FN Thomson Reuters Web of Science™ VR 1.0 PT J AU TASSANEEYAKUL, W BIRKETT, DJ VERONESE, ME MCMANUS, ME TUKEY, RH QUATTROCHI, LC GELBOIN, HV MINERS, JO AF TASSANEEYAKUL, W BIRKETT, DJ VERONESE, ME MCMANUS, ME TUKEY, RH QUATTROCHI, LC GELBOIN, HV MINERS, JO TI SPECIFICITY OF SUBSTRATE AND INHIBITOR PROBES FOR HUMAN CYTOCHROMES-P450 1A1 AND 1A2 SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID OXIDATIVE DRUG-METABOLISM; PHENACETIN O-DEETHYLASE; HUMAN-LIVER; CIGARETTE-SMOKING; CYTOCHROME-P450D P450IA2; MONOCLONAL-ANTIBODIES; GENETIC-POLYMORPHISM; CDNA EXPRESSION; MESSENGER-RNA; RAT AB Kinetic and inhibitor studies using cDNA-expressed enzymes and human liver microsomes have characterized the specificity of a range of cytochrome P450 (CYP) 1 A substrate and inhibitor probes towards the two isoforms comprising this subfamily. Expressed CYP1A1 and CYP1A2 both catalyzed the O-deethylation of phenacetin, although the apparent K(m) was about 4-fold lower for CYP1A2 (25 vs. 108 muM). Phenacetin 0-deethylation exhibited biphasic kinetics in human liver microsomes, and the apparent K(m) for the high-affinity component (9 +/- 6 muM) was consistent with the involvement of CYP1A2 in this reaction. The prototypic CYP1A xenobiotic inhibitor and substrate probes alpha-naphthoflavone, ellipticine, 7-ethoxycoumarin and 7-ethoxyresorufin all inhibited CYP1A1- and CYP1A2-mediated phenacetin O-deethylation as well as the high-affinity component of human liver phenacetin O-deethylase activity. Alpha-Naphthoflavone and 7-ethoxycoumarin were, however, approximately 1 0-fold more potent as inhibitors of CYP1A2 than CYP1A1. Other putative human CYP1A xenobiotic substrates and inhibitors, including caffeine, 5- and 8-methoxypsoralen, nifedipine, paraxanthine, propranolol and theophylline similarly inhibited CYP1A1- and 1A2-catalyzed phenacetin 0-deethylation and the high-affinity human liver phenacetin 0-deethylase. In contrast, the monoclonal antibody MAb 1-7-1, raised against 3-methylcholanthrene-inducible rat cytochromes 450, almost abolished CYP1A1-mediated phenacetin O-deethylation, but had no effect on human liver microsomal- or CYP1A2-catalyzed phenacetin dealkylation. Together with previous data, the results indicate that the majority of human CYP1A xenobiotic inhibitor and substrate probes are nonspecific in their recognition of CYP1A1 and CYP1A2, although selectivity is apparent for some compounds. C1 UCSD,CTR CANC,LA JOLLA,CA. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP MINERS, JO (reprint author), FLINDERS UNIV S AUSTRALIA,MED CTR,DEPT CLIN PHARMACOL,BEDFORD PK,SA 5042,AUSTRALIA. FU NIGMS NIH HHS [GM36590] NR 35 TC 310 Z9 319 U1 3 U2 20 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 APR PY 1993 VL 265 IS 1 BP 401 EP 407 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KY066 UT WOS:A1993KY06600055 PM 8474022 ER PT J AU FOX, RI LUPPI, M KANG, HI ABLSHI, D JOSEPHS, S AF FOX, RI LUPPI, M KANG, HI ABLSHI, D JOSEPHS, S TI DETECTION OF HIGH-LEVELS OF HUMAN HERPES VIRUS-6 DNA IN A LYMPHOMA OF A PATIENT WITH SJOGRENS-SYNDROME SO JOURNAL OF RHEUMATOLOGY LA English DT Letter ID POLYMERASE CHAIN-REACTION; HUMAN HERPESVIRUS-6 DNA; SALIVA; IDENTIFICATION; HHV-6 C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. RP FOX, RI (reprint author), SCRIPPS CLIN & RES FDN,DEPT RHEUMATOL,10666 N TORREY PINES RD,LA JOLLA,CA 92037, USA. RI Luppi, Mario/J-3668-2016 OI Luppi, Mario/0000-0002-0373-1154 NR 13 TC 11 Z9 11 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD APR PY 1993 VL 20 IS 4 BP 764 EP 765 PG 2 WC Rheumatology SC Rheumatology GA KY515 UT WOS:A1993KY51500044 PM 8388465 ER PT J AU STAGER, SV LUDLOW, CL AF STAGER, SV LUDLOW, CL TI SPEECH PRODUCTION CHANGES UNDER FLUENCY-EVOKING CONDITIONS IN NONSTUTTERING SPEAKERS SO JOURNAL OF SPEECH AND HEARING RESEARCH LA English DT Article DE NORMALLY FLUENT SPEAKERS; FLUENCY-EVOKING CONDITIONS; AERODYNAMICS ID NOISE AB Changes in airflow and intraoral pressure between baseline and four fluency-evoking conditions-choral reading (CR), metronome pacing (MET), delayed auditory feedback (DAF), and masking noise (NOISE)-were studied in 12 American English nonstuttering speakers. The duration, amplitude, and velocity of airflow and intraoral pressure development during the initial plosive and the duration and intensity of the following vowel were measured in eight target CVC words. Speech rate was computed for each sentence. Comparisons between baseline and the corresponding production in each condition revealed significant changes in peak flow, pressure rise time, peak instantaneous pressure velocity, speech rate, intensity, and vowel duration. Vowel duration increased under DAF, MET, and NOISE conditions. Peak pressure and pressure velocity decreased during CR and MET and increased during NOISE, but did not change during DAF. Subjects were consistent in the variables they modified across conditions. Changes in the aerodynamic variables were not related to intensity or rate changes. Thus, nonstuttering speakers modify intraoral pressure and flow under fluency-evoking conditions. RP STAGER, SV (reprint author), NIDCD,VSLB,VOICE & SPEECH SECT,BLDG 10,ROOM 5D-38,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. OI Stager, Sheila/0000-0002-4294-2114; Ludlow, Christy/0000-0002-2015-6171 NR 27 TC 19 Z9 19 U1 0 U2 0 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE RD, ROCKVILLE, MD 20852-3279 SN 0022-4685 J9 J SPEECH HEAR RES JI J. Speech Hear. Res. PD APR PY 1993 VL 36 IS 2 BP 245 EP 253 PG 9 WC Language & Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA KW998 UT WOS:A1993KW99800002 PM 8487517 ER PT J AU BENNAIM, E REDNER, S WEISS, GH AF BENNAIM, E REDNER, S WEISS, GH TI PARTIAL ABSORPTION AND VIRTUAL TRAPS SO JOURNAL OF STATISTICAL PHYSICS LA English DT Article DE PARTIAL ABSORPTION; VIRTUAL TRAP; RADIATION BOUNDARY CONDITION ID NEAREST-NEIGHBOR DISTANCES; DIFFUSING PARTICLES; SINGLE TRAP; DENSITY AB The spatial probability distribution associated with diffusion and attenuation in partially absorbing media is studied. An equivalence is established between a system with free diffusion for x > 0 and partial absorption for x < 0, and a semi-infinite system (x > 0) with a radiation boundary condition at x = 0. By exploiting this equivalence, it is shown that the effect of a partially absorbing medium in the long-time limit is equivalent to that of a perfect, ''virtual'' trap whose size is smaller than the original absorbing medium. For short times, however, there is substantial penetration of diffusing particles into the absorber. The virtual trap approach is readily generalized to higher dimensions. This allows one to obtain the density profile of diffusing particles around a partially absorbing spherical trap. An unusual crossover between short-time penetration and long-time trapping occurs in two dimensions; the size of the virtual trap is exponentially small in the case of weak absorption, corresponding to an absorption time which is exponentially large. C1 BOSTON UNIV, DEPT PHYS, BOSTON, MA 02215 USA. NIH, DCRT, PSL, BETHESDA, MD 20205 USA. RP BENNAIM, E (reprint author), BOSTON UNIV, CTR POLYMER STUDIES, BOSTON, MA 02215 USA. RI Ben-Naim, Eli/C-7542-2009 OI Ben-Naim, Eli/0000-0002-2444-7304 NR 12 TC 12 Z9 12 U1 1 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0022-4715 J9 J STAT PHYS JI J. Stat. Phys. PD APR PY 1993 VL 71 IS 1-2 BP 75 EP 88 DI 10.1007/BF01048089 PG 14 WC Physics, Mathematical SC Physics GA LA470 UT WOS:A1993LA47000005 ER PT J AU AGUILERA, G AF AGUILERA, G TI FACTORS CONTROLLING STEROID-BIOSYNTHESIS IN THE ZONA GLOMERULOSA OF THE ADRENAL SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article; Proceedings Paper CT SYMP IN TRIBUTE TO PAL VECSEI - ADRENAL STEROIDS : CURRENT VIEWS AND NEW FRONTIERS CY JUN 04-06, 1992 CL HEIDELBERG, GERMANY ID ATRIAL NATRIURETIC FACTOR; ALDOSTERONE SECRETION; ANGIOTENSIN-II; CYCLIC-AMP; CELLS; RAT; ADRENOCORTICOTROPIN; INHIBITION; SOMATOSTATIN; POTASSIUM AB The biosynthesis of aldosterone in the adrenal zona glomerulosa is influenced by a number of factors of which the main physiological regulator is the octapeptide, angiotensin II (AII). Sodium restriction increases plasma aldosterone, adrenal glomerulosa AII receptors and the activity of enzymes of the early and late aldosterone biosynthetic pathway. The effects of sodium restriction are mimicked by prolonged administration of low doses of AII, and prevented by blockade of AII formation using converting enzyme inhibitors, indicating that the effects of sodium restriction are mediated by AII. However, the adrenal glomerulotrophic actions of AII are impaired in rats on high sodium diet indicating that other factors are modulating the effects of AII in these conditions. A number of factors are known to influence aldosterone secretion, several of which have been shown to preferentially modulate the effect of AII. While the stimulatory effect of AII is potentiated by serotonin or increases in extracellular potassium, it is inhibited by dopamine, somatostatin and atrial natriuretic peptide. Future investigations will be important to understand the relative role of the individual regulators in the physiological control of adrenal sensitivity to AII, and how activation of various intracellular messenger systems results in changes in activity of the enzymes of the aldosterone biosynthetic pathway. RP AGUILERA, G (reprint author), NICHHD,ENDOCRINE PHYSIOL SECT,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892, USA. NR 26 TC 53 Z9 53 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-0760 J9 J STEROID BIOCHEM JI J. Steroid Biochem. Mol. Biol. PD APR PY 1993 VL 45 IS 1-3 BP 147 EP 151 DI 10.1016/0960-0760(93)90134-I PG 5 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA LA454 UT WOS:A1993LA45400022 PM 8481339 ER PT J AU MCNAMARA, MJ NORTON, JA NAUTA, RJ ALEXANDER, HR AF MCNAMARA, MJ NORTON, JA NAUTA, RJ ALEXANDER, HR TI INTERLEUKIN-1 RECEPTOR ANTIBODY (IL-1RAB) PROTECTION AND TREATMENT AGAINST LETHAL ENDOTOXEMIA IN MICE SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 1992 Annual Meeting of the Association-for-Academic-Surgery CY NOV 18-21, 1992 CL MONTREAL, CANADA SP ASSOC ACAD SURG ID TUMOR-NECROSIS-FACTOR; SEPTIC SHOCK; FACTOR-ALPHA; MONOCLONAL-ANTIBODIES; IMPROVES SURVIVAL; CACHECTIN; CYTOKINES; BACTEREMIA; ANTAGONIST; APPEARANCE C1 GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. RP MCNAMARA, MJ (reprint author), NCI,SURG BRANCH,BETHESDA,MD 20892, USA. NR 28 TC 28 Z9 28 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD APR PY 1993 VL 54 IS 4 BP 316 EP 321 DI 10.1006/jsre.1993.1050 PG 6 WC Surgery SC Surgery GA LM667 UT WOS:A1993LM66700009 PM 8331925 ER PT J AU THOM, AK FRAKER, DL NORTON, JA AF THOM, AK FRAKER, DL NORTON, JA TI IL-1 RECEPTOR ANTAGONIST (IL-1RA) AUGMENTS IL-2-INDUCED PULMONARY VASCULAR LEAK SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 1992 Annual Meeting of the Association-for-Academic-Surgery CY NOV 18-21, 1992 CL MONTREAL, CANADA SP ASSOC ACAD SURG ID TUMOR-NECROSIS-FACTOR; ACTIVATED KILLER-CELLS; GENE-EXPRESSION; INFILTRATING LYMPHOCYTES; INTERLEUKIN-2; INHIBITION; MICE; INVIVO; IMMUNOTHERAPY; PREVENTION RP THOM, AK (reprint author), NCI,SURG BRANCH,SURG METAB SECT,BETHESDA,MD 20894, USA. NR 26 TC 4 Z9 4 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD APR PY 1993 VL 54 IS 4 BP 336 EP 341 DI 10.1006/jsre.1993.1054 PG 6 WC Surgery SC Surgery GA LM667 UT WOS:A1993LM66700013 PM 8331927 ER PT J AU TUCKER, MA CRUTCHER, WA HARTGE, P SAGEBIEL, RW AF TUCKER, MA CRUTCHER, WA HARTGE, P SAGEBIEL, RW TI FAMILIAL AND CUTANEOUS FEATURES OF DYSPLASTIC NEVI - A CASE-CONTROL STUDY SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID MALIGNANT-MELANOMA; MELANOCYTIC NEVI; RISK FACTOR; NAEVI; DIAGNOSIS; MOLES AB Background. Although dysplastic nevi are- an important risk factor for melanoma, little is understood about the epidemiology of these nevi. To further characterize some of the correlates of dysplastic nevi, we reexamined patients from one of the original prevalence reports and their first-degree relatives. Objective: Our purpose was to characterize the prevalence and correlates of dysplastic nevi. Methods. We studied 25 persons originally diagnosed with dysplastic nevi in 1980 and 1981, 28 controls stratified by age, sex, race, and date of initial examination, and all willing first-degree relatives of both patients (n = 78) and control subjects (n = 76). Each study subject underwent a full skin examination and biopsy of nevi suspected of being dysplastic nevi, if willing. Results: Eighty percent of the case kindreds were multiplex (2 members or more affected) for dysplastic nevi; the relative risk of having dysplastic nevi was 7.2 (95% confidence interval 2.1 to 24) if one or more relatives had dysplastic nevi. Three of the cases (12%) in multiplex families also had a first-degree relative with melanoma. Cases and relatives with dysplastic nevi of both patients and control subjects tended to have increased numbers of nevi. The risk of having dysplastic nevi rose 99-fold in persons with more than five nevi 4 mm or larger and/or scars on their back (p < 0.001). Conclusion: These data support the hypothesis that family members of unselected persons with dysplastic nevi are likely to have dysplastic nevi and may be at increased risk of melanoma. C1 UNIV CALIF SAN FRANCISCO,DEPT PATHOL,SAN FRANCISCO,CA 94143. RP TUCKER, MA (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,6130 EXECUT BLVD,SUITE 439,BETHESDA,MD 20892, USA. RI Tucker, Margaret/B-4297-2015 NR 28 TC 17 Z9 17 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD APR PY 1993 VL 28 IS 4 BP 558 EP 564 PG 7 WC Dermatology SC Dermatology GA KU482 UT WOS:A1993KU48200003 PM 8463456 ER PT J AU STERN, JB PECK, GL HAUPT, HM HOLLINGSWORTH, HC BECKERMAN, T AF STERN, JB PECK, GL HAUPT, HM HOLLINGSWORTH, HC BECKERMAN, T TI MALIGNANT-MELANOMA IN XERODERMA-PIGMENTOSUM - SEARCH FOR A PRECURSOR LESION SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID HISTOPATHOLOGIC FEATURES; LENTIGINES AB Background. Malignant melanomas occur with increased frequency and at an early age in patients with xeroderma pigmentosum (XP). Objective: The purpose of this study was to describe the histologic features of malignant melanomas in patients with XP and to search for a possible precursor lesion. Methods. Clinical records and hematoxylin-eosin-stained sections of 19 malignant melanomas from seven patients with XP were examined. A search was conducted for malignant melanoma precursor lesions (melanocytic nevi and solar lentigines lateral to and contiguous with the malignant melanomas). Basal cell carcinomas removed from the same patients were used as controls. Results. Malignant melanomas were characteristically found in biopsy specimens of small elevations and/or changed color foci arising in large, flat, darkly pigmented, gradually enlarging macules. Histologically, solar lentigo was lateral to and contiguous with malignant melanoma in 88% of the malignant melanomas. Transitional areas were present. A significantly lower number (22%) of contiguous solar lentigines, without transitional areas, were observed in the basal cell carcinoma controls. Most of the invasive malignant melanomas were spindle cell malignant melanomas. Conclusion: We propose that solar lentigo is the most common precursor lesion of malignant melanoma in patients with XP. C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. PENN HOSP,DEPT PATHOL,PHILADELPHIA,PA 19107. UNIV MARYLAND,SCH DENT,BALTIMORE,MD 21201. RP STERN, JB (reprint author), DERMATOPATHOL CONSULTAT SERV,POB 10,DAMASCUS,MD 20872, USA. NR 10 TC 16 Z9 16 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD APR PY 1993 VL 28 IS 4 BP 591 EP 594 PG 4 WC Dermatology SC Dermatology GA KU482 UT WOS:A1993KU48200008 PM 8463460 ER PT J AU PANZA, JA QUYYUMI, AA CALLAHAN, TS EPSTEIN, SE AF PANZA, JA QUYYUMI, AA CALLAHAN, TS EPSTEIN, SE TI EFFECT OF ANTIHYPERTENSIVE TREATMENT ON ENDOTHELIUM-DEPENDENT VASCULAR RELAXATION IN PATIENTS WITH ESSENTIAL-HYPERTENSION SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CANINE FEMORAL-ARTERY; SMOOTH-MUSCLE; CORONARY-ARTERIES; ACETYLCHOLINE; CELLS; RATS AB Objectives. This study was designed to determine whether antihypertensive treatment can restore the impaired endothelium-dependent vasodilation of patients with essential hypertension. Background. The endothelium regulates vascular tone through the release of vasoactive agents that act on the underlying vascular smooth muscle. This endothelial function is impaired in certain cardiovascular conditions, including essential hypertension. Methods. The vascular responses to acetylcholine (endothelium-dependent vasodilator, 7.5, 15 and 30 mug/min) and sodium nitroprusside (direct dilator of smooth muscle, 0.8, 1.6, 3.2 mug/min) were studied in 15 patients (11 men and 4 women with a mean age of 54.1 +/- 12 years) on two occasions: after withdrawal of medications, when the patients were hypertensive, and during the medical treatment that reduced blood pressure to within normal limits in each patient. The results were compared with those obtained in 15 normal control subjects (10 men and 5 women with a mean age of 52.3 +/- 7 years). Drugs were infused into the brachial artery, and forearm blood flow response was measured by strain gauge plethysmography. Results. The blood flow and vascular resistance responses to acetylcholine were significantly reduced in the hypertensive patients (p < 0.0001); maximal forearm flow (ml/min per 100 ml) was 7.0 +/- 4 ml in the patients and 16.7 +/- 5 in the control subjects (p < 0.005). However, no significant differences between groups were observed in the responses to sodium nitroprusside. In patients with essential hypertension, the vascular responses to acetylcholine and sodium nitroprusside were not modified by medical therapy. Maximal forearm flow with acetylcholine (ml/min per 100 ml) was 7.2 +/- 2 during antihypertensive therapy and 7.0 +/- 4 after medication withdrawal. Conclusions. Clinically effective antihypertensive therapy does not restore the impaired endothelium-dependent vascular relaxation of patients with essential hypertension. This indicates that such endothelial dysfunction is either primary or becomes irreversible once the hypertensive process has become established. RP PANZA, JA (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 22 TC 213 Z9 217 U1 0 U2 4 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 APR PY 1993 VL 21 IS 5 BP 1145 EP 1151 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KV708 UT WOS:A1993KV70800017 PM 8459069 ER PT J AU BRESLOW, RA HALLFRISCH, J GUY, DG CRAWLEY, B GOLDBERG, AP AF BRESLOW, RA HALLFRISCH, J GUY, DG CRAWLEY, B GOLDBERG, AP TI THE IMPORTANCE OF DIETARY-PROTEIN IN HEALING PRESSURE ULCERS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID NURSING-HOME PATIENTS; SORES; ZINC; THERAPY AB Objective: To determine the effect of dietary protein on healing of pressure ulcers in malnourished patients. Design: Nutritional intervention trial with the non-randomized assignment of patients by pressure ulcer stage and bed type. Setting: Long-term care facility. Patients: Twenty-eight malnourished patients (age = 72 18 years, mean +/- SD) with a total of 33 truncal pressure ulcers. Nine patients had stage II ulcers, eight had stage III ulcers, and 16 had stage IV ulcers. Methods: Patients received liquid nutritional formulas as tubefeedings or meal supplements containing either 24% protein (61 g protein/L; n = 15) or 14% protein (37 g protein/L; n = 13) for 8 weeks. Results: There was a significant decrease in total truncal pressure ulcer surface area of the 15 patients in the 24% protein group (-4.2 +/- 7.1 cm2, P < 0.02), but not in the 13 patients in the 14% protein group (-2.1 +/- 11.5 cm2, P = NS). The change in total ulcer area correlated with both dietary protein intake per kg body weight (r(s) = -0.50, P < 0.01) and caloric intake per kg body weight (r(s) = -0.41, P < 0.03). The decrease in stage IV ulcer area in eight patients in the 24% protein group (-7.6 +/- 5.8 cm2, P < 0.02) was significantly greater (P < 0.05) than in eight patients in the 14% protein group (-3.2 +/- 16.4, P = NS). In these 16 patients, the decrease in ulcer size also correlated with dietary protein intake per kg body weight (r(s) = -0.63, P < 0.01). Conclusion: High protein diets may improve the healing of pressure ulcers in malnourished nursing home patients. C1 UNIV MARYLAND,DEPT HUMAN NUTR & FOOD SYST,COLL PK,MD 20742. MEAD JOHNSON NUTR GRP,EVANSVILLE,IN. NIA,GERONTOL RES CTR,CLIN PHYSIOL LAB,METAB SECT,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DIV GERIATR,BALTIMORE,MD 21205. FU NCRR NIH HHS [M01-RR02719-04]; NIA NIH HHS [P01-AG-004402-06] NR 35 TC 110 Z9 113 U1 0 U2 8 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 1993 VL 41 IS 4 BP 357 EP 362 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA KW777 UT WOS:A1993KW77700001 PM 8463519 ER PT J AU MARKEY, SP MARKEY, CJ WANG, TCL RODRIGUEZ, JB AF MARKEY, SP MARKEY, CJ WANG, TCL RODRIGUEZ, JB TI GAS-CHROMATOGRAPHIC MASS-SPECTROMETRIC METHOD FOR THE ASSESSMENT OF OXIDATIVE DAMAGE TO DOUBLE-STRANDED DNA BY QUANTIFICATION OF THYMINE GLYCOL RESIDUES SO JOURNAL OF THE AMERICAN SOCIETY FOR MASS SPECTROMETRY LA English DT Article ID DEOXYRIBONUCLEIC-ACID; PERMANGANATE OXIDATION; ALZHEIMERS-DISEASE; THYMIDINE GLYCOL; RADIATION-DAMAGE; ESCHERICHIA-COLI; CELLS; IDENTIFICATION; ASSAY; ESTER AB A technique for the measurement of thymine glycol at parts per million concentrations in double-stranded polymeric DNA is described. The procedure utilizes base to ring-open DNA-bound thymine glycol in the presence of monomeric [(H-4)-H-2]thymine glycol as an internal standard, followed by reduction, solvolytic cleavage, and quantification of the characteristic methyl-2-methylglycerate released from polymeric DNA. Methyl-2-methylglycerate is derivatized to form the di-tert-butyldimethylsilyl [(TBDMS)2] ether to enhance its gas chromatographic properties and electron ionization detection. This assay was tested by measuring thymine glycol levels in native, undamaged DNA (not purposefully oxidized). The measured quantities of thymine glycol are proportional to the amount of DNA analyzed. Components of DNA not containing oxidizable thymine do not contribute to the measured signal from methyl-2-methylglycerate-(TBDMS)2. These results indicate that there is approximately one thymine glycol per 10(6) bases in undamaged DNA and that this value increases with storage of DNA in refrigerated aqueous solutions. RP MARKEY, SP (reprint author), NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BLDG 10,ROOM 3D40,BETHESDA,MD 20892, USA. OI Rodriguez, Juan Bautista/0000-0002-5180-096X NR 36 TC 6 Z9 6 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1044-0305 J9 J AM SOC MASS SPECTR JI J. Am. Soc. Mass Spectrom. PD APR PY 1993 VL 4 IS 4 BP 336 EP 342 DI 10.1016/1044-0305(93)85056-4 PG 7 WC Chemistry, Analytical; Chemistry, Physical; Spectroscopy SC Chemistry; Spectroscopy GA KV987 UT WOS:A1993KV98700007 PM 24234868 ER PT J AU HENNEIN, HA JONES, M STONE, CD CLARK, RE AF HENNEIN, HA JONES, M STONE, CD CLARK, RE TI LEFT-VENTRICULAR FUNCTION IN EXPERIMENTAL MITRAL REGURGITATION WITH INTACT CHORDAE TENDINEAE SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article; Proceedings Paper CT 72ND ANNUAL MEETING OF THE AMERICAN ASSOC FOR THORACIC SURGERY CY APR 26-29, 1992 CL LOS ANGELES, CA SP AMER ASSOC THORAC SURG ID CHRONIC VOLUME OVERLOAD; END-SYSTOLIC INDEXES; VALVE-REPLACEMENT; CONSCIOUS DOG; PERFORMANCE; APPARATUS; REPAIR; PRESERVATION; HYPERTROPHY; MECHANICS AB Left ventricular function in mitral regurgitation has typically been studied in models that either sever the chordae tendineae or create a ventriculoatrial shunt. These methods may have adverse effects on left ventricular function independent of the regurgitant lesion. An animal model of chronic mitral regurgitation was therefore developed that both preserves annuloventricular continuity and avoids the use of external shunts. A circular 0.16 to 0.24 mm/kg defect was created in the anterior mitral valve leaflet of weanling sheep under direct vision with the aid of cardiopulmonary bypass. Six animals were studied preoperatively and immediately postoperatively (acute regurgitation group), and 20 animals were studied 8.1 +/- 0.2 (mean +/- one standard deviation) months postoperatively (chronic regurgitation group). Animals with chronic mitral regurgitation were compared with an age- and weight-matched control group that was not operated on (n = 7). Volumetric data and ejection fraction were derived from digitalized cineangiographic images. Maximal elastance was calculated from pressure-volume loops obtained from the simultaneous recording of left ventricular pressure by micromanometer-tipped left ventricular catheters, and volumes were obtained from digitalized images of epicardial echocardiographic recordings. Mitral valve perforation resulted in 3+ to 4+ mitral regurgitation and a calculated regurgitant fraction of 37 % +/- 7 % (mean +/- one standard deviation). Acute mitral regurgitation was associated with an increase in left ventricular end-diastolic volume from 110 +/- 17 to 121 +/- 23 ml (p less-than-or-equal-to 0.05) and no change in end-systolic volume. These changes were associated with an increase in fractional shortening, from 29 % +/- 11 % to 40 % +/- 10 % (p less-than-or-equal-to 0.05), and an increase in velocity of circumferential shortening, from 1.5 +/- 0.7 to 2.9 +/- 0.7 circ/sec (p less-than-or-equal-to 0.05). However, there was no change in maximal elastance, a load-independent index of left ventricular function. Conversely, animals with chronic mitral regurgitation exhibited an elevated end-diastolic volume (202 +/- 32 versus 145 +/- 34, p less-than-or-equal-to 0.05), an elevated end-systolic volume (104 +/- 17 versus 63 +/- 20 ml, p less-than-or-equal-to 0.05), and a reduced ejection fraction (48 % +/- 6 % versus 57 % +/- 9 %, p less-than-or-equal-to 0.05) compared with controls. These changes were associated with a reduction in fractional shortening from 26 % +/- 3 % to 41 % +/- 9 % (p less-than-or-equal-to 0.05), velocity of circumferential shortening from 1.2 +/- 0.1 to 1.7 +/- 0.5 circ/sec (p less-than-or-equal-to 0.05), and maximal elastance from 8 +/- 1 to 10 +/- 1 mm Hg/ml (p less-than-or-equal-to 0.05). We conclude that acute mitral regurgitation with intact chordae tendineae is associated with modest left ventricular dilatation and preservation of left ventricular function, whereas chronic mitral regurgitation is associated with marked left ventricular dilatation and depressed left ventricular function. The chordae tendineae likely contribute more to preserving diastolic, rather than systolic, function in acute mitral regurgitation, whereas their role in preserving left ventricular function in the chronically dilated ventricle remains unknown. C1 NHLBI,SURG BRANCH,BETHESDA,MD 20894. NR 39 TC 6 Z9 6 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD APR PY 1993 VL 105 IS 4 BP 624 EP 632 PG 9 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA KW483 UT WOS:A1993KW48300006 PM 8468996 ER PT J AU SOLOMON, SD BRAVO, M RUBIOSTIPEC, M CANINO, G AF SOLOMON, SD BRAVO, M RUBIOSTIPEC, M CANINO, G TI EFFECT OF FAMILY ROLE ON RESPONSE TO DISASTER SO JOURNAL OF TRAUMATIC STRESS LA English DT Article DE DISASTER; FAMILY ROLE; PTSD; SOCIAL SUPPORT ID MARITAL-STATUS; VULNERABILITY; IMPACT; STRESS