HARIHARAN, K NARA, PL POSNER, MR KANG, CY AF HARIHARAN, K NARA, PL POSNER, MR KANG, CY TI IDENTIFICATION OF A NEW NEUTRALIZING EPITOPE CONFORMATIONALLY AFFECTED BY THE ATTACHMENT OF CD4 TO GP120 SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,BOSTON,MA 02215. NCI,FCRDC,DCE,BCP,LTCB,VIRUS BIOL UNIT,FREDERICK,MD 21701. IDEC PHARMACEUT CORP,LA JOLLA,CA 92037. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A241 EP A241 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601390 ER PT J AU HINES, KL ALLEN, JB IMAMICHI, T MCCARTHY, JB FURCHT, LT WAHL, SM AF HINES, KL ALLEN, JB IMAMICHI, T MCCARTHY, JB FURCHT, LT WAHL, SM TI FIBRONECTIN PEPTIDES INHIBIT INFLAMMATORY CELL INFILTRATION AND ARTHRITIS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NR 0 TC 2 Z9 2 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 APR 15 PY 1993 VL 150 IS 8 BP A139 EP A139 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600797 ER PT J AU HIOE, CE KLAPPER, DG DETERDING, L TOMER, K FRELINGER, J AF HIOE, CE KLAPPER, DG DETERDING, L TOMER, K FRELINGER, J TI ISOLATION AND IDENTIFICATION OF THE NATURAL CTL PEPTIDE EPITOPE DERIVED FROM THE NUCLEOPROTEIN OF LYMPHOCYTIC CHORIOMENINGITIS VIRUS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 UNIV N CAROLINA,CHAPEL HILL,NC 27599. NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A7 EP A7 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600034 ER PT J AU HULI, J TANAKA, T SEDER, RA LINSLEY, PS PAUL, WE AF HULI, J TANAKA, T SEDER, RA LINSLEY, PS PAUL, WE TI IL-4 SUPPRESSES IL-2 AND IFN-GAMMA PRODUCTION BY NAIVE T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. BRISTOL MYERS SQUIBB,SEATTLE,WA 98121. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A6 EP A6 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600028 ER PT J AU JOHNSON, LA MELCHER, WL THYPHRONITIS, G ELMOHANDES, A WAHL, LM KATONA, IM AF JOHNSON, LA MELCHER, WL THYPHRONITIS, G ELMOHANDES, A WAHL, LM KATONA, IM TI ANTIIMMUNOGLOBULIN (ANTI-IG) - STIMULATED HUMAN B-CELLS INDUCE INCREASED HLA-DR ANTIGEN EXPRESSION ON T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 CHNMC,WASHINGTON,DC 20010. NIH,BETHESDA,MD 20892. USUHS,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A277 EP A277 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601592 ER PT J AU JOHNSTON, JA FERRIS, DK WANG, JM LONGO, DL OPPENHEIM, JJ KELVIN, DJ AF JOHNSTON, JA FERRIS, DK WANG, JM LONGO, DL OPPENHEIM, JJ KELVIN, DJ TI THE ROLE OF PHOSPHORYLATION OF ERK-1 AND OTHER SUBSTRATES IN INTERLEUKIN-8-INDUCED CHEMOTACTIC DESENSITIZATION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,BRMP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A126 EP A126 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600722 ER PT J AU JONES, JM ALBORNOZ, L YERALAN, O VEECH, RL AF JONES, JM ALBORNOZ, L YERALAN, O VEECH, RL TI EFFECTS OF ETHANOL ON PRODUCTION OF LYMPHOCYTE INHIBITORS BY CULTURED RAT HEPATOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 UNIV ARKANSAS MED SCI HOSP,LITTLE ROCK,AR 72205. NIAAA,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A133 EP A133 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600762 ER PT J AU KANG, V HONG, JX KEHRL, JH AF KANG, V HONG, JX KEHRL, JH TI FURTHER STUDY OF A NOVEL B-CELL ACTIVATION GENE-BL34 SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A263 EP A263 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601512 ER PT J AU KARLHOFER, FM HUNZIKER, R MARGULIES, DH YOKOYAMA, WM AF KARLHOFER, FM HUNZIKER, R MARGULIES, DH YOKOYAMA, WM TI MHC CLASS I-DEPENDENT ABSENCE OF LY-49+ NK CELL SUBSET INVIVO SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. MT SINAI MED CTR,DEPT MED,NEW YORK,NY 10029. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A256 EP A256 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601472 ER PT J AU KATZ, P WHALEN, G KEHRL, JH AF KATZ, P WHALEN, G KEHRL, JH TI CHARACTERIZATION OF A NOVEL PROTEIN-KINASE EXPRESSED PREFERENTIALLY IN GERMINAL CENTER VERSUS MANTLE ZONE B-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. GEORGETOWN UNIV,WASHINGTON,DC 20057. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A262 EP A262 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601507 ER PT J AU KEEGAN, AD WANG, LM PIERCE, JH PAUL, WE AF KEEGAN, AD WANG, LM PIERCE, JH PAUL, WE TI IL-4 RECEPTOR - SIGNAL TRANSDUCING MECHANISMS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A91 EP A91 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600519 ER PT J AU KHILKO, S CORR, M BOYD, LF LEES, A INMAN, JK MARGULIES, DH AF KHILKO, S CORR, M BOYD, LF LEES, A INMAN, JK MARGULIES, DH TI INTERACTIONS OF MHC CLASS-I MOLECULES WITH IMMOBILIZED ANTIGENIC PEPTIDES - DIRECT STUDIES USING SURFACE-PLASMON RESONANCE FOR DETECTION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A40 EP A40 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600221 ER PT J AU KINZER, C KEEGAN, A PLAUT, M PAUL, WE AF KINZER, C KEEGAN, A PLAUT, M PAUL, WE TI LONG-TERM CULTURE OF IL-3-DEPENDENT CELLS EXPRESSING C-KIT, FC-GAMMA-RII/III AND P161 BUT LACKING FC-EPSILON-R - AN FC-EPSILON-RI(NEG) MAST-CELL SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LI & ASTHMA & ALLERGY BRANCH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 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 APR 15 PY 1993 VL 150 IS 8 BP A146 EP A146 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600836 ER PT J AU KOPP, W OCHOA, A CURTI, B LONGO, D URBA, W AF KOPP, W OCHOA, A CURTI, B LONGO, D URBA, W TI PHENOTYPIC CHARACTERIZATION OF REBOUND LEUKOCYTES OBTAINED FROM PATIENTS TREATED WITH ANTI-CD3 STIMULATED CELLS AND IL-2 SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 PROGRAM RESOURCES INC,DYNCORP,FREDERICK,MD 21702. NCI,FCRDC,BRMP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A219 EP A219 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601259 ER PT J AU KOZLOWSKI, S CORR, M SHIRAIT, M BOYD, LF PENDLETON, CD BERZOFSKY, JA MARGULIES, DH AF KOZLOWSKI, S CORR, M SHIRAIT, M BOYD, LF PENDLETON, CD BERZOFSKY, JA MARGULIES, DH TI EXTRACELLULAR PROCESSING OF MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I-RESTRICTED PEPTIDES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A119 EP A119 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600678 ER PT J AU KULKARNI, AB MORSE, HC BENNINK, JR YEWDELL, JW MURPHY, BR AF KULKARNI, AB MORSE, HC BENNINK, JR YEWDELL, JW MURPHY, BR TI THE M2 PROTEIN OF RESPIRATORY SYNCYTIAL VIRUS (RSV) CONTAINS ALLELE-SPECIFIC KD-RESTRICTED MOTIFS RECOGNIZED BY CYTOTOXIC T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A155 EP A155 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600888 ER PT J AU LEONARD, EJ SKEEL, A AF LEONARD, EJ SKEEL, A TI ACTIVITY AND TARGET-CELL SPECIFICITY OF PURE MACROPHAGE STIMULATING PROTEIN (MSP) SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A53 EP A53 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600299 ER PT J AU LITTLE, J WASH, F ASOFSKY, R AF LITTLE, J WASH, F ASOFSKY, R TI RESISTANCE TO INDUCTION BY LPS IN A B-CELL LINE - EPIGENETIC CONTROL OF MEMORY OF PRIOR TREATMENT SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A265 EP A265 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601525 ER PT J AU LLOYD, A JOHNSTON, J CHATTOPADHYAY, U SPRENGER, H OPPENHEIM, JJ KELVIN, D AF LLOYD, A JOHNSTON, J CHATTOPADHYAY, U SPRENGER, H OPPENHEIM, JJ KELVIN, D TI IL-8 RECEPTOR EXPRESSION AND REGULATION IN HEMATOPOIETIC-CELLS BY G-CSF AND LPS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP,BRMP,LMI,FREDERICK,MD 21702. NCI,FCRDC,PRI DYNCORP,BCDP,FREDERICK,MD 21702. RI Lloyd, Andrew/E-7334-2017 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A126 EP A126 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600723 ER PT J AU MAITY, R MUKHERJEE, R SKOLNICK, P AF MAITY, R MUKHERJEE, R SKOLNICK, P TI STEREOSELECTIVITY OF SIGMA-RECEPTOR LIGANDS ON NATURAL-KILLER-CELL ACTIVITY IN MURINE SPLENOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A198 EP A198 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601136 ER PT J AU MALNATI, MS WESTON, M LONG, EO AF MALNATI, MS WESTON, M LONG, EO TI POSITIVE AND NEGATIVE EFFECTS OF MHC CLASS-I MOLECULES ON TARGET-CELL RECOGNITION BY NK CLONES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A257 EP A257 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601480 ER PT J AU MANDLER, R CHU, CC PAUL, WE MAX, EE SNAPPER, CM AF MANDLER, R CHU, CC PAUL, WE MAX, EE SNAPPER, CM TI IL-5 INDUCES S-MU-S-GAMMA-1 DNA REARRANGEMENT BY B-CELLS ACTIVATED WITH DEXTRAN-LINKED ANTI-IGD ANTIBODIES AND IL-4 - A 3 SIGNAL MODEL FOR IG CLASS SWITCHING SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 USUHS,BETHESDA,MD 20814. NIH,BETHESDA,MD 20892. US FDA,BETHESDA,MD 20014. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A171 EP A171 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600986 ER PT J AU MANN, D NALEWAIK, R AF MANN, D NALEWAIK, R TI HIV-1 T-CELL INFECTION BY MACROPHAGES IS REGULATED BY CELL-SURFACE STRUCTURES THAT PARTICIPATE IN THE EVENTS OF THE NORMAL IMMUNE-RESPONSE SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FCRDF,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A179 EP A179 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601032 ER PT J AU MARSH, JW EIDEN, MV GARCIA, JV DE, SK AF MARSH, JW EIDEN, MV GARCIA, JV DE, SK TI HIV NEF ACTIVITY IS NOT SPECIES OR CELL RESTRICTED SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIMH, MOLEC BIOL LAB, CELL BIOL LAB, BETHESDA, MD 20892 USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1993 VL 150 IS 8 BP A318 EP A318 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601837 ER PT J AU MAURER, D RIEGER, A KILGUS, O REININGER, B OCHIAI, K KINET, JP STINGL, G AF MAURER, D RIEGER, A KILGUS, O REININGER, B OCHIAI, K KINET, JP STINGL, G TI HUMAN PERIPHERAL-BLOOD MONOCYTES EXPRESS THE HIGH-AFFINITY IGE RECEPTOR FC-EPSILON-RI SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 UNIV VIENNA,SCH MED,DEPT DERMATOL,DIAID,A-1090 VIENNA,AUSTRIA. NIAID,MOLEC ALLERGOL & IMMUNOL SECT,ROCKVILLE,MD 20892. NR 0 TC 3 Z9 3 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 APR 15 PY 1993 VL 150 IS 8 BP A222 EP A222 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601282 ER PT J AU MAY, RD MURPHY, MJ ERICKSONMILLER, CL TOMASZEWSKI, JE OSBORN, BL PAGE, JG AF MAY, RD MURPHY, MJ ERICKSONMILLER, CL TOMASZEWSKI, JE OSBORN, BL PAGE, JG TI MYELOTOXICITY OF 4 NUCLEOSIDE ANALOGS AS POTENTIAL ANTI-AIDS COMPOUNDS USING MURINE, CANINE, AND HUMAN INVITRO CFU-GM ASSAYS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 SO RES INST,BIRMINGHAM,AL 35205. HIPPLE CANC RES CTR,DAYTON,OH 45439. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A318 EP A318 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601833 ER PT J AU MCCARTNEYFRANCIS, N ALLEN, JB MIZEL, D XIE, Q NATHAN, C ALBINA, J WAHL, S AF MCCARTNEYFRANCIS, N ALLEN, JB MIZEL, D XIE, Q NATHAN, C ALBINA, J WAHL, S TI SUPPRESSION OF ARTHRITIS BY AN INHIBITOR OF THE NITRIC-OXIDE PATHWAY SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,IMMUNOL LAB,BETHESDA,MD 20892. CORNELL UNIV,MED CTR,COLL MED,NEW YORK,NY 10021. RHODE ISL HOSP,DEPT SURG,PROVIDENCE,RI 02903. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A139 EP A139 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600796 ER PT J AU MCCOY, KL INMAN, J STUTZMAN, R AF MCCOY, KL INMAN, J STUTZMAN, R TI DIFFERENCES IN PROCESSING OF EXOGENOUS ANTIGEN INTERNALIZED BY PINOCYTOSIS AND BY TRANSFERRIN RECEPTORS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 VIRGINIA COMMONWEALTH UNIV,RICHMOND,VA 23298. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A122 EP A122 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600698 ER PT J AU MCDONALD, AH MAINHART, C SOPHER, J SMITHGILL, SJ AF MCDONALD, AH MAINHART, C SOPHER, J SMITHGILL, SJ TI ENVIRONMENTAL EXPOSURE MODULATES TUMOR-INDUCTION AND ANTIGEN-DRIVEN IMMUNE-RESPONSES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A20 EP A20 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600104 ER PT J AU MEKORI, YA OH, C METCALFE, DD AF MEKORI, YA OH, C METCALFE, DD TI STEM-CELL FACTOR (SCF) PREVENTS APOPTOTIC CELL-DEATH IN IL-3 DEPRIVED MAST-CELLS (MC) SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A148 EP A148 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600848 ER PT J AU MELILLO, G COX, GW BIRAGYN, A SHEFFLER, LA VARESIO, L AF MELILLO, G COX, GW BIRAGYN, A SHEFFLER, LA VARESIO, L TI PICOLINIC-ACID AND INTERFERON-GAMMA SYNERGISTICALLY INDUCE NITRIC-OXIDE SYNTHASE MESSENGER-RNA EXPRESSION IN MURINE MACROPHAGES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,BRMP,LMI,FREDERICK,MD 21702. RI varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A54 EP A54 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600305 ER PT J AU METZGER, H MALISSEN, B AF METZGER, H MALISSEN, B TI SIGNAL TRANSDUCTION .1. EARLY EVENTS MEDIATED BY B-CELL AND T-CELL ANTIGEN RECEPTORS AND BY FC-RECEPTORS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAMS,BETHESDA,MD 20892. CNRS,INSERM,MARSEILLE,FRANCE. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A1 EP A1 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600002 ER PT J AU MICHALEK, MT GRANT, EP GRAMM, C GOLDBERG, AL ANDERSON, RW YEWDELL, JW BENNINK, JR ROCK, KL AF MICHALEK, MT GRANT, EP GRAMM, C GOLDBERG, AL ANDERSON, RW YEWDELL, JW BENNINK, JR ROCK, KL TI A ROLE FOR THE UBIQUITIN-DEPENDENT PROTEOLYTIC PATHWAY IN MHC CLASS-I-RESTRICTED ANTIGEN PRESENTATION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NIAID,BETHESDA,MD 20892. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A91 EP A91 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600518 ER PT J AU MINOGUCHI, K NISHIKATA, H SIRAGANIAN, RP AF MINOGUCHI, K NISHIKATA, H SIRAGANIAN, RP TI BACTERIALLY EXPRESSED RAT P56(LYN) BINDS SEVERAL PROTEINS IN RAT BASOPHILIC LEUKEMIA (RBL-2H3) CELLS INCLUDING PP72, A TYROSINE PHOSPHORYLATED PROTEIN PROMINENT IN ACTIVATED CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A222 EP A222 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601279 ER PT J AU MUEGGE, K VILA, M DURUM, SK AF MUEGGE, K VILA, M DURUM, SK TI INTERLEUKIN-7 IS A COFACTOR FOR V-DJ REARRANGEMENT OF THE TCR-BETA GENE SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 PRI,FREDERICK,MD 21702. NCI,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A11 EP A11 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600059 ER PT J AU NAKAJIMA, H HENKART, P AF NAKAJIMA, H HENKART, P TI THE ROLE OF GRANZYMES IN LYMPHOCYTE-MEDIATED CYTOTOXICITY - APROTININ-LOADED TARGETS SHOW REDUCED DNA BREAKDOWN AND LYSIS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A208 EP A208 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601199 ER PT J AU NAUSS, JL REID, RH SADEGHNASSERI, S AF NAUSS, JL REID, RH SADEGHNASSERI, S TI BINDING INTERACTIONS OF PEPTIDES IN A STRUCTURAL HOMOLOGY MODEL OF THE DR1 CLASS-II MHC SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 WALTER REED ARMY INST RES,DEPT GASTROENTEROL,WASHINGTON,DC 20307. NIAID,LI,BETHESDA,MD 20892. NR 2 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A41 EP A41 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600232 ER PT J AU NETA, R MCNIECE, I OPPENHEIM, JJ WANG, JM AF NETA, R MCNIECE, I OPPENHEIM, JJ WANG, JM TI SYNERGISTIC EFFECT OF IL-1 AND C-KIT LIGAND SCF IN RADIOPROTECTION OF MICE SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 AFRRI,BETHESDA,MD 20814. AMGEN INC,THOUSAND OAKS,CA 91320. NCI,BRMP,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A202 EP A202 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601165 ER PT J AU NORCROSS, MA YANAGISHITA, M RODERIQUEZ, G BOUHABIB, D ORAVECZ, T HASCALL, V PATEL, M AF NORCROSS, MA YANAGISHITA, M RODERIQUEZ, G BOUHABIB, D ORAVECZ, T HASCALL, V PATEL, M TI CELL-SURFACE HEPARAN-SULFATE PROTEOGLYCAN MEDIATES HIV-1 INFECTION OF CD4+ T-CELL LINES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. US FDA,CBER,ROCKVILLE,MD 20857. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A243 EP A243 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601404 ER PT J AU OPPENHEIM, JJ HOWARD, M AF OPPENHEIM, JJ HOWARD, M TI THE ROLE OF CYTOKINES IN INFLAMMATION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21702. DNAX RES INST MOLEC & CELLULAR BIOL INC,PALO ALTO,CA 94304. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A2 EP A2 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600008 ER PT J AU OSWALD, IP ELTOUM, I WYNN, TA SHER, A JAMES, SL AF OSWALD, IP ELTOUM, I WYNN, TA SHER, A JAMES, SL TI ENDOTHELIAL-CELL MEDIATED KILLING OF LARVAL SCHISTOSOMES - ROLE OF CYTOKINES IN EFFECTOR CELL ACTIVATION AND REGULATION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. RI Wynn, Thomas/C-2797-2011; OSWALD, Isabelle/A-8497-2013 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A7 EP A7 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600036 ER PT J AU PALIOGIANNI, F BALOW, JE BOUMPAS, DT AF PALIOGIANNI, F BALOW, JE BOUMPAS, DT TI PROSTAGLANDIN-E2 (PGE2) INHIBITS INTERLEUKIN-2 (IL-2) GENE-TRANSCRIPTION BY INTERFERING WITH NUCLEAR FACTORS AP-1 AND NF-AT SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A111 EP A111 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600636 ER PT J AU PANTALEO, G GRAZIOSI, C DEMAREST, JF BUTINI, L COHEN, OJ FAUCI, AS AF PANTALEO, G GRAZIOSI, C DEMAREST, JF BUTINI, L COHEN, OJ FAUCI, AS TI HIV-INFECTION IS ACTIVE AND PROGRESSIVE DURING THE PROLONGED PERIOD OF CLINICAL LATENCY SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A243 EP A243 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601402 ER PT J AU PARKER, KC COLIGAN, JE AF PARKER, KC COLIGAN, JE TI A SCHEME FOR RANKING POTENTIAL HLA-A2 BINDING PEPTIDES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A39 EP A39 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600218 ER PT J AU PONCET, P BLANPIED, C PRIGENT, P YANG, Y ASHWELL, JD FEVRIER, M ATEN, J DRUET, P HIRSCH, F AF PONCET, P BLANPIED, C PRIGENT, P YANG, Y ASHWELL, JD FEVRIER, M ATEN, J DRUET, P HIRSCH, F TI A T-CELL HYBRIDOMA MAY BE DRIVEN TO CELL-DEATH BY DIFFERENT PATHWAYS - COMPARATIVE EFFECT OF 2 STIMULI - HGCL2 AND ANTI-CD3 MONOCLONAL-ANTIBODY SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 HOP BROUSSAIS,INSERM,U28,F-75674 PARIS 14,FRANCE. INST PASTEUR,F-75724 PARIS 15,FRANCE. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A193 EP A193 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601111 ER PT J AU RABINOVICH, P CHEN, P SUGIYAMA, H SITKOVSKY, M AF RABINOVICH, P CHEN, P SUGIYAMA, H SITKOVSKY, M TI CAMP-DEPENDENT PROTEIN-KINASE INVOLVEMENT IN THE TCR-TRIGGERED FUNCTIONAL-RESPONSES OF CYTOTOXIC T-LYMPHOCYTES (CTL) AND T-HELPER CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A113 EP A113 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600645 ER PT J AU RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B AF RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B TI B-CELLS IN BEHCET PATIENTS CONTAIN A HEAT-SHOCK PROTEIN THAT BINDS TO A FRAGMENT OF IRBP SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A72 EP A72 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600410 ER PT J AU RIZZO, LV DEKRUYFF, RH UMETSU, DT CASPI, RR AF RIZZO, LV DEKRUYFF, RH UMETSU, DT CASPI, RR TI THE REGULATION OF THE INTERACTIONS BETWEEN TH1 AND TH2 CLONES INVIVO SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 STANFORD UNIV,STANFORD,CA 94305. NEI,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A274 EP A274 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601576 ER PT J AU ROSEN, J MACNAMARA, J BOTTOMLY, K CARDING, SR AF ROSEN, J MACNAMARA, J BOTTOMLY, K CARDING, SR TI EXPRESSION OF CD45 ISOFORMS BY HUMAN T-CELLS IS DEVELOPMENTALLY REGULATED SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,NEW HAVEN,CT 06510. UNIV PENN,PHILADELPHIA,PA 19104. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A109 EP A109 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600621 ER PT J AU RYAN, J KINZER, C PAUL, WE AF RYAN, J KINZER, C PAUL, WE TI K-1(POS), FC-EPSILON-R(NEG) LONG-TERM IL-3-DEPENDENT CELL-LINES EXPRESS FC-EPSILON-RI-ALPHA AND BETA BUT NOT GAMMA-MESSENGER RNA - EVIDENCE FOR FC-EPSILON-R(NEG) MAST-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A223 EP A223 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601283 ER PT J AU SARTOR, RB MCCALL, RD ALLEN, JB HASKILL, JS WAHL, SM AF SARTOR, RB MCCALL, RD ALLEN, JB HASKILL, JS WAHL, SM TI MECHANISMS OF DIFFERENTIAL SUSCEPTIBILITY OF INBRED RAT STRAINS TO EXPERIMENTAL ENTEROCOLITIS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 UNIV N CAROLINA,CHAPEL HILL,NC 27514. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A10 EP A10 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600049 ER PT J AU SCULLY, G MCCOY, SM COHEN, DI LANE, HC AF SCULLY, G MCCOY, SM COHEN, DI LANE, HC TI THE ROLE OF VPU IN THE PATHOGENESIS OF HIV-1 INFECTION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A179 EP A179 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601030 ER PT J AU SEDER, RA GERMAIN, RN LINSLEY, PS PAUL, WE AF SEDER, RA GERMAIN, RN LINSLEY, PS PAUL, WE TI PRIMING FOR LYMPHOKINE PRODUCTION CAN BE ACHIEVED IN THE ABSENCE OF B7/CD28 CO-STIMULATION IF IL-2 IS PRESENT SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 BRISTOL MYERS SQUIBB,SEATTLE,WA 98121. NIAID,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A252 EP A252 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601449 ER PT J AU SELVEY, LA MORSE, HC JUNE, CH HODES, RJ AF SELVEY, LA MORSE, HC JUNE, CH HODES, RJ TI SPLENIC B-CELLS FROM MAIDS MICE SHOW A SELECTIVE DEFECT IN TYROSINE PHOSPHORYLATION IN RESPONSE TO IGM CROSS-LINKING SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIAID,PATHOL LAB,BETHESDA,MD 20892. USN,MED RES INST,BETHESDA,MD 20814. RI Selvey, Linda/B-8473-2017 OI Selvey, Linda/0000-0001-8493-0974 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A265 EP A265 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601522 ER PT J AU SHIELDS, MJ COLIGAN, JE PARKER, KC AF SHIELDS, MJ COLIGAN, JE PARKER, KC TI LARGE-SCALE PREPARATION OF SOLUBLE HUMAN MHC CLASS I/BETA-2-MICROGLOBULIN PEPTIDE COMPLEXES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A39 EP A39 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600215 ER PT J AU SMITH, P REDEGELD, F SITKOVSKY, M AF SMITH, P REDEGELD, F SITKOVSKY, M TI PP1 CLASS OF ECTO-PROTEINPHOSPHATASES ON THE T-CELLS SURFACE SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. RI Redegeld, Frank/O-6534-2016 OI Redegeld, Frank/0000-0001-8830-7960 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A113 EP A113 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600647 ER PT J AU SOUDEYNS, H PANTALEO, GP BOGHOSSIAN, T CIURLI, C REBAI, N LANE, HC FAUCI, AS SEKALY, RP AF SOUDEYNS, H PANTALEO, GP BOGHOSSIAN, T CIURLI, C REBAI, N LANE, HC FAUCI, AS SEKALY, RP TI V-BETA-SPECIFIC VARIATIONS IN THE TCR REPERTOIRE OF HIV-INFECTED SUBJECTS SUGGEST THE PRESENCE OF AN HIV-ASSOCIATED SUPERANTIGEN SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 IRCM, IMMUNOL LAB, MONTREAL H2W 1R7, PQ, CANADA. NIAID, IMMUNOREGULAT LAB, BETHESDA, MD 20892 USA. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 EI 1550-6606 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1993 VL 150 IS 8 BP A104 EP A104 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600595 ER PT J AU SPECTOR, NH AF SPECTOR, NH TI A BRIEF HISTORICAL INTRODUCTION TO NEUROIMMUNOMODULATION - OLD AND NEW INFORMATION EXPLOSIONS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,DIV FUNDAMENTAL NEUROSCI,BETHESDA,MD 20892. NR 6 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A82 EP A82 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600467 ER PT J AU SPRENGER, H LLOYD, AR KELVIN, DJ AF SPRENGER, H LLOYD, AR KELVIN, DJ TI ISOLATION AND CHARACTERIZATION OF IL-8 TYPE-I AND TYPE-II RECEPTOR GENES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,DCT,BRMP,LMI,FREDERICK,MD. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A126 EP A126 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600720 ER PT J AU STANLEY, SK MCCUNE, JM KANESHIMA, H JUSTEMENT, SJ SULLIVAN, M BOONE, E BASELER, M ADELSBERGER, J FOX, C ORENSTEIN, J FAUCI, AS AF STANLEY, SK MCCUNE, JM KANESHIMA, H JUSTEMENT, SJ SULLIVAN, M BOONE, E BASELER, M ADELSBERGER, J FOX, C ORENSTEIN, J FAUCI, AS TI INFECTION OF HUMAN THYMUS WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) IN THE SCID-HU MOUSE MODEL SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. SYSTEMIX INC,PALO ALTO,CA 94303. PRI DYNCORP,FREDERICK,MD 21702. AMER HISTOLABS,ROCKVILLE,MD 20879. GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC 20052. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A244 EP A244 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601408 ER PT J AU STERNBERG, EM AF STERNBERG, EM TI REGULATION OF NEUROENDOCRINE CIRCUITS, INFLAMMATORY RESPONSES AND BEHAVIOR IN LEWIS RATS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A248 EP A248 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601430 ER PT J AU STUMHOFEL, K VALAS, RB COLIGAN, JE AF STUMHOFEL, K VALAS, RB COLIGAN, JE TI BETA(2)-MICROGLOBULIN IS NOT REQUIRED FOR AUTOSTIMULATION OF V-GAMMA-1.1/C-GAMMA-4-V-DELTA-6 C-DELTA-1 EXPRESSING GAMMA/DELTA-T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A267 EP A267 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601535 ER PT J AU SULLIVAN, KE MULLEN, CA BLAESE, RM WINKELSTEIN, JA AF SULLIVAN, KE MULLEN, CA BLAESE, RM WINKELSTEIN, JA TI A REAPPRAISAL OF THE NATURAL-HISTORY OF THE WISKOTT-ALDRICH SYNDROME - A MULTIINSTITUTIONAL SURVEY SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,BALTIMORE,MD 21230. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 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 APR 15 PY 1993 VL 150 IS 8 BP A163 EP A163 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600937 ER PT J AU TAUB, DD LLOYD, AL CONLON, K MURPHY, W LONGO, DL KELVIN, DJ OPPENHEIM, JJ AF TAUB, DD LLOYD, AL CONLON, K MURPHY, W LONGO, DL KELVIN, DJ OPPENHEIM, JJ TI PREFERENTIAL CHEMOTAXIS AND ADHESION OF T-CELL SUBSETS IN RESPONSE TO MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA (MIP-1-ALPHA), MIP-1-BETA, AND RANTES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,DCT,BRMP,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. RI Lloyd, Andrew/E-7334-2017 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A46 EP A46 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600257 ER PT J AU THEVENIN, C KEHRL, JH AF THEVENIN, C KEHRL, JH TI CHARACTERIZATION OF THE HUMAN CD20 PROMOTER BY INVIVO FOOTPRINTING AND GEL RETARDATION ASSAYS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A264 EP A264 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601516 ER PT J AU THIBODEAU, J FLEURY, S LABRECQUE, N CANTIN, C ARONSON, HE HENDRICKSON, W YACHOU, A LONG, E SEKALY, RP AF THIBODEAU, J FLEURY, S LABRECQUE, N CANTIN, C ARONSON, HE HENDRICKSON, W YACHOU, A LONG, E SEKALY, RP TI POLYMORPHISM IN THE BETA-CHAIN OF HLA-DR AFFECTS THE INTERACTION WITH CD4 SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 IRCM, IMMUNOL LAB, MONTREAL H2W 1R7, PQ, CANADA. COLUMBIA UNIV, DEPT BIOCHEM MOLEC BIOPHYS, NEW YORK, NY 10032 USA. NIAID, ROCKVILLE, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 EI 1550-6606 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1993 VL 150 IS 8 BP A288 EP A288 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601656 ER PT J AU TIAN, H WAHL, L COHEN, D AF TIAN, H WAHL, L COHEN, D TI INTRACELLULAR SIGNALS FOLLOWING HIV-1 ENVELOPE/CD4 PROTEIN-INTERACTION ALTER NORMAL EVENTS IN CELL-CYCLE PROGRESSION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A241 EP A241 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601388 ER PT J AU TOSATO, G SGADARI, C TAGA, K LOVE, LA BATHIA, K AF TOSATO, G SGADARI, C TAGA, K LOVE, LA BATHIA, K TI REGRESSION OF EXPERIMENTAL BURKITTS-LYMPHOMA INDUCED BY EBV-IMMORTALIZED B-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 US FDA,CBER,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. RI Sgadari, Cecilia/H-4302-2016 OI Sgadari, Cecilia/0000-0003-0364-4912 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A309 EP A309 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601779 ER PT J AU TROTTER, J BRYAN, J PELFREY, C MCFARLAND, H AF TROTTER, J BRYAN, J PELFREY, C MCFARLAND, H TI MYELIN PROTEOLIPID PROTEIN-PEPTIDES WHICH ARE RECOGNIZED BY T-CELL LINES FROM HUMAN-SUBJECTS WITH MS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 WASHINGTON UNIV,ST LOUIS,MO 63130. NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR 15 PY 1993 VL 150 IS 8 BP A196 EP A196 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601126 ER PT J AU TUSCANO, JM KEHRL, JH AF TUSCANO, JM KEHRL, JH TI DEVELOPMENT AND INITIAL CHARACTERIZATION OF 12 MONOCLONAL-ANTIBODIES RAISED AGAINST ACTIVATED HUMAN B-LYMPHOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A263 EP A263 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601514 ER PT J AU UDEY, MC TANG, A AMAGAI, M STANLEY, JR LEE, MG AF UDEY, MC TANG, A AMAGAI, M STANLEY, JR LEE, MG TI ADHESION OF RESIDENT EPIDERMAL LEUKOCYTES TO KERATINOCYTES (KC) MEDIATED BY E-CADHERIN (E-CAD) SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A284 EP A284 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601637 ER PT J AU UTZ, U BROOKS, JA FLERLAGE, M MCFARLAND, HF BIDDISON, WE AF UTZ, U BROOKS, JA FLERLAGE, M MCFARLAND, HF BIDDISON, WE TI DIVERSITY OF TCR ALPHA-CHAINS IN MBP-SPECIFIC T-CELLS FROM MS PATIENTS AND NORMALS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A256 EP A256 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601470 ER PT J AU VACCAREZZA, M PANTALEO, G COHEN, OJ HOHMAN, RH FAUCI, AS AF VACCAREZZA, M PANTALEO, G COHEN, OJ HOHMAN, RH FAUCI, AS TI CYCLOSPORINE-A SUPPRESSES HIV-1 INFECTION IN PRIMARY T-LYMPHOCYTES ACUTELY INFECTED INVITRO SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT & CLIN IMMUNOL LAB,BETHESDA,MD 20892. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A179 EP A179 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601031 ER PT J AU VASILE, S COLIGAN, JE YOSHIDA, M SEON, BK AF VASILE, S COLIGAN, JE YOSHIDA, M SEON, BK TI HUMAN B29 AND MB-1 PROTEINS OF THE B-CELL ANTIGEN RECEPTOR COMPLEX - ISOLATION AND IDENTIFICATION BY AMINO-TERMINAL AMINO-ACID-SEQUENCE DETERMINATION SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 ROSWELL PK CANC INST,DEPT MOLEC IMMUNOL,BUFFALO,NY 14263. NIAID,BIOL RESOURCE BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A255 EP A255 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601467 ER PT J AU VILA, M DURUM, SK MUEGGE, K AF VILA, M DURUM, SK MUEGGE, K TI HYPOMETHYLATION OF THE TCR-BETA LOCUS PRECEDES REARRANGEMENT SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 PRI,FREDERICK,MD. NCI,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A108 EP A108 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600615 ER PT J AU WANG, MH SKEEL, A YOSHIMURA, T COPELAND, TD SAKAGUCHI, K LEONARD, EJ AF WANG, MH SKEEL, A YOSHIMURA, T COPELAND, TD SAKAGUCHI, K LEONARD, EJ TI CHARACTERIZATION OF ANTIBODIES TO HUMAN MACROPHAGE STIMULATING PROTEIN (MSP) SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A52 EP A52 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600293 ER PT J AU WANIDWORANUN, CC STROBER, W AF WANIDWORANUN, CC STROBER, W TI TNF-ALPHA UP-REGULATES IL-10 EXPRESSION IN HUMAN PERIPHERAL-BLOOD MONOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A180 EP A180 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601037 ER PT J AU WILLIAMS, MS HENKART, P AF WILLIAMS, MS HENKART, P TI INTRACELLULAR PROTEOLYSIS TRIGGERS CELL-DEATH GENERALLY ACCOMPANIED BY APOPTOTIC MORPHOLOGY AND DNA BREAKDOWN SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A208 EP A208 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601196 ER PT J AU WILSON, GL RIVA, A KEHRL, JH AF WILSON, GL RIVA, A KEHRL, JH TI DEVELOPMENT OF HUMAN B-CELL LINES DEFICIENT IN CD19, CD20, OR CD22 SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A99 EP A99 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600561 ER PT J AU ZIMMERMAN, PA CARRINGTON, M NUTMAN, TB AF ZIMMERMAN, PA CARRINGTON, M NUTMAN, TB TI DIRECTED HETERODUPLEX ANALYSIS SIMPLIFIES HLA-TYPING SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LPD,BETHESDA,MD 20892. NCI,FCRDC,PRI DYNCORP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A326 EP A326 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601881 ER PT J AU SHIRABE, S STEVENS, JR SCHWARTZ, JP AF SHIRABE, S STEVENS, JR SCHWARTZ, JP TI CHARACTERIZATION OF A TRANSMISSIBLE GROWTH-PROMOTING AGENT DERIVED FROM CSF OF SCHIZOPHRENIC-PATIENTS WHICH IS ACTIVE ON HUMAN NEUROBLASTOMA-CELLS SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE SCHIZOPHRENIA; SH-EP NEUROBLASTOMA CELL; TRANSFORMATION; TRANSMISSION ID NEURO-BLASTOMA CELLS; EXPRESSION; VIRUS; DISEASES AB A growth-promoting agent for the human neuroblastoma cell line SK-N-SH(EP) (SH-EP) has been detected in human cerebrospinal fluid (CSF) derived from schizophrenic patients. Following treatment with the CSF, a number of properties of the SH-EP cells changed permanently. These included an accelerated rate of growth, an increased cell density at confluence, a change of cell shape, and an increased ability to form colonies in soft agar. All of these changes are consistent with further cellular transformation of the SH-EP cells. Once the cells' properties had changed following CSF treatment, the growth-promoting activity was found to be present in freeze-thawed cell extracts and in the culture medium, and could be passed to untreated SH-EP cells. The activity could be detected in culture media diluted as high as 108. It was inactivated by proteinases, chloroform, or heat but passed through a 0.22-mum filter. The growth-promoting activity can be banded on a Percoll gradient, suggesting that it is particulate rather than a soluble growth factor. C1 NIMH,ST ELIZABETHS HOSP,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. RP SHIRABE, S (reprint author), NINCDS,CLIN NEUROSCI BRANCH,BLDG 9,ROOM 1W115,BETHESDA,MD 20892, USA. NR 26 TC 4 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR 15 PY 1993 VL 34 IS 6 BP 622 EP 628 DI 10.1002/jnr.490340604 PG 7 WC Neurosciences SC Neurosciences & Neurology GA KZ704 UT WOS:A1993KZ70400003 PM 8315662 ER PT J AU SACRISTAN, MP VESTAL, DJ DOURSZIMMERMANN, MT RANSCHT, B AF SACRISTAN, MP VESTAL, DJ DOURSZIMMERMANN, MT RANSCHT, B TI T-CADHERIN-2 - MOLECULAR CHARACTERIZATION, FUNCTION IN CELL-ADHESION, AND COEXPRESSION WITH T-CADHERIN AND N-CADHERIN SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Note DE CELL ADHESION MOLECULE; CALCIUM DEPENDENCE; GPI ANCHOR; HOMOPHILIC BINDING; T-CADHERIN ISOFORMS ID UVOMORULIN-CATENIN COMPLEX; ACTIVE RIBONUCLEIC-ACID; CYTOPLASMIC BETA-ACTIN; NEURITE OUTGROWTH; SEQUENCE-ANALYSIS; XENOPUS EMBRYOS; AVIAN EMBRYO; GENE FAMILY; R-CADHERIN; EXPRESSION AB Cadherins are integral membrane glycoproteins that mediate calcium-dependent, homophilic cell-cell adhesion and are implicated in controlling tissue morphogenesis. T-cadherin is anchored to the membrane through a glycosyl phosphatidylinositol (Ranscht B, Dours-Zimmermann MT: Neuron 7:391-402, 1991) and expressed in a restricted pattern in developing embryos (Ranscht B, Bronner-Fraser M: Development 111: 15-22, 1991). We report here the molecular and functional characterization of the T-cadherin isoform, T-cadherin 2 (Tcad-2) and the expression of the corresponding mRNA. Tcad-2 cDNA differs in its 3' nucleotide sequence from T-cadherin cDNA and encodes a protein in which the carboxy terminal Leu of T-cadherin is substituted by Lys and extended by the amino acids SerPheProTyrVal. By RNase protection, mRNAs encoding the T-cadherin isoforms are coexpressed in heart, muscle, liver, skin, somites, and in neural tissue. Many tissues contain both T-cadherin and Tcad-2 mRNAs in conjunction with N-cadherin transcripts, and T-cadherins and N-cadherin proteins are coexpressed on the surface of individual neurons in vitro. Expression in Chinese hamster ovary cells (CHO) revealed that Tcad-2 is a glycosyl phosphatidylinositol-anchored membrane protein that functions in calcium-dependent, homophilic cell adhesion. The identification of a functional T-cadherin isoform and the coexpression of T-cadherins and N-cadherin by individual cells suggest that specific adhesive interactions of embryonic cells may involve a complex interplay between multiple cadherins. C1 NCI,LA JOLLA CANC RES FDN,10901 N TORREY PINES RD,LA JOLLA,CA 92037. RI Sacristan, Maria/A-9587-2016 OI Sacristan, Maria/0000-0003-2314-8430 FU NCI NIH HHS [CA 09579-04]; NICHD NIH HHS [HD25938] NR 67 TC 27 Z9 29 U1 0 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR 15 PY 1993 VL 34 IS 6 BP 664 EP 680 DI 10.1002/jnr.490340610 PG 17 WC Neurosciences SC Neurosciences & Neurology GA KZ704 UT WOS:A1993KZ70400009 PM 8315665 ER PT J AU MASOLIVER, J WEISS, GH AF MASOLIVER, J WEISS, GH TI ON THE MAXIMUM DISPLACEMENT OF A ONE-DIMENSIONAL DIFFUSION PROCESS DESCRIBED BY THE TELEGRAPHERS EQUATION SO PHYSICA A LA English DT Article ID HEAT WAVES AB Recently Orsingher (1990) has derived bounds on the probability distribution of the maximum displacement of a one-dimensional diffusion process whose evolution is described by a telegrapher's equation. Foong has given more precise results for related variables. In this paper we derive an exact expression for this distribution as well as the joint distribution of the minimum and maximum displacements. C1 NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. RP MASOLIVER, J (reprint author), UNIV BARCELONA,DEPT FIS FONAMENTAL,DIAGONAL 647,E-08028 BARCELONA,SPAIN. RI Masoliver, Jaume/F-7198-2016 OI Masoliver, Jaume/0000-0002-5810-879X NR 11 TC 6 Z9 6 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4371 J9 PHYSICA A JI Physica A PD APR 15 PY 1993 VL 195 IS 1-2 BP 93 EP 100 DI 10.1016/0378-4371(93)90255-3 PG 8 WC Physics, Multidisciplinary SC Physics GA KY958 UT WOS:A1993KY95800006 ER PT J AU MENOTTIRAYMOND, M OBRIEN, SJ AF MENOTTIRAYMOND, M OBRIEN, SJ TI DATING THE GENETIC BOTTLENECK OF THE AFRICAN CHEETAH SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DNA FINGERPRINT; MTDNA ID MITOCHONDRIAL-DNA; ACINONYX-JUBATUS; MUTATION-RATES; POPULATIONS; DIVERSITY; AMERICAN; LIONS; INDIVIDUALIZATION; FINGERPRINTS; VARIABILITY AB The cheetah is unusual among felids in exhibiting near genetic uniformity at a variety of loci previously screened to measure population genetic diversity. It has been hypothesized that a demographic crash or population bottleneck in the recent history of the species is causal to the observed monomorphic profiles for nuclear coding loci. The timing of a bottleneck is difficult to assess, but certain aspects of the cheetah's natural history suggest it may have occurred near the end of the last ice age (late Pleistocene, approximately 10,000 years ago), when a remarkable extinction of large vertebrates occurred on several continents. To further define the timing of such a bottleneck, the character of genetic diversity for two rapidly evolving DNA sequences, mitochondrial DNA and hypervariable minisatellite loci, was examined. Moderate levels of genetic diversity were observed for both of these indices in surveys of two cheetah subspecies, one from South Africa and one from East Africa. Back calculation from the extent of accumulation of DNA diversity based on observed mutation rates for VNTR (variable number of tandem repeats) loci and mitochondrial DNA supports a hypothesis of an ancient Pleistocene bottleneck that rendered the cheetah depauperate in genetic variation for nuclear coding loci but would allow sufficient time for partial reconstitution of more rapidly evolving genomic DNA segments. C1 NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. RP MENOTTIRAYMOND, M (reprint author), NCI,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 48 TC 107 Z9 113 U1 8 U2 69 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 15 PY 1993 VL 90 IS 8 BP 3172 EP 3176 DI 10.1073/pnas.90.8.3172 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX816 UT WOS:A1993KX81600013 PM 8475057 ER PT J AU KIM, YH BUCHHOLZ, MJ NORDIN, AA AF KIM, YH BUCHHOLZ, MJ NORDIN, AA TI MURINE T-LYMPHOCYTE PROLIFERATION INDUCED BY INTERLEUKIN-2 CORRELATES WITH A TRANSIENT INCREASE IN P56(LCK) KINASE-ACTIVITY AND THE TYROSINE PHOSPHORYLATION OF A 97-KDA PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID IL-2 RECEPTOR; BETA-CHAIN; BIOCHEMICAL-EVIDENCE; SIGNAL TRANSDUCTION; NUCLEOTIDE-SEQUENCE; ACTIVATION; EXPRESSION; INDUCTION; CELLS; GENE AB The addition of recombinant interleukin 2 (rIL-2) to anti-CD3-activated murine G0 phase T cells results in an increased level of tyrosine phosphorylation of a single 97-kDa protein. The degree of tyrosine phosphorylation paralleled the amount of rIL-2 added and correlated with the extent of DNA synthesis. IL-2 treatment resulted in a transient increase in p56lck kinase activity without detectable modification of its level of tyrosine phosphorylation and gel mobility. When G0 T cells were activated by phorbol dibutyrate in the absence of IL-2, the high-affinity IL-2 receptor (IL-2R) expressed failed to induce a proliferative signal, and neither the tyrosine phosphorylation of the 97-kDa protein nor the transient increase in p56lck kinase activity was detected. Northern analysis of the total RNA extracted from these cells showed the accumulation of IL-2R alpha chain-specific mRNA but neither c-myc nor cdc2 mRNA was expressed. The addition of 100 nM rIL-2 to T cells activated by phorbol dibutyrate was able to induce a proliferative response, and under these conditions tyrosine phosphorylation of the 97-kDa protein, the transient increase in p56lck kinase activity, and specific mRNA for IL-2R alpha chain, c-myc, and cdc2 were detected. Unstimulated G0 T cells responded to 100 nM rIL-2 in the same manner as phorbol dibutyrate-activated cells. Irrespective of the signal-transducing structures involved, the IL-2-induced proliferative response closely correlates with an increase in p56lck kinase activity along with the tyrosine phophorylation of a 97-kDa protein. C1 NIA,GERONTOL RES CTR,CLIN IMMUNOL SECT,4940 EASTERN AVE,BALTIMORE,MD 21224. NR 41 TC 17 Z9 17 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 15 PY 1993 VL 90 IS 8 BP 3187 EP 3191 DI 10.1073/pnas.90.8.3187 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX816 UT WOS:A1993KX81600016 PM 7682694 ER PT J AU DAWSON, VL DAWSON, TM UHL, GR SNYDER, SH AF DAWSON, VL DAWSON, TM UHL, GR SNYDER, SH TI HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 COAT PROTEIN NEUROTOXICITY MEDIATED BY NITRIC-OXIDE IN PRIMARY CORTICAL CULTURES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GP120; AIDS; GLUTAMATE; N-METHYL-D-ASPARTATE; MICROGLIA ID AIDS DEMENTIA COMPLEX; CALCIUM-CHANNEL ANTAGONISTS; NERVOUS-SYSTEM; HIV-1; PEROXYNITRITE; SUPEROXIDE; INFECTION; BRAIN; GLUTAMATE; INJURY AB The human immunodeficiency virus type 1 coat protein, gp120, kills neurons in primary cortical cultures at low picomolar concentrations. The toxicity requires external glutamate and calcium and is blocked by glutamate receptor antagonists. Nitric oxide (NO) contributes to gp120 toxicity, since nitroarginine, an inhibitor of NO synthase, prevents toxicity as does deletion of arginine from the incubation medium and hemoglobin, which binds NO. Superoxide dismutase also attenuates toxicity, implying a role for superoxide anions. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,725 N WOLFE ST,BALTIMORE,MD 21205. NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. OI Dawson, Valina/0000-0002-2915-3970 FU NIDA NIH HHS [DA-00074, DA-00266, DA-271-90-7408] NR 46 TC 333 Z9 333 U1 1 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 15 PY 1993 VL 90 IS 8 BP 3256 EP 3259 DI 10.1073/pnas.90.8.3256 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX816 UT WOS:A1993KX81600030 PM 8097316 ER PT J AU BUSHMAN, FD ENGELMAN, A PALMER, I WINGFIELD, P CRAIGIE, R AF BUSHMAN, FD ENGELMAN, A PALMER, I WINGFIELD, P CRAIGIE, R TI DOMAINS OF THE INTEGRASE PROTEIN OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 RESPONSIBLE FOR POLYNUCLEOTIDYL TRANSFER AND ZINC-BINDING SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE RETROVIRUS; RECOMBINATION; IN PROTEIN; ZINC FINGER ID RETROVIRAL DNA INTEGRATION; VIRAL-DNA; INSERTION SEQUENCES; TRANSPOSITION; INVITRO; INTERMEDIATE; RECOGNITION; EXPRESSION; CLEAVAGE; ENDS AB The integrase protein of human immunodeficiency virus type 1 carries out a set of polynucleotidyl transfer reactions that result in the covalent attachment of the retroviral cDNA to host DNA. We have analyzed the activities of a set of deletion derivatives of the integrase protein. The analysis reveals that a central domain of only 137 amino acids is sufficient in vitro to catalyze a subset of the reactions carried out by the complete protein. This polypeptide contains an amino acid sequence motif, Asp-Xaa39-58-Asp-Xaa35-Glu (DX39-58DX35E, where X and the subscript indicate the intervening amino acids between the invariant acidic residues), that is found in the integrases of retroviruses and retrotransposons and also the transposase proteins of some bacterial transposable elements. We also find that the integrase protein can bind Zn2+, and the histidine and cysteine residues of another conserved motif (HX3-7HX23-32CX2C) are required for efficient Zn2+ binding. The activities displayed by deletion mutants suggest to us possible functions for the various parts of integrase. C1 NIDDKD, MOLEC BIOL LAB, BETHESDA, MD 20892 USA. NIH, PROT EXPRESS LAB, OFF DIRECTOR, BETHESDA, MD 20892 USA. NR 40 TC 330 Z9 335 U1 1 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 15 PY 1993 VL 90 IS 8 BP 3428 EP 3432 DI 10.1073/pnas.90.8.3428 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX816 UT WOS:A1993KX81600065 PM 8386373 ER PT J AU LEE, YJ QUAN, H AF LEE, YJ QUAN, H TI P-VALUES AFTER REPEATED SIGNIFICANCE TESTING - A SIMPLE APPROXIMATION METHOD SO STATISTICS IN MEDICINE LA English DT Article ID GROUP SEQUENTIAL TEST; CLINICAL-TRIALS; CONFIDENCE-INTERVALS; DESIGN AB The P-value after a repeated significance test is a useful measure of the strength of evidence against the null hypothesis. Its computation, however, requires a computer-intensive numerical integration method. The P-value is not conceptually straightforward, because it depends on how the sample space is ordered, which can be arbitrary. We look at two orderings of the sample space, one proposed by Tsiatis et al. and the other by Rosner and Tsiatis, and Chang. Although studies have shown that the latter ordering gives more reasonable confidence intervals than the former, the former gives a conservative and therefore more reasonable P-value. Both, however, should yield an identical P-value in most applications. In this paper we present a simple method of approximating P-values. We provide tables to implement the method for two to ten stages with alpha = 0.1, 0.05 and 0.01 for the Pocock and O'Brien-Fleming procedures. The proposed method can be applied to both orderings. RP LEE, YJ (reprint author), NICHHD,DIV PREVENT RES,BIOMETRY & MATH STAT BRANCH,EXECUT PL N,BETHESDA,MD 20892, USA. NR 18 TC 2 Z9 2 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD APR 15 PY 1993 VL 12 IS 7 BP 675 EP 684 DI 10.1002/sim.4780120706 PG 10 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA KZ509 UT WOS:A1993KZ50900005 PM 8511443 ER PT J AU BLACKWELDER, WC AF BLACKWELDER, WC TI SAMPLE-SIZE AND POWER FOR PROSPECTIVE ANALYSIS OF RELATIVE RISK SO STATISTICS IN MEDICINE LA English DT Article ID CONFIDENCE-INTERVALS; NULL HYPOTHESIS; WALDS TEST; RATIO; TRIALS AB In a placebo-controlled vaccine efficacy trial or a trial of equivalence of vaccines, one may wish to show that relative risk of disease is less than a specified value R0, not equal to one. This paper compares three methods for estimating relative risk in the binomial setting, based on a logarithmic transformation, likelihood scores, and a Poisson approximation. Exact power and size of test are calculated by enumeration of possible binomial outcomes, and power is approximated from asymptotic formulations. Although the score method is generally preferable, for most studies of practical interest the log and score methods are comparable, and the Poisson method is also appropriate for small risks, up to about 0.05. When true and null relative risks are less than one, unequal allocation of study individuals can increase power, and the asymptotic formula for the log method may substantially underestimate power; in such a study the power approximation for the score method is more reliable, even if the log method is used in analysis. Exact power calculations are helpful in planning studies. The log and Poisson methods, but not the score method, apply readily in the case of unequal follow-up. RP BLACKWELDER, WC (reprint author), NIAID,SOLAR BLDG 3,ROOM 3A24,BETHESDA,MD 20892, USA. NR 27 TC 28 Z9 29 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD APR 15 PY 1993 VL 12 IS 7 BP 691 EP 698 DI 10.1002/sim.4780120708 PG 8 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA KZ509 UT WOS:A1993KZ50900007 PM 8511445 ER PT J AU STRAUS, SE AF STRAUS, SE TI SHINGLES - SORROWS, SALVES, AND SOLUTIONS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Discussion ID VARICELLA-ZOSTER VIRUS; POST-HERPETIC NEURALGIA; ORAL ACYCLOVIR; IMMUNOCOMPROMISED PATIENTS; THERAPY; INFECTION; COMPLICATIONS; VIDARABINE; CHILDREN; IMMUNITY RP STRAUS, SE (reprint author), NIAID,CLIN INVEST LAB,BLDG 10,ROOM 11N-228,BETHESDA,MD 20892, USA. NR 32 TC 24 Z9 26 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 APR 14 PY 1993 VL 269 IS 14 BP 1836 EP 1839 DI 10.1001/jama.269.14.1836 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA KW250 UT WOS:A1993KW25000040 PM 8459517 ER PT J AU STANCATO, LF HUTCHISON, KA CHAKRABORTI, PK SIMONS, SS PRATT, WB AF STANCATO, LF HUTCHISON, KA CHAKRABORTI, PK SIMONS, SS PRATT, WB TI DIFFERENTIAL-EFFECTS OF THE REVERSIBLE THIOL-REACTIVE AGENTS ARSENITE AND METHYL METHANETHIOSULFONATE ON STEROID BINDING BY THE GLUCOCORTICOID RECEPTOR SO BIOCHEMISTRY LA English DT Article ID HEAT-SHOCK PROTEIN; DNA-BINDING; SULFHYDRYL-GROUPS; ACTIVATING FACTOR; HORMONE; DOMAIN; RECONSTITUTION; TRANSFORMATION; LOCALIZATION; THIOREDOXIN AB The hormone binding domain of the glucocorticoid receptor contains a unique vicinally spaced dithiol, and when it is bound by arsenite under conditions that are specific for reaction with vicinally spaced dithiols versus monothiols, steroid binding activity is eliminated [Simons, S. S., Jr., Chakraborti, P. K., & Cavanaugh, A. H. (1990) J. Biol. Chem. 265, 1938-1945]. The vicinally spaced dithiol lies in a region of the receptor that appears to be a contact site for hsp90, which is required for the high-affinity steroid binding conformation of the glucocorticoid receptor [Dalman, F. C., Scherrer, L. C., Taylor, L. P., Akil, H., & Pratt, W. B. (1991) J. Biol. Chem. 266, 3482-3490]. As part of a long-term project to develop a vicinal dithiol-specific agent that will permit studies of ligand-induced conformational changes in this region of the receptor, we have examined here the differential effects of two reversible thiol-reactive agents, arsenite and MMTS. At low concentration, arsenite inactivates the steroid binding activity of the unliganded receptor in a vicinal dithiol-specific manner, whereas dissociation of steroid from untransformed, transformed, or DNA-bound transformed receptors occurs only at concentrations typical of monothiol interactions. MMTS produces a unique bimodal effect on the steroid binding capacity of the unliganded receptor at pH 9 that is pH-dependent and becomes essentially unimodal at physiological pH. Whereas arsenite disrupts the dexamethasone-receptor complex more readily than the triamcinolone acetonide-receptor complex , MMTS has the opposite effect. During treatment for 1 h at 0-degrees-C, neither reagent causes dissociation of hsp90 from the receptor. Also, pretreatment of the hsp90-free unliganded receptor with the covalent sulfhydryl-modifying agents N-ethylmalemide or iodoacetamide does not affect the ability of the receptor to be enzymatically refolded into a heterocomplex with hsp90 by reticulocyte lysate. The observations of this work are consistent with the concept that the vicinally spaced dithiol lies in a portion of the binding pocket that is critical for binding the D-ring region of the steroid, and they suggest that labeling of the receptor with a vicinally spaced dithiol-specific derivatizing agent may allow detection of conformational changes likely to occur in a critical region of the hormone binding domain on dissociation of hsp90. C1 UNIV MICHIGAN,SCH MED,DEPT PHARMACOL,ANN ARBOR,MI 48109. NIDDK,LMCB,STEROID HORMONES SECT,BETHESDA,MD 20814. FU NIDDK NIH HHS [DK31573] NR 36 TC 31 Z9 33 U1 0 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 13 PY 1993 VL 32 IS 14 BP 3729 EP 3736 DI 10.1021/bi00065a027 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX179 UT WOS:A1993KX17900027 PM 8466913 ER PT J AU PUTILINA, T SITTENFELD, D CHADER, GJ WIGGERT, B AF PUTILINA, T SITTENFELD, D CHADER, GJ WIGGERT, B TI STUDY OF A FATTY-ACID BINDING-SITE OF INTERPHOTORECEPTOR RETINOID-BINDING PROTEIN USING FLUORESCENT FATTY-ACIDS SO BIOCHEMISTRY LA English DT Article ID RAT-LIVER; TRANSPORT; LIGANDS; HEART AB Interphotoreceptor retinoid-binding protein (IRBP) is a 140-kDa glycolipoprotein which constitutes about 70% of the soluble protein of the retinal interphotoreceptor matrix. Much is known concerning its role in the transport of retinoids between photoreceptor cells and pigment epithelium but little is known about its interactions with lipids. Here we have examined the physicochemical characteristics of a fatty acid binding site of IRBP using a set of fluorescent fatty acid analogs with an anthracene moiety attached at different positions along the hydrocarbon chain. The results show that fatty acids are bound in a hydrophobic environment as indicated by a blue shift in fluorescence maxima and by a increase in quantum yield of the bound ligand. There is a single specific fatty acid binding site for each molecule of IRBP with an apparent K(d) = 3.6 X 10(-7) M. There is a nonradiative energy transfer from tryptophan residues to bound ligand. The interactions of IRBP and bound fatty acid are sensitive to denaturation by increasing concentrations of urea as judged by changes in nonradiative energy transfer efficiency and the quantum yield of bound probe. Quantum yields of bound fatty acid analogs varied with position of the fluorophore along the hydrocarbon chain and had the lowest values for the fluorophore located at the midpoint. Probing of the microenvironment of bound fluorophore with a quencher indicated a highly structured binding site. RP PUTILINA, T (reprint author), NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 37 TC 18 Z9 19 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 13 PY 1993 VL 32 IS 14 BP 3797 EP 3803 DI 10.1021/bi00065a036 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX179 UT WOS:A1993KX17900036 PM 8466918 ER PT J AU STEVENS, VJ CORRIGAN, SA OBARZANEK, E BERNAUER, E COOK, NR HEBERT, P MATTFELDTBEMAN, M OBERMAN, A SUGARS, C DALCIN, AT WHELTON, PK AF STEVENS, VJ CORRIGAN, SA OBARZANEK, E BERNAUER, E COOK, NR HEBERT, P MATTFELDTBEMAN, M OBERMAN, A SUGARS, C DALCIN, AT WHELTON, PK TI WEIGHT-LOSS INTERVENTION IN PHASE-1 OF THE TRIALS OF HYPERTENSION PREVENTION SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID BLOOD-PRESSURE; FINAL REPORT; REDUCTION; OBESITY; THERAPY; DRUG; RESTRICTION; PROGRAM; DIET; MEN AB Background: Phase 1 of the Trials of Hypertension Prevention was a collaborative, randomized controlled clinical trial designed to determine the feasibility and efficacy of selected nonpharmacologic interventions in reducing or preventing an increase in diastolic blood pressure. Methods: Participants aged 30 to 54 years who had a high-normal diastolic blood pressure (80 to 89 mm Hg), and were between 115% and 165% of their desirable body weight, were randomly assigned to either an 18-month weight loss intervention (n=308) or a usual-care control condition (N=256). Intervention consisted of 14 weekly group meetings followed by monthly maintenance sessions. Intervention participants received training in behavioral self-management technique and were asked to make life-style changes aimed at achieving a moderate reduction in energy intake and an increase in physical activity. Results: The average weight losses in the intervention group at 6, 12, and 18 months of follow-up were 6.5, 5.6, and 4.7 kg for men and 3.7, 2.7, and 1.6 kg for women. The mean (+/- SE) change in diastolic blood pressure for intervention participants compared with controls at termination was -2.8 +/- 0.6 mm Hg for men and -1.1 +/- 0.9 mm Hg for women. For systolic blood pressure, the corresponding change was -3.1 +/- 0.7 mm Hg for men and -2.0 +/- 1.3 mm Hg for women. Blood pressure reductions were greater for those who lost larger amounts of weight. Sex-related differences in blood pressure response were largely due to the smaller amount of weight lost by women, and sex differences in weight loss could be accounted for by differences in baseline body weight. Conclusions: During an 18-month follow-up period, this weight reduction program was shown to be an effective nonpharmacologic intervention for reducing blood pressure in overweight adults with high-normal blood pressure. C1 KAISER PERMANENTE CTR HLTH RES,PORTLAND,OR. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. NHLBI,BETHESDA,MD 20892. ST LOUIS UNIV,SCH MED,ST LOUIS,MO 63104. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD 21218. UNIV CALIF DAVIS,SACRAMENTO MED CTR,SACRAMENTO,CA 95817. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. UNIV ALABAMA,BIRMINGHAM,AL 35294. NR 39 TC 156 Z9 161 U1 0 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD APR 12 PY 1993 VL 153 IS 7 BP 849 EP 858 DI 10.1001/archinte.153.7.849 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA KW475 UT WOS:A1993KW47500006 PM 8466377 ER PT J AU BEZRUKOV, SM KASIANOWICZ, JJ AF BEZRUKOV, SM KASIANOWICZ, JJ TI CURRENT NOISE REVEALS PROTONATION KINETICS AND NUMBER OF IONIZABLE SITES IN AN OPEN PROTEIN ION CHANNEL SO PHYSICAL REVIEW LETTERS LA English DT Article ID AUREUS ALPHA-TOXIN; QUANTUM JUMPS; BINDING AB In analogy to current fluctuations found in solid state electronic microstructure devices, excess noise generated by the reversible ionization of sites in a transmembrane ionic channel was observed. By analyzing the pH-dependent fluctuations in the current through fully open single channels formed by the alpha-toxin protein, we were able to evaluate the protonation rate constants, the number of sites participating in the protonation process, and the effect of recharging a single site on the channel conductance. C1 NIDDK,LBM,BIOPHYS UNIT,BETHESDA,MD 20892. NATL INST STAND & TECHNOL,DEPT PHYS,DIV BIOTECHNOL,BIOSENSORS GRP,GAITHERSBURG,MD 20899. RP BEZRUKOV, SM (reprint author), UNIV MARYLAND,COLL PK,MD 20742, USA. NR 29 TC 123 Z9 125 U1 3 U2 12 PU AMERICAN PHYSICAL SOC PI COLLEGE PK PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA SN 0031-9007 J9 PHYS REV LETT JI Phys. Rev. Lett. PD APR 12 PY 1993 VL 70 IS 15 BP 2352 EP 2355 DI 10.1103/PhysRevLett.70.2352 PG 4 WC Physics, Multidisciplinary SC Physics GA KW756 UT WOS:A1993KW75600039 ER PT J AU ERZURUM, SC LEMARCHAND, P ROSENFELD, MA YOO, JH CRYSTAL, RG AF ERZURUM, SC LEMARCHAND, P ROSENFELD, MA YOO, JH CRYSTAL, RG TI PROTECTION OF HUMAN ENDOTHELIAL-CELLS FROM OXIDANT INJURY BY ADENOVIRUS-MEDIATED TRANSFER OF THE HUMAN CATALASE CDNA SO NUCLEIC ACIDS RESEARCH LA English DT Article ID GLUTATHIONE REDOX CYCLE; HYDROGEN-PEROXIDE; SUPEROXIDE-DISMUTASE; REPERFUSION INJURY; XANTHINE-OXIDASE; OXYGEN-TOXICITY; TISSUE-INJURY; FREE-RADICALS; NEUTROPHILS; DNA AB In a variety of disorders, endothelial cells are exposed to high levels of oxidants, generated within the cells and/or consequent to local inflammation. In the context of the sensitivity of endothelial cells to oxidant stress, particularly related to H2O2, we have designed a replication deficient recombinant adenovirus containing the human catalase cDNA (AdCL) to transfer the catalase cDNA to the endothelial cells, in order to augment intracellular anti-H2O2 protection. Human umbilical vein endothelial cells that were not infected or infected with control adenovirus maintained low levels of catalase mRNA. Endothelial cells infected with AdCL expressed AdCL-driven exogenous catalase mRNA, as early as 24 hr and at least for 7 days. Catalase protein levels were increased significantly over controls in cells infected with AdCL, as were catalase activity levels, with catalase activity correlated closely with levels of catalase protein. Importantly, when the endothelial cells were exposed to 500 muM H2O2, all the AdCL infected endothelial cells survived, compared to only 37% of the control cells. Thus, a recombinant adenovirus containing the human catalase cDNA is able to infect human endothelial cells in vitro and express high levels of functional intracellular catalase, protecting the cells against H2O2-mediated oxidant stress. These observations support the feasibility of the transfer of catalase cDNA to human endothelium to protect against oxidant injury. C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. RI lemarchand, patricia/C-3247-2011 NR 40 TC 82 Z9 82 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 APR 11 PY 1993 VL 21 IS 7 BP 1607 EP 1612 DI 10.1093/nar/21.7.1607 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX756 UT WOS:A1993KX75600016 PM 8479912 ER PT J AU BAUMANN, MH ROTHMAN, RB AF BAUMANN, MH ROTHMAN, RB TI EFFECTS OF ACUTE AND CHRONIC COCAINE ON THE ACTIVITY OF TUBEROINFUNDIBULAR DOPAMINE NEURONS IN THE RAT SO BRAIN RESEARCH LA English DT Article DE COCAINE; DOPAMINE SYNTHESIS; TUBEROINFUNDIBULAR DOPAMINE NEURON; MEDIAN EMINENCE; PROLACTIN ID MEDIAN-EMINENCE; PROLACTIN; SYSTEM; AUTORECEPTORS; HYPOTHESIS; WITHDRAWAL; PITUITARY; STRIATUM; BINDING; RELEASE AB We investigated the effects of acute and chronic cocaine on dopamine (DA) synthesis in tuberoinfundibular dopamine (TIDA) neurons by measuring the accumulation of 3,4-dihydroxyphenylalanine (DOPA) in the median eminence (ME). Cocaine-induced prolactin (PRL) responses were evaluated for comparison. Acute cocaine inhibited DA synthesis in the ME and decreased circulating PRL. Chronic cocaine did not after basal DOPA levels in TIDA nerve terminals or PRL levels in plasma. After repeated cocaine injections, cocaine's inhibitory effect on DA synthesis was abolished in the ME while the PRL response to drug was unchanged. These results suggest that TIDA neurons become tolerant to cocaine-induced suppression of DA synthesis after chronic cocaine exposure, but the altered sensitivity of TIDA neurons is not revealed by plasma PRL measures. RP BAUMANN, MH (reprint author), NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,BLDG C,4940 EASTERN AVE,POB 5180,BALTIMORE,MD 21224, USA. NR 36 TC 22 Z9 22 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 APR 9 PY 1993 VL 608 IS 1 BP 175 EP 179 DI 10.1016/0006-8993(93)90792-L PG 5 WC Neurosciences SC Neurosciences & Neurology GA KW778 UT WOS:A1993KW77800028 PM 8495344 ER PT J AU NOGUCHI, M YI, HF ROSENBLATT, HM FILIPOVICH, AH ADELSTEIN, S MODI, WS MCBRIDE, OW LEONARD, WJ AF NOGUCHI, M YI, HF ROSENBLATT, HM FILIPOVICH, AH ADELSTEIN, S MODI, WS MCBRIDE, OW LEONARD, WJ TI INTERLEUKIN-2 RECEPTOR GAMMA CHAIN MUTATION RESULTS IN X-LINKED SEVERE COMBINED IMMUNODEFICIENCY IN HUMANS SO CELL LA English DT Article ID B-CELLS; MOLECULAR-CLONING; ALPHA-CHAIN; CHROMOSOME INACTIVATION; IMMATURE THYMOCYTES; IL-2 RECEPTOR; HUMAN GENOME; LINKAGE MAP; BONE-MARROW; T-CELLS AB The interleukin-2 (IL-2) receptor gamma chain (IL-2Rgamma) is a component of high and intermediate affinity IL-2 receptors that is required to achieve full ligand binding affinity and internalization. We have localized the IL-2Rgamma gene to human chromosome Xq13. Genetic linkage analysis indicates that the IL-2Rgamma gene and the locus for X-linked severe combined immunodeficiency (XSCID) appear to be at the same position. Moreover, we demonstrate that each of three unrelated patients with XSCID has a different mutation in his IL-2Rgamma gene resulting in a different premature stop codon and predicted C-terminal truncation. These data establish that XSCID is associated with mutations of the IL-2Rgamma gene product. Since XSCID is characterized by absent or markedly reduced numbers of T cells, our findings imply that IL-2Rgamma plays a vital role in thymic maturation of T cells. These results also have important implications for prenatal and postnatal diagnosis, carrier female detection, and gene therapy for XSCID. C1 NCI,DIV CANC BIOL & DIAG,BIOCHEM LAB,BETHESDA,MD 20892. BAYLOR COLL MED,DEPT PEDIAT,DIV ALLERGY & IMMUNOL,HOUSTON,TX 77030. UNIV MINNESOTA HOSP & CLIN,DEPT PEDIAT,DIV IMMUNOL,MINNEAPOLIS,MN 55455. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21701. RP NOGUCHI, M (reprint author), NHLBI,INTRAMURAL RES PROGRAM,OFF DIRECTOR,PULM & MOLEC IMMUNOL SECT,BETHESDA,MD 20892, USA. RI Adelstein, Stephen/I-7936-2016 OI Adelstein, Stephen/0000-0001-7221-6298 FU NCRR NIH HHS [M01 RR00188] NR 65 TC 959 Z9 980 U1 8 U2 26 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD APR 9 PY 1993 VL 73 IS 1 BP 147 EP 157 DI 10.1016/0092-8674(93)90167-O PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KW753 UT WOS:A1993KW75300015 PM 8462096 ER PT J AU SMITH, RH WLADKOWSKI, BD TAYLOR, JE THOMPSON, EJ PRUSKI, B KLOSE, JR ANDREWS, AW MICHEJDA, CJ AF SMITH, RH WLADKOWSKI, BD TAYLOR, JE THOMPSON, EJ PRUSKI, B KLOSE, JR ANDREWS, AW MICHEJDA, CJ TI ACID-CATALYZED DECOMPOSITION OF 1-ALKYLTRIAZOLINES - A MECHANISTIC STUDY SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Article ID 1,3-DIALKYLTRIAZENES; TRIALKYLTRIAZENES; MUTAGENICITY; TRIAZENES AB 1-Alkyltriazolines are five-membered cyclic triazenes containing the unusual Z-configuration for the triazene moiety. The hydrolytic decomposition of these compounds in aqueous or mixed acetonitrile-aqueous buffers leads predominantly to the formation of the corresponding 1-alkylaziridines and lesser amounts of 2-(alkylamino)ethanols, alkylamines, and acetaldehyde. The latter two products presumably result from hydrolysis of a rearrangement product, N-ethylidenealkylamine. Neither the nature of the 1-alkyl group nor the pH of the medium greatly influences the product distribution, although decomposition in purely aqueous buffers slightly reduces the aziridine yields. The rate of hydrolysis of 1-alkyltriazolines is about twice as fast as that of the analogous acyclic 1,3,3-trialkyltriazenes and varies in the order tert-butyl > isopropyl > ethyl > butyl > methyl > propyl > benzyl. The mechanism of the decomposition is specific acid-catalyzed (A1) involving rapid reversible protonation followed by rate-limiting formation of a 2-(alkylamino)ethyldiazonium ion. The slopes of the log k(obs) versus pH plots are near -1.0. The solvent deuterium isotope effect, k(H2O)/k(D2O), is in all cases <1.0 and ranges from 0.58 for 1-methyltriazoline to 0.86 for 1-benzyltriazoline. The rate of decomposition shows no significant dependence on the concentration of the buffer acid. The proposed mechanism involves rate-limiting formation of a 2-(alkylamino)ethyldiazonium ion, which is then partitioned among several competing product formation pathways. 