AB This study hypothesized that family role (marital and parental status) would moderate the effect of disaster exposure on the mental health of victims. The study included St. Louis residents exposed to floods and dioxin, as well as Puerto Rican respondents exposed to floods and mudslides. In St. Louis, worst outcomes were found for single and married parents exposed to disaster, substantially exceeding the symptomatology of all unexposed respondents except non-victim single parents. In Puerto Rico, victims without families had higher levels of alcohol abuse symptoms than did any other subgroup. Perceived emotional support was found to be an important moderator of disaster's effect on psychiatric distress in this site, generally overriding the effect of family role. Single parents in both sites who were exposed to disaster had substantially reduced levels of emotional support available to them, as compared to unexposed single parents, suggesting that single parents are at particularly high risk for losing access to emotional support following a disaster. This study suggests that both single and married parents constitute important high-risk victim groups. The findings also suggest that those perceiving they lack adequate emotional support, regardless of family role, may be in special need of services. C1 UNIV PUERTO RICO,DEPT GRAD STUDIES EDUC,RIO PIEDRAS,PR 00931. UNIV PUERTO RICO,BEHAV SCI RES INST,RIO PIEDRAS,PR 00931. UNIV PUERTO RICO,DEPT ECON,RIO PIEDRAS,PR 00931. RP SOLOMON, SD (reprint author), NIMH,DIV EPIDEMIOL & SERV RES,ROCKVILLE,MD 20857, USA. NR 21 TC 27 Z9 28 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0894-9867 J9 J TRAUMA STRESS JI J. Trauma Stress PD APR PY 1993 VL 6 IS 2 BP 255 EP 269 DI 10.1002/jts.2490060208 PG 15 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA KY263 UT WOS:A1993KY26300007 ER PT J AU SUBBARAO, EK LONDON, W MURPHY, BR AF SUBBARAO, EK LONDON, W MURPHY, BR TI A SINGLE AMINO-ACID IN THE PB2-GENE OF INFLUENZA-A VIRUS IS A DETERMINANT OF HOST RANGE SO JOURNAL OF VIROLOGY LA English DT Article ID NUCLEOTIDE-SEQUENCE; POLYMERASE GENES; MONKEYS; NUCLEOPROTEIN; ORIGIN AB The single gene reassortant virus that derives its PB2 gene from the avian influenza A/Mallard/NY/78 virus and remaining genes from the human influenza A/Los Angeles/2/87 virus exhibits a host range restriction (hr) phenotype characterized by efficient replication in avian tissue and failure to produce plaques in mammalian Madin-Darby canine kidney cells. The hr phenotype is associated with restriction of viral replication in the respiratory tract of squirrel monkeys and humans. To identify the genetic basis of the hr phenotype, we isolated four phenotypic hr mutant viruses that acquired the ability to replicate efficiently in mammalian tissue. Segregational analysis indicated that the loss of the hr phenotype was due to a mutation in the PB2 gene itself. The nucleotide sequences of the PB2 gene of each of the four hr mutants revealed that a single amino acid substitution at position 627 (Glu --> Lys) was responsible for the restoration of the ability of the PB2 single gene reassortant to replicate in Madin-Darby canine kidney cells. Interestingly, the amino acid at position 627 in every avian influenza A virus PB2 protein analyzed to date is glutamic acid, and in every human influenza A virus PB2 protein, it is lysine. Thus, the amino acid at residue 627 of PB2 is an important determinant of host range of influenza A viruses. C1 GEORGETOWN UNIV,DEPT MICROBIOL,DIV MOLEC VIROL & IMMUNOL,ROCKVILLE,MD 20852. RP SUBBARAO, EK (reprint author), NIAID,INFECT DIS LAB,RESP VIRUSES SECT,BETHESDA,MD 20892, USA. NR 16 TC 482 Z9 534 U1 2 U2 19 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 APR PY 1993 VL 67 IS 4 BP 1761 EP 1764 PG 4 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000003 PM 8445709 ER PT J AU HIJIKATA, M SHIMIZU, YK KATO, H IWAMOTO, A SHIH, JW ALTER, HJ PURCELL, RH YOSHIKURA, H AF HIJIKATA, M SHIMIZU, YK KATO, H IWAMOTO, A SHIH, JW ALTER, HJ PURCELL, RH YOSHIKURA, H TI EQUILIBRIUM CENTRIFUGATION STUDIES OF HEPATITIS-C VIRUS - EVIDENCE FOR CIRCULATING IMMUNE-COMPLEXES SO JOURNAL OF VIROLOGY LA English DT Article ID NON-B-HEPATITIS; NON-A; SEQUENCE; CHIMPANZEES; ANTIGEN; GENOME AB The buoyant density of hepatitis C virus (HCV), with high in vivo infectivity (strain H) or low in vivo infectivity (strain F), was determined by sucrose gradient equilibrium centrifugation. Viral RNA of strain H was detected in fractions with densities of less-than-or-equal-to 1.09 g/ml (principally approximately 1.06 g/ml), while that of strain F was found in fractions with densities of approximately 1.06 and approximately 1.17 g/ml. The observed difference was confirmed by differential flotation centrifugation; in NaCl solution with a density of 1.063 g/ml, most of the HCV RNA of strain H was detected in the top fraction, while that of strain F appeared in the bottom. The same relationship between buoyant density and infectivity was observed in flotation centrifugation experiments with other HCV strains. In immunoprecipitation experiments with anti-human immunoglobulin, HCV (as measured by HCV RNA) was precipitated from the samples with low infectivity and high density but not from those with high infectivity and low density. Examination of serial sera from a chimpanzee infected with HCV revealed parallel changes in the buoyant density and immunoprecipitability of HCV-associated RNA during the course of infection. These data suggest that HCV is bound to anti-HCV antibodies as antigen-antibody complexes in chronic hepatitis C. C1 UNIV TOKYO,DEPT BACTERIOL,7-3-1 HONGO,BUNKYO KU,TOKYO 113,JAPAN. UNIV TOKYO,DEPT INTERNAL MED 1,BUNKYO KU,TOKYO 113,JAPAN. UNIV TOKYO,FAC MED,BUNKYO KU,TOKYO 113,JAPAN. NATL INST HLTH,DEPT VIRAL DIS & VACCINE CONTROL,MUSASHIMURAYAMA,TOKYO 208,JAPAN. NIH,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892. NIH,DEPT TRANSFUS MED,BETHESDA,MD 20892. NR 25 TC 299 Z9 307 U1 2 U2 6 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 APR PY 1993 VL 67 IS 4 BP 1953 EP 1958 PG 6 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000026 PM 8383220 ER PT J AU FALGOUT, B MILLER, RH LAI, CJ AF FALGOUT, B MILLER, RH LAI, CJ TI DELETION ANALYSIS OF DENGUE VIRUS TYPE-4 NONSTRUCTURAL PROTEIN NS2B - IDENTIFICATION OF A DOMAIN REQUIRED FOR NS2B-NS3 PROTEASE ACTIVITY SO JOURNAL OF VIROLOGY LA English DT Article ID YELLOW-FEVER VIRUS; COMPLETE NUCLEOTIDE-SEQUENCE; STRUCTURAL PROTEINS; VIRAL POLYPROTEIN; EXPRESSION SYSTEM; VACCINIA VIRUS; GENOME RNA; INVITRO; NS3; TRANSLATION AB Most proteolytic cleavages in the nonstructural protein (NS) region of the flavivirus polyprotein are effected by a virus-encoded protease composed of two viral proteins, NS2B and NS3. The N-terminal 180-amino-acid-region of NS3 includes sequences with homology to the active sites of serine proteases, and there is evidence that this portion of NS3 can mediate proteolytic cleavages. In contrast, nothing is known about required sequences in NS2B. We constructed a series of deletion mutations in the NS2B portion of plasmid pTM/NS2B-30%NS3, which expresses dengue virus type 4 (DEN4) cDNA encoding NS2B and the N-terminal 184 residues of NS3 from the T7 RNA polymerase promoter. Mutant or wild-type plasmids were transfected into cells that had been infected with a recombinant vaccinia virus expressing T7 RNA polymerase, and the protease activities of the expressed polyproteins were assayed by examining the extent of self-cleavage at the NS2B-NS3 junction. The results identify a 40-amino-acid segment of NS2B (DEN4 amino acids 1396 to 1435) essential for protease activity. A hydrophobicity profile of DEN4 NS2B predicts this segment constitutes a hydrophilic domain surrounded by hydrophobic regions. Hydrophobicity profiles of the NS2B proteins of other flaviviruses show similar patterns. Amino acid sequence alignment of this domain of DEN4 NS2B with comparable regions of other proteins of flaviviruses indicates significant sequence conservation, especially at the N-terminal end. These observations suggest that the central hydrophilic domain of NS2B of these other flaviviruses will also prove to be essential for protease activity. C1 NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892. RP FALGOUT, B (reprint author), NIAID,INFECT DIS LAB,MOLEC URAL BIOL SECT,BETHESDA,MD 20892, USA. NR 36 TC 167 Z9 172 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1993 VL 67 IS 4 BP 2034 EP 2042 PG 9 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000035 PM 8383225 ER PT J AU CARVALHO, M DERSE, D AF CARVALHO, M DERSE, D TI PHYSICAL AND FUNCTIONAL-CHARACTERIZATION OF TRANSCRIPTIONAL CONTROL ELEMENTS IN THE EQUINE INFECTIOUS-ANEMIA VIRUS PROMOTER SO JOURNAL OF VIROLOGY LA English DT Article ID LONG TERMINAL REPEAT; HUMAN IMMUNODEFICIENCY VIRUS; DNA-BINDING PROTEIN; NUCLEAR FACTOR; GENE-EXPRESSION; ENHANCER REGION; C-JUN; SITES; AP-1; FOS AB Equine infectious anemia virus (EIAV) is a lentivirus that causes a chronic disease of horses characterized by cyclic episodes of fever, anemia, and viremia. Although the genome and promoter of EIAV are much less complex than those of its relatives the primate immunodeficiency viruses, the cellular proteins that activate and regulate transcription of EIAV have not yet been identified. In this report, we show by electrophoretic mobility shift assays and DNase I footprinting that the EIAV promoter contains multiple binding sites for ubiquitous, cell type-specific, and inducible cellular proteins. Functional analysis by transient transfection of canine osteosarcoma (D17) and human epithelial carcinoma (HeLa) cells with EIAV promoters containing deletions or individually mutated DNA-binding sites demonstrated that these DNA-binding elements cooperatively regulate transcriptional activity. A methylated DNA-binding site (MDBP; also designated EF-C or EP) acts as either a positive or negative regulator of promoter activity, depending on the cell type or condition. Two PEA2 elements, an AP-1 site, and an ets/PEA3 motif confer a positive effect on promoter activity. The EIAV promoter is shown to be activated by treatment of HeLa cells with phorbol myristate acetate (PMA). DNA-binding activities were induced in PMA-treated HeLa cells and formed complexes on oligonucleotides that contain the EIAV AP-1 and ets/PEA3 elements. Functional analysis of mutated promoters indicated that the ets/PEA3 motif was the principal mediator of PMA activation. C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 40 TC 28 Z9 30 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 APR PY 1993 VL 67 IS 4 BP 2064 EP 2074 PG 11 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000038 PM 8383228 ER PT J AU KANNO, H WOLFINBARGER, JB BLOOM, ME AF KANNO, H WOLFINBARGER, JB BLOOM, ME TI ALEUTIAN MINK DISEASE PARVOVIRUS INFECTION OF MINK PERITONEAL-MACROPHAGES AND HUMAN MACROPHAGE CELL-LINES SO JOURNAL OF VIROLOGY LA English DT Article ID MINUTE VIRUS; INTERSTITIAL PNEUMONIA; NEUTRALIZING ANTIBODY; RHEUMATOID-ARTHRITIS; NUCLEOTIDE-SEQUENCE; VIRAL REPLICATION; LEUKEMIA-CELLS; ADULT MINK; MICE; DIFFERENTIATION AB Aleutian mink disease parvovirus (ADV) mRNAs are found in macrophages in lymph nodes and peritoneal exudate cells from ADV-infected mink. Therefore, we developed an in vitro infection system for ADV by using primary cultures of mink macrophages or macrophage cell lines. In peritoneal macrophage cultures from adult mink, virulent ADV-Utah I strain showed nuclear expression of viral antigens with fluorescein isothiocyanate-labeled ADV-infected mink serum, but delineation of specific viral proteins could not be confirmed by immunoblot analysis. Amplification of ADV DNA and production of replicative-form DNA were observed in mink macrophages by Southern blot analysis; however, virus could not be serially propagated. The human macrophage cell line U937 exhibited clear nuclear expression of viral antigens after infection with ADV-Utah I but not with tissue culture-adapted ADV-G. In U937 cells, ADV-Utah I produced mRNA, replicative-form DNA, virion DNA, and structural and nonstructural proteins; however, virus could not be serially passaged nor could [H-3]thymidine-labeled virions be observed by density gradient analysis. These findings indicated that ADV-Utah I infection in U937 cells was not fully permissive and that there is another restricted step between gene amplification and/or viral protein expression and production of infectious virions. Treatment with the macrophage activator phorbol 12-myristate 13-acetate after adsorption of virus reduced the frequency of ADV-positive U937 cells but clearly increased that of human macrophage line THP-1 cells. These results suggested that ADV replication may depend on conditions influenced by the differentiation state of macrophages. U937 cells may be useful as an in vitro model system for the analysis of the immune disorder caused by ADV infection of macrophages. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 47 TC 28 Z9 28 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1993 VL 67 IS 4 BP 2075 EP 2085 PG 11 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000039 PM 8383229 ER PT J AU GILBERT, DJ NEUMANN, PE TAYLOR, BA JENKINS, NA COPELAND, NG AF GILBERT, DJ NEUMANN, PE TAYLOR, BA JENKINS, NA COPELAND, NG TI SUSCEPTIBILITY OF AKXD RECOMBINANT INBRED MOUSE STRAINS TO LYMPHOMAS SO JOURNAL OF VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; FOCUS-FORMING VIRUSES; T-CELL; AKR/J MICE; VIRAL INTEGRATION; POLYTROPIC MULVS; GENETIC-ANALYSIS; BALB/C MICE; B-CELL; C-MYC AB We analyzed the susceptibility of 10 AKXD recombinant inbred (RI) mouse strains to lymphomas. These strains were derived from crosses of AKR/J, a highly lymphomatous strain, and DBA/2J, a weakly lymphomatous strain. Of the 10 strains analyzed, nine showed a high incidence of lymphoma development. As with the other 13 AKXD strains analyzed previously (M. L. Mucenski, B. A. Taylor, N. A. Jenkins, and N. G. Copeland, Mol. Cell. Biol. 6:4236-4243, 1986), the mean age at onset of lymphomas and lymphoma types varied among the strains. Whereas some strains were susceptible to T-cell lymphomas, as was the AKR/J parent, other strains were susceptible to B-cell lymphomas or to a combination of T- and B-cell lymphomas. Somatic mink cell focus-forming proviruses appeared causally associated with T-cell lymphomas, whereas somatic ecotropic proviruses appeared causally associated with B-cell lymphomas. Mice with T-cell lymphomas died significantly earlier than mice with other lymphoma types (stem, pre-B, or B cell and myeloid). The numbers of effective loci influencing the mean age at onset of lymphomas, the presence or absence of mink cell focus-forming viruses in tumors, and the frequency of T-cell lymphomas were estimated to be 3.9, 1.8, and 2.7, respectively. Tests of association with marker loci already typed in the AKXD RI strains suggested that two loci, Rmcf and Pmv-25 (or a locus linked to Pmv-25), influence all three trait variables. Finally, D21S16h, a marker locus on distal chromosome 16, showed 50% probability of linkage to a locus that influences the mean age at onset of lymphomas. Additional studies in combination with classical genetic crosses should be helpful in confirming these linkages and in identifying other loci influencing tumor susceptibility in AKXD RI strains. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. JACKSON LAB,BAR HARBOR,ME 04609. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. FU NCI NIH HHS [CA-33093, N01-CO-74101]; NICHD NIH HHS [P30-HD-18655] NR 51 TC 54 Z9 55 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1993 VL 67 IS 4 BP 2083 EP 2090 PG 8 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000040 PM 8383230 ER PT J AU DIMITROV, DS WILLEY, RL SATO, H CHANG, LJ BLUMENTHAL, R MARTIN, MA AF DIMITROV, DS WILLEY, RL SATO, H CHANG, LJ BLUMENTHAL, R MARTIN, MA TI QUANTITATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION KINETICS SO JOURNAL OF VIROLOGY LA English DT Article ID CELL-FUSION; HIV-1; RETROVIRUS; GP120; GENE; AIDS; EXPRESSION; PLASMA; REGION; ASSAY AB Tissue culture infections of CD4-positive human T cells by human immunodeficiency virus type 1 (HIV-1) proceed in three stages: (i) a period following the initiation of an infection during which no detectable virus is produced; (ii) a phase in which a sharp increase followed by a peak of released progeny virions can be measured; and (iii) a final period when virus production declines. In this study, we have derived equations describing the kinetics of HIV-1 accumulation in cell culture supernatants during multiple rounds of infection. Our analyses indicated that the critical parameter affecting the kinetics of HIV-1 infection is the infection rate constant k = Inn/t(i), where n is the number of infectious virions produced by one cell (about 10(2)) and t(i) is the time required for one complete cycle of virus infection (typically 3 to 4 days). Of particular note was our finding that the infectivity of HIV-1 during cell-to-cell transmission is 10(2) to 10(3) times greater than the infectivity of cell-free virus stocks, the inocula commonly used to initiate tissue culture infections. We also demonstrated that the slow infection kinetics of an HIV-1 tat mutant is not due to a longer replication time but reflects the small number of infectious particles produced per cycle. C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RP DIMITROV, DS (reprint author), NCI,MEMBRANE STRUCT & FUNCT SECT,BETHESDA,MD 20892, USA. NR 34 TC 361 Z9 364 U1 1 U2 6 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 APR PY 1993 VL 67 IS 4 BP 2182 EP 2190 PG 9 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000052 PM 8445728 ER PT J AU KORALNIK, IJ FULLEN, J FRANCHINI, G AF KORALNIK, IJ FULLEN, J FRANCHINI, G TI THE P12I, P13II, AND P30II PROTEINS ENCODED BY HUMAN T-CELL LEUKEMIA LYMPHOTROPIC VIRUS TYPE-I OPEN READING FRAME-I AND FRAME-II ARE LOCALIZED IN 3 DIFFERENT CELLULAR COMPARTMENTS SO JOURNAL OF VIROLOGY LA English DT Article ID TROPICAL SPASTIC PARAPARESIS; HTLV-I; LYMPHOCYTES-T; MESSENGER-RNA; EXPRESSION; RETROVIRUS; ANTIBODIES; GENES; PX; REPLICATION AB Three protein isoforms are encoded by the human T-cell leukemia/lymphotropic virus type I pX region open reading frames (ORF) I and II through alternative splicing. Both the singly and doubly spliced mRNAs from ORF I encode a single 12-kDa protein (p12I), whereas two distinct proteins of 13 kDa (p13II) and 30 kDa (p30II) are encoded from the ORF II alternatively spliced mRNA. Because the p12I protein is very hydrophobic and poorly immunogenic, we genetically engineered its cDNA by adding a short stretch of amino acids from the highly immunogenic epitope HA1 of influenza virus or the AU1 epitope of bovine papillomavirus. The HA1 epitope was also added to the p13II and p30II proteins, albeit rabbit immune sera raised against synthetic peptides were also available. To determine in which cellular compartments these proteins reside, we transfected the tagged and wild-type cDNAs in HeLa/Tat cells and studied their localization by indirect immunofluorescence. The p12I protein was identified in the cellular endomembranes and, particularly, in the perinuclear area. p13II and p30II were found in the nuclei and nucleoli of the transfected cells, respectively. The presence of the HA1 epitope at the carboxy terminus of p13II and p30II did not interfere with their cellular localization, since the rabbit immune sera demonstrated their presence in the same cellular compartments when the untagged proteins were expressed. The defined localization of these proteins in specific cellular compartments warrants further study of their function. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 32 TC 104 Z9 106 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 APR PY 1993 VL 67 IS 4 BP 2360 EP 2366 PG 7 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000072 PM 8445734 ER PT J AU WU, EW CLEMENS, KE HECK, DV MUNGER, K AF WU, EW CLEMENS, KE HECK, DV MUNGER, K TI THE HUMAN PAPILLOMAVIRUS E7 ONCOPROTEIN AND THE CELLULAR TRANSCRIPTION FACTOR E2F BIND TO SEPARATE SITES ON THE RETINOBLASTOMA TUMOR SUPPRESSOR PROTEIN SO JOURNAL OF VIROLOGY LA English DT Article ID TYPE-16 E7; ADENOVIRUS E1A; MUTATIONAL ANALYSIS; GENE-PRODUCT; LARGE-T; TRANSACTIVATION; TRANSFORMATION; KERATINOCYTES; MECHANISM; DOMAINS AB The ability of the high-risk and low-risk human papillomavirus E7 oncoproteins to disrupt complexes of the retinoblastoma tumor suppressor protein pRB and the cellular transcription factor E2F was studied. The ability of E7 to disrupt this transcription factor complex correlated with the different pRB binding efficiencies of the high-risk and low-risk human papillomavirus-encoded E7 proteins. The pRB binding site was the sole determinant for these observed differences. The phosphorylation status of the casein kinase II site that is immediately adjacent to the pRB binding site in E7 had no marked effect on this biochemical property of E7. Peptides consisting of the pRB binding site of E7, however, were not able to disrupt the pRB/E2F complex. These data suggest that additional carboxy-terminal sequences in E7 are also required for the efficient disruption of the pRB/E2F complex and that E7 and E2F may interact with nonidentical sites of pRB. C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. OI Munger, Karl/0000-0003-3288-9935 NR 40 TC 87 Z9 88 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 APR PY 1993 VL 67 IS 4 BP 2402 EP 2407 PG 6 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000080 PM 8445736 ER PT J AU BOYER, PL CURRENS, MJ MCMAHON, JB BOYD, MR HUGHES, SH AF BOYER, PL CURRENS, MJ MCMAHON, JB BOYD, MR HUGHES, SH TI ANALYSIS OF NONNUCLEOSIDE DRUG-RESISTANT VARIANTS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 REVERSE-TRANSCRIPTASE SO JOURNAL OF VIROLOGY LA English DT Article ID ANTI-HIV AGENTS; SELECTIVE-INHIBITION; DERIVATIVES; REPLICATION; INVITRO; 1H,3H-THIAZOLO<3,4-A>BENZIMIDAZOLES; SENSITIVITY; MUTANTS; POTENT; AZT AB A number of chemically distinct nonnucleoside inhibitors of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) have been reported. Several lines of evidence, including the isolation of RT mutants that show cross resistance, suggest that, despite their structural diversity, many of these inhibitors bind to a common site on HIV-1 RT. We have recently reported that, on the basis of analyses of HIV-1/HIV-2 chimeras, the natural product calanolide A may interact with a different site or sites in HIV-1 RT. We have used BspMI cassette mutagenesis to prepare a collection of HIV-1 RT mutants that show resistance to the known members of the general class of nonnucleoside inhibitors. This collection of mutants can be used to determine whether a new drug will show cross resistance with known inhibitors and to define amino acid positions critical for the action of the drugs. The mutants were used to analyze calanolide A, 1H,3H-thiazolo[3,4-a]benzimidazole(4i), and the acyclic nucleoside analog 1-[(2-hydroxyethoxy)methyl]-6-(phenylthio)thymine. These analyses suggest that all three drugs interact with HIV-1 RT within the previously defined common binding site for nonnucleoside inhibitors. However, the drugs respond differently to the panel of drug-resistant HIV-1 RTs, indicating that while the binding sites of the drugs overlap they are not identical. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,POB B,FREDERICK,MD 21702. NCI,DCT,DTP,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 36 TC 103 Z9 104 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 APR PY 1993 VL 67 IS 4 BP 2412 EP 2420 PG 9 WC Virology SC Virology GA KT980 UT WOS:A1993KT98000082 PM 7680393 ER PT J AU LUTZ, W SANDERS, M SALISBURY, J LOLAIT, S OCARROLL, AM KUMAR, R AF LUTZ, W SANDERS, M SALISBURY, J LOLAIT, S OCARROLL, AM KUMAR, R TI VASOPRESSIN RECEPTOR-MEDIATED ENDOCYTOSIS IN CELLS TRANSFECTED WITH V1-TYPE VASOPRESSIN RECEPTORS SO KIDNEY INTERNATIONAL LA English DT Article ID EPIDERMAL GROWTH-FACTOR; LIGAND-INDUCED INTERNALIZATION; 12-AMINO ACID SEQUENCE; COATED PIT FORMATION; INSULIN-RECEPTOR; CYTOPLASMIC DOMAIN; DOWN-REGULATION; JUXTAMEMBRANE REGION; ARGININE-VASOPRESSIN; BETA-SUBUNIT AB We examined the process of receptor-mediated endocytosis in A-9 lung fibroblast and chinese hamster ovary (CHO) cells transfected with the recently cloned vasopressin V1a receptor (51). We used a fluorescent labeled vasopressin analog (rhodamine-mercaptopropionic acid lysine vasopressin) and radiolabeled vasopressin to examine this process in the two transfected cell lines. Both A-9 and CHO cells internalize vasopressin in a manner consistent with receptor-mediated endocytosis. A-9 cells internalize vasopressin more rapidly than CHO cells. The process is inhibited by vasopressin and by specific vasopressin V1 receptor antagonists but not by specific V2 receptor antagonists. Hypertonic sucrose inhibits endocytosis in both cell types suggesting a role of clathrin coated pits in the endocytosis of receptor in these cells. These cells are excellent models in which to examine the effect of receptor mutations on vasopressin receptor-mediated endocytosis. C1 MAYO CLIN & MAYO FDN,DEPT MED,NEPHROL RES UNIT,911A GUGGENHEIM BLDG,200 1ST ST SW,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,DEPT BIOCHEM & MOLEC BIOL,ROCHESTER,MN 55905. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. FU NIDDK NIH HHS [R01 DK058546, DK 42791, R01 DK025409, DK 25409] NR 56 TC 12 Z9 12 U1 0 U2 3 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD APR PY 1993 VL 43 IS 4 BP 845 EP 852 DI 10.1038/ki.1993.119 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA KT675 UT WOS:A1993KT67500009 PM 8479120 ER PT J AU KREITMAN, RJ CHAUDHARY, VK WALDMANN, TA HANCHARD, B CRANSTON, B FITZGERALD, DJP PASTAN, I AF KREITMAN, RJ CHAUDHARY, VK WALDMANN, TA HANCHARD, B CRANSTON, B FITZGERALD, DJP PASTAN, I TI CYTOTOXIC ACTIVITIES OF RECOMBINANT IMMUNOTOXINS COMPOSED OF PSEUDOMONAS TOXIN OR DIPHTHERIA-TOXIN TOWARD LYMPHOCYTES FROM PATIENTS WITH ADULT T-CELL LEUKEMIA SO LEUKEMIA LA English DT Article ID INTERLEUKIN-2 FUSION PROTEIN; CYTO-TOXICITY; LYMPHOTROPIC RETROVIRUSES; GENETIC CONSTRUCTION; MUTANT PROTEINS; EXOTOXIN-A; RECEPTOR; EXPRESSION; AERUGINOSA; FRAGMENT AB We have previously shown that the recombinant single-chain immunotoxin anti-Tac(Fv)-PE40, composed of the variable domains of the anti-Tac monoclonal antibody in a single-chain form joined to a derivative of Pseudomonas exotoxin (PE), is cytotoxic toward malignant cells from adult T-cell leukemia (ATL) patients. Using this assay, we have now compared the activity of anti-Tac(Fv)-PE40 with that of an improved version, anti-Tac(Fv)-PE40KDEL which contains an altered carboxyl terminus, and also with two chimeric toxins made with diphtheria toxin (DT). One of these is a fusion of amino acids 1-388 of DT with anti-Tac(Fv) and is termed DT388-anti-Tac(Fv). The other, DT388-IL2, contains interleukin 2 (IL2) at the carboxyl terminus of the same DT derivative. We incubated these toxins with malignant ATL peripheral blood mononuclear cells (PBMCs) for 1-3 days and then measured [H-3]leucine incorporation. We found that anti-Tac(Fv)-PE40KDEL was the most cytotoxic agent and was followed in decreasing order of activity by anti-Tac(Fv)-PE40, DT388-anti-Tac(Fv), and finally DT388-L2. Trypan blue staining showed that inhibition of protein synthesis correlated with cell death. Time course studies showed that tha recombinant toxins containing anti-Tac(Fv) were cytotoxic even if exposed to the cells for only one hour. After intravenous injection into mice, the half-life of anti-Tac(Fv)-PE40 or anti-Tac(Fv)-PE40KDEL was 30 minutes. Normal PBMCs were resistant to all four toxins. Recombinant immunotoxins made with anti-Tac merit further study as potential reagents in the treatment of ATL. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NCI,DIV CANC BIOL DIAG & CTR,METAB BRANCH,BETHESDA,MD 20892. UNIV W INDIES,DEPT PATHOL,KINGSTON 7,JAMAICA. UNIV DELHI,DEPT BIOCHEM,NEW DELHI 110021,INDIA. NR 30 TC 38 Z9 39 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 1993 VL 7 IS 4 BP 553 EP 562 PG 10 WC Oncology; Hematology SC Oncology; Hematology GA KY973 UT WOS:A1993KY97300011 PM 8464234 ER PT J AU BLATTNER, WA AF BLATTNER, WA TI HTLV-I AND ADULT T-CELL LEUKEMIA SO LEUKEMIA RESEARCH LA English DT Letter ID C RETROVIRUS; LYMPHOMA VIRUS; HUMAN-SERA; ANTIBODIES; LINE; LYMPHOCYTES; PARTICLES; PATIENT; BLACKS; AIDS RP BLATTNER, WA (reprint author), NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 19 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD APR PY 1993 VL 17 IS 4 BP 385 EP 386 DI 10.1016/0145-2126(93)90029-K PG 2 WC Oncology; Hematology SC Oncology; Hematology GA LA568 UT WOS:A1993LA56800015 PM 8487589 ER PT J AU JOSHI, M DWYER, DM NAKHASI, HL AF JOSHI, M DWYER, DM NAKHASI, HL TI CLONING AND CHARACTERIZATION OF DIFFERENTIALLY EXPRESSED GENES FROM INVITRO-GROWN AMASTIGOTES OF LEISHMANIA-DONOVANI SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE LEISHMANIA-DONOVANI; INVITRO AMASTIGOTE; DIFFERENTIAL GENE REGULATION; RIBOSOMAL PROTEIN; STRESS-INDUCIBLE PROTEIN; IMMUNOREACTIVITY; VISCERAL LEISHMANIASIS ID RIBOSOMAL PROTEIN-S11; SURFACE GLYCOPROTEIN; NUCLEOTIDE-SEQUENCE; PROMASTIGOTES; STAGE; MACROPHAGES; MEXICANA; CULTURE AB Leishmanial parasites routinely undergo cyclic differentiation from promastigotes to amastigotes during their life cycle. This process involves both morphological and macromolecular changes. To study such changes, we used a axenic culture system which permits the continuous generation and cycling of Leishmania donovani from promastigotes to 'amastigotes' in vitro. cDNA libraries were constructed from poly(A)+ RNA isolated from both the pro- and amastigote forms. Using differential cDNA hybridization techniques, 3 unique cDNAs clones (P17, A41 and A45) were isolated from the amastigote library. To assess whether these clones were differentially expressed by the pro-or 'amastigotes' forms, they were hybridized to RNA isolated from each of these parasite forms in Northern and slot-blots. Results of these analyses showed that 'amastigotes' had approx. 2-fold higher levels of the A41 and A45 RNAs compared to the promastigotes. Conversely, promastigotes showed approx. 2-fold higher levels of the P17 RNA than 'amastigotes'. Nucleotide sequence analysis and comparison with those in Gene bank, revealed that the 3 cDNAs represent unique leishmanial genes. Comparison of the deduced amino acid sequences revealed that: P17 open reading frame (ORF) had significant similarity with a soybean ribosomal protein S11; A41 ORF with a Bacillus subtilis spore germination gene (gerC) and A45 ORF with yeast stress-inducible protein (STI1). It is of interest to note that. of the 3 cDNAs identified, the A45-encoded protein was recognized by sera from patients with clinically active visceral leishmaniasis and was encoded by a single copy gene. C1 CBER,FOOD & DRUG ADM,DIV BIOCHEM & BIOPHYS,BIOCHEM LAB,BLDG 29,RM 107,8800 ROCKVILLE PIKE,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 30 TC 90 Z9 92 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-6851 J9 MOL BIOCHEM PARASIT JI Mol. Biochem. Parasitol. PD APR PY 1993 VL 58 IS 2 BP 345 EP 354 DI 10.1016/0166-6851(93)90057-5 PG 10 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA KU715 UT WOS:A1993KU71500017 PM 8479459 ER PT J AU WILLIAMSON, KC CRISCIO, MD KASLOW, DC AF WILLIAMSON, KC CRISCIO, MD KASLOW, DC TI CLONING AND EXPRESSION OF THE GENE FOR PLASMODIUM-FALCIPARUM TRANSMISSION-BLOCKING TARGET ANTIGEN, PFS230 SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Note DE PLASMODIUM-FALCIPARUM; MALARIA; TRANSMISSION-BLOCKING IMMUNITY; PFS230; GAMETE; ZYGOTE ID SURFACE-ANTIGENS; PROTEIN; ANTIBODIES C1 NIAID,MALARIA RES LAB,MOLEC VACCINE SECT,BLDG 4,RM B1-37,BETHESDA,MD 20892. NR 11 TC 70 Z9 72 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-6851 J9 MOL BIOCHEM PARASIT JI Mol. Biochem. Parasitol. PD APR PY 1993 VL 58 IS 2 BP 355 EP 358 DI 10.1016/0166-6851(93)90058-6 PG 4 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA KU715 UT WOS:A1993KU71500018 PM 8479460 ER PT J AU GATIGNOL, A BUCKLER, C JEANG, KT AF GATIGNOL, A BUCKLER, C JEANG, KT TI RELATEDNESS OF AN RNA-BINDING MOTIF IN HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TAR RNA-BINDING PROTEIN TRBP TO HUMAN P1/DSI KINASE AND DROSOPHILA STAUFEN SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HIV-1 REV PROTEIN; RESPONSIVE ELEMENT; TRANSACTIVATING REGION; SECONDARY STRUCTURE; NUCLEAR-PROTEIN; GENE-EXPRESSION; BASIC DOMAIN; RECOGNITION; SEQUENCE; IDENTIFICATION AB TRBP is a human cellular protein that binds the human immunodeficiency virus type 1 TAR RNA. Here, we show that the intact presence of amino acids 247 to 267 in TRBP correlates with its ability to bind RNA. This region contains a lysine- and arginine-rich motif, KKLAKRNAAAKMLLRVHTVPLDAR. A 24-amino-acid synthetic peptide (TR1) of this sequence bound TAR RNA with affinities similar to that of the entire TRBP, thus suggesting that this short motif contains a sufficient RNA-binding activity. Using RNA probe-shift analysis, we determined that TR1 does not bind all double-stranded RNAs but prefers TAR and other double-stranded RNAs with G+C-rich characteristics. Immunoprecipitation of TRBP from human immunodeficiency virus type 1-infected T lymphocytes recovered TAR RNA. This is consistent with a TRBP-TAR ribonucleoprotein during viral infection. Computer alignment revealed that TR1 is highly homologous to the RNA-binding domain of human P1/dsI protein kinase and two regions within Drosophila Staufen. We suggest that these proteins are related by virtue of sharing a common RNA-binding moiety. RP GATIGNOL, A (reprint author), NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892, USA. RI Jeang, Kuan-Teh/A-2424-2008 NR 73 TC 121 Z9 123 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1993 VL 13 IS 4 BP 2193 EP 2202 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KT913 UT WOS:A1993KT91300021 PM 8455607 ER PT J AU RABIN, SJ CLEGHON, V KAPLAN, DR AF RABIN, SJ CLEGHON, V KAPLAN, DR TI SNT, A DIFFERENTIATION-SPECIFIC TARGET OF NEUROTROPHIC FACTOR-INDUCED TYROSINE KINASE-ACTIVITY IN NEURONS AND PC12 CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID NERVE GROWTH-FACTOR; TRK PROTOONCOGENE PRODUCT; PHEOCHROMOCYTOMA CELLS; PROTEIN-KINASE; MOLECULAR-CLONING; SUBSTANTIA-NIGRA; DIVISION CYCLE; B-RAF; RECEPTOR; BRAIN AB To elucidate the signal transduction mechanisms used by ligands that induce differentiation and the cessation of cell division, we utilized p13suc1-agarose, a reagent that binds p34cdc2/cdk2. By using this reagent, we identified a 78- to 90-kDa species in PC12 pheochromocytoma cells that is rapidly phosphorylated on tyrosine following treatment with the differentiation factors nerve growth factor (NGF) and fibroblast growth factor but not by the mitogens epidermal growth factor or insulin. This species, called SNT (suc-associated neurotrophic factor-induced tyrosine-phosphorylated target), was also phosphorylated on tyrosine in primary rat cortical neurons treated with the neurotrophic factors neurotrophin-3, brain-derived neurotrophic factor, and fibroblast growth factor but not in those treated with epidermal growth factor. In neuronal and fibroblast cells, where NGF can also act as a mitogen, SNT was tyrosine phosphorylated to a much greater extent during NGF-induced differentiation than during NGF-induced proliferation. SNT was phosphorylated in vitro on serine, threonine, and tyrosine in p13suc1-agarose precipitates from NGF-treated PC12 cells, indicating that this protein may be a substrate of kinase activities associated with p13suc1-p34cdc2/cdk2 complexes. In addition, SNT was associated predominantly with nuclear fractions following subcellular fractionation of NGF-treated PC12 cells. Finally, in PC12 cells, NGF-stimulated tyrosine phosphorylation of SNT was dependent on the levels of Trk tyrosine kinase activity and was constitutively induced by expression of pp60v-src. However, Ras was not required for constitutive SNT tyrosine phosphorylation, suggesting that this protein functions distally to Trk and pp60v-src but in a pathway parallel to that of Ras. SNT is the first identified specific target of differentiation factor-induced tyrosine kinase activity in neuronal cells. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MOLEC MECHANISMS CARCINOGENESIS LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 77 TC 176 Z9 178 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1993 VL 13 IS 4 BP 2203 EP 2213 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KT913 UT WOS:A1993KT91300022 PM 7681142 ER PT J AU SEGARS, JH MARKS, MS HIRSCHFELD, S DRIGGERS, PH MARTINEZ, E GRIPPO, JF BROWN, M WAHLI, W OZATO, K AF SEGARS, JH MARKS, MS HIRSCHFELD, S DRIGGERS, PH MARTINEZ, E GRIPPO, JF BROWN, M WAHLI, W OZATO, K TI INHIBITION OF ESTROGEN-RESPONSIVE GENE ACTIVATION BY THE RETINOID-X RECEPTOR-BETA - EVIDENCE FOR MULTIPLE INHIBITORY PATHWAYS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HUMAN-BREAST CANCER; 5' FLANKING REGION; THYROID-HORMONE; TRANSCRIPTIONAL ACTIVATION; GLUCOCORTICOID RECEPTORS; INVITRO TRANSCRIPTION; MAMMALIAN-CELLS; OVALBUMIN GENE; ACID RECEPTOR; V-ERBA AB The retinoid X receptor beta (RXRbeta; H-2RIIBP) forms heterodimers with various nuclear hormone receptors and binds multiple hormone response elements, including the estrogen response element (ERE). In this report, we show that endogenous RXRbeta contributes to ERE binding activity in nuclear extracts of the human breast cancer cell line MCF-7. To define a possible regulatory role of RXRbeta regarding estrogen-responsive transcription in breast cancer cells, RXRbeta and a reporter gene driven by the vitellogenin A2 ERE were transfected into estrogen-treated MCF-7 cells. RXRbeta inhibited ERE-driven reporter activity in a dose-dependent and element-specific fashion. This inhibition occurred in the absence of the RXR ligand 9-cis retinoic acid. The RXRbeta-induced inhibition was specific for estrogen receptor (ER)-mediated ERE activation because inhibition was observed in ER-negative MDA-MB-231 cells only following transfection of the estrogen-activated ER. No inhibition of the basal reporter activity was observed. The inhibition was not caused by simple competition of RXRbeta with the ER for ERE binding, since deletion mutants retaining DNA binding activity but lacking the N-terminal or C-terminal domain failed to inhibit reporter activity. In addition, cross-linking studies indicated the presence of an auxiliary nuclear factor present in MCF-7 cells that contributed to RXRbeta binding of the ERE. Studies using known heterodimerization partners of RXRbeta confirmed that RXRbeta/triiodothyronine receptor alpha heterodimers avidly bind the ERE but revealed the existence of another triiodothyronine-independent pathway of ERE inhibition. These results indicate that estrogen-responsive genes may be negatively regulated by RXRbeta through two distinct pathways. C1 NICHHD, MOLEC GROWTH REGULAT LAB, BETHESDA, MD 20892 USA. UNIV LAUSANNE, INST BIOL ANIM, CH-1015 LAUSANNE, SWITZERLAND. HOFFMANN LA ROCHE INC, DRUG METAB, NUTLEY, NJ 07110 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT MED, BOSTON, MA 02115 USA. RI Wahli, Walter/B-1398-2009; Hirschfeld, Steven/E-2987-2016 OI Wahli, Walter/0000-0002-5966-9089; Hirschfeld, Steven/0000-0003-0627-7249 FU NICHD NIH HHS [HD00849-02] NR 80 TC 85 Z9 85 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1993 VL 13 IS 4 BP 2258 EP 2268 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KT913 UT WOS:A1993KT91300027 PM 8384307 ER PT J AU KUANG, AA NOVAK, KD KANG, SM BRUHN, K LENARDO, MJ AF KUANG, AA NOVAK, KD KANG, SM BRUHN, K LENARDO, MJ TI INTERACTION BETWEEN NF-KAPPA-B AND SERUM RESPONSE FACTOR-BINDING ELEMENTS ACTIVATES AN INTERLEUKIN-2 RECEPTOR ALPHA-CHAIN ENHANCER SPECIFICALLY IN T-LYMPHOCYTES SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID C-FOS GENE; PROTEIN-BINDING; DNA-BINDING; TRANSCRIPTION FACTORS; IMMUNOGLOBULIN-KAPPA; 65-KD SUBUNIT; REL ONCOGENE; CELL LINES; INDUCIBILITY; EXPRESSION AB We find that a short enhancer element containing the NF-kappaB binding site from the interleukin-2 receptor alpha-chain gene (IL-2Ralpha) is preferentially activated in T cells. The IL-2Ralpha enhancer binds NF-kappaB poorly and is only weakly activated by the NF-kappaB site alone. Serum response factor (SRF) binds to a site adjacent to the NF-kappaB site in the IL-2R enhancer, and both sites together have strong transcriptional activity specifically in T cells. Surprisingly, the levels of SPF constitutively expressed in T cells are consistently higher than in other cell types. Overexpression of SRF in B cells causes the IL-2R enhancer to function as well as it does in T cells, suggesting that the high level of SRF binding in T cells is functionally important. C1 NIAID,IMMUNOL LAB,ROOM 11D09,BLDG 10,BETHESDA,MD 20892. RI Bruhn, Kevin/F-9772-2013 NR 66 TC 38 Z9 39 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1993 VL 13 IS 4 BP 2536 EP 2545 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KT913 UT WOS:A1993KT91300055 PM 8455627 ER PT J AU POSADA, J YEW, N AHN, NG VANDEWOUDE, GF COOPER, JA AF POSADA, J YEW, N AHN, NG VANDEWOUDE, GF COOPER, JA TI MOS STIMULATES MAP KINASE IN XENOPUS OOCYTES AND ACTIVATES A MAP KINASE KINASE INVITRO SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MATURATION-PROMOTING FACTOR; PROTO-ONCOGENE PRODUCT; CDC2 PROTEIN; TYROSINE PHOSPHORYLATION; S6 KINASE; MPF; COMPONENT; HOMOLOG; EGGS; FIBROBLASTS AB Several protein kinases, including Mos, maturation-promoting factor (MPF), mitogen-activated protein (MAP) kinase, and MAP kinase kinase (MAPKK), are activated when Xenopus oocytes enter meiosis. De novo synthesis of the Mos protein is required for progesterone-induced meiotic maturation. Recently, bacterially synthesized maltose-binding protein (MBP)-Mos fusion protein was shown to be sufficient to initiate meiosis I and MPF activation in fully grown oocytes in the absence of protein synthesis. Here we show that MAP kinase is rapidly phosphorylated and activated following injection of wild-type, but not kinase-inactive mutant, MBP-Mos into fully grown oocytes. MAP kinase activation by MBP-Mos occurs within 20 min, much more rapidly than in progesterone-treated oocytes. The MBP-Mos fusion protein also activates MPF, but MPF activation does not occur until approximately 2 h after injection. Extracts from oocytes injected with wild-type but not kinase-inactive MBP-Mos contain an activity that can phosphorylate MAP kinase, suggesting that Mos directly or indirectly activates a MAPKK. Furthermore, activated MBP-Mos fusion protein is able to phosphorylate and activate a purified, phosphatase-treated, rabbit muscle MAPKK in vitro. Thus, in oocytes, Mos is an upstream activator of MAP kinase which may function through direct phosphorylation of MAPKK. C1 FRED HUTCHINSON CANC RES CTR,1124 COLUMBIA ST,SEATTLE,WA 98104. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. UNIV COLORADO,DEPT CHEM & BIOCHEM,BOULDER,CO 80309. FU NCI NIH HHS [F32 CA08860, N01CO-74101]; NIGMS NIH HHS [GM48521] NR 57 TC 370 Z9 372 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1993 VL 13 IS 4 BP 2546 EP 2553 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KT913 UT WOS:A1993KT91300056 PM 8384311 ER PT J AU WEISSINGER, EM MISCHAK, H GOODNIGHT, J DAVIDSON, WF MUSHINSKI, JF AF WEISSINGER, EM MISCHAK, H GOODNIGHT, J DAVIDSON, WF MUSHINSKI, JF TI ADDITION OF CONSTITUTIVE C-MYC EXPRESSION TO ABELSON MURINE LEUKEMIA-VIRUS CHANGES THE PHENOTYPE OF THE CELLS TRANSFORMED BY THE VIRUS FROM PRE-B-CELL LYMPHOMAS TO PLASMACYTOMAS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PRIMED BALB/C MICE; V-ABL; BONE-MARROW; MOUSE; GENE; PRISTANE; RETROVIRUS; ONCOGENES; INDUCTION; RNA AB Abelson murine leukemia virus (A-MuLV), a retrovirus that expresses the v-abl oncogene, characteristically induces pre-B-cell lymphomas following in vivo infection of BALB/c mice or in vitro infection of suspensions of fetal liver or bone marrow cells. ABL-MYC, a retrovirus that expresses both v-abl and c-myc, induces solely plasmacytomas in BALB/c mice. To investigate how the addition of overexpression of c-myc to that of v-abl accomplishes this dramatic change in the phenotype of the cells transformed by these closely related retroviruses, we utilized helper-free A-MuLV(PSI2) and ABL-MYC(PSI2) in vitro to infect suspensions of cells from different lymphoid tissues and purified immature and purified mature B cells. As expected, A-MuLV(PSI2) induced only pre-B-cell lymphomas in vivo and in vitro when immature B cells were present. ABL-MYC(PSI2), on the other hand, produced only plasmacytomas, even when purified immature B lymphocytes were infected in vitro. Although the A-MuLV(PSI2)-induced pre-B-cell lymphomas express easily detectable levels of c-myc mRNA, maturation into more-mature forms of B lymphocytes is blocked. The constitutively overexpressed c-myc in the ABL-MYC retrovirus abrogates this block, permits maturation of infected immature B cells, and yields transformed plasma cells. C1 NCI,GENET LAB,MOLEC GENET SECT,BLDG 37,ROOM 2B04,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. RI Mischak, Harald/E-8685-2011 NR 38 TC 14 Z9 14 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1993 VL 13 IS 4 BP 2578 EP 2585 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KT913 UT WOS:A1993KT91300059 PM 8455630 ER PT J AU HONDA, T WADA, E BATTEY, JF WANK, SA AF HONDA, T WADA, E BATTEY, JF WANK, SA TI DIFFERENTIAL GENE-EXPRESSION OF CCK(A) AND CCK(B) RECEPTORS IN THE RAT-BRAIN SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID PANCREATIC ACINAR-CELLS; CHOLECYSTOKININ RECEPTORS; INSITU HYBRIDIZATION; NUCLEUS-ACCUMBENS; BINDING-SITES; MESSENGER-RNA; AUTORADIOGRAPHIC LOCALIZATION; ANTAGONISTS; DOPAMINE; PEPTIDE C1 NIH,DIGEST DIS BRANCH,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,BIOL CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NR 43 TC 107 Z9 108 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 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell Neurosci. PD APR PY 1993 VL 4 IS 2 BP 143 EP 154 DI 10.1006/mcne.1993.1018 PG 12 WC Neurosciences SC Neurosciences & Neurology GA KU018 UT WOS:A1993KU01800002 PM 19912917 ER PT J AU VAUGHAN, RA UHL, G KUHAR, MJ AF VAUGHAN, RA UHL, G KUHAR, MJ TI RECOGNITION OF DOPAMINE TRANSPORTERS BY ANTIPEPTIDE ANTIBODIES SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID CLONING; EXPRESSION C1 NIDA,ADDICT RES CTR,MOLEC NEUROBIOL SECT,BALTIMORE,MD 21224. RP VAUGHAN, RA (reprint author), NIDA,ADDICT RES CTR,MOLEC PHARMACOL SECT,BALTIMORE,MD 21224, USA. NR 15 TC 28 Z9 29 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell Neurosci. PD APR PY 1993 VL 4 IS 2 BP 209 EP 215 DI 10.1006/mcne.1993.1025 PG 7 WC Neurosciences SC Neurosciences & Neurology GA KU018 UT WOS:A1993KU01800009 PM 19912924 ER PT J AU BARLETTA, JM KINGMA, DW LING, Y CHARACHE, P MANN, RB AMBINDER, RF AF BARLETTA, JM KINGMA, DW LING, Y CHARACHE, P MANN, RB AMBINDER, RF TI RAPID INSITU HYBRIDIZATION FOR THE DIAGNOSIS OF LATENT EPSTEIN-BARR-VIRUS INFECTION SO MOLECULAR AND CELLULAR PROBES LA English DT Article DE EPSTEIN-BARR VIRUS; INSITU HYBRIDIZATION; LYMPHOMA; NASOPHARYNGEAL CARCINOMA; HODGKINS DISEASE; RAPID DIAGNOSIS; EBER; RIBOPROBE ID SMALL RNAS; EXPRESSION; CELLS C1 JOHNS HOPKINS UNIV,SCH MED,DEPT LAB MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT ONCOL,BALTIMORE,MD 21205. NCI,DEPT HEMATOPATHOL,BETHESDA,MD 20892. FU NCI NIH HHS [R01 CA55529] NR 13 TC 53 Z9 55 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0890-8508 J9 MOL CELL PROBE JI Mol. Cell. Probes PD APR PY 1993 VL 7 IS 2 BP 105 EP 109 DI 10.1006/mcpr.1993.1014 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology GA LB940 UT WOS:A1993LB94000003 PM 8391639 ER PT J AU CERRUTI, C WALTHER, DM KUHAR, MJ UHL, GR AF CERRUTI, C WALTHER, DM KUHAR, MJ UHL, GR TI DOPAMINE TRANSPORTER MESSENGER-RNA EXPRESSION IS INTENSE IN RAT MIDBRAIN NEURONS AND MODEST OUTSIDE MIDBRAIN SO MOLECULAR BRAIN RESEARCH LA English DT Article DE DOPAMINE; DOPAMINE TRANSPORTER MESSENGER RNA; MIDBRAIN; RAT ID PARKINSONS-DISEASE; MEDIAN-EMINENCE; COCAINE; CLONING; PHYSIOLOGY; RECEPTORS AB Dopamine transporter mRNA expression in individual neurons from the substantia nigra pars compacta, 'A11' area, arcuate nucleus of the hypothalamus, retina, and olfactory bulb was assessed by in situ hybridization. High levels of expression were noted over individual neurons in midbrain nuclei; much lower expression was found in cells of the inner nuclear layer of the retina, glomerular cell layer of the olfactory bulb, and medial aspect of the arcuate nucleus of the hypothalamus. The low levels of expression in the latter nuclei are consistent with the paucity of effects of cocaine in visual and olfactory systems, failure to detect photoaffinity-labelled transporter protein in hypothalamus or olfactory bulb, and observations that little or no damage is found in dopaminergic neurons outside the basal midbrain in idiopathic Parkinsonism. C1 NIDA,ADDICT RES CTR,BOX 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21224. NR 28 TC 87 Z9 88 U1 2 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD APR PY 1993 VL 18 IS 1-2 BP 181 EP 186 DI 10.1016/0169-328X(93)90187-T PG 6 WC Neurosciences SC Neurosciences & Neurology GA KU590 UT WOS:A1993KU59000020 ER PT J AU CHU, E KOELLER, DM JOHNSTON, PG ZINN, S ALLEGRA, CJ AF CHU, E KOELLER, DM JOHNSTON, PG ZINN, S ALLEGRA, CJ TI REGULATION OF THYMIDYLATE SYNTHASE IN HUMAN COLON CANCER-CELLS TREATED WITH 5-FLUOROURACIL AND INTERFERON-GAMMA SO MOLECULAR PHARMACOLOGY LA English DT Article ID HUMAN COLORECTAL-CARCINOMA; MESSENGER-RNA TRANSLATION; CULTURED MAMMALIAN-CELLS; DIHYDROFOLATE-REDUCTASE; GENE-EXPRESSION; SYNTHETASE-ACTIVITY; MOUSE FIBROBLASTS; THYMIDINE KINASE; BREAST-CANCER; LINES AB The effects of fluorouracil (5-FU) and interferon-gamma (IFN-gamma) on the regulation of thymidylate synthase (TS) gene expression were investigated in the human colon cancer H630 cell line. By Western immunoblot analysis, TS protein levels in H630 cells were increased 3-, 5.5-, 5-, and 2.5-fold after 8-, 16-, 24-, and 36-hr exposure to 1 mum 5-FU, respectively. When H630 cells were exposed to varying concentrations of 5-FU (0.3-10 muM) for 24 hr, increases in TS protein up to 5.5-fold were observed. A 24-hr exposure to 1 muM 5-FU resulted in a 4.5-fold increase in the level of TS protein, whereas in 5-FU/IFN-gamma-treated cells TS protein was increased by only 1.8-fold, compared with control cells. IFN-gamma treatment alone did not affect TS protein levels, relative to control. Northern blot analysis revealed no changes in TS mRNA levels when H630 cells were exposed either to 1 muM 5-FU for 8-36 hr, to varying concentrations of 5-FU (0.3-10 muM) for 24 hr, or to the combination of 5-FU and IFN-gamma. Pulse-labeling studies with [S-35]methionine demonstrated a 3.5-fold increase in net synthesis of TS in cells treated with 1 muM 5-FU, whereas the level of newly synthesized TS increased only 1.5-fold in cells treated with 5-FU/IFN-gamma, compared with control cells. Pulse-chase studies revealed that the half-lives of TS protein in control and 5-FU-treated cells were equivalent. These findings demonstrate that the increase in TS protein after 5-FU exposure and the subsequent inhibitory effect of IFN-gamma on TS protein expression are both regulated at the post-transcriptional level. C1 UNIV WASHINGTON,DEPT MED,DIV MED GENET,SEATTLE,WA 98105. RP CHU, E (reprint author), USN,NCI,DIV CANC TREATMENT,MED ONCOL BRANCH,BLDG 8,ROOM 5101,BETHESDA,MD 20889, USA. NR 46 TC 136 Z9 139 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 1993 VL 43 IS 4 BP 527 EP 533 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KY669 UT WOS:A1993KY66900006 PM 8474431 ER PT J AU LLOYD, RV SHUSTER, L MASON, RP AF LLOYD, RV SHUSTER, L MASON, RP TI REEXAMINATION OF THE MICROSOMAL TRANSFORMATION OF N-HYDROXYNORCOCAINE TO NORCOCAINE NITROXIDE SO MOLECULAR PHARMACOLOGY LA English DT Article ID INDUCED HEPATIC-NECROSIS; LIPID-PEROXIDATION; OXIDATIVE DAMAGE; LINOLEIC-ACID; FREE-RADICALS; RAT-BRAIN; COCAINE; HEPATOTOXICITY; METABOLISM; SUPEROXIDE AB Cocaine is known to be associated with hepatotoxicity in laboratory animals, and there is recent evidence that it also induces liver damage in humans. In both cases an N-oxidative pathway is responsible. Cocaine (NCN) is first N-demethylated to norcocaine, followed by oxidation to N-hydroxynorcocaine (NCNOH) and norcocaine nitroxide (NCNO.). On the basis of ESR studies of NCNOH with rat liver microsomes, it has been proposed that NCNO. induces hepatotoxicity by futile redox cycling between NCNO. and NCNOH at the expense of NADPH. The reaction is reported to be accompanied by formation of superoxide and lipid peroxyl radicals. It has also been reported that the same toxic sequence occurs with rat brain microsomes, leading to the formation of reactive free radicals in the brain. We have reexamined the microsomal metabolism of NCNOH to investigate the mechanism more thoroughly. Spin traps [5,5-dimethyl-1-pyrroline N-oxide and alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone] were used to investigate the formation of reactive free radicals, including superoxide, in liver and brain microsomal incubations. In agreement with the literature, we detected a six-line spectrum of a radical adduct of alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone from liver microsome incubations. In contrast, our results showed that brain microsomes were completely inactive, contrary to the literature. In addition, we did not find any NCNO.- or NCNOH-dependent formation of superoxide with either brain or liver microsomes. C1 NIEHS,MOLEC BIOPHYS LAB,POB 12233,MD 10-03,RES TRIANGLE PK,NC 27709. NR 36 TC 25 Z9 25 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 1993 VL 43 IS 4 BP 645 EP 648 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KY669 UT WOS:A1993KY66900019 PM 8386313 ER PT J AU JONG, SC MCMANUS, C AF JONG, SC MCMANUS, C TI COMPUTER CODING OF STRAIN FEATURES OF THE GENUS RHIZOPUS SO MYCOTAXON LA English DT Article ID DNA COMPLEMENTARITY; VARIETIES AB Members of the fungal genus Rhizopus play important roles in human, animal, and plant disease and in the fermentation industry. Identification of Rhizopus species is based primarily on the morphology of sporangiosporogenous structures, zygospores, and asexual reproductive structures. The standardized coding system, the RKC Code, used for computer storage and analysis of microbial strain data was expanded to include features specific to the identification of Rhizopus species. C1 NIDR,MICROBIAL SYSTEMAT SECT,BETHESDA,MD 20892. RP JONG, SC (reprint author), AMER TYPE CULTURE COLLECT,12031 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 25 TC 1 Z9 1 U1 0 U2 0 PU MYCOTAXON LTD PI ITHACA PA PO BOX 264, ITHACA, NY 14851-0264 SN 0093-4666 J9 MYCOTAXON JI Mycotaxon PD APR-JUN PY 1993 VL 47 BP 161 EP 176 PG 16 WC Mycology SC Mycology GA LJ151 UT WOS:A1993LJ15100014 ER PT J AU RALL, JE AF RALL, JE TI RALL FAREWELL TO FRONTIERS SO NATURE LA English DT Letter RP RALL, JE (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD APR 1 PY 1993 VL 362 IS 6419 BP 390 EP 390 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV424 UT WOS:A1993KV42400024 PM 8464463 ER PT J AU LUSSO, P MALNATI, MS GARZINODEMO, A CROWLEY, RW LONG, EO GALLO, RC AF LUSSO, P MALNATI, MS GARZINODEMO, A CROWLEY, RW LONG, EO GALLO, RC TI INFECTION OF NATURAL-KILLER-CELLS BY HUMAN HERPESVIRUS-6 SO NATURE LA English DT Article ID CHRONIC FATIGUE SYNDROME; HUMAN-IMMUNODEFICIENCY-VIRUS; INVITRO; AIDS; DEFICIENCY; MECHANISM; ANTIGEN AB NATURAL killer (NK) cells are a functionally defined subset of non-T, non-B lymphocytes of bone marrow origin, which induce lysis of selected target cells, including neoplastic and virus-infected cells1-3. The NK cell function provides an important mechanism of primary defence against viruses in vivo, as demonstrated by the occurrence of multiple herpesvirus infections in patients congenitally lacking NK cells4,5. Here we show that functionally competent CD3- NK clones can be productively infected by human herpesvirus 6 (HHV-6)6, a T-lymphotropic DNA virus7 that may play a role in the acquired immunodeficiency syndrome (AIDS)8 and in the chronic fatigue syndrome9, two disorders associated with a defective NK cell activity10-15. The infection is cytopathic and induces de novo expression of CD4, an antigen not expressed within the NK lineage16,17, thereby predisposing NK cells to infection by human immunodeficiency virus type 1 (HIV-1). These results provide evidence that a herpesvirus can directly target and kill NK cells, a potential strategy to suppress the natural anti-viral immunity of the host. C1 NIAID,IMMUNOGENET LAB,BETHESDA,MD 20892. RP LUSSO, P (reprint author), NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892, USA. RI Long, Eric/G-5475-2011 OI Long, Eric/0000-0002-7793-3728 NR 29 TC 154 Z9 156 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD APR 1 PY 1993 VL 362 IS 6419 BP 458 EP 462 DI 10.1038/362458a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV424 UT WOS:A1993KV42400087 PM 7681936 ER PT J AU MIKI, T SMITH, CL LONG, JE EVA, A FLEMING, TP AF MIKI, T SMITH, CL LONG, JE EVA, A FLEMING, TP TI ONCOGENE ECT2 IS RELATED TO REGULATORS OF SMALL GTP-BINDING PROTEINS SO NATURE LA English DT Article ID EXPRESSION CDNA CLONING; CELL-DIVISION-CYCLE; SACCHAROMYCES-CEREVISIAE; NUCLEOTIDE-SEQUENCE; MOLECULAR-CLONING; HUMAN HOMOLOG; ABL-ONCOGENE; GENE; YEAST; BCR AB WE have developed an efficient expression cloning system that allows rapid isolation of complementary DNAs able to induce the transformed phenotype1,2. We searched for molecules expressed in epithelial cells and possessing transforming potential to fibroblasts, and cloned a cDNA for the normal receptor of a growth factor secreted by NIH/3T3 cells3,4. Here we report a second novel transforming gene, ect2. The isolated cDNA is activated by amino-terminal truncation of the normal product. The Ect2 protein has sequence similarity within a central core of 255 amino acids with the products of the breakpoint cluster gene, bcr (ref. 5), the yeast cell cycle gene, CDC24 (ref. 6), and the dbl oncogene7. Each of these genes encodes regulatory molecules or effectors for Rho-like small GTP-binding proteins8-10. The baculovirus-expressed Ect2 protein could bind highly specifically to Rho and Rac proteins, whereas the dbl product showed broader binding specificity to Rho family proteins. Thus ect2 is a new member of an expanding family, whose products have transforming properties and interact with Rho-like proteins of the Ras superfamily. RP MIKI, T (reprint author), NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37-1E24,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Eva, Alessandra/J-8268-2016 OI Eva, Alessandra/0000-0003-2949-078X NR 27 TC 225 Z9 233 U1 0 U2 3 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD APR 1 PY 1993 VL 362 IS 6419 BP 462 EP 465 DI 10.1038/362462a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV424 UT WOS:A1993KV42400088 PM 8464478 ER PT J AU GAO, XM FUKAMAUCHI, F CHUANG, DM AF GAO, XM FUKAMAUCHI, F CHUANG, DM TI LONG-TERM BIPHASIC EFFECTS OF LITHIUM TREATMENT ON PHOSPHOLIPASE-C-COUPLED M(3)-MUSCARINIC ACETYLCHOLINE-RECEPTORS IN CULTURED CEREBELLAR GRANULE CELLS SO NEUROCHEMISTRY INTERNATIONAL LA English DT Article ID CEREBRAL-CORTEX; RAT CORTEX; AGONIST; BRAIN; HYDROLYSIS; BINDING; ACCUMULATION; METABOLISM; EXPRESSION; SLICES AB We have studied the long-term effects of lithium on neuronal morphology and the functional expression of phospholipase C-coupled m3-muscarinic acetylcholine receptors (mAChRs) in cerebellar granule cells. There was a biphasic dose-dependent effect on cell morphology following treatment with lithium for 7 days. At low concentrations (less-than-or-equal-to 2 mM), this drug elicited an increase in the number and thickness of connecting nerve fibers, and the size of neuronal aggregates. At high concentrations (5 10 mM), lithium induced a severe deterioration of cell morphology, which ultimately resulted in neuronal death. Carbachol-induced phosphoinositide (PI) turnover was similarly affected by lithium treatment with a significant potentiation at concentrations up to 2 mM and a marked inhibition at doses higher than 5 mM due to lithium-induced neurotoxicity, The biphasic effect on mAChR-mediated PI hydrolysis was associated with corresponding changes in the maximal extent of carbachol-induced inositol phosphate accumulation, and was accompanied by similar changes in [H-3]N-methyl-scopolamine binding to mAChRs and the levels of mRNAs for m3-mAChR and c-Fos. The up-regulation of m3-mAChR mRNA induced by low concentrations of lithium was associated with a down-regulation of m2-mAChR mRNA and no change in either total RNA or beta-actin mRNA. Lithium's effects on m2- and m3-mAChR mRNAs were time-dependent, requiring a pretreatment time of greater-than-or-equal-to 3 days. The biphasic effect was also demonstrated by the binding of [H-3]ouabain to Na+, K+-ATPase, which was shown to be a convenient method for quantifying viable neurons. The neurotoxic effect induced by treatment with high concentrations of lithium was not prevented by known neuroprotective/neurotrophic substances such as 9-amino-tetrahydroacridine or N-methyl-D-aspartate, or the co-presence of excess myo-inositol. Since the neurotrophic influence was induced by concentrations of lithium which overlap the clinical dose range and require long-term treatment, this effect might be relevant to the efficacy of this drug in the treatment of manic-depressive illness. C1 NIMH,BIOL PSYCHIAT BRANCH,MOLEC NEUROBIOL SECT,BETHESDA,MD 20892. NR 31 TC 27 Z9 27 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-0186 J9 NEUROCHEM INT JI Neurochem. Int. PD APR PY 1993 VL 22 IS 4 BP 395 EP 403 DI 10.1016/0197-0186(93)90021-V PG 9 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KU608 UT WOS:A1993KU60800006 PM 8384505 ER PT J AU PACAK, K PALKOVITS, M KVETNANSKY, R FUKUHARA, K ARMANDO, I KOPIN, IJ GOLDSTEIN, DS AF PACAK, K PALKOVITS, M KVETNANSKY, R FUKUHARA, K ARMANDO, I KOPIN, IJ GOLDSTEIN, DS TI EFFECTS OF SINGLE OR REPEATED IMMOBILIZATION ON RELEASE OF NOREPINEPHRINE AND ITS METABOLITES IN THE CENTRAL NUCLEUS OF THE AMYGDALA IN CONSCIOUS RATS SO NEUROENDOCRINOLOGY LA English DT Article DE NOREPINEPHRINE; DIHYDROXYPHENYLGLYCOL; METHOXYHYDROXYPHENYLGLYCOL; DIHYDROXYPHENYLACETIC ACID ID ADRENOCORTICOTROPIN SECRETION; INTRACEREBRAL MICRODIALYSIS; INTRANEURONAL DISPOSITION; PARAVENTRICULAR NUCLEUS; NORADRENALINE RELEASE; INVIVO MICRODIALYSIS; STRESS; PLASMA; BRAIN; RESPONSES AB The release of norepinephrine (NE) and its metabolites in the central nucleus of the amygdala was measured using in vivo microdialysis during immobilization (IMMO) stress in conscious rats. Animals underwent 2-hour periods of IMMO either once or daily for 7 days. Extracellular fluid concentrations of NE, dihydroxyphenylglycol (DHPG), methoxyhydroxyphenylglycol (MHPG), and the dopamine metabolite dihydroxyphenylacetic acid (DOPAC) were measured before, during, and after IMMO. Microdialysate levels of NE and DHPG attained 2- to 3-fold increments during the 1 h of IMMO and declined thereafter, whereas MHPG and DOPAC levels attained maximal levels of about twice basal concentrations during the 2- or 3-h after initiation of IMMO. After the sixth IMMO basal levels of NE, DHPG, MHPG, and DOPAC were decreased, and NE, DHPG, and DOPAC responses during the seventh IMMO failed to attain levels found during the first IMMO, although the absolute changes during IMMO were similar between animals subjected to IMMO once or seven times. The results indicate that acute IMMO increases synthesis, release, and metabolism of NE in the central nucleus of the amygdala and that repetition of IMMO decreases basal catecholamine synthesis and noradrenergic turnover in this brain region, without inhibiting acute noradrenergic responses. C1 NINCDS,CLIN NEUROSCI BRANCH,BLDG 10,ROOM 5N214,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RI Palkovits, Miklos/F-2707-2013 NR 42 TC 43 Z9 44 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD APR PY 1993 VL 57 IS 4 BP 626 EP 633 DI 10.1159/000126417 PG 8 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA LP392 UT WOS:A1993LP39200010 PM 8367029 ER PT J AU WANG, XJ RINZEL, J AF WANG, XJ RINZEL, J TI SPINDLE RHYTHMICITY IN THE RETICULARIS-THALAMI NUCLEUS - SYNCHRONIZATION AMONG MUTUALLY INHIBITORY NEURONS SO NEUROSCIENCE LA English DT Letter ID LATERAL GENICULATE-NUCLEUS; CENTRAL-NERVOUS-SYSTEM; ELECTROPHYSIOLOGICAL PROPERTIES; CALCIUM CURRENTS; RAT; CAT; INVITRO; MORPHOLOGY; PACEMAKER; EPILEPSY AB The sleep spindle rhythm of thalamic origin (7-14 Hz) displays widespread synchronization among thalamic nuclei and over most of the neocortex.1 The mechanisms which mediate such global synchrony are not yet well understood. Here, we theoretically address the hypothesis of Steriade and colleagues that the reticularis thalami nucleus may be considered as a genuine pacemaker for thalamocortical spindles.29-31 Interestingly, the reticularis consists of a population of neurons15,25 which are GABAergic and synaptically Coupled.9,21,23,35 These cells, as do thalamic relay cells,10,17-18 exhibit a transient depolarization following release from sustained hyperpolarization.2,19,22,28 This postinhibitory rebound property is due to a T-type calcium ionic current which is inactivated at rest but de-inactivated by hyperpolarization. Theoretically, rebound-capable cells coupled by inhibition can generate rhythmic activity, although such oscillations are usually alternating (out-of-phase), rather than synchronous (in-phase).'' Here, we develop and apply to Steriade's pacemaker hypothesis our earlier finding34 that mutual inhibition can in fact synchronize cells, provided that the postsynaptic conductance decays sufficiently slowly. Indeed, postsynaptic receptors of the GABA(B) subtype mediate inhibition with a large decay time-constant (congruent-to 200 ms).13 In contrast, chloride-dependent, GABA(A)-mediated inhibitory postsynaptic potentials are fast and brief. Both GABA(A) and GABA(B) receptor binding sites are present in most thalamic regions, including the reticularis.4,6 We suggest that if GABA(B) receptors exist postsynaptically in the reticularis, they may play a critical role in the rhythmic synchronization among reticular neurons, hence in the thalamocortical system. C1 UNIV CHICAGO,JAMES FRANCK INST,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MATH,CHICAGO,IL 60637. RP WANG, XJ (reprint author), NIDDK,MATH RES BRANCH,NATL INST HLTH BLDG 31,ROOM 4B-54,BETHESDA,MD 20892, USA. RI Wang, Xiao-Jing/D-2722-2009 NR 35 TC 175 Z9 176 U1 1 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD APR PY 1993 VL 53 IS 4 BP 899 EP 904 DI 10.1016/0306-4522(93)90474-T PG 6 WC Neurosciences SC Neurosciences & Neurology GA KY904 UT WOS:A1993KY90400001 PM 8389430 ER PT J AU POULTER, MO BARKER, JL OCARROLL, AM LOLAIT, SJ MAHAN, LC AF POULTER, MO BARKER, JL OCARROLL, AM LOLAIT, SJ MAHAN, LC TI COEXISTENT EXPRESSION OF GABA-A RECEPTOR BETA-2, BETA-3 AND GAMMA-2 SUBUNIT MESSENGER-RNAS DURING EMBRYOGENESIS AND EARLY POSTNATAL-DEVELOPMENT OF THE RAT CENTRAL-NERVOUS-SYSTEM SO NEUROSCIENCE LA English DT Article ID REGION-SPECIFIC EXPRESSION; A-RECEPTOR; BENZODIAZEPINE RECEPTORS; ACETYLCHOLINE-RECEPTORS; XENOPUS OOCYTES; BRAIN; SENSITIVITY; DISTINCT; NEURONS; CELLS AB The expression of beta1, beta2, beta3, gamma2 and delta subunit messenger RNAs of the GABA(A) receptor was followed by in situ hybridization histochemistry using radiolabeled oligodeoxynucleotide probes in sections of embryonic (E12-21) and early postnatal (P1-5) rat. Beta2, beta3 and gamma2 subunit messenger RNAs were first detectable at E15 in the spinal cord (ventral > dorsal) and lower central nervous system regions (e.g. pons, medulla and thalamus). Beta3 subunit messenger RNA was abundantly expressed in olfactory bulb neurons at E15. At E17, the expression pattern of these subunit messenger RNAs continued in the lower central nervous system. In the upper central nervous system, beta2, beta3 and 2 subunit messenger RNAs were first detectable in the outer layer of the hippocampal and entire cortical neuroepithelium. The expression for both beta3 and gamma2 subunit messenger RNAs increased significantly over that observed at E15, whereas beta2 subunit messenger RNA increased to a lesser extent and was more discretely expressed in inferior colliculus, cerebellar neuroepithelium and spinal cord (ventral = dorsal). By E19, messenger RNAs for beta2, beta3 and gamma2 subunits displayed a widespread and abundant co-existent distribution throughout the central nervous system. Exceptions to this co-expression were the absence of beta2 messenger RNA in the dentate gyrus and beta3 messenger RNA in entorhinal cortex, areas in which they are present in adult. There was also a differential distribution of subunit messenger RNAs in developing olfactory bulb at E19-20: the glomerular cells preferentially expressed beta3 and gamma2 subunit messenger RNAs; the mitral cells preferentially expressed beta2 subunit messenger RNA; inner granule cells expressed moderate levels of beta2, beta3 and gamma2 subunit messenger RNAs. Expression of beta2, beta3 and gamma2 messenger RNAs was also anatomically co-existent at P5. In addition, significant expression of beta1 and delta subunit messenger RNAs was apparent in hippocampus and entorhinal cortex. The identity of the gamma2 expressed between E15 and E21 was shown to be mostly the short isoform of gamma2 subunit messenger RNA. Expression of both forms was evident beginning around P3-5. These results indicate that during the late embryonic and early postnatal period of development, beta2, beta2 and gamma2 subunit messenger RNAs are abundantly expressed and co-localized to most central nervous system regions. The anatomical and cellular distribution of these GABA, subunit messenger RNAs, as well as those coding for specific alpha subunits [Poulter M. O. et al. (1992) J. Neurosci. 12, 2888-28901 indicates that the expression of GABA, receptor subunit messenger RNA is a complex and dynamic process, giving rise to a pattern that has constant and variable features which often differ from distributions seen in the adult CNS. This ontogenetic profile is consistent with the evidence that GABA(A) receptors play a role in synaptogenesis and/or cellular differentiation. C1 NINCDS,NEUROPHYSIOL LAB,BETHESDA,MD 20892. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RI Poulter, Michael/K-3909-2013 OI Poulter, Michael/0000-0001-7469-8462 NR 42 TC 90 Z9 91 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD APR PY 1993 VL 53 IS 4 BP 1019 EP 1033 DI 10.1016/0306-4522(93)90486-Y PG 15 WC Neurosciences SC Neurosciences & Neurology GA KY904 UT WOS:A1993KY90400013 PM 8389426 ER PT J AU JUWEID, M SATO, J PAIK, C ONAYBASARAN, S WEINSTEIN, JN NEUMANN, RD AF JUWEID, M SATO, J PAIK, C ONAYBASARAN, S WEINSTEIN, JN NEUMANN, RD TI A SIMPLE METHOD FOR AFFINITY PURIFICATION OF RADIOLABELED MONOCLONAL-ANTIBODIES SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article ID IMMUNOREACTIVITY; MODEL; TUMOR AB A simple method is described for affinity purification of radiolabeled antibodies using glutaraldehyde-fixed tumor target cells. The cell-bound antibody fraction is removed from the cells by an acid wash and then immediately subjected to buffer-exchange chromatography. The method was applied to the D3 murine monoclonal antibody which binds to a 290 kDa antigen on the surface of Line 10 guinea pig carcinoma cells. No alteration in the molecular size profile was detected after acid washing. Purification resulted in a significant increase in immunoreactivity by an average of 14 +/- 47% (SD; range 4-30%). C1 NCI, CTR CLIN,DEPT NUCL MED,10-1 C-496, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NCI, MATH BIOL LAB, BETHESDA, MD 20892 USA. NR 17 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0969-8051 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD APR PY 1993 VL 20 IS 3 BP 311 EP 315 DI 10.1016/0969-8051(93)90053-W PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KQ858 UT WOS:A1993KQ85800010 PM 8485490 ER PT J AU SALBE, AD HILL, CH VEILLON, C HOWE, M LONGNECKER, MP TAYLOR, PR LEVANDER, OA AF SALBE, AD HILL, CH VEILLON, C HOWE, M LONGNECKER, MP TAYLOR, PR LEVANDER, OA TI RELATIONSHIP BETWEEN SERUM SOMATOMEDIN-C LEVELS AND TISSUE SELENIUM CONTENT AMONG ADULTS LIVING IN A SELENIFEROUS AREA SO NUTRITION RESEARCH LA English DT Article DE SOMATOMEDIN-C; SELENIUM STATUS; SELENIUM TOXICITY; TISSUE SELENIUM LEVELS; HUMANS ID DIETARY SELENIUM; BLOOD; TOENAILS AB Depressed serum somatomedin C levels have been suggested by others as an early indicator of selenium (Se) toxicity. In both human and animal studies, somatomedin C levels were lower in Se supplemented as compared to control subjects. The present study examined Se and somatomedin C levels in 44 adult long-term residents of seleniferous areas in South Dakota. Serum Se (SSe) and whole blood Se (WBSe) levels were analyzed by GC/MS. Toenail Se (TSe) was measured by neutron activation analysis. Somatomedin C was analyzed by RIA assay. Subjects were divided into 3 groups based on the following criteria: group I, SSe < 200, WBSe <320 ng/ml; group II, SSe 201-240, WBSe 321-400 ng/ml; group III, SSe >240, WBSe >400 ng/ml. Data were pooled across gender (20 males, 24 females). Somatomedin C levels were not different despite greater than 50% differences in SSe, WBSe, and TSe levels among the groups. In these subjects, somatomedin C was not a sensitive index of elevated Se exposure. C1 USDA ARS, BELTSVILLE AGR RES CTR, HUMAN NUTR RES CTR, BELTSVILLE, MD 20705 USA. N CAROLINA STATE UNIV, DEPT POULTRY SCI, RALEIGH, NC 27650 USA. S DAKOTA SCH MINES & TECHNOL, RAPID CITY, SD 57702 USA. UNIV CALIF LOS ANGELES, SCH PUBL HLTH, DEPT EPIDEMIOL, LOS ANGELES, CA 90024 USA. NCI, DIV CANC PREVENT & CONTROL, BETHESDA, MD 20892 USA. NR 18 TC 5 Z9 5 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0271-5317 J9 NUTR RES JI Nutr. Res. PD APR PY 1993 VL 13 IS 4 BP 399 EP 405 DI 10.1016/S0271-5317(05)80704-3 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA KW064 UT WOS:A1993KW06400004 ER PT J AU CNATTINGIUS, S BERENDES, HW FORMAN, MR AF CNATTINGIUS, S BERENDES, HW FORMAN, MR TI DO DELAYED CHILDBEARERS FACE INCREASED RISKS OF ADVERSE PREGNANCY OUTCOMES AFTER THE 1ST BIRTH SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID GESTATIONAL-AGE; WEIGHT; OLDER AB Objective: To investigate whether the age-related risk of adverse pregnancy outcomes in the first birth persisted in the second birth, before and after adjusting for the influence of an adverse pregnancy outcome in the first birth and for other possible confounders. Methods: Prospectively collected longitudinal data from the Swedish Medical Birth Registry (n = 210,735 women) were analyzed to contrast the effects of maternal age at the first birth on the risk of adverse pregnancy outcomes in the first and second successive births. Results: Rates of adverse pregnancy outcomes were substantially higher in first than in second births. Compared with women aged 20-24, women aged 30-34 years had significantly higher odds ratios (ORs) of late fetal death (OR 1.4) and early neonatal death (OR 1.4) for the first but not for second births; women aged 35+ had a significantly higher OR of late fetal death (OR 2.2) for the first but not for second births. Women over 35 also had a significantly higher OR of early neonatal death for the first birth (OR 2.8) and less of an increase for second births (OR 1.8), a higher OR of low birth weight (LBW) for the first (OR 1.5) and second births (OR 1.6), and a higher OR of preterm birth for the first (OR 1.4) and second births (OR 1.7). Despite the strong tendency to repeat an adverse pregnancy outcome in second births, the age-related ORs did not change with adjustment for the previous pregnancy outcome. Conclusion: Women aged 30+ at their first births have increased risks of adverse pregnancy outcomes in first births. However, second births showed no age-related increase in late fetal death and a smaller increase in early neonatal death. Increased risks for LBW and preterm birth were similar for first and second births of delayed child-bearers. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. UPPSALA UNIV HOSP,DEPT SOCIAL MED,UPPSALA,SWEDEN. NCI,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. NR 20 TC 31 Z9 32 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD APR PY 1993 VL 81 IS 4 BP 512 EP 516 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KT965 UT WOS:A1993KT96500007 PM 8459958 ER PT J AU HICKEY, CA CLIVER, SP GOLDENBERG, RL KOHATSU, J HOFFMAN, HJ AF HICKEY, CA CLIVER, SP GOLDENBERG, RL KOHATSU, J HOFFMAN, HJ TI PRENATAL WEIGHT-GAIN, TERM BIRTH-WEIGHT, AND FETAL GROWTH-RETARDATION AMONG HIGH-RISK MULTIPAROUS BLACK-AND-WHITE WOMEN SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID PREPREGNANCY WEIGHT; UNDERWEIGHT WOMAN; PREGNANCY; PATTERNS; INFANT AB Objective: To examine the association of prenatal weight gain below, within, and above the Institute of Medicine guidelines with birth weight and fetal growth restriction (FGR) among low-income, high-risk black and white women. Methods: Eight hundred three black and 365 white women were grouped by pregravid body mass index (BMI): low (below 19.8), normal (19.8-26), high (above 26-29), and very high (above 29). The impact of maternal weight gain on birth weight and race-specific FGR was determined while controlling for sociodemographic and reproductive variables and for time between last weight observation and delivery. Results: One-third of both black and white women failed to achieve the Institute of Medicine minimum recommended gain for pregravid BMI. More women with low BMI gained less than the recommended weight as compared with those having normal, high, or very high BMI. Nonobese black women (BMI 29 or below) delivered fewer infants with FGR as weight gain increased from below the recommended range (17.9% FGR) to within (10.3% FGR) or above (3.8% FGR) the range; corresponding data for nonobese white women were 20.9, 19.1, and 10.5% FGR, respectively. Obese black women (BMI above 29) also delivered fewer infants with FGR (4.2%) when they exceeded the minimum gain (6 kg) than did white women (11.8%). When analysis of covariance was used to adjust mean birth weight, black women in each pregravid BMI category delivered increasingly larger infants (P less-than-or-equal-to .01 for each category) as they met or exceeded the guidelines; among white women this trend was attenuated. Conclusion: These observations support the Institute of Medicine suggestion that black women strive for prenatal weight gain at the upper end of the recommended range for pregravid BMI. C1 NIDOCD,EPIDEMIOL STAT & DATA SYST BRANCH,BETHESDA,MD. UNIV ALABAMA,SCH PUBL HLTH,DEPT PUBL HLTH SCI,BIRMINGHAM,AL 35294. UNIV BIRMINGHAM,SCH MED,DEPT OBSTET & GYNECOL,PERINATAL EPIDEMIOL UNIT,BIRMINGHAM B15 2TT,W MIDLANDS,ENGLAND. RP HICKEY, CA (reprint author), UNIV ALABAMA,SCH PUBL HLTH,DIV MATERNAL & CHILD HLTH,315 TIDWELL HALL,BIRMINGHAM,AL 35294, USA. FU BHP HRSA HHS [DHHS 282-92-0055]; NICHD NIH HHS [1-HD-4-2811]; PHS HHS [MCJ-9040] NR 22 TC 36 Z9 36 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 APR PY 1993 VL 81 IS 4 BP 529 EP 535 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KT965 UT WOS:A1993KT96500010 PM 8459961 ER PT J AU LEONE, A SEEGER, RC HONG, CM HU, YY ARBOLEDA, MJ BRODEUR, GM STRAM, D SLAMON, DJ STEEG, PS AF LEONE, A SEEGER, RC HONG, CM HU, YY ARBOLEDA, MJ BRODEUR, GM STRAM, D SLAMON, DJ STEEG, PS TI EVIDENCE FOR NM23 RNA OVEREXPRESSION, DNA AMPLIFICATION AND MUTATION IN AGGRESSIVE CHILDHOOD NEUROBLASTOMAS SO ONCOGENE LA English DT Article ID NUCLEOSIDE DIPHOSPHATE KINASE; DUCTAL BREAST CARCINOMAS; TUMOR-METASTASIS; N-MYC; DROSOPHILA DEVELOPMENT; PROTEIN-KINASE; GENE; EXPRESSION; ASSOCIATION; CANCER AB Reduced expression of nm23 RNAs/proteins has been associated previously with high tumor metastatic potential. In contrast, we report that regional (state III) and metastatic (stage IV) childhood neuroblastomas exhibit elevated nm23 RNA levels as compared with localized tumors. Elevated neuroblastoma nm23 RNA levels were associated with significant reductions in patient survival in the overall (n = 75) and N-myc non-amplified (n = 61) portion of the cohort. Amplification of the chromosomal nm23-H1 gene was observed in 6/18 stage III and IV tumors; amplification of nm23-H2 was not demonstrated. Genomic amplification of nm23-H1 was associated with increased tumor nm23 RNA expression and reduced patient survival. Single-strand conformational polymorphism (SSCP) analysis was performed on seven neuroblastomas. Minor subpopulations of cDNAs exhibiting altered mobility were apparent in both nm23-H1 and nm23-H2 translated regions of stage III and IV tumors, suggestive.of mutations. Confirmation of the SSCP data was provided by direct sequencing of nm23-H2 in a stage IV tumor, revealing a leucine to valine mutation at position 48. The data indicate that molecular alterations to nm23 other than its reduced expression can be associated with tumor aggressiveness, and provide the first evidence for nm23 mutation in a human cancer. C1 NCI, PATHOL LAB, BLDG 10, ROOM 2A33, BETHESDA, MD 20892 USA. CHILDRENS HOSP LOS ANGELES, DEPT PEDIAT, DIV HEMATOL ONCOL, LOS ANGELES, CA 90027 USA. UNIV SO CALIF, SCH MED, LOS ANGELES, CA 90027 USA. CHILDRENS CANC GRP, ARCADIA, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DIV HEMATOL ONCOL, LOS ANGELES, CA 90027 USA. WASHINGTON UNIV, SCH MED, DEPT PEDIAT, DIV HEMATOL ONCOL, ST LOUIS, MO 63110 USA. RI Leone, Alvaro/K-6410-2016 OI Leone, Alvaro/0000-0003-3815-9052 FU NCI NIH HHS [CA 02649, CA22794, CA49712] NR 43 TC 207 Z9 208 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1993 VL 8 IS 4 BP 855 EP 865 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KT220 UT WOS:A1993KT22000006 PM 8384356 ER PT J AU BROWN, PH ALANI, R PREIS, LH SZABO, E BIRRER, MJ AF BROWN, PH ALANI, R PREIS, LH SZABO, E BIRRER, MJ TI SUPPRESSION OF ONCOGENE-INDUCED TRANSFORMATION