1-Alkyltriazolines are potent direct-acting mutagens in the alkylation-sensitive TA 1535 strain of Salmonella typhimurium. A clear, dose-dependent mutagenicity is observed. At the highest dose level, various 1-alkyltriazolines have activities roughly equivalent to that of the potent methylating agent, 1,3-dimethyltriazene. At low levels of substrate, 1-alkyltriazolines are significantly more active than 1,3-dimethyltriazene, with mutagenicity following the order benzyl > methyl > ethyl. C1 NCI,FREDERICK CANC RES & DEV CTR,MOLEC ASPECTS DRUG DESIGN SECT,ABL,BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DYN CORP,PROGRAM RESOURCES INC,CHEM SYNTH & ANAL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DYN CORP,PROGRAM RESOURCES INC,FREDERICK,MD 21702. RP SMITH, RH (reprint author), WESTERN MARYLAND COLL,DEPT CHEM,WESTMINSTER,MD 21157, USA. NR 34 TC 15 Z9 15 U1 2 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 APR 9 PY 1993 VL 58 IS 8 BP 2097 EP 2103 DI 10.1021/jo00060a027 PG 7 WC Chemistry, Organic SC Chemistry GA KX348 UT WOS:A1993KX34800027 ER PT J AU STANTON, GB BRUCE, CJ GOLDBERG, ME AF STANTON, GB BRUCE, CJ GOLDBERG, ME TI TOPOGRAPHY OF PROJECTIONS TO THE FRONTAL-LOBE FROM THE MACAQUE FRONTAL EYE FIELDS SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE AUTORADIOGRAPHY; MONKEY; NEURAL CONNECTIVITY; SACCADES; EYE MOVEMENTS ID DORSOLATERAL PREFRONTAL CORTEX; RHESUS-MONKEY; INTRACORTICAL MICROSTIMULATION; CORTICAL CONNECTIONS; SQUIRREL-MONKEYS; TERMINAL FIELDS; UNIT-ACTIVITY; OWL MONKEYS; NEURONS; MOVEMENTS AB Efferents from the frontal eye fields (FEF) to the ipsilateral frontal lobe were studied by autoradiography of tritiated tracers (leucine, proline, and fucose) in seven macaque monkeys that were used previously to describe subcortical connections. In four of the cases, tracer injection sites were confirmed by low thresholds for the electrical elicitation of saccadic eye movements. Cases were grouped as IFEF or sFEF cases according to large or small saccades that were characteristic of the injection site. Projections from the FEF terminated in five frontal regions: 1) area FD on the dorsomedial convexity; 2) area FC (containing SEF) medial to the upper limb of the arcuate sulcus; 3) areas FD and FDDELTA along the walls of the principal sulcus; 4) area FCBm on the deep, posterior wall of the arcuate sulcus inferior to the sulcal spur; and 5) the inferolateral cortex (area FDi) on the convexity and lateral two thirds of the anterior wall of the arcuate sulcus. Projections in sFEF cases tended to be confined to medial parts of dorsomedial FD and FC and the lateral wall of the principal sulcus and inferolateral convexity. Neither IFEF nor sFEF appeared to project to the SMA or pericingulate cortex. Label in these areas was found only in the cases in which tracer spread into non-FEF areas. FEF projections terminated in column-like patches of about 500-600 mum in diameter. Labeled axons and terminals were seen in all cortical layers regardless of location in the frontal lobe. C1 YALE UNIV,SCH MED,NEUROBIOL SECT,NEW HAVEN,CT 06510. NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. RP STANTON, GB (reprint author), HOWARD UNIV,COLL MED,DEPT ANAT,WASHINGTON,DC 20059, USA. OI Bruce, Charles/0000-0002-7481-5793 FU NEI NIH HHS [EY-04740, EY-03763] NR 52 TC 83 Z9 83 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD APR 8 PY 1993 VL 330 IS 2 BP 286 EP 301 DI 10.1002/cne.903300209 PG 16 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA KT099 UT WOS:A1993KT09900008 PM 8491870 ER PT J AU HAUSER, P ZAMETKIN, AJ MARTINEZ, P VITIELLO, B MATOCHIK, JA MIXSON, AJ WEINTRAUB, BD AF HAUSER, P ZAMETKIN, AJ MARTINEZ, P VITIELLO, B MATOCHIK, JA MIXSON, AJ WEINTRAUB, BD TI ATTENTION-DEFICIT HYPERACTIVITY DISORDER IN PEOPLE WITH GENERALIZED RESISTANCE TO THYROID-HORMONE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID ERBA-BETA GENE; RECEPTOR; KINDREDS; BINDING; BRAIN; TRIIODOTHYRONINE; INTERVIEW; MUTATION; CHILDREN; PROTEIN AB Background. Attention deficit-hyperactivity disorder is a well-recognized psychiatric disorder of childhood. Its cause is unknown, but there is evidence of a familial predisposition. Symptoms suggestive of this disorder have been reported in subjects with generalized resistance to thyroid hormone, a disease caused by mutations in the thyroid receptor-beta gene and characterized by reduced responsiveness of peripheral and pituitary tissues to the actions of thyroid hormone. We systematically evaluated the presence and severity of attention deficit-hyperactivity disorder in 18 families with a history of generalized resistance to thyroid hormone. Methods. We studied 49 affected and 55 unaffected family members; 52 were adults, and 52 were children. All subjects were evaluated with structured psychiatric questionnaires by interviewers who were unaware of the medical diagnosis. The number of symptoms of attention deficit-hyperactivity disorder was calculated for each subject. Results. Among the adults, 11 of 22 subjects with generalized resistance to thyroid hormone (50 percent) and 2 of 30 unaffected subjects (7 percent) had met the criteria for attention deficit-hyperactivity disorder as children (P less-than-or-equal-to 0.001). Among the children, 19 of 27 subjects resistant to thyroid hormone (70 percent) and 5 of 25 unaffected subjects (20 percent) met the criteria for the disorder (P<0.001). The odds of having attention deficit-hyperactivity disorder were 3.2 times higher for affected male subjects than for affected female subjects and 2.7 times higher for unaffected male subjects than for unaffected female subjects. The mean symptom score was 2.5 times higher in the affected group than in the unaffected group (7.0 vs. 2.8, P<0.001). The frequency of other psychiatric diagnoses was similar in the two groups. Conclusions. In our study sample, attention deficit-hyperactivity disorder is strongly associated with generalized resistance to thyroid hormone. C1 NIMH,CEREBRAL METAB LAB,CLIN BRAIN IMAGING SECT,BETHESDA,MD 20892. NIMH,DEV PSYCHOL LAB,BETHESDA,MD 20892. NIMH,DIV BASIC BRAIN & BEHAV SCI,BETHESDA,MD 20892. RP HAUSER, P (reprint author), NIDDKD,MOLEC & CELLULAR ENDOCRINOL BRANCH,RM 8D-14,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 32 TC 215 Z9 216 U1 2 U2 3 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 APR 8 PY 1993 VL 328 IS 14 BP 997 EP 1001 DI 10.1056/NEJM199304083281403 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA KW282 UT WOS:A1993KW28200003 PM 8450877 ER PT J AU BREWSTER, ME HUANG, MJ POP, E PITHA, J DEWAR, MJS KAMINSKI, JJ BODOR, N AF BREWSTER, ME HUANG, MJ POP, E PITHA, J DEWAR, MJS KAMINSKI, JJ BODOR, N TI AN AM1 MOLECULAR-ORBITAL STUDY OF ALPHA-D-GLUCOPYRANOSE AND BETA-MALTOSE - EVALUATION AND IMPLICATIONS SO CARBOHYDRATE RESEARCH LA English DT Article ID NEUTRON-DIFFRACTION; CARBOHYDRATE-CHEMISTRY; MAIZE STARCHES; SUBSTITUTION; CRYSTAL; MODELS; CYCLODEXTRIN; MONOHYDRATE; REFINEMENT; GLUCOSE AB Chemical reactivity and other characteristics of alpha-D-glucopyranose and beta-maltose were evaluated within a semiempirical molecular orbital (AM1) framework. Theoretically generated structures compared well to those determined by X-ray crystallographic techniques. Calculations suggested that the secondary hydroxy functions (OH-2 and OH-3) of the mono- and di-saccharides were more acidic than the primary alcohol (OH-6), which is consistent with experimental findings. In addition, the enhanced reactivity of the OH-3 locus, which is observed upon OH-2 alkylation of the object sugars, was rationalized in terms of increased OH-3 acidity. The chemical behavior of the monomers examined may be insightful in explaining the reactivity of glucopyranose polymers. C1 SCHERING PLOUGH CORP, BLOOMFIELD, NJ 07003 USA. UNIV FLORIDA, DEPT CHEM, GAINESVILLE, FL 32610 USA. UNIV FLORIDA, COLL PHARM, CTR DRUG DISCOVERY, GAINESVILLE, FL 32610 USA. NIA, BETHESDA, MD 20892 USA. RP BREWSTER, ME (reprint author), PHARMOS INC, POB 730, ALACHUA, FL 32615 USA. NR 43 TC 24 Z9 24 U1 0 U2 7 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0008-6215 EI 1873-426X J9 CARBOHYD RES JI Carbohydr. Res. PD APR 7 PY 1993 VL 242 BP 53 EP 67 DI 10.1016/0008-6215(93)80021-6 PG 15 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA KX487 UT WOS:A1993KX48700005 PM 8495446 ER PT J AU HEALY, B AF HEALY, B TI MUCOSAL IMMUNITY, VACCINE DEVELOPMENTS NEW FRONTIER SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material C1 NIH,BETHESDA,MD 20892. NR 2 TC 3 Z9 3 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 APR 7 PY 1993 VL 269 IS 13 BP 1612 EP 1612 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KV349 UT WOS:A1993KV34900006 PM 8455284 ER PT J AU CSAKO, G ELIN, RJ AF CSAKO, G ELIN, RJ TI UNRECOGNIZED FALSE-POSITIVE KETONES FROM DRUGS CONTAINING FREE-SULFHYDRYL GROUP(S) SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter ID THERAPY; MESNA RP CSAKO, G (reprint author), NIH,BETHESDA,MD 20892, USA. NR 5 TC 7 Z9 7 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 APR 7 PY 1993 VL 269 IS 13 BP 1634 EP 1634 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KV349 UT WOS:A1993KV34900013 PM 8455289 ER PT J AU GELERNTER, J GOLDMAN, D RISCH, N AF GELERNTER, J GOLDMAN, D RISCH, N TI THE A1 ALLELE AT THE D2-DOPAMINE RECEPTOR GENE AND ALCOHOLISM - A REAPPRAISAL SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID ASSOCIATION; LOCUS; DRD2 AB Objective.-An allelic association between the Taq I ''A'' system A1 allele at the D2 dopamine receptor locus (DRD2) and either alcoholism or severe alcoholism has been proposed. Our purpose was to evaluate whether, based on all of the accumulated evidence, this association could be considered to be proven. Data Sources.-We considered data from all published reports of DRD2 allele frequency in alcoholics, controls, or both. Study Selection.-We concentrated on the issue of replication. We therefore considered all data reported (on white samples, because DRD2 allele frequency varies by race and ethnicity) since the first report by Blum et al in 1990. Data Synthesis.-We analyzed the set of data for differences in allele frequencies between alcoholics and controls, and for heterogeneity among samples. We also investigated the influence of the data from the first group to report an association (including a subsequent report from that group) on the findings. Our analysis shows that, when all studies subsequent to the original study are considered, there is no significant difference in DRD2 A1 allele frequency between alcoholics and controls, there is significant heterogeneity among reported alcoholics and reported controls, and there is no significant difference in DRD2A1 allele frequency between severe and not severe alcoholics. Also, the two reports of Blum et al account for all of the (nonsignificant) differences seen between controls, alcoholics, and severe alcoholics. Conclusions.-In general, heterogeneity among studies (for alcoholics or controls) is considerably greater than differences between alcoholics and controls overall. The findings to date can best be explained by more conservative interpretations than a confirmed physiologically important allelic association between DRD2 alleles and alcoholism. These other possibilities include sampling error and ethnic variation in those studies that individually showed a large effect. C1 YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT EPIDEMIOL & PUBL HLTH,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06510. NIAAA,NEUROGENET LAB,ROCKVILLE,MD 20852. RP GELERNTER, J (reprint author), W HAVEN DEPT VET AFFAIRS MED CTR,950 CAMPBELL AVE,W HAVEN,CT 06516, USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 FU NHGRI NIH HHS [HG00348]; NIMH NIH HHS [MH00931] NR 22 TC 251 Z9 252 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 7 PY 1993 VL 269 IS 13 BP 1673 EP 1677 DI 10.1001/jama.269.13.1673 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA KV349 UT WOS:A1993KV34900033 PM 8095994 ER PT J AU MORRISON, PF DEDRICK, RL AF MORRISON, PF DEDRICK, RL TI DISCOVERING SWITCH PHARMACEUTICALS FROM MULTISTATIONARY BIOCHEMICAL NETWORKS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID PHOSPHOFRUCTOKINASE; OSCILLATIONS; STATES; SYSTEM RP MORRISON, PF (reprint author), NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13,BETHESDA,MD 20892, USA. NR 12 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 APR 7 PY 1993 VL 85 IS 7 BP 518 EP 518 DI 10.1093/jnci/85.7.518 PG 1 WC Oncology SC Oncology GA KV467 UT WOS:A1993KV46700001 PM 8455193 ER PT J AU MONFARDINI, S YANCIK, R AF MONFARDINI, S YANCIK, R TI CANCER IN THE ELDERLY - MEETING THE CHALLENGE OF AN AGING POPULATION SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID ONCOLOGY-GROUP; BREAST-CANCER; AGE; CHEMOTHERAPY; STAGE; DIAGNOSIS; THERAPY; PATIENT; VARIES; WOMEN C1 NIA,9000 ROCKVILLE PIKE,BLDG 31,RM 5C05,BETHESDA,MD 20892. IST NAZL TUMORI,CTR RIFERIMENTO ONCOL,DIV MED ONCOL,AVIANO,ITALY. NR 35 TC 67 Z9 67 U1 0 U2 1 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 7 PY 1993 VL 85 IS 7 BP 532 EP 538 DI 10.1093/jnci/85.7.532 PG 7 WC Oncology SC Oncology GA KV467 UT WOS:A1993KV46700008 PM 8455199 ER PT J AU SMITH, MA RUBINSTEIN, L CAZENAVE, L UNGERLEIDER, RS MAURER, HM HEYN, R KHAN, FM GEHAN, E AF SMITH, MA RUBINSTEIN, L CAZENAVE, L UNGERLEIDER, RS MAURER, HM HEYN, R KHAN, FM GEHAN, E TI REPORT OF THE CANCER-THERAPY EVALUATION PROGRAM MONITORING PLAN FOR SECONDARY ACUTE MYELOID-LEUKEMIA FOLLOWING TREATMENT WITH EPIPODOPHYLLOTOXINS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ACUTE NONLYMPHOCYTIC LEUKEMIA; SMALL-CELL-CARCINOMA; COMPLICATING HODGKINS-DISEASE; SEMUSTINE METHYL-CCNU; BREAST-CANCER; MYELODYSPLASTIC SYNDROME; ADJUVANT CHEMOTHERAPY; OVARIAN-CARCINOMA; ALKYLATING-AGENTS; 2ND MALIGNANCIES AB Background: Recent reports have documented the occurrence of treatment-related acute myeloid leukemia (AML) following therapy with epipodophyllotoxins. These reports have led to growing concern among oncologists, which could lead to premature abandonment of these agents at a time when the relationship between cumulative dose of epipodophyllotoxin and risk of treatment-related AML has not been determined. Purpose: Because of the increasingly important role of epipodophyllotoxins in the treatment of several types of adult and pediatric tumors, the Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute (NCI) has developed a monitoring plan to obtain reliable estimates of the risk of treatment-related AML following epipodophyllotoxin treatment. Methods: We identified 12 NCI-supported Cooperative Group clinical trials in which patients with solid tumors are being treated with epipodophyllotoxins at different cumulative doses. One trial is using a moderate dose of teniposide (900 mg/m2), and 11 trials are using etoposide at a low