BY A DELETION MUTANT OF C-JUN SO ONCOGENE LA English DT Article ID TRANSCRIPTION FACTOR AP-1; DNA-BINDING ACTIVITY; RAT EMBRYO CELLS; LEUCINE ZIPPER; HETERODIMER FORMATION; ENHANCER ELEMENTS; PROTO-ONCOGENE; V-JUN; FOS; ACTIVATION AB Jun and Fos proteins are DNA-binding proteins that are involved in the control of gene expression through transcriptional regulation. We have made a deletion mutant of the c-jun gene that lacks amino acids 3-122 of c-jun, and thus is missing the major transactivation domain of c-jun, but retains the DNA-binding and leucine zipper domains. Unlike c-Jun, the mutant protein is unable to stimulate the transcription of an AP-1 responsive gene, and unlike c-jun this mutant gene is unable to transform rat embryo celts in cooperation with an activated ras gene. However, this mutant protein blocks in vitro DNA binding of Jun-Jun homodimers and Jun-Fos heterodimers, transcriptional activation induced by c-jun or c-fos and transformation of rat embryo cells induced by an activated ras gene and a deregulated c-jun or c-fos gene. In addition, transformation of rat embryo cells induced by an activated ras gene in the presence of the tumor promoter 12-0-tetradecanoyl phorbol 13-acetate (TPA) or by ras plus SV40 large T antigen is also inhibited by this dominant-negative mutant, suggesting that a member of the jun or fos family is involved in the pathways leading to transformation in these systems as well. The possible molecular mechanisms by which this dominant-negative mutant of c-jun blocks the functions of wild-type jun and fos family members are discussed. C1 NCI,DIV CANC PREVENT & CONTROL,BIOMARKERS & PREVENT RES BRANCH,5516 NICHOLSON LANE,ROOM 100,KENSINGTON,MD 20895. UNIV HLTH SCI,UNIFORMED SERV,BETHESDA,MD 20814. HOWARD HUGHES MED INST,BETHESDA,MD 20814. NR 54 TC 238 Z9 239 U1 1 U2 7 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1993 VL 8 IS 4 BP 877 EP 886 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KT220 UT WOS:A1993KT22000008 PM 8455942 ER PT J AU MAGLIONE, D GUERRIERO, V VIGLIETTO, G FERRARO, MG APRELIKOVA, O ALITALO, K DELVECCHIO, S LEI, KJ CHOU, JY PERSICO, MG AF MAGLIONE, D GUERRIERO, V VIGLIETTO, G FERRARO, MG APRELIKOVA, O ALITALO, K DELVECCHIO, S LEI, KJ CHOU, JY PERSICO, MG TI 2 ALTERNATIVE MESSENGER-RNAS CODING FOR THE ANGIOGENIC FACTOR, PLACENTA GROWTH-FACTOR (PIGF), ARE TRANSCRIBED FROM A SINGLE GENE OF CHROMOSOME-14 SO ONCOGENE LA English DT Article ID ENDOTHELIAL-CELL MITOGEN; VASCULAR-PERMEABILITY FACTOR; FACTOR-A-CHAIN; ACID; CDNA; HYBRIDIZATION; SEQUENCES; INDUCTION AB We have previously reported on the identification of a cDNA (placenta growth factor, PIGF) coding for a novel angiogenic factor expressed in placental tissue that is similar to vascular permeability factor/vascular endothelial growth factor (VPF/VEGF). Biochemical and functional characterization of PIGF derived from transfected COS-1 celts revealed that it is a glycosylated dimeric secreted protein able to stimulate endothelial cell growth in vitro. Here, we report the isolation and characterization of the PIGF gene located on chromosome 14. At least two different mRNAs are produced from this single-copy gene in different cell lines and tissues. Sequence comparison of the polypeptides encoded by the two different isolated cDNAs indicates that they are identical except for the insertion of a highly basic 21 amino acid stretch at the carboxyl end of the protein. RNA expression analysis of several tissues, tumors and cell tines indicates differential distribution of the two PlGF mRNAs. Finally, preliminary results indicate that the PlGF gene has been conserved in evolution, since the human PlGF cDNA hybridizes to sequences present in the genomic DNA of Drosophila, Xenopus, chicken and mouse. C1 CNR,INT INST GENET & BIOPHYS,VIA G MARCONI 12,I-80125 NAPLES,ITALY. SIFI SPA,I-95020 LAVINAIO,ITALY. UNIV HELSINKI,DEPT PATHOL,SF-00290 HELSINKI 29,FINLAND. FDN G PASCALE,IST NAZL STUDIO CURA TUMORI,I-80131 NAPLES,ITALY. NICHHD,HUMAN GENET LAB,BETHESDA,MD 20892. RI Del Vecchio, Silvana/F-4972-2012; Alitalo, Kari/J-5013-2014; OI Alitalo, Kari/0000-0002-7331-0902; DEL VECCHIO, Silvana/0000-0002-5466-1213 NR 35 TC 245 Z9 256 U1 0 U2 17 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1993 VL 8 IS 4 BP 925 EP 931 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KT220 UT WOS:A1993KT22000014 PM 7681160 ER PT J AU OTTERSON, GA KRATZKE, RA LIN, AY JOHNSTON, PG KAYE, FJ AF OTTERSON, GA KRATZKE, RA LIN, AY JOHNSTON, PG KAYE, FJ TI ALTERNATIVE SPLICING OF THE RBP1 GENE CLUSTERS IN AN INTERNAL EXON THAT ENCODES POTENTIAL PHOSPHORYLATION SITES SO ONCOGENE LA English DT Article ID RETINOBLASTOMA SUSCEPTIBILITY GENE; CELL-CYCLE; TRANSCRIPTION FACTOR; PRODUCT; PROTEINS; BINDING; EXPRESSION; CARCINOMA; COMPLEX; IDENTIFICATION AB We have isolated cDNA and genomic clones for the human retinoblastoma binding protein 1 (RBP1) gene, and have identified alternative splicing of RBP1 clustered within a 207-nucleotide internal exon. Three of the predicted RPB1 peptides share amino-terminal and carboxy-terminal domains, while a fourth species encodes a distinct carboxy-terminal domain. Functional analysis of these peptides demonstrated that they are capable of precipitating retinoblastoma (RB) protein in vitro from K562 cell lysates, but cannot bind to mutant RB protein. However, each of the RBP1 peptides differed within an internal exon that contains potential casein kinase II and p34cdc2 phosphorylation sites. Immunoblot analysis using polyclonal alpha-RBP1 antiserum revealed that the RBP1 protein is expressed in a wide range of cell lines of differing histologic type and migrates on sodium dodecyl sulfate-polyacrylamide gel electrophoresis predominantly as a 200-kDa protein. Immunohistochemical analysis using the alpha-RBP1 antiserum demonstrated a distinct nuclear staining pattern that was eliminated when the antiserum was preabsorbed with RBP1 peptide. The RBP1 gene encodes a widely expressed 200-kDa nuclear protein and undergoes alternative splicing that predicts a family of RB-binding peptides. C1 USN HOSP,NCI,NAVY ONCOL BRANCH,BLDG 8,RM 5101,BETHESDA,MD 20889. UNIV HLTH SCI,UNIFORMED SERV,BETHESDA,MD 20889. RI kaye, frederic/E-2437-2011 NR 38 TC 20 Z9 21 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1993 VL 8 IS 4 BP 949 EP 957 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KT220 UT WOS:A1993KT22000017 PM 8455946 ER PT J AU MEINERT, C STERNBERG, A AMENDLIBERCCI, D DODGE, J GERCZAK, C HAYNES, V ISAACSON, M LEVINE, C MAGUIRE, M MEINERT, J TONASCIA, J TONASCIA, S WETZEL, D HAWKINS, B BONDS, B CANNER, J CONNOR, K DICKERSIN, K GUNTHER, G THOMAS, B TU, N XU, C SPAETH, G KATZ, LJ BECKERSHOFF, C DEPIANO, D SLAGLE, S BARONE, L GROSS, P JACKSON, M MORGANSTERN, S SAMMARTINO, M STRONG, C WILENSKY, J FROHLICHSTEIN, D BECKMAN, H CRABTREE, J CZEDIK, C SUNDERMEYER, S KURINIJ, N DUDLEY, P SURAN, A KRUG, J CHIAVELLI, M BERRY, I EVANS, C JOYNER, M KITTAY, R MELANSON, A STOUT, K WAY, R EPSTEIN, D BERSON, F LATINA, M MELAMED, S JOHNSON, E LINDERMEYER, A MCGEE, R PIVABOWE, D SMITH, TJ WILENSKY, J TESSLER, H FROHLICHSTEIN, D ANDERSON, J JEDNOCK, N PETERSON, R NAIL, C MILLMAN, K SIEGEL, H SPIGELMAN, V SPRINCZ, M BECKMAN, H CYRLIN, M CZEDIK, C RITCH, R PODOLSKY, M STEINBERGER, D STOCK, L ABDULAZIM, J JOHNSON, M KRANTZ, J SWEENEY, V CUNNINGHAM, J MARANAN, L TERRERO, A THEERTHAM, M SPAETH, G KATZ, LJ BECKERSHOFF, C DEPIANO, D MOLINEAUX, J NICHOLS, J PETRAKIS, P SLAGLE, J CAPRIOLI, J SIMMONS, S STRANG, S CAPONE, M SAMMARTINO, M SANDY, R WILSON, R WITTKOWSKI, D VELATHOMAS, MA HARBIN, T LEEF, D GOMEZ, S GEMMILL, M GILMAN, J MOORE, K SWORDS, R WRIGHT, J CAMPBELL, D CARLTON, S FRANK, MK LASALLE, J MAIO, M NICHOLAS, P SNIPES, C WEBER, P KAPETANSKY, F MCKINNEY, K CLARK, M MOORE, D SIMMONS, L JONES, S RADIUS, R KLEWIN, K SOPA, J GUNDERSEN, B RICHIE, M WIPPLINGER, W BAUER, D LANGE, C BENCE, D HELT, P KAVANAGH, J WOLF, C AF MEINERT, C STERNBERG, A AMENDLIBERCCI, D DODGE, J GERCZAK, C HAYNES, V ISAACSON, M LEVINE, C MAGUIRE, M MEINERT, J TONASCIA, J TONASCIA, S WETZEL, D HAWKINS, B BONDS, B CANNER, J CONNOR, K DICKERSIN, K GUNTHER, G THOMAS, B TU, N XU, C SPAETH, G KATZ, LJ BECKERSHOFF, C DEPIANO, D SLAGLE, S BARONE, L GROSS, P JACKSON, M MORGANSTERN, S SAMMARTINO, M STRONG, C WILENSKY, J FROHLICHSTEIN, D BECKMAN, H CRABTREE, J CZEDIK, C SUNDERMEYER, S KURINIJ, N DUDLEY, P SURAN, A KRUG, J CHIAVELLI, M BERRY, I EVANS, C JOYNER, M KITTAY, R MELANSON, A STOUT, K WAY, R EPSTEIN, D BERSON, F LATINA, M MELAMED, S JOHNSON, E LINDERMEYER, A MCGEE, R PIVABOWE, D SMITH, TJ WILENSKY, J TESSLER, H FROHLICHSTEIN, D ANDERSON, J JEDNOCK, N PETERSON, R NAIL, C MILLMAN, K SIEGEL, H SPIGELMAN, V SPRINCZ, M BECKMAN, H CYRLIN, M CZEDIK, C RITCH, R PODOLSKY, M STEINBERGER, D STOCK, L ABDULAZIM, J JOHNSON, M KRANTZ, J SWEENEY, V CUNNINGHAM, J MARANAN, L TERRERO, A THEERTHAM, M SPAETH, G KATZ, LJ BECKERSHOFF, C DEPIANO, D MOLINEAUX, J NICHOLS, J PETRAKIS, P SLAGLE, J CAPRIOLI, J SIMMONS, S STRANG, S CAPONE, M SAMMARTINO, M SANDY, R WILSON, R WITTKOWSKI, D VELATHOMAS, MA HARBIN, T LEEF, D GOMEZ, S GEMMILL, M GILMAN, J MOORE, K SWORDS, R WRIGHT, J CAMPBELL, D CARLTON, S FRANK, MK LASALLE, J MAIO, M NICHOLAS, P SNIPES, C WEBER, P KAPETANSKY, F MCKINNEY, K CLARK, M MOORE, D SIMMONS, L JONES, S RADIUS, R KLEWIN, K SOPA, J GUNDERSEN, B RICHIE, M WIPPLINGER, W BAUER, D LANGE, C BENCE, D HELT, P KAVANAGH, J WOLF, C TI THE GLAUCOMA LASER TRIAL (GLT) .5. SUBGROUP DIFFERENCES AT ENROLLMENT SO OPHTHALMIC SURGERY AND LASERS LA English DT Article ID OPEN-ANGLE GLAUCOMA; LONGITUDINAL DATA-ANALYSIS; VISUAL-FIELD DEFECTS; RISK-FACTORS; OCULAR HYPERTENSION; CLINICAL RESEARCH; PREVALENCE; CHARTS; RACE AB Data collected at enrollment on the 271 patients (542 eyes) who participated in the Glaucoma Laser Trial (GLT) were analyzed for subgroup differences. The subgrouping variables included four patient characteristics (race, sex, age, and history of a vascular disease) and one ocular characteristic (myopia). The strongest differences observed were between blacks and whites. As compared with the eyes of the white patients, those of the black patients had lower mean decibels per test location in the visual field (P < .001), greater mean defect (P < .001), number of abnormal test locations (P < .001), and corrected loss variance (P = .009), as well as greater cup depth (P < .001), and larger mean horizontal (P = .002) and vertical (P < .001) cup/disc ratios. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. UNIV ILLINOIS,EYE & EAR INFIRM,CTR VISUAL FIELD READING,CHICAGO,IL 60612. NEW YORK EYE & EAR INFIRM,NEW YORK,NY 10003. WILLS EYE HOSP & RES INST,CTR DISC STEREOPHOTOG READING,PHILADELPHIA,PA 19107. MED COLL WISCONSIN,MILWAUKEE,WI 53226. OHIO STATE UNIV,COLUMBUS,OH 43210. NEI,PROJECT OFF,BETHESDA,MD 20892. RP MEINERT, C (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,615 N WOLFE ST,BALTIMORE,MD 21205, USA. RI Dickersin, Kay/A-4576-2008 NR 33 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0022-023X J9 OPHTHALMIC SURG LAS JI Ophthalmic Surg. Lasers PD APR PY 1993 VL 24 IS 4 BP 232 EP 241 PG 10 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA KX368 UT WOS:A1993KX36800002 ER PT J AU SHIP, JA ATKINSON, JC AF SHIP, JA ATKINSON, JC TI WISKOTT-ALDRICH SYNDROME, RENAL-FAILURE, AND OSTEOSCLEROSIS SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS LA English DT Article RP SHIP, JA (reprint author), NIDR,9000 ROCKVILLE PIKE,BLDG 10,ROOM 1N-113,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1079-2104 J9 ORAL SURG ORAL MED O JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. PD APR PY 1993 VL 75 IS 4 BP 534 EP 534 DI 10.1016/0030-4220(93)90186-8 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KW553 UT WOS:A1993KW55300024 PM 8464623 ER PT J AU SNOW, JB AF SNOW, JB TI FROM THE NATIONAL-INSTITUTE-ON-DEAFNESS AND OTHER COMMUNICATION DISORDERS SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article RP SNOW, JB (reprint author), NIDCD,BLDG 31,ROOM 3C-02,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD APR PY 1993 VL 108 IS 4 BP 380 EP 383 PG 4 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA KY324 UT WOS:A1993KY32400013 PM 8483612 ER PT J AU RUDA, MA AF RUDA, MA TI GENDER AND PAIN SO PAIN LA English DT Editorial Material RP RUDA, MA (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892, USA. NR 4 TC 27 Z9 27 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD APR PY 1993 VL 53 IS 1 BP 1 EP 2 DI 10.1016/0304-3959(93)90048-T PG 2 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA LB102 UT WOS:A1993LB10200001 PM 8316380 ER PT J AU JAMES, SL AF JAMES, SL TI IMMUNITY TO HELMINTHS SO PARASITOLOGY TODAY LA English DT Letter ID SCHISTOSOMA-MANSONI; NITROGEN-OXIDES RP JAMES, SL (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0169-4758 J9 PARASITOL TODAY JI Parasitol. Today PD APR PY 1993 VL 9 IS 4 BP 128 EP 128 DI 10.1016/0169-4758(93)90172-C PG 1 WC Parasitology SC Parasitology GA KT341 UT WOS:A1993KT34100007 PM 15463733 ER PT J AU LEDLEY, FD ADAMS, RM SORIANO, HE DARLINGTON, G FINEGOLD, M LANFORD, R CAREY, D LEWIS, D BALEY, PA ROTHENBERG, S KAY, M BRANDT, M MOEN, R ANDERSON, WF WHITINGTON, P POKORNY, W WOO, SLC AF LEDLEY, FD ADAMS, RM SORIANO, HE DARLINGTON, G FINEGOLD, M LANFORD, R CAREY, D LEWIS, D BALEY, PA ROTHENBERG, S KAY, M BRANDT, M MOEN, R ANDERSON, WF WHITINGTON, P POKORNY, W WOO, SLC TI DEVELOPMENT OF A CLINICAL PROTOCOL FOR HEPATIC GENE-TRANSFER - LESSONS LEARNED IN PRECLINICAL STUDIES SO PEDIATRIC RESEARCH LA English DT Article ID ACUTE LIVER-FAILURE; HEPATOCELLULAR TRANSPLANTATION; MOUSE HEPATOCYTES; PRIMARY CULTURES; CIRRHOTIC DOGS; EXPRESSION; SURVIVAL; THERAPY; CELLS; RATS AB Strategies for hepatic gene therapy have been proposed that involve isolation of primary hepatocytes and introduction of recombinant genes into these cells in culture, followed by autologous hepatocellular transplantation (HCT). Consideration of clinical applications requires data suggesting that HCT can be performed safely in human subjects in addition to data indicating that recombinant gene expression can reverse a disease process. This report describes preclinical studies that underlie a clinical trial of HCT in which hepatocytes would be labeled with a marker gene to facilitate assessment of engraftment in the recipient. Human hepatocytes were harvested from liver segments preserved in Belzar's solution and transduced with an amphotropic retroviral vector carrying a recombinant marker gene (neomycin phosphotransferase II). Human hepatocytes were recovered from monolayer culture, stained with the fluorescent dye 1,1'-dioctadecyl-3,3,3,3'-tetra-methylindo-carbocyanine perchlorate (Dil) and transplanted into severe combined immunodeficient mice by splenic injection. Engrafted hepatocytes were identified in the liver and spleen of severe combined immunodeficient mice but not immunocompetent controls. Two large animal models of HCT are described. In a dog model, neomycin phosphotransferase II-containing hepatocytes were identified in the liver 7 wk after transplantation. In a baboon model, autologous HCT with DiI-stained cells demonstrated that transplanted cells assume a normal morphology and constitute up to 5% of hepatocytes. These data demonstrate transduction and transplantation of human hepatocytes and the feasibility of HCT in large animals. On the basis of these studies, the proposed clinical trial for gene transfer and transplantation in human subjects has been approved by the National Institutes of Health and the Food and Drug Administration. These studies illustrate the nature and extent of preclinical data required to gain approval for clinical trials involving gene transfer into human subjects. These data also illustrate the limitations of existing methods that may be used for hepatic gene therapy in the future. C1 BAYLOR COLL MED,DEPT PEDIAT,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MOLEC GENET,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT IMMUNOL,HOUSTON,TX 77030. UNIV CHICAGO,DEPT PEDIAT,CHICAGO,IL 60639. GENET THERAPY INC,GAITHERSBURG,MD 20878. SW FDN BIOMED RES,SAN ANTONIO,TX 78284. NIH,BETHESDA,MD 20892. RP LEDLEY, FD (reprint author), BAYLOR COLL MED,DEPT CELL BIOL,HOUSTON,TX 77030, USA. FU NICHD NIH HHS [P30-HD-24064, 1P30-HD-27823]; NIDDK NIH HHS [P01-DK-44080] NR 56 TC 15 Z9 15 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1993 VL 33 IS 4 BP 313 EP 320 PN 1 PG 8 WC Pediatrics SC Pediatrics GA KV791 UT WOS:A1993KV79100001 PM 8386832 ER PT J AU BRENNER, RE NERLICH, A HEINZE, E VETTER, U TELLER, WM AF BRENNER, RE NERLICH, A HEINZE, E VETTER, U TELLER, WM TI DIFFERENT REGULATION OF CLONAL GROWTH BY TRANSFORMING GROWTH-FACTOR-BETA-1 IN HUMAN FETAL ARTICULAR AND COSTAL CHONDROCYTES SO PEDIATRIC RESEARCH LA English DT Article ID FACTOR-BINDING PROTEIN-1; FACTOR-BETA; FACTOR-I; HUMAN-FETUS; TGF-BETA; INSULIN; HORMONE; SERUM AB The variable affection of rib and limb growth in human skeletal dysplasias suggests the presence of site-specific regulatory mechanisms for chondrocyte proliferation. We therefore studied the clonal growth of normal human costal and articular chondrocytes from the same four fetuses (15 to 30 wk of gestation) in a semisolid medium (0.8% methylcellulose) with a basal supplementation of 5% heat-inactivated FCS. IGF-I [0.3-12.5 ng/mL (0.04-1.6 nmol/L)], IGF-II [0.3-12.5 ng/mL (0.04-1.7 nmol/L)], and hGH [0.5-25 ng/mL (0.02-1.1 nmol/L)] stimulated clonal growth of articular and costal chondrocytes without site-specific difference. In contrast, a significant difference was found for transforming growth factor-beta1, which proved to be a potent growth factor for fetal articular chondrocytes but did not stimulate or only minimally stimulated fetal costal chondrocytes [p < 0.05 for 0.3 ng/mL (0.01 nmol/L) TGF-beta1 and p < 0.01 for 1.25 ng/mL (0.05 nmol/L) TGF-beta1 using paired t test]. Preincubation with an IGF-I receptor antibody (alphaIR-3) completely prevented the proliferative effect of IGF-I, IGF-II, and hGH, indicating that hGH acts via autocrine or paracrine induction of IGF. The antibody partly reduced TGF-beta1 action on articular chondrocytes [p < 0.05 for 0.3 ng/mL (0.01 nmol/L) TGF-beta1, NS for 1.25 ng/mL (0.05 nmol/L) TGF-beta1 using paired t test]. These results indicate that TGF-beta1 is involved in the regulation of human fetal growth and has a different effect in ribs and limbs. C1 UNIV MUNICH,INST PATHOL,W-8900 MUNICH,GERMANY. NIDR,BETHESDA,MD 20892. RP BRENNER, RE (reprint author), UNIV ULM,KINDERKLIN,ABT 1,PRITTWITZSTR 43,W-7900 ULM,GERMANY. NR 32 TC 14 Z9 14 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1993 VL 33 IS 4 BP 390 EP 393 PN 1 PG 4 WC Pediatrics SC Pediatrics GA KV791 UT WOS:A1993KV79100015 PM 8479821 ER PT J AU SWEDO, SE LEONARD, HL SCHAPIRO, MB CASEY, BJ MANNHEIM, GB LENANE, MC RETTEW, DC AF SWEDO, SE LEONARD, HL SCHAPIRO, MB CASEY, BJ MANNHEIM, GB LENANE, MC RETTEW, DC TI SYDENHAM CHOREA - PHYSICAL AND PSYCHOLOGICAL SYMPTOMS OF ST-VITUS-DANCE SO PEDIATRICS LA English DT Article DE SYDENHAM CHOREA; MOVEMENT DISORDERS; OBSESSIVE-COMPULSIVE DISORDER; ATTENTION DEFICIT HYPERACTIVITY DISORDER; NEUROPSYCHOLOGY ID ACUTE RHEUMATIC-FEVER; RELIABILITY; ADOLESCENTS; CHILDREN AB Eleven children with Sydenham's chorea (8 girls and 3 boys, mean age = 8.4 +/- 2.2 [SD] years) underwent comprehensive physical, neuropsychologic, and psychiatric examination. The chorea was manifested as dysarthria, gait disturbances, and frequent adventitious movements of the face, neck, trunk, and extremities. Antineuronal antibodies were present in 10 of 11 children. All children exhibited concomitant psychologic dysfunction, specifically obsessive-compulsive symptomatology, increased emotional lability, motoric hyperactivity, irritability, distractibility, and age-regressed behavior. Obsessive-compulsive symptoms were observed in 9 (82%) children, 4 of whom met diagnostic criteria for obsessive-compulsive disorder. These behavioral symptoms began several days to weeks before the chorea was observed, and they waxed and waned in severity along with the motoric abnormalities. These results suggest that psychologic, particularly obsessive-compulsive, symptoms are accompanying manifestations of Sydenham's chorea which may require medical attention. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. RP SWEDO, SE (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 47 TC 198 Z9 202 U1 1 U2 8 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 APR PY 1993 VL 91 IS 4 BP 706 EP 713 PG 8 WC Pediatrics SC Pediatrics GA KW567 UT WOS:A1993KW56700003 PM 8464654 ER PT J AU BUTLER, KM VENZON, D HENRY, N HUSSON, RN MUELLER, BU BALIS, FM JACOBSEN, F LEWIS, LL PIZZO, PA AF BUTLER, KM VENZON, D HENRY, N HUSSON, RN MUELLER, BU BALIS, FM JACOBSEN, F LEWIS, LL PIZZO, PA TI PANCREATITIS IN HUMAN IMMUNODEFICIENCY VIRUS-INFECTED CHILDREN RECEIVING DIDEOXYINOSINE SO PEDIATRICS LA English DT Article DE PANCREATITIS; DIDEOXYINOSINE; HUMAN IMMUNODEFICIENCY VIRUS; ANTIRETROVIRAL THERAPY ID AIDS-RELATED COMPLEX; PHASE-I TRIAL; 2',3'-DIDEOXYINOSINE DDI AB To define predictive or contributory risk factors for pancreatitis in human immunodeficiency virus-infected children receiving dideoxyinosine (ddI), the authors evaluated 95 children, 3 months to 18 years of age, who had received ddl at 60 to 540 Mg/M2 per day for a mean of 56 weeks. Pancreatitis developed in 7 patients (7%) but resolved in all upon withdrawal of ddl. Neither age, sex, nor CD4 count at study entry was predictive of pancreatitis, but pancreatitis appeared more likely to develop in hemophiliacs than in other patients (4 of 23 vs 3 of 72). Pancreatitis developed only in patients who received ddl at the highest dose levels (7 of 60 patients who received ddl at a dose greater-than-or-equal-to 360 mg/m2 per day vs 0 of 35 patients who received less-than-or-equal-to 270 mg/m2 per day). Patients in whom pancreatitis developed had received a higher mean daily dose of ddl than patients with normal amylase and lipase levels throughout the study (348 mg/m2 vs 282 mg/m2), but no relationship with the cumulative dose or the duration of ddI therapy was observed. Although a statistically significant relationship between ddI plasma concentration (area under the curve) and pancreatitis was not conclusively demonstrated, as the number of patients in whom pancreatitis actually developed was small, such a relationship may have been obscured. The mean interval from initiation of ddl to onset of symptoms of pancreatitis (25 weeks) was significantly shorter than the average duration of ddI therapy (56 weeks), and, consequently, patients in whom pancreatitis developed had been exposed to a lower cumulative dose of ddl than those with normal amylase and lipase levels (64.5 g/m2 vs 119.06 g/m2). Although baseline amylase values did not correlate with the later development of pancreatitis, elevation of baseline aspartate aminotransferase and alanine aminotransferase levels was significantly associated with the later development of pancreatitis. C1 NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N240,BETHESDA,MD 20892. NCI,CLIN ONCOL PROGRAM,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 6 TC 37 Z9 37 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 APR PY 1993 VL 91 IS 4 BP 747 EP 751 PG 5 WC Pediatrics SC Pediatrics GA KW567 UT WOS:A1993KW56700011 PM 7681940 ER PT J AU MAYES, LC GRANGER, RH FRANK, MA SCHOTTENFELD, R BORNSTEIN, MH AF MAYES, LC GRANGER, RH FRANK, MA SCHOTTENFELD, R BORNSTEIN, MH TI NEUROBEHAVIORAL PROFILES OF NEONATES EXPOSED TO COCAINE PRENATALLY SO PEDIATRICS LA English DT Article DE COCAINE; NEONATE; NEUROBEHAVIORAL PROFILE ID BEHAVIORAL ORGANIZATION; MENTAL-DEVELOPMENT; INFANT BEHAVIOR; PREGNANCY; CONSEQUENCES; PATTERNS; SCALE; TERM AB This study examined the effects of maternal cocaine use on performance on the Neonatal Behavioral Assessment Scale (NBAS). Cocaine-exposed newborns (n = 56) were compared with a non-cocaine-exposed group (n = 30) born to mothers with similar sociodemographic characteristics. Cocaine-exposed newborns showed significant reduction in birth weight but did not experience greater obstetric or postnatal complications. On neurobehavioral assessments using the NBAS, cocaine-exposed newborns showed significantly depressed performance on the habituation cluster but not on other NBAS clusters when differences in birth weight were controlled. In a sample of 30 cocaine-exposed newborns matched on birth weight, gestational age, and race to the 30 non-cocaine-exposed newborns, cocaine-exposed newborns continued to show depressed habituation performance. The significance of a selective effect of cocaine exposure on early habituation performance is discussed in terms of the implications for attentional regulation in the first year of life. C1 YALE UNIV,SCH MED,NEW HAVEN,CT 06510. RP MAYES, LC (reprint author), NICHHD,YALE CHILD STUDY CTR,230 S FRONTAGE RD,NEW HAVEN,CT 06510, USA. NR 49 TC 103 Z9 103 U1 1 U2 2 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 APR PY 1993 VL 91 IS 4 BP 778 EP 783 PG 6 WC Pediatrics SC Pediatrics GA KW567 UT WOS:A1993KW56700017 PM 8464666 ER PT J AU RANA, SR SEKHSARIA, S CASTRO, OL AF RANA, SR SEKHSARIA, S CASTRO, OL TI HEMOGLOBIN S-TRAIT AND C-TRAIT - CONTRIBUTING CAUSES FOR DECREASED MEAN HEMATOCRIT IN AFRICAN-AMERICAN CHILDREN SO PEDIATRICS LA English DT Article DE HEMOGLOBIN-S TRAIT; HEMOGLOBIN-C TRAIT; HEMATOCRIT; AFRICAN-AMERICANS; BLACK RACE ID UNITED-STATES; ANEMIA; WHITE; BLACK; CRITERIA AB Several nutritional surveys have shown that African-American children have lower mean hematocrit and hemoglobin values than white children. While the high prevalence of both alpha and beta thalassemias in African-American children can partly account for the lower hematologic values, the remaining differences cannot be explained. African-American individuals have a high prevalence of traits for hemoglobin S (HbAS) and hemoglobin C (HbAC). The mean hematocrit of children with normal hemoglobin AA (HbAA) (n = 15637) was compared with that of children with traits for HbAS (n = 1197) and HbAC (n = 440). For both sexes, the mean hematocrit of subjects with HbAC and HbAS was 1.5 and 1 point lower, respectively, than that of subjects with HbAA. These differences were highly significant statistically. When the data were examined with regard to age and sex, statistically significant differences were present for all groups analyzed except the 11- through 14-year-old male group for HbAC and the 15- through 19-year-old male group for HbAS. Thus, the presence of Hb S and C traits is associated with a lower hematocrit. This reduced hematocrit may significantly contribute to the racial differences in mean hematocrit due to the high prevalence of these traits in African-American children. C1 HOWARD UNIV,COLL MED,DEPT PEDIAT & CHILD HLTH,WASHINGTON,DC 20001. HOWARD UNIV,COLL MED,CTR SICKLE CELL DIS,WASHINGTON,DC 20001. NIAID,BETHESDA,MD 20892. NR 21 TC 11 Z9 11 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 APR PY 1993 VL 91 IS 4 BP 800 EP 802 PG 3 WC Pediatrics SC Pediatrics GA KW567 UT WOS:A1993KW56700021 PM 8464670 ER PT J AU WESTERGAARD, GC AF WESTERGAARD, GC TI HAND PREFERENCE IN THE USE OF TOOLS BY INFANT BABOONS (PAPIO-CYNOCEPHALUS-ANUBIS) SO PERCEPTUAL AND MOTOR SKILLS LA English DT Article ID HANDEDNESS AB Hand preference in the use of tools was examined in a peer group of five infant baboons, Papio cynocephalus anubis. Hand preference was noted for all subjects on a sponging task and for one subject on