dose (<1500 mg/m2), a moderate dose (1500-3999 mg/m2), or a high dose (greater-than-or-equal-to 4000 mg/m2). Cases of treatment-related AML and treatment-related myelodysplastic syndrome (MDS) (hereafter referred to as treatment-related AML/MDS) occurring in these trials are reported to CTEP, with initial analysis for each cumulative dose group triggered by the reporting of four cases of treatment-related AML/MDS in that group. For each analysis, total patient follow-up for the group is determined and cumulative 6-year incidence rate is calculated. Results: Three cases of treatment-related AML and one case of treatment-related MDS (with documented monosomy 7) were reported in a group of 207 patients who received etoposide at a low cumulative dose. The calculated 6-year rate of development of treatment-related AML/MDS was 3.2% (95% upper confidence interval bounded by 7.2%). Conclusions: The 6-year cumulative rate of treatment-related AML/MDS (3.2%) is within the range previously reported for alkylator-based regimens that did not include epipodophyllotoxins. Implications: Previous reports have suggested that higher cumulative doses of alkylators are associated with increased risk of treatment-related AML, and a critical goal of the monitoring plan is to determine whether a similar relationship exists for the epipodophyllotoxins. Estimates will be developed for leukemogenic risk for the moderate- and high-cumulative-dose groups when four cases of treatment-related AML/MDS have been identified within each group. C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. MOTT CHILDRENS HOSP,ANN ARBOR,MI. PEDIAT INTERGRP STAT CTR,HOUSTON,TX. RP SMITH, MA (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,RM 741,EXECUT PLAZA N,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA-30138, CA-30969, CA-24507] NR 46 TC 60 Z9 61 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 APR 7 PY 1993 VL 85 IS 7 BP 554 EP 558 DI 10.1093/jnci/85.7.554 PG 5 WC Oncology SC Oncology GA KV467 UT WOS:A1993KV46700011 PM 8455202 ER PT J AU MILLER, MS BUZARD, GS MCDOWELL, AE AF MILLER, MS BUZARD, GS MCDOWELL, AE TI INVIVO INHIBITION OF GLUCOCORTICOID-INDUCIBLE GENE-EXPRESSION BY DIMETHYLNITROSAMINE IN RAT-LIVER SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID HEPATOMA-CELLS; MESSENGER-RNA; C-JUN; DNA; BINDING; RECEPTOR; HORMONE; N-METHYL-N'-NITRO-N-NITROSOGUANIDINE; HEPATOCYTES; PROMOTER AB Sprague-Dawley rats were pretreated with a single i.p. injection of either 2.25 mL/kg of phosphate-buffered saline (PBS) or 22.5 mg/kg of dimethylnitrosamine (DMN) followed 2 hr later by a single i.p. injection of either 1.35 mg/kg of dexamethasone (DEX) or the vehicle, a 50% ethanol solution, both delivered in a volume of 3 mL/kg. RNA levels of the hormone-inducible. specialized liver function genes, tyrosine aminotransferase (TAT) and glutamine synthetase (GS), were monitored 4, 5, 6, 7, 8, and 10 hr after the DEX injection. Maximal induction of both the TAT (26-fold) and GS (6-fold) RNAs occurred 6 hr after DEX administration in PBS-pretreated animals. Pretreatment with DMN caused at least a 42% inhibition of DEX-induced RNA accumulation at every time point examined, with greater than 90% inhibition occurring when the genes were maximally induced at 6 hr. This inhibition was not due to any alterations of the glucocorticoid receptors as DMN had no effect on the binding affinity or amounts of glucocorticoid receptors present in rat hepatic cytosols. These results suggest that chemical carcinogens such as DMN may affect normal gene function in vivo by inhibiting the cellular response to hormone receptors mediating differentiation-associated, specialized cell functions. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21701. NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21701. NR 44 TC 14 Z9 15 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD APR 6 PY 1993 VL 45 IS 7 BP 1465 EP 1470 DI 10.1016/0006-2952(93)90046-Y PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KX573 UT WOS:A1993KX57300012 PM 8097092 ER PT J AU BLANEY, SM GREM, JL BALIS, FM COLE, DE ADAMSON, PC POPLACK, DG AF BLANEY, SM GREM, JL BALIS, FM COLE, DE ADAMSON, PC POPLACK, DG TI MECHANISM OF RESISTANCE TO CYCLOPENTENYL CYTOSINE (CPE-C) IN MOLT-4 LYMPHOBLASTS SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID CYTIDINE DEAMINASE; 1-BETA-D-ARABINOFURANOSYLCYTOSINE 5'-TRIPHOSPHATE; CTP SYNTHETASE; CELLS; TRIPHOSPHATE; LEUKEMIA; PHARMACOLOGY; QUANTITATION; PURIFICATION; INHIBITION AB Cyclopentenyl cytosine (CPE-C), a carbocyclic analogue of cytidine. has preclinical anti-neoplastic activity against ara-C resistant murine leukemias and a broad spectrum of human tumor xenografts. CPE-C is a prodrug and requires intracellular phosphorylation to cyclopentenyl cytosine triphosphate (CPE-CTP) which depletes endogenous CTP pools. The initial step in this activation process is catalyzed by uridine/cytidine kinase. We studied the mechanism of resistance to CPE-C in a Molt-4 T-cell leukemia line made resistant to CPE-C (Molt-4R) by culturing it in the continuous presence of increasing concentrations of CPE-C. Using a tetrazolium based colorimetric assay to assess cytotoxicity, the IC90 for the parent Molt-4 cells (Molt-4WT) was 0.5 muM after a 24 hr drug exposure. In contrast, cytotoxicity was not observed at concentrations as high as 1 mM in the Molt-4R cells. Following a brief exposure to 1 muM CPE-C, parent drug could be detected intracellularly in the resistant and sensitive cell lines. However, CPE-CTP formation was reduced markedly in the resistant cell line. Measurement of the activity of anabolic and catabolic enzymes in the Molt-4WT and Molt-4R cells revealed equivalent activities of alkaline and acid phosphatases as well as cytidine and dCMP deaminase but there was a significant reduction in uridine/cytidine kinase activity in Molt-4R cells. Endogenous ribonucleotide pools and CPE-CTP pools were measured in the absence and presence of CPE-C. CTP pools were reduced markedly in Molt-4WT cells following exposure to CPE-C. However, CTP pools in Molt-4R cells exposed to 100 muM CPE-C were two times greater than in the untreated Molt-4WT cells. At high concentrations of CPE-C (10 and 100 muM), Molt-4R cells were able to generate amounts of CPE-CTP equivalent to that seen in Molt-4WT cells exposed to 1 muM CPE-C (a cytotoxic concentration of drug in Molt-4WT cells), but no cytotoxic effect was seen in Molt-4R cells. Therefore, in addition to decreased uridine/cytidine kinase activity, a second mechanism of resistance that is the result of alterations in CTP synthetase activity also appears to be operative. Elucidation of the mechanism of resistance in vitro may provide insight into the mechanism of action of the drug and potential mechanisms of resistance in vivo. C1 WALTER REED ARMY MED CTR, WASHINGTON, DC 20307 USA. NATL NAVAL MED CTR, NCI, NAVY MED ONCOL BRANCH, BETHESDA, MD 20899 USA. RP BLANEY, SM (reprint author), NCI, PEDIAT BRANCH, BLDG 10, ROOM 13N240, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 26 TC 11 Z9 11 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 APR 6 PY 1993 VL 45 IS 7 BP 1493 EP 1501 DI 10.1016/0006-2952(93)90050-7 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KX573 UT WOS:A1993KX57300016 PM 8471071 ER PT J AU BAI, R ROACH, MC JAYARAM, SK BARKOCZY, J PETTIT, GR LUDUENA, RF HAMEL, E AF BAI, R ROACH, MC JAYARAM, SK BARKOCZY, J PETTIT, GR LUDUENA, RF HAMEL, E TI DIFFERENTIAL-EFFECTS OF ACTIVE ISOMERS, SEGMENTS, AND ANALOGS OF DOLASTATIN-10 ON LIGAND INTERACTIONS WITH TUBULIN - CORRELATION WITH CYTOTOXICITY SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID BOVINE BRAIN TUBULIN; PHOMOPSIN-A; ANTINEOPLASTIC AGENTS; MICROTUBULE ENDS; BINDING; POLYMERIZATION; DERIVATIVES; NUCLEOTIDE; SITE; BETA-1-TUBULIN AB Dolastatin 10 is a potent antimitotic peptide isolated from the marine mollusk Dolabella auricularia. Four of its five residues are modified amino acids (in sequence, dolavaline, valine, dolaisoleuine, dolaproine, dolaphenine). Besides inhibiting tubulin polymerization, dolastatin 10 non-competitively inhibits vinca alkaloid binding to tubulin, inhibits nucleotide exchange and formation of the beta(s) cross-link, and stabilizes the colchicine binding activity of tubulin. To examine the mechanism of action of dolastatin 10 we prepared six chiral isomers, one tri- and one tetrapeptide segment, and one pentapeptide analog of dolastatin 10, all of which differ little from dolastatin 10 as inhibitors of tubulin polymerization. However, only two of the chiral isomers were similar to dolastatin 10 in their cytotoxicity for L1210 murine leukemia cells and in their effects on vinblastine binding, nucleotide exchange, beta(s) cross-link formation, and colchicine binding. These were isomer 2, with reversal of configuration at position C(19a) in the dolaisoleuine moiety, and isomer 19, with reversal of configuration at position C(6) in the dolaphenine moiety. The pentapeptides with reduced cytotoxicity and reduced effects on tubulin interactions with other ligands were all modified in the dolaproine moiety at positions C(9) and/or C(10). The tripeptide and tetrapeptide segments which inhibited polymerization but not ligand interactions were the amino terminal tripeptide (lacking dolaproine and dolaphenine) and the carboxyl terminal tetrapeptide (lacking dolavaline). We speculate that strong inhibition of other ligand interactions with tubulin requires stable peptide binding to tubulin (i.e. slow dissociation), but that inhibition of polymerization requires only rapid binding to tubulin. C1 NCI,DIV CANC,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78284. ARIZONA STATE UNIV,DEPT CHEM,TEMPE,AZ 85287. ARIZONA STATE UNIV,CANC RES INST,TEMPE,AZ 85287. FU NCI NIH HHS [CA-443440-1A1-02, CA26376] NR 39 TC 75 Z9 76 U1 0 U2 4 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 APR 6 PY 1993 VL 45 IS 7 BP 1503 EP 1515 DI 10.1016/0006-2952(93)90051-W PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KX573 UT WOS:A1993KX57300017 PM 8471072 ER PT J AU TOZSER, J FRIEDMAN, D WEBER, IT BLAHA, I OROSZLAN, S AF TOZSER, J FRIEDMAN, D WEBER, IT BLAHA, I OROSZLAN, S TI STUDIES ON THE SUBSTRATE-SPECIFICITY OF THE PROTEINASE OF EQUINE INFECTIOUS-ANEMIA VIRUS USING OLIGOPEPTIDE SUBSTRATES SO BIOCHEMISTRY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-1 PROTEASE; REVERSE-TRANSCRIPTASE; RETROVIRAL PROTEASE; NUCLEOTIDE-SEQUENCE; CHEMICAL SYNTHESIS; VIRAL PROTEINASES; ESCHERICHIA-COLI; POL POLYPROTEINS; LEUKEMIA-VIRUS AB The proteinase of the equine infectious anemia virus (EIAV), a lentivirus closely related to human immunodeficiency virus (HIV), was purified from concentrated virus. The specificity of the enzyme was characterized using oligopeptides representing naturally occurring cleavage sites in the Gag and Gag-Pol polyproteins. The length of the substrate binding pocket was found to be 1-2 residues longer than that of HIV proteinases. Although the EIAV and HIV proteinases cleaved most of the peptides at the same bond, some were hydrolyzed by only the EIAV enzyme. Oligopeptides representing cleavage sites in the nucleocapsid protein were also found to be substrates of the EIAV proteinase. However, these peptides were not hydrolyzed by the HIV proteinases. While peptides representing the corresponding sequences in the first cysteine arrays of the nucleocapsid proteins of HIV-1 and HIV-2 were substrates of the proteinases, peptides representing the homologous sequences in the second Cys arrays were resistant against the proteolytic attack. A three-dimensional model of the EIAV proteinase built on the basis of homology with HIV-1 proteinase was used to interpret the differences. In addition to the oligopeptides representing cleavage sites in the Gag and Gag-Pol polyproteins, the EIAV proteinase was also able to cleave an oligopeptide mimicking a cleavage site in the transmembrane protein. Our results suggest that the specificity of lentiviral proteinases share common characteristics, although substantial differences may exist in hydrolysis of some peptides. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MOLEC VIROL & CARCINOGENESIS LAB, FREDERICK, MD 21702 USA. THOMAS JEFFERSON UNIV, JEFFERSON CANC INST, DEPT PHARMACOL, PHILADELPHIA, PA 19107 USA. DEBRECEN UNIV MED, DEPT BIOCHEM, H-4012 DEBRECEN, HUNGARY. CZECHOSLOVAK ACAD SCI, INST ORGAN CHEM & BIOCHEM, CS-16610 PRAGUE 6, CZECHOSLOVAKIA. 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 58 TC 36 Z9 36 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 6 PY 1993 VL 32 IS 13 BP 3347 EP 3353 DI 10.1021/bi00064a018 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW112 UT WOS:A1993KW11200018 PM 8384879 ER PT J AU WEBER, IT TOZSER, J WU, J FRIEDMAN, D OROSZLAN, S AF WEBER, IT TOZSER, J WU, J FRIEDMAN, D OROSZLAN, S TI MOLECULAR-MODEL OF EQUINE INFECTIOUS-ANEMIA VIRUS PROTEINASE AND KINETIC MEASUREMENTS FOR PEPTIDE-SUBSTRATES WITH SINGLE AMINO-ACID SUBSTITUTIONS SO BIOCHEMISTRY LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS-1; SYNTHETIC HIV-1 PROTEASE; RETROVIRAL PROTEASES; CRYSTAL-STRUCTURE; TYPE-1 PROTEASE; BINDING-SITE; INHIBITOR; RESOLUTION; COMPLEX; FAMILY AB A molecular model has been built of the equine infectious anemia virus (EIAV) proteinase on the basis of the crystal structures of the related Rous sarcoma virus (RSV) and human immunodeficiency virus (HIV) proteinases. The 104 residue long EIAV proteinase has 30 identical and 11 similar amino acids compared to those in HIV-1 proteinase and 25 identical and 18 similar amino acids compared to RSV proteinase. The overall structure is predicted to be close to that of HIV-1 proteinase. Two regions show differences: there are 6 additional residues leading to the tip of the flap, which is predicted to be involved in interactions with substrate, and there is a single residue deletion in the beta b' strand at a position equivalent to residue 60 in HIV-1 proteinase. The conformation of the residues leading to the flap was modeled by analogy to the corresponding region of RSV proteinase. The peptide substrate, VSQNYPIVQ, was modeled by analogy to the inhibitors in the cocrystal structures of HIV-1 proteinase, and the residues forming the substrate binding sites of EIAV proteinase were identified. EIAV proteinase showed several nonconservative substitutions in these residues compared to HIV-1 proteinase: Thr 30 instead of Asp in subsites S2, S2', S4, and S4', Ile 54 instead of Gly 48 in subsites S1, S1', S3, and S3', Arg 79 instead of Thr 74 in S4 and S4', and Ile 85 instead of Thr 80 in subsites S1 and S1'. The presence of additional residues in the flaps which lie over the substrate at S4 and S4' and the substitutions in the individual subsites can be correlated with differences in specificity of HIV and EIAV proteinases for various substrate peptides. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MOLEC VIROL & CARCINOGENESIS LAB, FREDERICK, MD 21702 USA. DEBRECEN UNIV MED, DEPT BIOCHEM, H-4012 DEBRECEN, HUNGARY. RP WEBER, IT (reprint author), THOMAS JEFFERSON UNIV, JEFFERSON CANC INST, DEPT PHARMACOL, PHILADELPHIA, PA 19107 USA. RI Tozser, Jozsef/A-7840-2008 OI Tozser, Jozsef/0000-0003-0274-0056 FU NCI NIH HHS [N01-CO-74101] NR 41 TC 16 Z9 17 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 6 PY 1993 VL 32 IS 13 BP 3354 EP 3362 DI 10.1021/bi00064a019 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW112 UT WOS:A1993KW11200019 PM 8384880 ER PT J AU HAMAWY, MM MERGENHAGEN, SE SIRAGANIAN, RP AF HAMAWY, MM MERGENHAGEN, SE SIRAGANIAN, RP TI TYROSINE PHOSPHORYLATION OF PP125(FAK) BY THE AGGREGATION OF HIGH-AFFINITY IMMUNOGLOBULIN-E RECEPTORS REQUIRES CELL ADHERENCE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID BASOPHILIC LEUKEMIA-CELLS; VIRUS-TRANSFORMED CELLS; PROTEIN KINASE-C; SIGNAL TRANSDUCTION; HISTAMINE-RELEASE; PHORBOL ESTER; 2H3 CELLS; CALCIUM SIGNAL; INTEGRIN; TALIN AB The aggregation of the high affinity IgE receptor (FcespilsonRI) in adherent rat basophilic leukemia (RBL-2H3) cells induces the tyrosine phosphorylation of several proteins. We examined whether focal adhesion-associated tyrosine kinase, pp125FAK, is one of these proteins. Anti-pp125FAK monoclonal antibody immunoblotted and precipitated a 115-kDa tyrosine-phosphorylated protein. In the absence of FcepsilonRI aggregation, pp125FAK was tyrosine-phosphorylated only in adherent cells. Aggregating FcepsilonRI in adherent cells markedly enhanced tyrosine phosphorylation of pp125FAK. This increase was detectable within 1 min of FcepsilonRI aggregation and was maximal by 15 min. In contrast, in nonadherent cells FcepsilonRI aggregation did not induce tyrosine phosphorylation of pp125FAK. The enhanced influx of calcium by calcium ionophore or the activation of protein kinase C by phorbol myristate acetate induced tyrosine phosphorylation of pp125FAK only in adherent cells. Thus, FcepsilonRI-induced tyrosine phosphorylation of pp125FAK could be mediated by the activation of protein kinase C and/or the induction of calcium influx. The data indicate that cell adherence is essential for FcepsilonRI-induced tyrosine phosphorylation of pp125FAK. RP HAMAWY, MM (reprint author), NIDR,IMMUNOL LAB,BLDG 10,RM 1N106,BETHESDA,MD 20892, USA. NR 48 TC 112 Z9 112 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1993 VL 268 IS 10 BP 6851 EP 6854 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV141 UT WOS:A1993KV14100008 PM 8463210 ER PT J AU HAUN, RS TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M AF HAUN, RS TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M TI EFFECT OF MYRISTOYLATION ON GTP-DEPENDENT BINDING OF ADP-RIBOSYLATION FACTOR TO GOLGI SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN ALPHA-SUBUNIT; CHOLERA-TOXIN; NUCLEOTIDE-BINDING; MEMBRANE ATTACHMENT; ADENYLATE-CYCLASE; BOVINE BRAIN; EXPRESSION; TRANSPORT; ACTIVATOR; VESICLES AB ADP-ribosylation factors (ARFs), a family of approximately 20-kDa guanine nucleotide-binding proteins that activate cholera toxin ADP-ribosyltransferase in vitro, have been implicated in intracellular protein trafficking and are thought to cycle between cytosolic and membrane compartments. Although isolated predominantly as soluble proteins, ARFs associate with membranes and phospholipids in a GTP-dependent manner. In contrast to other small GTP-binding proteins, ARFs are NH2 terminally myristoylated. Using a bacterial expression system, recombinant myristoylated and non-myristoylated human ARF5 were produced to investigate the role of myristoylation in its association with Golgi. The recombinant ARFs (myristoylated and non-myristoylated) exhibited similar biochemical activity as measured by GTP binding and in vitro activation of cholera toxin. Myristoylated ARF5, however, demonstrated a temperature- and GTP-dependent association with Golgi membranes, whereas non-myristoylated ARF did not bind to Golgi under any of the experimental conditions. These data indicate that myristoylation is necessary, although not sufficient, for membrane attachment, but is not necessary for activation of cholera toxin. RP HAUN, RS (reprint author), NHLBI,CELLULAR METAB LAB,BLDG 10,RM 5N307,BETHESDA,MD 20892, USA. NR 43 TC 82 Z9 83 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 APR 5 PY 1993 VL 268 IS 10 BP 7064 EP 7068 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV141 UT WOS:A1993KV14100039 PM 8463239 ER PT J AU GENTRYWEEKS, CR KEITH, JM THOMPSON, J AF GENTRYWEEKS, CR KEITH, JM THOMPSON, J TI TOXICITY OF BORDETELLA-AVIUM BETA-CYSTATHIONASE TOWARD MC3T3-E1 OSTEOGENIC CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID POSSIBLE REGULATORY ROLE; TRACHEAL CYTO-TOXIN; ESCHERICHIA-COLI; L-CANALINE; RHODOPSEUDOMONAS-SPHEROIDES; METHIONINE SYNTHESIS; DERMONECROTIC TOXIN; NUCLEOTIDE-SEQUENCE; PROTEIN SECRETION; GAMMA-SYNTHASE AB Bordetella avium is the etiological agent of an upper respiratory disease in birds which, symptomatically and pathologically, resembles bordetellosis in humans. Studies of the virulence of this organism revealed a novel cytotoxic protein, designated osteotoxin, that was lethal for MC3T3-E1 osteogenic cells, fetal bovine trabecular cells, UMR106-01(BSP) rat osteosarcoma cells, and embryonic bovine tracheal cells. The osteotoxin lacked dermonecrotic toxin activity, exhibited no cross-reactivity with antibody against B. avium dermonecrotic toxin, and was non-proteolytic. Osteotoxin (M(r) approximately 80,000 by gel filtration, pI 5.4) was purified to electrophoretic homogeneity from B. avium 197. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and spectrophotometric analyses showed that the native protein was a homodimer and that each of the non-covalently linked subunits (M(r) approximately 41,000) contained one molecule of pyridoxal 5'-phosphate. Microsequencing of the first 32 amino acids from the NH2 terminus allowed the synthesis of two oligonucleotide probes, which, together with polyclonal antibody to the purified protein, facilitated cloning, sequencing, and expression of the osteotoxin gene product in Escherichia coli. The open reading frame encodes a polypeptide of 396 amino acid residues (M(r) = 42,606, calculated pI 5.9), whose sequence exhibits approximately 38% identity (approximately 60% similarity) to pyridoxal 5'-phosphate-dependent beta-cystathionase(s) from E. coli, Salmonella typhimurium, and rat liver. The characteristic motif, TKYXXGHSD, associated with binding the cofactor in these enzymes is also present in osteotoxin. Physicochemical and enzymatic analyses established the coidentity of osteotoxin with beta-cystathionase. The region upstream of the beta-cystathionase (metC) gene in B. avium 197 lacked regulatory sequences (''Met boxes'') described for metC in enteric species, and enzyme production was not repressed by methionine. Incubation of MC3T3-E1 osteogenic cells in medium containing L-[S-35]cystine and purified beta-cystathionase resulted in S-35-labeling of the enzyme and at least one major MC3T3-E1 cell protein (M(r) approximately 50,000). Cytotoxicity can be attributed to: 1) beta-cystathionase-catalyzed cleavage of L-cystine in the medium and formation of reactive sulfane-containing derivative(s), and 2) transfer of sulfane sulfur to metabolically sensitive or structurally important proteins in the osteogenic cells. RP GENTRYWEEKS, CR (reprint author), NIDR,MICROBIAL ECOL LAB,BLDG 30,RM 532,BETHESDA,MD 20892, USA. NR 66 TC 34 Z9 35 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 APR 5 PY 1993 VL 268 IS 10 BP 7298 EP 7314 PG 17 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV141 UT WOS:A1993KV14100070 PM 8463265 ER PT J AU OKAMOTO, K WAKAMIYA, M NOJI, S KOYAMA, E TANIGUCHI, S TAKEMURA, R COPELAND, NG GILBERT, DJ JENKINS, NA MURAMATSU, M HAMADA, H AF OKAMOTO, K WAKAMIYA, M NOJI, S KOYAMA, E TANIGUCHI, S TAKEMURA, R COPELAND, NG GILBERT, DJ JENKINS, NA MURAMATSU, M HAMADA, H TI A NOVEL CLASS OF MURINE POU GENE PREDOMINANTLY EXPRESSED IN CENTRAL-NERVOUS-SYSTEM SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PRE-MESSENGER RNA; TRANSCRIPTION FACTOR; DNA-BINDING; DOMAIN; PROTEIN; SEQUENCE; OCT-1; CELLS; DROSOPHILA; REGION AB A mouse gene (referred to as Emb) encoding a novel class of POU domain is described. The Emb POU domain shares only 40-50% homology to that of any other POU proteins. Nonetheless, the Emb POU domain can bind to the octamer sequence like other POU domains. Emb is a single-copy gene, located on the distal region of mouse chromosome 15. It is expressed in embryo throughout post-implantation stages, where the most prominent expression is seen in developing central nervous system. In the adult, it is highly expressed in brain, whereas weaker expression can be detected in other organs such as testis, skeletal muscle, and kidney. The expression in adult brain is most evident in neurons of hypocampus formation. Two types of Emb mRNA are expressed in brain; one type encodes a protein of 301 amino acids residues, whereas the other codes for a protein with two extra amino acids residues added at the amino-terminal end of POU domain. These two mRNA species are generated by alternative splicing by utilizing an unusual splice acceptor site: CCTCCCTCTG/. Emb mRNA expressed in testis, on the other hand, encodes a smaller protein lacking most of the amino-terminal region. C1 UNIV TOKYO,FAC MED,DEPT BIOCHEM,HONGO 7-3-1,BUNKYO KU,TOKYO 113,JAPAN. OKAYAMA UNIV,SCH DENT,DEPT BIOCHEM,OKAYAMA 700,JAPAN. TORANOMON GEN HOSP,OKINAKA MEM RES INST,TOKYO 113,JAPAN. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 32 TC 36 Z9 37 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 APR 5 PY 1993 VL 268 IS 10 BP 7449 EP 7457 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV141 UT WOS:A1993KV14100089 PM 8463278 ER PT J AU HOLMES, KA CHAFFINS, S OSBORN, BL LIOTTA, LA KOHN, EC AF HOLMES, KA CHAFFINS, S OSBORN, BL LIOTTA, LA KOHN, EC TI QUANTITATION OF HUMAN PLASMA-LEVELS OF THE ANTICANCER AGENT CARBOXYAMIDOTRIAZOLE BY HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS LA English DT Article ID L651582 AB The predominant cause of death of cancer patients is growth and metastasis of their tumors. By targeting signal transduction pathways as sites of therapeutic intervention, we have identified a novel anticancer drug carboxyamidotriazole (CAI). A straight-forward and reliable method of detection and quantitation of human CAI plasma levels using solid-phase organic extraction followed by isocratic reversed-phase chromatography is now reported. This assay detected CAI over the concentration range 0.04-10.0 mug/ml, which brackets the range shown to be physiologically and biochemically effective. Linearity was demonstrated by linear regression analysis of calibration curves (r2 = 0.999). Equivalence of recovery of extracted versus non-extracted CAI over a broad concentration range was demonstrated (r2 = 0.998, coefficients of variability <10%). The method was applied to quantitate CAI plasma levels from patients now entered on the Phase I clinical, trial underway at the National Cancer Institute. C1 NCI,PATHOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. BATTELLE MEM INST,COLUMBUS,OH 43201. NCI,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NR 9 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR-BIOMED JI J. Chromatogr.-Biomed. Appl. PD APR 2 PY 1993 VL 613 IS 2 BP 317 EP 325 DI 10.1016/0378-4347(93)80148-W PG 9 WC Chemistry, Analytical SC Chemistry GA KW510 UT WOS:A1993KW51000016 PM 8491819 ER PT J AU MILLSTEIN, RA AF MILLSTEIN, RA TI DRUG-ABUSE RESEARCH SO SCIENCE LA English DT Letter RP MILLSTEIN, RA (reprint author), NIDA,ROCKVILLE,MD 20857, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 2 PY 1993 VL 260 IS 5104 BP 16 EP 16 DI 10.1126/science.8465192 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV423 UT WOS:A1993KV42300004 PM 8465192 ER PT J AU BAX, A GRZESIEK, S AF BAX, A GRZESIEK, S TI METHODOLOGICAL ADVANCES IN PROTEIN NMR SO ACCOUNTS OF CHEMICAL RESEARCH LA English DT Review ID TWO-DIMENSIONAL NMR; MAGNETIC-RESONANCE SPECTROSCOPY; HETERONUCLEAR NMR; LARGER PROTEINS; SEQUENTIAL ASSIGNMENT; SECONDARY STRUCTURE; CHEMICAL-SHIFTS; SPECTRA; C-13; INTERLEUKIN-1-BETA RP BAX, A (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA. NR 49 TC 713 Z9 718 U1 3 U2 31 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0001-4842 J9 ACCOUNTS CHEM RES JI Accounts Chem. Res. PD APR PY 1993 VL 26 IS 4 BP 131 EP 138 DI 10.1021/ar00028a001 PG 8 WC Chemistry, Multidisciplinary SC Chemistry GA KY068 UT WOS:A1993KY06800001 ER EF