a probing task. The baboons exhibited the highest percentage of bimanual actions on the initial segment of each three-component task. These results are consistent with the hypothesis that immature nonhuman primates exhibit lateral asymmetries when they use tools and bimanual coordination when they perform complex manipulative tasks. C1 NICHHD,COMPARAT ETHOL LAB,BETHESDA,MD 20892. FU NCRR NIH HHS [RR00166]; NICHD NIH HHS [HDO2274] NR 7 TC 4 Z9 4 U1 0 U2 0 PU PERCEPTUAL MOTOR SKILLS PI MISSOULA PA PO BOX 9229, MISSOULA, MT 59807 SN 0031-5125 J9 PERCEPT MOTOR SKILL JI Percept. Mot. Skills PD APR PY 1993 VL 76 IS 2 BP 447 EP 450 PG 4 WC Psychology, Experimental SC Psychology GA KY257 UT WOS:A1993KY25700021 PM 8483654 ER PT J AU ELMALLAKH, RS WYATT, RJ LOONEY, SW AF ELMALLAKH, RS WYATT, RJ LOONEY, SW TI DOES MOTOR CEREBRAL-DOMINANCE DEVELOP SECONDARY TO SENSORY DOMINANCE SO PERCEPTUAL AND MOTOR SKILLS LA English DT Article ID HANDEDNESS; BIRTH AB Current research and theoretical frameworks for understanding motor dominance assume that motor dominance is primary. Various developmental clues, however, suggest that the maturation of proprioceptive sensory processing predates that of motor control. We hypothesized that the observed adult pattern of lateralized motor dominance may develop as a consequence of preexisting lateralized ''sensory'' or ''proprioceptive dominance.'' To test whether motor preference could develop in response to sensory dominance, we investigated sighting eye dominance, eye lid winking, and handedness in 164 individuals. Subjects winked the nondominant eye significantly more frequently than the dominant eye and independently of their handedness, lending partial support to the idea that motor function can develop in response to sensory function. Specific investigation of the development of the proprioceptive system would be needed to evaluate whether lateralization of motor handedness develops as a consequence of ''proprioceptive'' lateralization. C1 NIMH,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. NR 26 TC 6 Z9 6 U1 0 U2 0 PU PERCEPTUAL MOTOR SKILLS PI MISSOULA PA PO BOX 9229, MISSOULA, MT 59807 SN 0031-5125 J9 PERCEPT MOTOR SKILL JI Percept. Mot. Skills PD APR PY 1993 VL 76 IS 2 BP 647 EP 652 PG 6 WC Psychology, Experimental SC Psychology GA KY257 UT WOS:A1993KY25700058 PM 8483682 ER PT J AU TELLA, SR SCHINDLER, CW GOLDBERG, SR AF TELLA, SR SCHINDLER, CW GOLDBERG, SR TI CHLORISONDAMINE, A NONCOMPETITIVE GANGLIONIC BLOCKER, ANTAGONIZES THE CARDIOVASCULAR EFFECTS OF COCAINE IN CONSCIOUS SQUIRREL-MONKEYS SO PHARMACOLOGICAL RESEARCH LA English DT Article DE COCAINE; BLOOD PRESSURE; HEART RATE; GANGLIONIC BLOCKADE; CHLORISONDAMINE; CENTRAL NERVOUS SYSTEM (SQUIRREL MONKEYS) ID CENTRAL-NERVOUS-SYSTEM; RESPONSES; ABUSE; DOGS; RATS C1 GEORGETOWN UNIV,SCH MED,DEPT PHARMACOL,WASHINGTON,DC 20007. RP TELLA, SR (reprint author), NIDA,ADDICT RES CTR,BEHAV PHARMACOL & GENET SECT,PRECLIN PHARMACOL LAB,POB 5180,BALTIMORE,MD 21224, USA. NR 16 TC 9 Z9 9 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 1043-6618 J9 PHARMACOL RES JI Pharmacol. Res. PD APR PY 1993 VL 27 IS 3 BP 233 EP 239 DI 10.1006/phrs.1993.1022 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LE134 UT WOS:A1993LE13400004 PM 8100996 ER PT J AU ANDERSON, SM KANT, GJ DESOUZA, EB AF ANDERSON, SM KANT, GJ DESOUZA, EB TI EFFECTS OF CHRONIC STRESS ON ANTERIOR-PITUITARY AND BRAIN CORTICOTROPIN-RELEASING FACTOR RECEPTORS SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE STRESS; CORTICOTROPIN-RELEASING FACTOR; CRF RECEPTORS; NEUROHUMOR RECEPTORS; ANTERIOR PITUITARY GLAND ID FACTOR-LIKE IMMUNOREACTIVITY; RAT-BRAIN; FACTOR CRF; DIFFERENTIAL REGULATION; HORMONE CRH; ALZHEIMERS-DISEASE; DEPRESSED-PATIENTS; BETA-ENDORPHIN; CYCLIC-AMP; CORTICOSTERONE AB [I-125]Corticotropin-releasing factor binding was measured in membrane homogenates prepared from the anterior pituitary, frontal cortex, motor cortex, somatosensory cortex, mesolimbic area (olfactory tubercle and nucleus accumbens), caudate putamen, hypothalamus, midbrain, and cerebellum from control and chronically stressed rats. The stressor consisted of 3 or 14 days of around-the-clock intermittent foot-shock (approximately one trial per 5-min frequency) that could be avoided or escaped on 90% of the trials presented by pulling a ceiling chain. Plasma corticosterone levels were almost doubled in stressed rats following 3 days of chronic stress and remained significantly elevated in rats stressed for 14 days as compared to controls. Plasma corticotropin levels were similar in controls and stressed animals in both the 3- and 14-day experiments. [I-125]Corticotropin-releasing factor binding was decreased in anterior pituitary and frontal cortex following 3 days of chronic stress; binding affinity of anterior pituitary membranes was not different between control and stressed animals. [I-125]Corticotropin-releasing factor binding was similar in control and 3-day-stressed animals in the other brain areas examined. After 14 days of chronic stress, hypothalamic [I-125]corticotropin-releasing factor binding was decreased in stressed rats as compared to control animals but no other differences were seen. The decrease in the apparent number of anterior pituitary corticotropin-releasing factor receptors following 3 days of stress may be due, in part, to increased plasma corticosterone levels and/or increased corticotropin-releasing factor secretion during that time. The downregulation of frontal cortex and hypothalamic corticotropin-releasing factor receptors, however, is more likely to be primarily in response to sustained stress-induced corticotropin-releasing factor release at those sites. C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205. RP ANDERSON, SM (reprint author), WALTER REED ARMY INST RES,DEPT MED NEUROSCI,WASHINGTON,DC 20307, USA. NR 51 TC 59 Z9 59 U1 0 U2 3 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 APR PY 1993 VL 44 IS 4 BP 755 EP 761 DI 10.1016/0091-3057(93)90002-B PG 7 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA KU641 UT WOS:A1993KU64100002 PM 8385781 ER PT J AU MCLENIGAN, M LEVINE, AS PROTIC, M AF MCLENIGAN, M LEVINE, AS PROTIC, M TI DIFFERENTIAL EXPRESSION OF PYRIMIDINE DIMER-BINDING PROTEINS IN NORMAL AND UV LIGHT-TREATED VERTEBRATE CELLS SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID XERODERMA PIGMENTOSUM-CELLS; COLI DNA PHOTOLYASE; DAMAGED PLASMID DNA; ESCHERICHIA-COLI; PHOTOREACTIVATING ENZYME; ULTRAVIOLET-LIGHT; EXCISION-REPAIR; HELA-CELLS; 6-4 PHOTOPRODUCTS; MAMMALIAN-CELLS AB The expression of UV damage-specific DNA-binding proteins was examined in various phylogenetically distant species with differing DNA repair phenotypes. Two distinct constitutive DNA-binding activities, one specific for cyclobutane pyrimidine dimers and the other for non-cyclobutane dimer photoproducts, were detected. The expression of these binding activities was found to be variable throughout the animal kingdom: cold-blooded vertebrates show a constitutive cyclobutane dimer-binding activity exclusively, and primates reveal only non-cyclobutane binding activity. In contrast, birds and marsupials appear to express both types of binding activities. The kinetics of expression (rather than the constitutive presence) of these UV damage-specific DNA-binding activities after UV treatment correlate with the cell's capacity for DNA repair. In addition, cyclobutane pyrimidine dimer-binding activities could be detected only in cells with established photoreactivating activity. C1 NATL INST CHILD HLTH & HUMAN DEV,VIRUSES & CELLULAR BIOL SECT,BETHESDA,MD 20892. NR 44 TC 10 Z9 10 U1 0 U2 0 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 APR PY 1993 VL 57 IS 4 BP 655 EP 662 DI 10.1111/j.1751-1097.1993.tb02932.x PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LB366 UT WOS:A1993LB36600012 PM 8506394 ER PT J AU MASOLIVER, J PORRA, JM WEISS, GH AF MASOLIVER, J PORRA, JM WEISS, GH TI SOME 2-DIMENSIONAL AND 3-DIMENSIONAL PERSISTENT RANDOM-WALKS SO PHYSICA A LA English DT Article AB We formulate non-Markovian versions of the persistent random walk in two and three dimensions and in continuous time. These models can be regarded as being generalizations of the original Pearson random walk and of the freely jointed chain which has been of some importance in polymer physics. Solutions for the probability density of the displacement of the random walker can be furnished for a restricted (essentially Markovian) set of these models. It is shown that in two dimensions the solution to one of these models is equivalent to the solution to an inhomogeneous telegrapher's equation. It does not appear to be possible, starting from a similar model in three dimensions, to find any form of the telegrapher's equation that follows from our solution of the equations in the Fourier-Laplace transform domains. 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 9 TC 40 Z9 40 U1 1 U2 6 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 1 PY 1993 VL 193 IS 3-4 BP 469 EP 482 DI 10.1016/0378-4371(93)90488-P PG 14 WC Physics, Multidisciplinary SC Physics GA KW834 UT WOS:A1993KW83400012 ER PT J AU LAKATTA, EG AF LAKATTA, EG TI CARDIOVASCULAR REGULATORY MECHANISMS IN ADVANCED AGE SO PHYSIOLOGICAL REVIEWS LA English DT Review ID BETA-ADRENERGIC-RECEPTOR; CONGESTIVE-HEART-FAILURE; VASCULAR SMOOTH-MUSCLE; LEFT-VENTRICULAR MASS; RAT CARDIAC MYOCYTES; DEPENDENT PROTEIN-KINASE; AORTIC INPUT IMPEDANCE; INTRACELLULAR CALCIUM TRANSIENTS; ADENYLATE-CYCLASE SYSTEM; BODY NEGATIVE-PRESSURE RP LAKATTA, EG (reprint author), NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BALTIMORE,MD 21224, USA. NR 564 TC 515 Z9 525 U1 1 U2 18 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0031-9333 J9 PHYSIOL REV JI Physiol. Rev. PD APR PY 1993 VL 73 IS 2 BP 413 EP 467 PG 55 WC Physiology SC Physiology GA KX818 UT WOS:A1993KX81800004 PM 8475195 ER PT J AU SCHWARTZ, LK WEIFFENBACH, JM VALDEZ, IH FOX, PC AF SCHWARTZ, LK WEIFFENBACH, JM VALDEZ, IH FOX, PC TI TASTE INTENSITY PERFORMANCE IN PATIENTS IRRADIATED TO THE HEAD AND NECK SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE TASTE; THERAPEUTIC RADIATION; CANCER; AGING; SUPRATHRESHOLD; INTENSITY ID CANCER-PATIENTS; ABNORMALITIES; RECOVERY; ACUITY AB Decrements in taste-detection thresholds during radiotherapy and subsequent recovery in the months after therapy are well documented. However, few studies have explored suprathreshold taste intensity perception in radiation patients. This cross-sectional study compared taste function in 15 men postradiation with a group of 23 healthy, nonirradiated male volunteers. A direct-scaling procedure was used to assess taste intensity perception of the four basic taste qualities. Patients performed nearly as well as control subjects on objective measures of suprathreshold functioning. Postradiation intensity judgments of salty (sodium chloride), sweet (sucrose), and bitter (quinine sulfate) solutions were not significantly reduced. Subtle, age-related taste impairments were identified for sour perception (citric acid) postradiotherapy. Younger patients judged citric acid to be more intense than did age-appropriate control subjects, whereas older patients judged it to be less intense. Moreover, younger patients were likely to be mildly dysgeusic, whereas older patients appeared to be hypogeusic for citric acid. This study provides evidence for near normal suprathreshold taste intensity perception in patients who have received head and neck irradiation. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. NR 25 TC 19 Z9 19 U1 0 U2 3 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 APR PY 1993 VL 53 IS 4 BP 671 EP 677 DI 10.1016/0031-9384(93)90172-C PG 7 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA KY316 UT WOS:A1993KY31600008 PM 8511171 ER PT J AU HANSON, AD HUANG, ZH GAGE, DA AF HANSON, AD HUANG, ZH GAGE, DA TI EVIDENCE THAT THE PUTATIVE COMPATIBLE SOLUTE 5-DIMETHYLSULFONIOPENTANOATE IS AN EXTRACTION ARTIFACT SO PLANT PHYSIOLOGY LA English DT Note ID MASS-SPECTROMETRY; CHROMATOGRAPHY AB A novel gas chromatography-mass spectrometry method for analyzing sulfonium compounds as their S-demethylated silyl derivatives has clarified the origin of 5-dimethylsulfoniopentanoate. This compound, previously reported from flowers of Diplotaxis tenuifolia (L.) DC. (Cruciferae), is generated from glucoerucin during treatment with hot 6 N HCl. Glucoerucin is the characteristic glucosinolate of D. tenuifolia. C1 MICHIGAN STATE UNIV,NIH,DEPT BIOCHEM,MASS SPECTROMETRY FACIL,E LANSING,MI 48824. RP HANSON, AD (reprint author), UNIV MONTREAL,INST RECH BIOL VEGETALE,4101 RUE SHERBROOKE EST,MONTREAL H1X 2B2,PQ,CANADA. FU NCRR NIH HHS [RR 00484] NR 12 TC 3 Z9 3 U1 0 U2 1 PU AMER SOC PLANT PHYSIOLOGISTS PI ROCKVILLE PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 SN 0032-0889 J9 PLANT PHYSIOL JI Plant Physiol. PD APR PY 1993 VL 101 IS 4 BP 1391 EP 1393 DI 10.1104/pp.101.4.1391 PG 3 WC Plant Sciences SC Plant Sciences GA KX043 UT WOS:A1993KX04300037 PM 8310067 ER PT J AU FREY, MW NOSSAL, NG CAPSON, TL BENKOVIC, SJ AF FREY, MW NOSSAL, NG CAPSON, TL BENKOVIC, SJ TI CONSTRUCTION AND CHARACTERIZATION OF A BACTERIOPHAGE-T4 DNA-POLYMERASE DEFICIENT IN 3'-]5' EXONUCLEASE ACTIVITY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CELL NUCLEAR ANTIGEN; ESCHERICHIA-COLI; AMINO-ACID; ACCESSORY PROTEINS; 3'-5' EXONUCLEASE; KINETIC-ANALYSIS; REPLICATION; SITE; FRAGMENT; INVITRO AB Bacteriophage T4 DNA polymerase has a proofreading 3' --> 5' exonuclease that plays an important role in maintaining the accuracy of DNA replication. We have constructed a T4 DNA polymerase deficient in this exonuclease by converting Asp-219 to Ala. The exonuclease activity of the mutant T4 DNA polymerase has been reduced by a factor of at least 10(7), but it retains a polymerase activity whose kinetic parameters, k(cat), K(d) DNA, and K(d) dATP, are very close to those of the wild-type enzyme. Bacteriophage T4 with the mutant polymerase gene has a markedly increased mutation frequency. Asp-219 in T4 DNA polymerase is within a sequence similar to those surrounding Asp residues previously shown to be essential for the exonuclease activities of the Klenow fragment of Escherichia coli DNA polymerase I (Asp-424), bacteriophage phi29 DNA polymerase (Asp-66), and Saccharomyces cerevisiae DNA polymerase delta (Asp-405). Thus, these studies support the proposal that there are similar sequences in the active sites for the proofreading exonucleases of these and related DNA polymerases. C1 NIDDKD,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. RP FREY, MW (reprint author), PENN STATE UNIV,DEPT CHEM,152 DAVEY LAB,UNIV PK,PA 16802, USA. FU NIGMS NIH HHS [GM13306] NR 36 TC 120 Z9 120 U1 0 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 1 PY 1993 VL 90 IS 7 BP 2579 EP 2583 DI 10.1073/pnas.90.7.2579 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500006 PM 8464864 ER PT J AU PERNECKY, SJ LARSON, JR PHILPOT, RM COON, MJ AF PERNECKY, SJ LARSON, JR PHILPOT, RM COON, MJ TI EXPRESSION OF TRUNCATED FORMS OF LIVER MICROSOMAL P450 CYTOCHROMES 2B4 AND 2E1 IN ESCHERICHIA-COLI - INFLUENCE OF NH2-TERMINAL REGION ON LOCALIZATION IN CYTOSOL AND MEMBRANES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE LIVER MICROSOMAL CYTOCHROME-P450; MEMBRANE BINDING; HETEROLOGOUS EXPRESSION ID AMINO-ACID-SEQUENCE; PHENOBARBITAL-INDUCED CYTOCHROME-P-450; TERMINAL SEQUENCE; INSERTION SIGNAL; LACZ GENE; TOPOLOGY; PROTEINS; PURIFICATION; PREDICTION; SEGMENT AB The currently accepted model for the membrane topology of microsomal cytochrome P450 is that of a largely cytoplasmic domain bound by only one or two transmembrane segments at the NH2 terminus. However, as we have reported previously, P450 2E1 lacking the hydrophobic NH2-terminal signal peptide, like the full-length protein, is located in the inner cell membrane when expressed in Escherichia coli and is active with typical substrates. In the present study, additional variants of alcohol-inducible P450 2E1 as well as truncated forms of phenobarbital-inducible P450 2B4 were similarly expressed to determine the influence of the NH2-terminal region on the membrane-binding properties. After deletion of S1 (the NH2-terminal hydrophobic segment), or both Sl and L1 (the following hydrophilic region, expected to be lumenal or cytosolic), one-third of the resulting P450 2B4 (DELTA2-20) and 2B4 (DELTA2-27) remained membrane bound. Furthermore, the idea that the first two hydrophobic segments are required for attachment by a hairpin loop is not supported by the finding that after deletion of the S1, LI, and S2 segments about half of the P450 2E1 (DELTA3-48) remained membrane bound. Since Na2CO3 treatment of the membrane fraction had no significant effect, the findings are apparently not attributable to a loose attachment or occlusion of the truncated proteins. The replacement of neutral amino acids by positively charged residues in positions 3 and 8 of P450 2E1 (DELTA3-29) changed the amount in the cytosol from 35% to 50%, and the deletion of residues 2-20 or 2-27 from P450 2B4, which resulted in positive charges occurring in the NH2-terminal region, changed the amount in the cytosol from 27% to 67%. We conclude that alterations in the NH2-terminal region can change the location of the cytochrome from largely membranous to largely cytosolic and that the first two hydrophobic segments are not uniquely involved in membrane attachment. C1 NIEHS,DIV CELLULAR & MOLEC PHARMACOL,RES TRIANGLE PK,NC 27709. RP PERNECKY, SJ (reprint author), UNIV MICHIGAN,SCH MED,DEPT BIOL CHEM,ANN ARBOR,MI 48109, USA. FU NIAAA NIH HHS [AA-06221]; NIDDK NIH HHS [DK-10339]; NIEHS NIH HHS [ES-07062] NR 40 TC 97 Z9 98 U1 1 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 APR 1 PY 1993 VL 90 IS 7 BP 2651 EP 2655 DI 10.1073/pnas.90.7.2651 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500021 PM 8464872 ER PT J AU MARTIN, OC COMLY, ME BLANCHETTEMACKIE, EJ PENTCHEV, PG PAGANO, RE AF MARTIN, OC COMLY, ME BLANCHETTEMACKIE, EJ PENTCHEV, PG PAGANO, RE TI CHOLESTEROL DEPRIVATION AFFECTS THE FLUORESCENCE PROPERTIES OF A CERAMIDE ANALOG AT THE GOLGI-APPARATUS OF LIVING CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID PORCINE SUBMAXILLARY-GLANDS; PLASMA-MEMBRANE; GLUCOSYLCERAMIDE SYNTHESIS; CULTURED FIBROBLASTS; RAT-LIVER; TRANSPORT; SPHINGOMYELIN; CISTERNAE; SPHINGOLIPIDS; ACCUMULATION AB Previous studies have established that a fluorescent analog of ceramide, N-[7-(4-nitrobenzo-2-oxa-1,3-diazole)]-6-aminohexanoyl-D-erythro-sphingosine C6-NBD-Cer), is a vital stain for the Golgi apparatus and a useful tool for studying the sorting and transport of sphingolipids along the secretory pathway in animal cells. Here, we examine the effects of various culture conditions on labeling of the Golgi apparatus of human skin fibroblasts by C6-NBD-Cer and demonstrate that cholesterol deprivation affects the fluorescence properties of the probe at this organelle. Labeling of the Golgi apparatus by C6-NBD-Cer was dramatically reduced in cells grown in medium containing lipoprotein-deficient serum compared to cells grown in medium containing normal serum. Quantitative fluorescence microscopy showed that this apparent reduction in labeling resulted from accelerated photobleaching of the fluorescent analog. C6-NBD-Cer labeling of the Golgi apparatus was restored in cholesterol-deprived cells by stimulating endogenous cholesterol biosynthesis with mevalonic acid or by adding exogenous nonlipoprotein cholesterol or low density lipoprotein to the culture medium. In addition, when cells grown in medium containing normal serum were perforated and treated with cholesterol oxidase, an apparent reduction in labeling resulted, further implicating an intracellular pool of cholesterol in the potentiation of C6-NBD-Cer fluorescence. These results demonstrate that cytological studies using C6-NBD-Cer are affected by cholesterol deprivation and suggest that this fluorescent lipid may be used to monitor cholesterol at the Golgi apparatus of living cells. C1 CARNEGIE INST WASHINGTON,DEPT EMBRYOL,BALTIMORE,MD 21210. NINCDS,DEV & METAB NEUROL BRANCH,BETHESDA,MD 20892. NIDDKD,CELLULAR & DEV BIOL LAB,ENDOCRINOL LAB,BETHESDA,MD 20892. FU NIGMS NIH HHS [R37 GM-22942, GM-37434] NR 33 TC 42 Z9 42 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 APR 1 PY 1993 VL 90 IS 7 BP 2661 EP 2665 DI 10.1073/pnas.90.7.2661 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500023 PM 8464873 ER PT J AU SUN, Y NAKAMURA, K WENDEL, E COLBURN, N AF SUN, Y NAKAMURA, K WENDEL, E COLBURN, N TI PROGRESSION TOWARD TUMOR-CELL PHENOTYPE IS ENHANCED BY OVEREXPRESSION OF A MUTANT P53 TUMOR-SUPPRESSOR GENE ISOLATED FROM NASOPHARYNGEAL CARCINOMA SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE NEOPLASTIC PHENOTYPE; NEGATIVE DOMINANCE; DNA TRANSFECTION; MOUSE JB6 CELLS; HUMAN SAOS-2 CELLS ID WILD-TYPE P53; TRANSFORMATION; MUTATIONS; PROMOTION; ONCOGENE; CLONING; PROTEIN; GROWTH; LINES; RAS AB We recently reported the detection of a heterozygous G --> C point mutation at codon 280 of p53 in nasopharyngeal carcinoma, which causes an Arg --> Thr substitution. To test whether this mutant p53 has gained function as an oncogene, we overexpressed the mutant p53 in nontumorigenic cells of two model systems: (i) human Saos-2 cells lacking endogenous p53 and (ii) mouse JB6 variants that bear endogenous wild-type p53. Although they have no growth advantage over the neomycin controls in monolayer culture, human Saos-2 transfectants overexpressing mutant p53 do show enhanced progression to tumor cell phenotype, as assayed by anchorage-independent growth and in vivo tumorigenicity. The enhancement is seen only in transfectants expressing higher levels of p53 protein. In the mouse JB6 system, the mutant p53 functions dominantly in the presence of endogenous wild-type p53 to enhance progression of preneoplastic promotion-sensitive cells toward anchorage-independent phenotype. Mouse JB6 transfectants of mutant p53 are, however, not tumorigenic in nude mice. We conclude from these studies that the G --> C point mutation of p53 at codon 280 is a gain-of-function mutation that appears to operate dominantly and that the mutant p53-thr280 has only moderate oncogenic activity. This mutation may cooperate with other yet-to-be isolated genes in the genesis of nasopharyngeal carcinoma. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RP SUN, Y (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,CELL BIOL SECT,BLDG 560,ROOM 21-89,FREDERICK,MD 21702, USA. NR 31 TC 71 Z9 72 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 APR 1 PY 1993 VL 90 IS 7 BP 2827 EP 2831 DI 10.1073/pnas.90.7.2827 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500057 PM 8464896 ER PT J AU APASOV, S SITKOVSKY, M AF APASOV, S SITKOVSKY, M TI HIGHLY LYTIC CD8+, ALPHA,BETA T-CELL RECEPTOR CYTOTOXIC T-CELLS WITH MAJOR HISTOCOMPATIBILITY COMPLEX (MHC) CLASS-I ANTIGEN-DIRECTED CYTOTOXICITY IN BETA(2)-MICROGLOBULIN, MHC CLASS-I-DEFICIENT MICE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GENE KNOCKOUT ID BETA-2-MICROGLOBULIN; EXPRESSION; ANTIBODY AB Targeted disruption of the beta2-microglobulin (beta2m) gene results in major histocompatibility complex (MHC) class I deficiency and virtual disappearance of functional CD8+ cytotoxic T lymphocytes (CTLs) in beta2m-deficient (beta2m -/-) mice. We asked whether the beta2m -/- mice are able to reject tumor cells injected i.p. and what is the cellular composition of peritoneal exudate leukocytes (PELs) from such mice. We found that beta2m -/- mice do reject MHC class I-bearing tumor cells injected i.p. Surprisingly, analysis of PEL CTLs obtained from i.p. tumor-injected beta2m -/- mice revealed the presence of a large proportion of functional, tumor-destroying CD8+, CD4-, alphabeta T-cell receptor-positive, CD3+, Thy-1+, MHC class I-negative CTLs with strong MHC class I-directed cytotoxic activity. These results call for careful studies of local accumulation of CD8+ CTLs in beta2m -/- mouse models and suggest that the dramatic decrease in MHC class I expression caused by beta2m gene disruption does not prevent CD8+/CD4-cell selection and expansion. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 21 TC 77 Z9 77 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 APR 1 PY 1993 VL 90 IS 7 BP 2837 EP 2841 DI 10.1073/pnas.90.7.2837 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500059 PM 8464897 ER PT J AU BHATIADEY, N ADELSTEIN, RS DAWID, IB AF BHATIADEY, N ADELSTEIN, RS DAWID, IB TI CLONING OF THE CDNA-ENCODING A MYOSIN HEAVY CHAIN-B ISOFORM OF XENOPUS NONMUSCLE MYOSIN WITH AN INSERT IN THE HEAD REGION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CELL MOTILITY; CYTOSKELETON ID GENE-EXPRESSION; NERVOUS-SYSTEM; LAEVIS; SEQUENCES; DIVISION; RNAS AB The complete amino acid sequence of Xenopus laevis nonmuscle myosin heavy chain B (MHC-B) has been deduced from overlapping cDNA clones isolated from an XTC cell library. RNA blots of various developmental stages, adult tissues, and XTC cells detect a single transcript of 7.5 kb which is expressed at similar levels throughout development. MHC-B mRNA was detected in XTC cells, heart, lung, spleen, and brain, at lower levels in ovary, testis, pancreas, stomach, liver, and eye, but not in kidney and skeletal muscle. Protein expression in adult tissues, as detected by immunoblot analysis, correlates well with mRNA expression. In chickens and humans, a fraction of the mRNA encoding the MHC-B isoform was found previously to contain a 10-amino acid insert at amino acid 211 near the ATP-binding site. As reported elsewhere, in the chicken this insert-bearing isoform is nervous system-specific. The Xenopus sequence shows a 16-amino acid insertion at the same position; 7 of 16 residues are identical to those in the chicken and human insertion, and these identical residues include a consensus target sequence for cyclin-p34cdc2 kinase. In contrast to chicken, all frog tissues and embryonic stages tested contained the insert-bearing form, and no evidence for a non-insert-bearing MHC-B isoform was found in Xenopus. C1 NICHHD, MOLEC GENET LAB, BLDG 6B, ROOM 413, BETHESDA, MD 20892 USA. NHLBI, MOLEC CARDIOL LAB, BETHESDA, MD 20892 USA. OI Adelstein, Robert/0000-0002-8683-2144 NR 29 TC 24 Z9 24 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1993 VL 90 IS 7 BP 2856 EP 2859 DI 10.1073/pnas.90.7.2856 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500063 PM 8464900 ER PT J AU HARRIS, N ROSALES, R MOSS, B AF HARRIS, N ROSALES, R MOSS, B TI TRANSCRIPTION INITIATION-FACTOR ACTIVITY OF VACCINIA VIRUS CAPPING ENZYME IS INDEPENDENT OF MESSENGER-RNA GUANYLYLATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE POXVIRUS; GENE REGULATION; RNA POLYMERASE ID ESCHERICHIA-COLI; DNA-REPLICATION; LATE GENES; POLYMERASE; GUANYLYLTRANSFERASE; INVITRO; VIRIONS; INTERMEDIATE; PURIFICATION; SUBUNIT AB Cytoplasmic extracts of vaccinia virus-infected HeLa cells blocked in DNA replication were capable of transcribing templates containing the minimal promoter sequences derived from three viral intermediate-stage genes (A1L, A2L, and G8R) but not promoters from early or late genes. One of three isolated components required for transcription copurified with the viral capping enzyme, a heterodimeric protein responsible for forming the 7-methyl-guanosine(5')triphospho(5')nucleoside [m7G(5')ppp(5')N-] structure at the 5' end of mRNAs, as had been reported using a template with another intermediate promoter [Vos, J. C., Sasker, M. & Stunnenberg, H. G. (1991) EMBO J. 10, 2553-2558]. Transcription factor activity was associated with partially purified capping enzyme from infected cell extracts, homogeneous enzyme from purified virions, and recombinant viral enzyme from Escherichia coli. By transcribing truncated templates of different sizes, we determined that RNA chains of 35 nt were capped whereas those of 15 nt were not. Nevertheless, the capping enzyme was required for formation of short uncapped transcripts, indicating that capping and transcription initiation factor activities are independent functions. RP HARRIS, N (reprint author), NIAID,VIRAL DIS LAB,BETHESDA,MD 20892, USA. NR 38 TC 25 Z9 25 U1 1 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 1 PY 1993 VL 90 IS 7 BP 2860 EP 2864 DI 10.1073/pnas.90.7.2860 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500064 PM 8385346 ER PT J AU KRAUS, MH FEDI, P STARKS, V MURARO, R AARONSON, SA AF KRAUS, MH FEDI, P STARKS, V MURARO, R AARONSON, SA TI DEMONSTRATION OF LIGAND-DEPENDENT SIGNALING BY THE ERBB-3 TYROSINE KINASE AND ITS CONSTITUTIVE ACTIVATION IN HUMAN BREAST-TUMOR CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GP180(ERBB-3); RECEPTOR TYROSINE KINASE; TYROSINE PHOSPHORYLATION; MITOGENIC SIGNALING; NEOPLASIA ID EPIDERMAL GROWTH-FACTOR; HUMAN MAMMARY-TUMORS; EGF RECEPTOR GENE; PROTO-ONCOGENE; EXPRESSION; AMPLIFICATION; OVEREXPRESSION; PHENOTYPE; DOMAINS; MEMBER AB The predicted human erbB-3 gene product is closely related to epidermal growth factor receptor (EGFR) and erbB-2, which have been implicated as oncogenes in model systems and human neoplasia. We expressed the erbB-3 coding sequence in NIH 3T3 fibroblasts and identified its product as a 180-kDa glycoprotein, gp180erbB-3. Tunicamycin and pulse-chase experiments revealed that the mature protein was processed by N-linked glycosylation of a 145-kDa erbB-3 core polypeptide. The intrinsic catalytic function of gp180erbB-3 was shown by its ability to autophosphorylate in vitro. Ligand-dependent signaling of its cytoplasmic domain was established employing transfectants that express a chimeric EGFR/erbB-3 protein, gp180EGFR/erbB-3. EGF induced tyrosine phosphorylation of the chimera and promoted soft agar colony formation of such transfectants. These findings combined with the detection of constitutive tyrosine phosphorylation of gp180erbB-3 in 4 of 12 human mammary tumor cell lines implicate the activated erbB-3 product in the pathogenesis of some human malignancies. C1 UNIV ROMA LA SAPIENZA,DIPARTIMENTO MED SPERIMENTALE,I-00161 ROME,ITALY. RP KRAUS, MH (reprint author), NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 32 TC 129 Z9 130 U1 0 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 1 PY 1993 VL 90 IS 7 BP 2900 EP 2904 DI 10.1073/pnas.90.7.2900 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500072 PM 8464905 ER PT J AU LAVORGNA, G KARIM, FD THUMMEL, CS WU, C AF LAVORGNA, G KARIM, FD THUMMEL, CS WU, C TI POTENTIAL ROLE FOR A FTZ-F1 STEROID-RECEPTOR SUPERFAMILY MEMBER IN THE CONTROL OF DROSOPHILA METAMORPHOSIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID SEQUENTIAL GENE ACTIVATION; ECDYSONE-INDUCIBLE GENE; HEAT-SHOCK FACTOR; POLYTENE CHROMOSOMES; NUCLEAR RECEPTORS; FUSHI-TARAZU; EARLY PUFF; ENCODES 2; MELANOGASTER; EXPRESSION AB FTZ-F1, a member of the steroid receptor superfamily, has been implicated in the activation of the homeobox segmentation gene fushi tarazu early in Drosophila embryogenesis. We have cloned a developmental isoform of FTZ-F1 and found that it is expressed as a product of the previously identified, midprepupal chromosome puff at 75CD. The 75CD puff occurs in the midst of a period of intense puffing activity that is triggered in response to the steroid hormone ecdysone at the onset of metamorphosis. Indirect immunofluorescent staining for FTZ-F1 on Drosophila polytene chromosomes reveals binding to over 150 chromosomal targets, which include 75CD itself and prominent late prepupal puffs that are predicted to be regulated by midprepupal puff proteins. These results suggest a role for FTZ-F1 as a regulator of insect metamorphosis and underscore the repeated utilization of a regulatory protein for widely separate developmental pathways. C1 NCI,BIOCHEM LAB,BLDG 37,ROOM 4C-09,BETHESDA,MD 20892. UNIV UTAH,HOWARD HUGHES MED INST,SALT LAKE CITY,UT 84112. FU NIGMS NIH HHS [GM40905, 5T32GM07464] NR 27 TC 132 Z9 136 U1 0 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 APR 1 PY 1993 VL 90 IS 7 BP 3004 EP 3008 DI 10.1073/pnas.90.7.3004 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500093 PM 8096644 ER PT J AU OGATA, N OSTBERG, L EHRLICH, PH WONG, DC MILLER, RH PURCELL, RH AF OGATA, N OSTBERG, L EHRLICH, PH WONG, DC MILLER, RH PURCELL, RH TI MARKEDLY PROLONGED INCUBATION PERIOD OF HEPATITIS-B IN A CHIMPANZEE PASSIVELY IMMUNIZED WITH A HUMAN MONOCLONAL-ANTIBODY TO THE ALPHA-DETERMINANT OF HEPATITIS-B SURFACE-ANTIGEN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID LIVER-TRANSPLANTATION; NUCLEOTIDE-SEQUENCE; FINAL REPORT; HEPATOCELLULAR-CARCINOMA; SYNTHETIC-PEPTIDE; VIRUS REINFECTION; RECOMBINANT YEAST; ESCHERICHIA-COLI; CONTROLLED TRIAL; CARRIER STATE AB The protective efficacy of a human monoclonal antibody directed against the a determinant of hepatitis B virus (HBV) surface antigen was studied in a chimpanzee. A single high dose of 5 mg/kg (body weight) of monoclonal antibody SDZ OST 577 was intravenously administered to a chimpanzee, followed by intravenous challenge with 10(3.5) chimpanzee infectious doses of a wild-type HBV, the MS-2 strain (ayw subtype). The passively acquired antibody to HBV surface antigen could be detected for 40 weeks. Serum HBV DNA tested by a ''nested'' polymerase chain reaction assay was negative through the 36th week after virus challenge but became positive by the 38th week. The chimpanzee subsequently developed acute hepatitis B almost-equal-to 1 year after challenge. The nucleotide sequence of the a determinant of the surface gene of the replicated virus was identical with that of the inoculated wild-type virus. Thus, a human monoclonal antibody directed against the a determinant of HBV surface antigen delayed but did not prevent experimental infection of HBV and hepatitis in the chimpanzee. Our results indicate an incomplete ability of this antibody to protect against HBV infection in vivo after a single infusion. C1 SANDOZ INC,RES INST,E HANOVER,NJ 07936. RP OGATA, N (reprint author), NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892, USA. NR 53 TC 47 Z9 49 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 APR 1 PY 1993 VL 90 IS 7 BP 3014 EP 3018 DI 10.1073/pnas.90.7.3014 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500095 PM 8464917 ER PT J AU GREGOR, P REEVES, RH JABS, EW YANG, XD DACKOWSKI, W ROCHELLE, JM BROWN, RH HAINES, JL OHARA, BF UHL, GR SELDIN, MF AF GREGOR, P REEVES, RH JABS, EW YANG, XD DACKOWSKI, W ROCHELLE, JM BROWN, RH HAINES, JL OHARA, BF UHL, GR SELDIN, MF TI CHROMOSOMAL LOCALIZATION OF GLUTAMATE RECEPTOR GENES - RELATIONSHIP TO FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS AND OTHER NEUROLOGICAL DISORDERS OF MICE AND HUMANS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CONSERVED LINKAGE GROUP; MOLECULAR-CLONING; FUNCTIONAL EXPRESSION; MOUSE CHROMOSOME-16; ALZHEIMER-DISEASE; MESSENGER-RNA; X-CHROMOSOME; KAINATE; PROTEIN; SUBUNIT AB Receptors for the major excitatory neurotransmitter glutamate may play key roles in neurodegeneration. The mouse Glur-5 gene maps to chromosome 16 between App and Sod-1. The homologous human GLUR5 gene maps to the corresponding region of human chromosome 21, which contains the locus for familial amyotrophic lateral sclerosis. This location, and other features, render GLUR5 a possible candidate gene for familial amyotrophic lateral sclerosis. In addition, dosage imbalance of GLUR5 may have a role in the trisomy 21 (Down syndrome). Further characterization of the murine glutamate receptor family includes mapping of Glur-1 to the same region as neurological mutants spasmodic, shaker-2, tipsy, and vibrator on chromosome 11; Glur-2 near spastic on chromosome 3; Glur-6 near waltzer and Jackson circler on chromosome 10; and Glur-7 near clasper on chromosome 4. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT & MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL & NEUROSCI,BALTIMORE,MD 21205. INTEGRATED GENET INC,FRAMINGHAM,MA 01701. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT MICROBIOL,DURHAM,NC 27710. MASSACHUSETTS GEN HOSP,DAY NEUROMUSCULAR RES CTR,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. STANFORD UNIV,DEPT BIOL SCI,STANFORD,CA 94305. RP GREGOR, P (reprint author), NIDA,ADDICT RES CTR,MOLEC NEUROBIOL SECT,POB 5180,BALTIMORE,MD 21224, USA. RI Haines, Jonathan/C-3374-2012; OI Jabs, Ethylin/0000-0001-8983-5466 FU NHGRI NIH HHS [HG00324, HG00101, HG00465] NR 77 TC 55 Z9 56 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 1 PY 1993 VL 90 IS 7 BP 3053 EP 3057 DI 10.1073/pnas.90.7.3053 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500103 PM 8464923 ER PT J AU SAVARINO, SJ FASANO, A WATSON, J MARTIN, BM LEVINE, MM GUANDALINI, S GUERRY, P AF SAVARINO, SJ FASANO, A WATSON, J MARTIN, BM LEVINE, MM GUANDALINI, S GUERRY, P TI ENTEROAGGREGATIVE ESCHERICHIA-COLI HEAT-STABLE ENTEROTOXIN-1 REPRESENTS ANOTHER SUBFAMILY OF ESCHERICHIA-COLI HEAT-STABLE TOXIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DIARRHEA; BACTERIAL PATHOGENESIS ID AMINO-ACID-SEQUENCE; ENTERO-TOXIN; PERSISTENT DIARRHEA; GUANYLATE-CYCLASE; ION-TRANSPORT; INVITRO; INTESTINE AB Enteroaggregative Escherichia coli (EAggEC) are associated with persistent diarrhea in young children. Some of these organisms produce a low-molecular-weight, heat-stable, plasmid-encoded enterotoxin that has been named EAggEC heat-stable enterotoxin 1 (EAST1). We have cloned a 4.4-kb DNA fragment from the virulence plasmid of prototype EAggEC strain 17-2, which expresses enterotoxic activity as measured by electrogenic response in Ussing chambers mounted with rabbit ileal tissue. DNA-sequence analysis of this fragment identified an open reading frame (ORF) encoding a cysteine-rich polypeptide of 38 amino acids (M(r), 4100). Insertional and deletional mutations in this ORF resulted in loss of enterotoxic activity. The ORF was cloned into a T7 expression vector, and postinduction culture filtrates exhibited enterotoxic activity and increased ileal tissue cGMP levels. A synthetic peptide consisting of predicted amino acid residues 8-29 also showed enterotoxic activity. These data indicate that this ORF, named ast4 (EAggEC heat-stable enterotoxin), represents the EAST1 structural gene. EAST1 shows significant homology with the enterotoxic domain of heat-stable enterotoxin a (STa) of enterotoxigenic E. coli and with guanylin, a mammalian analog of STa. Unlike STa, which requires six cysteines and three disulfide linkages for full biological activity, both EASTI and guanylin contain four cysteine residues. Based on the cGMP data and the sequence homology to STa and guanylin, it is predicted that EAST1 stimulates the particulate form of guanylate cyclase through the same receptor-binding region as STa and guanylin. C1 FAC MED & CHIRURG CATANZARO,INST SCI PEDIAT & GINECOL,I-88100 CATANZARO,ITALY. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DEPT MED,DIV GEOG MED,CTR VACCINE DEV,BALTIMORE,MD 21201. RP SAVARINO, SJ (reprint author), USN,MED RES INST,ENTER DIS PROGRAM,BETHESDA,MD 20892, USA. NR 33 TC 179 Z9 185 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 APR 1 PY 1993 VL 90 IS 7 BP 3093 EP 3097 DI 10.1073/pnas.90.7.3093 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV975 UT WOS:A1993KV97500111 PM 8385356 ER PT J AU HONG, JS MCGINTY, JF LEE, PHK XIE, CW MITCHELL, CL AF HONG, JS MCGINTY, JF LEE, PHK XIE, CW MITCHELL, CL TI RELATIONSHIP BETWEEN HIPPOCAMPAL OPIOID-PEPTIDES AND SEIZURES SO PROGRESS IN NEUROBIOLOGY LA English DT Review ID WET-DOG SHAKES; PERFORANT PATH STIMULATION; PRODYNORPHIN MESSENGER-RNA; ENKEPHALIN-LIKE IMMUNOREACTIVITY; TEMPORAL-LOBE EPILEPSY; DENTATE GRANULE CELLS; REPEATED ELECTROCONVULSIVE SHOCKS; LONG-TERM POTENTIATION; KAINIC ACID; RAT HIPPOCAMPUS C1 E CAROLINA UNIV,SCH MED,DEPT ANAT & CELL BIOL,GREENVILLE,NC 27858. RP HONG, JS (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU SAMHSA HHS [OA 03982] NR 154 TC 57 Z9 66 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0301-0082 J9 PROG NEUROBIOL JI Prog. Neurobiol. PD APR PY 1993 VL 40 IS 4 BP 507 EP 528 DI 10.1016/0301-0082(93)90020-S PG 22 WC Neurosciences SC Neurosciences & Neurology GA KL531 UT WOS:A1993KL53100004 PM 8446760 ER PT J AU FERRETTI, A JUDD, JT TAYLOR, PR NAIR, PP FLANAGAN, VP AF FERRETTI, A JUDD, JT TAYLOR, PR NAIR, PP FLANAGAN, VP TI INGESTION OF MARINE OIL REDUCES EXCRETION OF 11-DEHYDROTHROMBOXANE -B(2), AN INDEX OF INTRAVASCULAR PRODUCTION OF THROMBOXANE -A(2) SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID OMEGA-3 FATTY-ACIDS; FISH-OIL; EICOSAPENTAENOIC ACID; IMMUNE-RESPONSE; PLATELET; PROSTAGLANDINS; DIET; DISEASE; BALANCE; INVIVO AB We evaluated the effect of anchovy oil supplementation on the endogenous production of thromboxane A2 by measuring the excretion of its stable metabolite, 11-dehydrothromboxane B2 (11-DTXB2), in 24-h urine. In a longitudinal study, 35 male volunteers consumed a controlled basal diet for two experimental periods lasting a total of 20 weeks. During period 1 (10 weeks) the diet was supplemented with placebo (PO) capsules (15 x 1 g/d) consisting of a blend of fats approaching the fatty acid profile of the basal diet. During period 2 the subjects received 15 x 1 g/d capsules of fish oil concentrate (FOC). PO and FOC capsules contained 1 mg alpha-tocopherol per gram of fat as antioxidant. A 38% reduction of 11-DTXB, excretion was observed after 10 weeks of FOC supplementation (period 2, n-6/n-3 PUFA ratio = 2.3), compared to an identical period of PO supplementation (period 1, n-6/n-3 = 12.5), p = 0.0001. The 11-DTXB2 excretion reduction (DELTA) fits the quadratic equation DELTA = 136.0038 - 0.3178(tx1) - 0.0002(tx1)2, (R2 =0.8944), where tx1 is the excretion rate at the end of period 1. This finding supports the hypothesis that the antithrombotic effect of marine oil is mediated, at least in part, by diet-induced shifts in the eicosanoid system. C1 NCI,DIV CANC PREVENT & CONTROL,DHHS,BETHESDA,MD 20892. RP FERRETTI, A (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE HUMAN NUTR RES CTR,LIPID NUTR LAB,ROOM 122,BLDG 308,BELTSVILLE,MD 20705, USA. NR 27 TC 10 Z9 10 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0952-3278 J9 PROSTAG LEUKOTR ESS JI Prostaglandins Leukot. Essent. Fatty Acids PD APR PY 1993 VL 48 IS 4 BP 305 EP 308 DI 10.1016/0952-3278(93)90220-Q PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA KW747 UT WOS:A1993KW74700004 PM 8497491 ER PT J AU MIYAZAWA, S JERNIGAN, RL AF MIYAZAWA, S JERNIGAN, RL TI A NEW SUBSTITUTION MATRIX FOR PROTEIN-SEQUENCE SEARCHES BASED ON CONTACT FREQUENCIES IN PROTEIN STRUCTURES SO PROTEIN ENGINEERING LA English DT Article DE CONTACT ENERGIES; CONTACT FREQUENCIES; HOMOLOGY SEARCH; SEQUENCE COMPARISON; SUBSTITUTION MATRIX ID AMINO-ACID SEQUENCES; HYDROPHOBICITY; SIMILARITY AB The instabilities of the native structures of mutant proteins with an amino acid exchange are estimated by using the contact energy and the number of contacts for each type of amino acid pair, which were estimated from 18 192 residue - residue contacts observed in 42 crystals of globular proteins. They were then used to evaluate a transition probability matrix of codon substitutions and a log relatedness odds matrix, which is used as a scoring matrix to measure the similarity between protein sequences. To consider amino acid substitutions in homologous proteins, base mutation rates and the effects of the genetic code are also taken into account. The average fitness of an amino acid exchange is approximated to be proportional to the structural stability of the mutant protein, which is then approximated by the average energy change of the protein native structure expected for the amino acid exchange with neglect of the energy change of the denatured state. In global and local homology searches, this scoring matrix tends to yield significantly higher alignment scores than either the unitary matrix or the genetic code matrix, and also may yield higher alignment scores for distantly related protein pairs than MDM78. One of advantages of this scoring matrix is that the equilibrium frequencies of codons and also base mutation rates can be adjusted. C1 NCI,BETHESDA,MD 20892. RP MIYAZAWA, S (reprint author), GUNMA UNIV,FAC TECHNOL,KIRYU,GUNMA 376,JAPAN. RI Jernigan, Robert/A-5421-2012 NR 20 TC 57 Z9 58 U1 0 U2 6 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PD APR PY 1993 VL 6 IS 3 BP 267 EP 278 DI 10.1093/protein/6.3.267 PG 12 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA KZ974 UT WOS:A1993KZ97400004 PM 8506261 ER PT J AU BACHAR, O FISCHER, D NUSSINOV, R WOLFSON, H AF BACHAR, O FISCHER, D NUSSINOV, R WOLFSON, H TI A COMPUTER VISION-BASED TECHNIQUE FOR 3-D SEQUENCE-INDEPENDENT STRUCTURAL COMPARISON OF PROTEINS SO PROTEIN ENGINEERING LA English DT Article DE COMPUTER VISION; 3-D PROTEIN MOTIFS; GEOMETRIC HASHING; PROTEIN FOLDING; PROTEIN STRUCTURAL COMPARISON ID AMINO-ACID SEQUENCE; STRUCTURE ALIGNMENT; BACTERIAL FERREDOXIN; GENERAL METHOD; RECOGNITION; EVOLUTION; TAXONOMY AB A detailed description of an efficient approach to comparison of protein structures is presented. Given the 3-D coordinate data of the structures to be compared, the system automatically identifies every region of structural similarity between the structures without prior knowledge of an initial alignment. The method uses the geometric hashing technique which was originally developed for model-based object recognition problems in the area of computer vision. It exploits a rotationally and translationally invariant representation of rigid objects, resulting in a highly efficient, fully automated tool. The method is independent of the amino acid sequence and, thus, insensitive to insertions, deletions and displacements of equivalent substructures between the molecules being compared. The method described here is general, identifies 'real' 3-D substructures and is not constrained by the order imposed by the primary chain of the amino acids. Typical structure comparison problems are examined and the results of the new method are compared with the published results from previous methods. These results, obtained without using the sequence order of the chains, confirm published structural analogies that use sequence-dependent techniques. Our results also extend previous analogies by detecting geometrically equivalent out-of-sequential-order structural elements which cannot be obtained by current techniques. C1 TEL AVIV UNIV,FAC MED,SACKLER INST MOLEC MED,IL-69978 TEL AVIV,ISRAEL. TEL AVIV UNIV,SCH MATH SCI,DEPT COMP SCI,IL-69978 TEL AVIV,ISRAEL. NCI,FCRF,PRI DYNACORP,MATH BIOL LAB,FREDERICK,MD 21702. NYU,COURANT INST MATH SCI,ROBOT RES LAB,NEW YORK,NY 10012. RI Wolfson, Haim/A-1837-2011 FU NCI NIH HHS [1-CO-74102] NR 31 TC 113 Z9 116 U1 1 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PD APR PY 1993 VL 6 IS 3 BP 279 EP 288 DI 10.1093/protein/6.3.279 PG 10 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA KZ974 UT WOS:A1993KZ97400005 PM 8506262 ER PT J AU PETERKOFSKY, A GOLLOP, N AF PETERKOFSKY, A GOLLOP, N TI THE ESCHERICHIA-COLI ADENYLYL CYCLASE COMPLEX - STIMULATION BY GTP AND OTHER NUCLEOTIDES SO PROTEIN SCIENCE LA English DT Article DE ALLOSTERIC REGULATION; AMPPNP; GTP; NUCLEOTIDES; SIGNAL TRANSDUCTION ID GLUCOSE AB Escherichia coli cells permeabilized by treatment with low concentrations of toluene contain an adenylyl cyclase activity that can be stimulated 3.6-7.6-fold by GTP. The stimulatory effect of GTP is maximal at concentrations of the nucleotide in the physiological range (above 0.7 mM). Studies of the dependence of velocity on substrate (ATP) concentration indicate that the velocity vs. substrate plots are sigmoid in the absence of GTP but hyperbolic in the presence of GTP, suggesting an allosteric regulatory site that can be occupied by either ATP or GTP. Replacement of ATP by AMPPNP as substrate results in velocity vs. substrate plots that are hyperbolic in the absence or presence of GTP, although GTP increases the V(max) by a factor of 2.2; these findings indicate that AMPPNP specifically occupies the substrate site and GTP exclusively occupies the regulatory site. A test of the capacity of other guanine nucleotides to stimulate adenylyl cyclase activity showed that 2'-deoxy-GTP was almost as effective as GTP, but that GDP, GMP, ppGpp, and 3,5'-cGMP were not stimulatory effectors; GTP-gamma-S and GMPPNP stimulated adenylyl cyclase activity but to a lesser degree than did GTP. In addition to the previous indication that ATP can occupy the regulatory site on adenylyl cyclase, it was found that CTP and UTP were potent stimulators. Thus, all the naturally occurring RNA precursor nucleoside triphosphates are capable of stimulating adenylyl cyclase activity. In contrast, PPPi inhibits adenylyl cyclase activity. Additional studies showed that there is only one regulatory site for all the nucleotide stimulators and that the nucleotide occupying the substrate site can influence the properties of the regulatory site. These observations suggest a mechanism by which adenylyl cyclase activity can be regulated by the availability of nucleic acid precursors. RP PETERKOFSKY, A (reprint author), NHLBI,BIOCHEM GENET LAB,BLDG 36,ROOM 4C-11,BETHESDA,MD 20892, USA. NR 16 TC 4 Z9 4 U1 0 U2 1 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 APR PY 1993 VL 2 IS 4 BP 498 EP 505 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV394 UT WOS:A1993KV39400002 PM 8518728 ER PT J AU PELTON, JG TORCHIA, DA MEADOW, ND ROSEMAN, S AF PELTON, JG TORCHIA, DA MEADOW, ND ROSEMAN, S TI TAUTOMERIC STATES OF THE ACTIVE-SITE HISTIDINES OF PHOSPHORYLATED AND UNPHOSPHORYLATED III(GLC), A SIGNAL-TRANSDUCING PROTEIN FROM ESCHERICHIA-COLI, USING 2-DIMENSIONAL HETERONUCLEAR NMR TECHNIQUES SO PROTEIN SCIENCE LA English DT Article DE HISTIDINE TAUTOMER; LOW HISTIDINE PK(A); PHOSPHOENOLPYRUVATE PHOSPHOTRANSFERASE SYSTEM; PHOSPHOHISTIDINE ID NUCLEAR MAGNETIC-RESONANCE; BACTERIAL PHOSPHOTRANSFERASE SYSTEM; HYDROGEN-BONDING INTERACTIONS; ALPHA-LYTIC PROTEASE; L-ALA-OH; PHOSPHOCARRIER PROTEIN; SALMONELLA-TYPHIMURIUM; SUGAR-TRANSPORT; CHEMICAL-SHIFTS; SECONDARY STRUCTURE AB III(Glc) is an 18.1-kDa signal-transducing phosphocarrier protein of the phosphoenolpyruvate:glycose phosphotransferase system from Escherichia coli. The H-1, N-15, and C-13 histidine ring NMR signals of both the phosphorylated and unphosphorylated forms of III(Glc) have been assigned using two-dimensional H-1-N-15 and H-1-C-13 heteronuclear multiple-quantum coherence (HMQC) experiments and a two-dimensional C-13-C-13-H-1 correlation spectroscopy via J(CC) coupling experiment. The data were acquired on uniformly N-15-labeled and uniformly N-15/C-13-labeled protein samples. The experiments rely on one-bond and two-bond J couplings that allowed for assignment of the signals without the need for the analysis of through-space (nuclear Overhauser effect spectroscopy) correlations. The N-15 and C-13 chemical shifts were used to determine that His-75 exists predominantly in the N(epsilon2)-H tautomeric state in both the phosphorylated and unphosphorylated forms of III(Glc), and that His-90 exists primarily in the N(delta1)-H state in the unphosphorylated protein. Upon phosphorylation of the N(epsilon2) nitrogen of His-90, the N(delta1) nitrogen remains protonated, resulting in the formation of a charged phospho-His-90 moiety. The H-1, N-15, and C-13 signals of the phosphorylated and unphosphorylated proteins showed only minor shifts in the pH range from 6.0 to 9.0. These data indicate that the pK(a) values for both His-75 and His-90 in III(Glc) and His-75 in phospho-III(Glc) are less than 5.0, and that the pK(a) value for phospho-His-90 is greater than 10. The results are presented in relation to previously obtained structural data on III(Glc), and implications for proposed mechanisms of phosphoryl transfer are discussed. C1 NIDR,BONE RES BRANCH,BLDG 30,ROOM 106,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,MCCOLLUM PRATT INST,BALTIMORE,MD 21218. FU NIGMS NIH HHS [GM38759] NR 76 TC 260 Z9 261 U1 1 U2 17 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 APR PY 1993 VL 2 IS 4 BP 543 EP 558 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV394 UT WOS:A1993KV39400006 PM 8518729 ER PT J AU DANISHEFSKY, AT HOUSSET, D KIM, KS TAO, F FUCHS, J WOODWARD, C WLODAWER, A AF DANISHEFSKY, AT HOUSSET, D KIM, KS TAO, F FUCHS, J WOODWARD, C WLODAWER, A TI CREVICE-FORMING MUTANTS IN THE RIGID CORE OF BOVINE PANCREATIC TRYPSIN-INHIBITOR - CRYSTAL-STRUCTURES OF F22A, Y23A, N43G, AND F45A SO PROTEIN SCIENCE LA English DT Article DE BPTI; CREVICES; CRYSTAL STRUCTURE; MUTANTS; RIGID CORE ID THERMODYNAMIC STABILITY; ALZHEIMERS-DISEASE; PROTEIN-PRECURSOR; REFINEMENT; DOMAIN; CONFORMATION; DYNAMICS; EXCHANGE; SHOWS AB Crystal structures of four mutants of bovine pancreatic trypsin inhibitor (F22A, Y23A, N43G, and F45A), engineered to alter their stability properties, have been determined. The mutated residues, which are highly conserved among Kunitz-type inhibitors, are located in the rigid core of the molecule. Replacement of the partially buried bulky residues of the wild-type protein with smaller residues resulted in crevices open to the exterior of the molecule. The overall three-dimensional structure of these mutants is very similar to that of the wild-type protein and only small rearrangements are observed among the atoms lining the crevices. C1 UNIV MINNESOTA,DEPT BIOCHEM,ST PAUL,MN 55108. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOLEC STRUCT LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101]; NIGMS NIH HHS [GM26246] NR 39 TC 27 Z9 27 U1 0 U2 0 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 APR PY 1993 VL 2 IS 4 BP 577 EP 587 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV394 UT WOS:A1993KV39400009 PM 8518731 ER PT J AU KIM, KS TAO, F FUCHS, J DANISHEFSKY, AT HOUSSET, D WLODAWER, A WOODWARD, C AF KIM, KS TAO, F FUCHS, J DANISHEFSKY, AT HOUSSET, D WLODAWER, A WOODWARD, C TI CREVICE-FORMING MUTANTS OF BOVINE PANCREATIC TRYPSIN-INHIBITOR - STABILITY CHANGES AND NEW HYDROPHOBIC SURFACE SO PROTEIN SCIENCE LA English DT Article DE BPTI; CRYSTAL STRUCTURE; HYDROGEN EXCHANGE; PROTEIN FOLDING; THERMOSTABILITY ID COLD DENATURATION; THERMODYNAMICS; PARAMETERS; MYOGLOBIN; PROTEINS; KINETICS; EXCHANGE; SOLUTES; WATER; AREA AB Four mutants of bovine pancreatic trypsin inhibitor (BPTI) with replacements in the rigid core result in the creation of deep crevices on the surface of the protein. Other than crevices at the site of the mutation, few other differences are observed in the crystal structures of wild-type BPTI and the mutants F22A, Y23A, N43G, and F45A. These mutants are highly destabilized relative to wild type (WT). The differences between WT and mutants in the free energy change associated with cooperative folding/unfolding, DELTADELTAG0(WT --> mut), have been measured by calorimetry, and they are in good agreement with DELTADELTAG0(WT --> mut) values from hydrogen exchange rates. For F22A the change in free energy difference is about 1.7 kcal/mol at 25-degrees-C; for the other three mutants it is in the range of 5-7 kcal/mol at 25-degrees-C. The experimental DELTADELTAG0(WT --> mut) values of F22A, Y23A, and F45A are reasonably well accounted for as the sum of two terms: the difference in transfer free energy change, and a contribution from exposure to solvent of new surface (Eriksson, A.E., et al., 1992, Science 255, 178-183), if the recently corrected transfer free energies and surface hydrophobicities (De Young, L. & Dill, K., 1990, J. Phys. Chem. 94, 801-809; Sharp, K.A., et al., 1991a, Science 252, 106-109) are used and only nonpolar surface is taken into account. In N43G, three protein-protein hydrogen bonds are replaced by protein-water hydrogen bonds. The value of DELTADELTAG0(WT --> mut) computed from model transfer free energies and surface hydrophobicities is 4.0 kcal/mol less than observed, consistent with reports that one hydrogen bond contributes about 1.3 kcal/mol of stabilizing free energy (Shirley, B.A., et al., 1992, Biochemistry 31, 725-732). C1 UNIV MINNESOTA, DEPT BIOCHEM, ST PAUL, MN 55108 USA. NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MACROMOLEC STRUCT LAB, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N01-CO-74101]; NIGMS NIH HHS [GM26246] NR 40 TC 45 Z9 45 U1 0 U2 1 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 APR PY 1993 VL 2 IS 4 BP 588 EP 596 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV394 UT WOS:A1993KV39400010 PM 7686069 ER PT J AU VENABLE, RM BROOKS, BR CARSON, FW AF VENABLE, RM BROOKS, BR CARSON, FW TI THEORETICAL-STUDIES OF RELAXATION OF A MONOMERIC SUBUNIT OF HIV-1 PROTEASE IN WATER USING MOLECULAR-DYNAMICS SO PROTEINS-STRUCTURE FUNCTION AND GENETICS LA English DT Article DE AIDS; ENERGY MINIMIZATION; ENZYME INHIBITION; MOLECULAR MODELING; PROTEIN CONFORMATION; CROSS-CORRELATION MAP ID IMMUNODEFICIENCY-VIRUS PROTEASE; 3-DIMENSIONAL STRUCTURE; RETROVIRAL PROTEASES; CRYSTAL-STRUCTURE; ESCHERICHIA-COLI; TYPE-1 PROTEASE; RESOLUTION; INHIBITOR; COMPLEX; AIDS AB The dynamic behavior of one 99-residue subunit of the dimeric aspartyl protease of HIV-1 was studied in a 160 psec molecular dynamics simulation at 300 K in water. The crystal structure of one of the identical subunits of the dimer was the starting point, with the aqueous phase modeled by 4,331 explicit waters in a restrained spherical droplet. Analysis of the simulations showed that the monomer displayed considerable flexibility in the interfacial portions of the flap (the region which folds over the substrate), the N- and C-termini, and, to a lesser extent, the active site. The flap undergoes significant motion as an independent rigid finger, but without the cantilever previously reported in a simulation of the dimer. The N-terminus displayed the greatest fluctuational disorder whereas the C-terminus exhibited the greatest root mean square movement from the crystal structure. The central core of the monomer had a heavy-atom root mean square deviation from the initial structure of about 3.0 angstrom during the latter half of the simulation. Although this is larger than the 1.6 A found for comparable simulations of typical globular proteins, the general features of the tertiary structure were preserved over the course of the simulation. Overall, these results indicate that the relaxed structure obtained in these simulations may provide a better model for the tertiary structure of the solvated HIV-1 protease monomer than the subunit conformation seen in the X-ray crystallographic structure of the dimer. Except in the flap region, the design of compounds intended to interfere with dimerization should take this relaxation and the flexibility of the solvated monomer, especially at the termini, into account. C1 NIH,DIV COMP RES & TECHNOL,MOLEC GRAPH & SIMULAT LAB,BETHESDA,MD 20892. AMERICAN UNIV,DEPT CHEM,WASHINGTON,DC 20016. RP VENABLE, RM (reprint author), US FDA,CTR BIOL EVALUAT & RES,BIOPHYS LAB,8800 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [BBCA 1 R15 AI26307-01] NR 46 TC 21 Z9 21 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-3585 J9 PROTEINS JI Proteins PD APR PY 1993 VL 15 IS 4 BP 374 EP 384 DI 10.1002/prot.340150405 PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KT967 UT WOS:A1993KT96700004 PM 8460108 ER PT J AU BARBATO, G MOUL, DE SCHWARTZ, P ROSENTHAL, NE OREN, DA AF BARBATO, G MOUL, DE SCHWARTZ, P ROSENTHAL, NE OREN, DA TI SPONTANEOUS EYE BLINK RATE IN WINTER SEASONAL AFFECTIVE-DISORDER SO PSYCHIATRY RESEARCH LA English DT Article DE DEPRESSION; LIGHT THERAPY; CIRCANNUAL RHYTHMS; TREATMENT; SEX DIFFERENCES ID SCHIZOPHRENIA; INDEPENDENCE; EYEBLINK AB We investigated spontaneous eye-blink rates in 19 drug-free patients with winter seasonal affective disorder (SAD) and 18 normal control subjects. At baseline, there were no significant differences between the two groups (mean +/- SD blink rate: 15 / minute +/- 8 vs. 15 / minute +/- 7). Light therapy (10,000 lux: 1 hour each morning for 1 week) produced no significant change in mean (+/- SD) blink rates either in 10 SAD patients (13/minute +/- 8 vs. 10/minute +/- 7) or in 12 normal control subjects (15/minute +/- 6 vs. 14/minute +/- 6). A post hoc exploratory analysis of the effect of light therapy on premenopausal female subjects (5 patients and 9 control subjects) showed a significant decrease in mean (+/- SD) blink rate in the patients after treatment (17 +/- 6 vs. 12 +/- 8 compared with 15 +/- 7 vs. 16 +/- 5). These results do not support the ideal that an elevated blink rate may be a general biological marker in SAD, but they suggest a possible link between light treatment and mechanisms that regulate blink rate in premenopausal SAD patients. C1 NIMH,CLIN PSYCHOBIOL BRANCH,BLDG 10,RM 4S 239,BETHESDA,MD 20892. NIMH,ENVIRONM PSYCHIAT SECT,BETHESDA,MD 20892. OI Barbato, Giuseppe/0000-0001-6523-5327 NR 29 TC 20 Z9 20 U1 0 U2 1 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 APR PY 1993 VL 47 IS 1 BP 79 EP 85 DI 10.1016/0165-1781(93)90057-N PG 7 WC Psychiatry SC Psychiatry GA LB558 UT WOS:A1993LB55800008 PM 8516420 ER PT J AU GENHART, MJ KELLY, KA COURSEY, RD DATILES, M ROSENTHAL, NE AF GENHART, MJ KELLY, KA COURSEY, RD DATILES, M ROSENTHAL, NE TI EFFECTS OF BRIGHT LIGHT ON MOOD IN NORMAL ELDERLY WOMEN SO PSYCHIATRY RESEARCH LA English DT Article DE AGING; PHOTOTHERAPY; SEASONALITY; SLEEP ID SEASONAL AFFECTIVE-DISORDER; PHOTOTHERAPY; DEPRESSION; EXPOSURE; PATIENT; THERAPY; CYCLE AB Reduced light appears to be a key factor in seasonal affective disorder (SAD). This study asks whether the reduced levels of light experienced by elderly persons might result in depression and other SAD symptoms, and how normal elderly persons might respond to bright light interventions similar to those used to treat SAD. In interviews with 140 senior citizens, we found virtually no seasonal variation in mood and behavior and very little depressed affect. Seventeen of these seniors who had good mental and physical health, with no major eye problems, participated in a crossover study of the effects of bright light on both positive and negative affect and sleep. Although sleep did not appear to be affected, the bright light intervention tended to make these normal elderly persons feel worse-more irritable, anxious, and agitated. These findings confirm earlier reports that bright light is not beneficial for normal individuals who are unaffected by seasonal changes. C1 NIMH,OUTPATIENT SERV UNIT,RM 4S 239,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. CALIF PACIFIC MED CTR,CTR ADOLESCENT DAY TREATMENT,SAN FRANCISCO,CA. UNIV MARYLAND,DEPT PSYCHOL,COLL PK,MD 20742. NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892. NEI,CATARACT & CORNEA SECT,BETHESDA,MD 20892. OI Datiles, Manuel III B./0000-0003-4660-1664 NR 43 TC 24 Z9 24 U1 2 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 APR PY 1993 VL 47 IS 1 BP 87 EP 97 DI 10.1016/0165-1781(93)90058-O PG 11 WC Psychiatry SC Psychiatry GA LB558 UT WOS:A1993LB55800009 PM 8516421 ER PT J AU MINER, LL ELMER, GI PIEPER, JO MARLEY, RJ AF MINER, LL ELMER, GI PIEPER, JO MARLEY, RJ TI AGGRESSION MODULATES GENETIC INFLUENCES ON MORPHINE ANALGESIA AS ASSESSED USING A CLASSICAL MENDELIAN CROSS ANALYSIS SO PSYCHOPHARMACOLOGY LA English DT Article DE ANALGESIA; AGGRESSION; MORPHINE; PHARMACOGENETICS ID DBA/2 MICE; MOUSE; TOLERANCE; SENSITIVITY AB Pharmacogenetic techniques allow for the examination of genetic and environmental factors underlying phenotypes associated with drug response. Initial studies of mice bred at Jackson Laboratories (JAX) indicated that C57BL/6J mice were more sensitive to morphine-induced analgesia, as measured by latency to paw lick, than SJL/J mice. A classical Mendelian cross breeding program was initiated in which F1, F2 and backcross generations were derived from C57BL/6J and SJL/J breeding pairs purchased from JAX to examine the genetic factors underlying morphine analgesia. Genetic analysis indicated significant dominance or heterosis for a reduced drug response. The F1 generation was less sensitive to morphine-induced analgesia than either parental strain. Mathematical analysis of the generation means revealed that a simple dominance model with no epistatic interaction between genes best described the data. Environmental factors also affected sensitivity to morphine analgesia, in that C57BL and SJL mice raised in our facility did not differ in latency to paw lick. SJL mice from JAX exhibit a high degree of aggression, while SJL mice raised in our facilities show little or no aggression. The levels of aggression among groups of SJL mice were characterized and found to correlate with sensitivity to morphine analgesia. Mice exposed to increasingly greater levels of aggression were the least sensitive to morphine. Thus, the changes observed in sensitivity to morphine-induced analgesia appear to be related to the degree of aggression to which these mice are exposed, possibly resulting from the stress and/or prolonged exposure to painful stimuli associated with aggressive encounters. RP MINER, LL (reprint author), NIDA,ADDICT RES CTR,BEHAV PHARMACOL & GENET LAB,BOX 5180,BALTIMORE,MD 21224, USA. NR 24 TC 11 Z9 11 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD APR PY 1993 VL 111 IS 1 BP 17 EP 22 DI 10.1007/BF02257401 PG 6 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA KV797 UT WOS:A1993KV79700002 PM 7870928 ER PT J AU OLDEN, K AF OLDEN, K TI ENVIRONMENTAL-HEALTH SCIENCE RESEARCH AND HUMAN RISK ASSESSMENT SO REGULATORY TOXICOLOGY AND PHARMACOLOGY LA English DT Article C1 NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. RP OLDEN, K (reprint author), NATL INST ENVIRONM HLTH SCI,OFF DIRECTOR,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 1 Z9 1 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 0273-2300 J9 REGUL TOXICOL PHARM JI Regul. Toxicol. Pharmacol. PD APR PY 1993 VL 17 IS 2 BP 230 EP 233 DI 10.1006/rtph.1993.1021 PN 1 PG 4 WC Medicine, Legal; Pharmacology & Pharmacy; Toxicology SC Legal Medicine; Pharmacology & Pharmacy; Toxicology GA KY664 UT WOS:A1993KY66400010 PM 8484031 ER PT J AU ZAHM, SH WEISENBURGER, DD CANTOR, KP HOLMES, FF BLAIR, A AF ZAHM, SH WEISENBURGER, DD CANTOR, KP HOLMES, FF BLAIR, A TI ROLE OF THE HERBICIDE ATRAZINE IN THE DEVELOPMENT OF NON-HODGKINS-LYMPHOMA SO SCANDINAVIAN JOURNAL OF WORK ENVIRONMENT & HEALTH LA English DT Article DE AGRICULTURE; CANCER; CASE-REFERENT STUDY; EPIDEMIOLOGY; HERBICIDES; OCCUPATION; TRIAZINES ID SOFT-TISSUE SARCOMA; DIAGNOSES; LEUKEMIA; CANCER; RISK AB Atrazine is the most commonly used herbicide in the United States and is a widespread groundwater contaminant in the Midwest. The role of atrazine in the development of human non-Hodgkin's lymphoma (NHL) was investigated in three case-referent studies conducted in four midwestern states in the United States. A total of 993 white men with NHL and 2918 population-based referents were interviewed concerning their agricultural practices. When the results of the three studies were combined, atrazine use was associated with an odds ratio of 1.4 [95% confidence interval (95% CI) 1.1-1.8, 130 cases, 249 referents) for NHL. However, adjustments for the use of 2,4-dichlorophenoxyacetic acid and organophosphate insecticides reduced the apparent association between NHL and atrazine in all but one state and reduced the associations for the long-term and frequent users in Nebraska. Detailed analyses suggested that there was little or no increase in the risk of NHL attributable to the agricultural use of atrazine. C1 UNIV KANSAS,MED CTR,CANC DATA SERV,KANSAS CITY,KS 66103. UNIV NEBRASKA,MED CTR,DEPT PATHOL & MICROBIOL,OMAHA,NE 68105. RP ZAHM, SH (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,OCCUPAT STUDIES SECT,EXECUT PLAZA N,ROOM 418,ROCKVILLE,MD 20892, USA. RI Zahm, Shelia/B-5025-2015 NR 32 TC 38 Z9 38 U1 2 U2 4 PU SCAND J WORK ENV HEALTH PI HELSINKI PA TOPELIUKSENKATU 41A, SF-00250 HELSINKI, FINLAND SN 0355-3140 J9 SCAND J WORK ENV HEA JI Scand. J. Work Environ. Health PD APR PY 1993 VL 19 IS 2 BP 108 EP 114 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LB912 UT WOS:A1993LB91200006 ER PT J AU RICHARDSON, GE JOHNSON, BE AF RICHARDSON, GE JOHNSON, BE TI THE BIOLOGY OF LUNG-CANCER SO SEMINARS IN ONCOLOGY LA English DT Review ID HUMAN SMALL-CELL; EPIDERMAL GROWTH-FACTOR; GASTRIN-RELEASING PEPTIDE; NEOPLASTIC CEREBELLAR DEGENERATION; EATON MYASTHENIC SYNDROME; NEURON-SPECIFIC ENOLASE; RETINOBLASTOMA SUSCEPTIBILITY GENE; K-RAS ONCOGENE; BRONCHIAL EPITHELIAL-CELLS; BOMBESIN-LIKE PEPTIDES C1 UNIFORMED SERV UNIV HLTH SCI,DEPT MED,NCI,CLIN ONCOL PROGRAM,USN,MED ONCOL BRANCH,BETHESDA,MD 20814. RP RICHARDSON, GE (reprint author), USN,NATL MED CTR,MED ONCOL BRANCH,NCI,BLDG 8,ROOM 5015,BETHESDA,MD 20889, USA. NR 395 TC 117 Z9 119 U1 1 U2 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD APR PY 1993 VL 20 IS 2 BP 105 EP 127 PG 23 WC Oncology SC Oncology GA KX472 UT WOS:A1993KX47200002 PM 8480184 ER PT J AU FEIGAL, EG CHRISTIAN, M CHESON, B GREVER, M FRIEDMAN, MA AF FEIGAL, EG CHRISTIAN, M CHESON, B GREVER, M FRIEDMAN, MA TI NEW CHEMOTHERAPEUTIC-AGENTS IN NON-SMALL-CELL LUNG-CANCER SO SEMINARS IN ONCOLOGY LA English DT Review ID PHASE-I TRIAL; EVERY 21 DAYS; ANTITUMOR-ACTIVITY; TOPOISOMERASE-I; 10-DEAZA-AMINOPTERIN SERIES; FOLATE ANALOGS; STAGE-III; TAXOL; CAMPTOTHECIN; NAVELBINE C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. RP FEIGAL, EG (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,INVEST DRUG BRANCH,CLIN INVEST BRANCH,BETHESDA,MD 20892, USA. NR 113 TC 54 Z9 54 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD APR PY 1993 VL 20 IS 2 BP 185 EP 201 PG 17 WC Oncology SC Oncology GA KX472 UT WOS:A1993KX47200008 PM 7683142 ER PT J AU YEWDELL, JW ANDERSON, R COX, JH EISENLOHR, LC ESQUIVEL, F LAPHAM, C RESTIFO, NP BENNINK, JR AF YEWDELL, JW ANDERSON, R COX, JH EISENLOHR, LC ESQUIVEL, F LAPHAM, C RESTIFO, NP BENNINK, JR TI THE MULTIPLE USES OF VIRUSES FOR STUDYING ANTIGEN PROCESSING SO SEMINARS IN VIROLOGY LA English DT Article DE ANTIGEN PROCESSING; CELLULAR IMMUNITY; CYTOTOXIC T-LYMPHOCYTES; VACCINIA VIRUS; MHC CLASS-I MOLECULES ID TOXIC LYMPHOCYTES-T; RECOMBINANT VACCINIA VIRUS; CLASS-II REGION; INFLUENZA-VIRUS; INFECTED-CELLS; ENDOPLASMIC-RETICULUM; PROTEIN-SYNTHESIS; HUMAN CYTOMEGALOVIRUS; BETA-2 MICROGLOBULIN; TARGET-CELLS C1 NIAID, SURG BRANCH, BETHESDA, MD 20892 USA. RP YEWDELL, JW (reprint author), NIAID, VIRAL DIS LAB, BETHESDA, MD 20892 USA. RI Restifo, Nicholas/A-5713-2008; yewdell, jyewdell@nih.gov/A-1702-2012; OI Restifo, Nicholas P./0000-0003-4229-4580 NR 66 TC 4 Z9 4 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1044-5773 J9 SEMIN VIROL JI Semin. Virol. PD APR PY 1993 VL 4 IS 2 BP 109 EP 116 DI 10.1006/smvy.1993.1005 PG 8 WC Virology SC Virology GA KX298 UT WOS:A1993KX29800005 ER PT J AU HUNDT, GAL FORMAN, MR AF HUNDT, GAL FORMAN, MR TI INTERFACING ANTHROPOLOGY AND EPIDEMIOLOGY - THE BEDOUIN ARAB INFANT-FEEDING STUDY SO SOCIAL SCIENCE & MEDICINE LA English DT Article DE INTERDISCIPLINARY; TRIANGULATION OF DATA; GROWTH; BREAST-FEEDING AB This paper encapsulates a 10 year effort of multi-disciplinary research on the relationship between infant feeding, growth, and morbidity among the Negev Bedouin Arabs of Israel as they underwent a transition from semi-nomadism to urban settlement. The research team was multi-disciplinary including a nutritional epidemiologist and an anthropologist who both came to the study with previous experience in interdisciplinary work. The specific study objectives were (1) a description of infant feeding practices among Negev Bedouin Arab women at various stages of settlement, (2) an examination of the trend in these infant feeding practices, (3) a comparison of the extent to which different infant feeding practices are related to infant morbidity and growth after adjustment for exposure to social change and other covariates. The data collection took place in 1981-83 and the analysis from 1984-88. In this paper, two areas of the study are discussed in depth: the duration of exclusive breast feeding during the practice of the traditional postpartum 40 day rest period, and the development of a culture-specific scale of socioeconomic status. Through these examples, we highlight the use of ethnographic data and the merging of epidemiology and anthropology from hypothesis generation through data collection, data analysis and interpretation. C1 NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT RES PROGRAM,BETHESDA,MD 20892. RP HUNDT, GAL (reprint author), UNIV BIRMINGHAM,DEPT SOCIAL WORK & SOCIAL POLICY,BIRMINGHAM B15 2TT,W MIDLANDS,ENGLAND. NR 23 TC 13 Z9 13 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0277-9536 J9 SOC SCI MED JI Soc. Sci. Med. PD APR PY 1993 VL 36 IS 7 BP 957 EP 964 PG 8 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA KU282 UT WOS:A1993KU28200013 PM 8480241 ER PT J AU GROSS, CE BEDNAR, MM HOWARD, DB SPORN, MB AF GROSS, CE BEDNAR, MM HOWARD, DB SPORN, MB TI TRANSFORMING GROWTH-FACTOR-BETA-1 REDUCES INFARCT SIZE AFTER EXPERIMENTAL CEREBRAL-ISCHEMIA IN A RABBIT MODEL SO STROKE LA English DT Article DE CEREBRAL ISCHEMIA; TRANSFORMING GROWTH FACTORS; RABBITS ID FACTOR-BETA; BLOOD-FLOW; POLYMORPHONUCLEAR LEUKOCYTES; NEUTROPHILS; STIMULATION; INDUCTION; CLEARANCE; RAT AB Background and Purpose: The aim of this study was to examine the effect of transforming growth factor-beta1, a cytokine shown to amelioriate cardiac ischemia, in a rabbit model of thromboembolic stroke. Methods: An autologous clot embolus was introduced intracranially through the right internal carotid artery in 21 New Zealand White rabbits, with seven in each group receiving either vehicle control (albumin) or 10 or 50 mug transforming growth factor-beta1 administered as an intracarotid bolus immediately before autologous clot embolization. Multiple physiological parameters were monitored, including regional cerebral blood flow, arterial blood gases, hematocrit, glucose, core temperature, and mean arterial pressure. The brain was harvested 4 hours after embolization, and infarct size was determined planimetrically as a percentage of the entire hemisphere. Results: Brain infarct size was reduced in both the 10-mug (16.7+/-4.0% [mean +/- SEM], p < 0.05) and 50-mug (21.7+/-4.5%) transforming growth factor-beta1-treated groups when compared with the control group (31.9+/-6.6%). Regional cerebral blood flow did not show any significant intergroup or intragroup variation over time, although the 10-mug transforming growth factor-beta1 group experienced a greater return of cerebral blood flow in the first 2 hours after embolization. Conclusions: Transforming growth factor-beta1 reduced brain infarct size in a rabbit model of thromboembolic stroke. This effect was not related to a direct effect on blood flow. Studies are ongoing to determine the mechanism by which transforming growth factor-beta1 salvages ischemic brain. C1 UNIV VERMONT,DEPT MED BIOSTAT,BURLINGTON,VT 05401. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. RP GROSS, CE (reprint author), UNIV VERMONT,VERMONT CTR VASC RES,DIV NEUROSURG,1 S PROSPECT ST,BURLINGTON,VT 05401, USA. NR 26 TC 121 Z9 132 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD APR PY 1993 VL 24 IS 4 BP 558 EP 562 PG 5 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA KV419 UT WOS:A1993KV41900009 PM 8465363 ER PT J AU HURD, YL HERKENHAM, M AF HURD, YL HERKENHAM, M TI MOLECULAR ALTERATIONS IN THE NEOSTRIATUM OF HUMAN COCAINE ADDICTS SO SYNAPSE LA English DT Article DE ADDICTION; OPIOIDS; DOPAMINE; SUBSTANCE-P; INSITU HYBRIDIZATION; OPIATE RECEPTORS ID H-3 MAZINDOL AUTORADIOGRAPHY; GLUTAMIC-ACID DECARBOXYLASE; NUCLEUS-ACCUMBENS; RAT-BRAIN; MESSENGER-RNAS; SUBSTANCE-P; INVIVO MICRODIALYSIS; DOPAMINE SYNTHESIS; VENTRAL PALLIDUM; OPIATE RECEPTORS AB Molecular changes in the neostriatum of human subjects who died with a history of cocaine abuse were revealed in discrete cell populations by means of the techniques of in situ hybridization histochemistry and in vitro receptor binding and autoradiography. Cocaine subjects had a history of repeated cocaine use and had cocaine and/or cocaine metabolites on board at the time of death. These subjects were compared to control subjects that had both a negative history and toxicology of cocaine use. Selective alterations in mRNA levels of striatal neuropeptides were detected in cocaine subjects compared to control subjects, especially for the opioid peptides. Marked reductions in the levels of enkephalin mRNA and mu opiate receptor binding were found in the caudate and putamen, concomitant with elevations in levels of dynorphin mRNA and kappa opiate receptor binding in the putamen and caudate, respectively. Dopamine uptake site binding was reduced in the caudate and putamen of cocaine subjects. The greater magnitude of changes in the dorsolateral striatum (caudate and putamen) as opposed to the ventromedial striatum (nucleus accumbens) suggests that cocaine abuse preferentially alters the biosynthetic activity of striatal systems associated with sensorimotor functioning. Additionally, an imbalance in the activity of the two major striatal output pathways in cocaine users is implicated because peptide mRNA levels were reduced in enkephalinergic striatopallidal neurons and increased in dynorphinergic striatonigral neurons. Another imbalance, that of reductions of transmitter mRNA and receptor expression associated with euphoria (enkephalin and mu opiate receptors), together with elevations in mRNAs of transmitter systems associated with dysphoria (dynorphin and kappa opiate receptors), suggests a model of dysphoria and craving in the human cocaine addict brain. C1 NIMH,FUNCT NEUROANAT SECT,BETHESDA,MD 20892. OI Herkenham, Miles/0000-0003-2228-4238 NR 81 TC 237 Z9 239 U1 3 U2 11 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 APR PY 1993 VL 13 IS 4 BP 357 EP 369 DI 10.1002/syn.890130408 PG 13 WC Neurosciences SC Neurosciences & Neurology GA KV343 UT WOS:A1993KV34300007 PM 7683144 ER PT J AU HORNE, MK AF HORNE, MK TI THE EFFECT OF SECRETED HEPARIN-BINDING PROTEINS ON HEPARIN-BINDING TO PLATELETS SO THROMBOSIS RESEARCH LA English DT Article DE HEPARIN; PLATELETS; PLATELET FACTOR-IV ID FACTOR-4 AB Heparin is known to bind to activated platelets at two classes of sites. However, the true affinities of these sites for heparin have been uncertain because the measurements have been made in the presence of heparin-binding proteins secreted by the platelets. Of these proteins platelet factor-4 (PF4) has the greatest affinity for heparin and is present in relatively high concentrations. Furthermore, a portion of the secreted PF4 binds to the platelet surface. Nevertheless, by gel-filtering platelets in the presence of 5 mug/ml heparin , we prepared platelets that were virtually free of PF4. The high and low affinities of these cells for heparin were respectively ten- and two-fold greater than the apparent affinities measured in the presence of the secreted platelet proteins. In contrast, neither the high- nor the low-affinity heparin binding capacity of these cells was altered, indicating that PF4, even though it binds to both heparin and platelets, appears not to link heparin to platelets. RP HORNE, MK (reprint author), NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT CLIN PATHOL,HEMATOL SECT,BETHESDA,MD 20892, USA. NR 13 TC 16 Z9 16 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0049-3848 J9 THROMB RES JI Thromb. Res. PD APR 1 PY 1993 VL 70 IS 1 BP 91 EP 98 PG 8 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA KZ153 UT WOS:A1993KZ15300006 PM 8511754 ER PT J AU ANDERSON, YB JACKSON, JA BIRNBAUM, LS AF ANDERSON, YB JACKSON, JA BIRNBAUM, LS TI MATURATIONAL CHANGES IN DERMAL ABSORPTION OF 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (TCDD) IN FISCHER 344 RATS SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID SKIN; ADULT C1 NIEHS,EXPTL TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. RP ANDERSON, YB (reprint author), US EPA,HLTH EFFECTS RES LAB,DIV ENVIRONM TOXICOL,MD 51,RES TRIANGLE PK,NC 27711, USA. NR 20 TC 18 Z9 18 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 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD APR PY 1993 VL 119 IS 2 BP 214 EP 220 DI 10.1006/taap.1993.1062 PG 7 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA KY218 UT WOS:A1993KY21800007 PM 8480330 ER PT J AU STORM, SM RAPP, UR AF STORM, SM RAPP, UR TI ONCOGENE ACTIVATION - C-RAF-1 GENE-MUTATIONS IN EXPERIMENTAL AND NATURALLY-OCCURRING TUMORS SO TOXICOLOGY LETTERS LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON APPROACHES FOR THE IDENTIFICATION OF LESIONS RELEVANT IN CARCINOGENESIS CY JUN 18-20, 1992 CL UNIV WURZBURG, INST PHARM & TOXICOL, WURZBURG, GERMANY HO UNIV WURZBURG, INST PHARM & TOXICOL DE ONCOGENE; RAF; POINT MUTATION; LUNG TUMOR; LYMPHOMA ID CELL LUNG-CANCER; RAS ONCOGENES; POINT MUTATIONS; CARCINOMA; MOUSE; MICE; DNA; 1-ETHYL-1-NITROSOUREA; CARCINOGENESIS; AMPLIFICATION AB We demonstrate here consistent point mutations of the c-raf-1 proto-oncogene, within a small region of the kinase domain, in a mouse model for chemical tumor induction. This is the first demonstration of point mutated raf genes in vivo, and the first isolation of activating in vivo point mutations in the kinase domain of a proto-oncogene. The specific region where these mutations are clustered also has biological significance. This is precisely the region where 5/5 independently generated monoclonal antibodies raised against Raf-I map to [29], and predictions based upon the crystal structure of A kinase identify this as the substrate pocket. The tumors examined show a selective specificity for Raf-1 mutations in that another family of genes, the ras proto-oncogenes which are frequently activated by point mutation in both animal and human tumors [I 5-21,26], is not involved. Our consistent finding of Raf-1 mutations in a mouse tumor model also has consequences for further evaluation of the role of Raf-I in human tumor development, as it emphasizes the need to examine c-raf-I at the sequence level. In fact preliminary screening of human lung tumors indicates point mutations at amino acid 533 (John Lyons, personal communication). Finally, the cumulative data on the critical role of Raf-1 in signal transduction and the occurrence of oncogenic Raf-1 in tumors [32-41] highlight this enzyme as an attractive target for development of novel anticancer regimens. C1 FREDERICK CANC RES & DEV CTR,FREDERICK,MD. NR 41 TC 44 Z9 45 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0378-4274 J9 TOXICOL LETT JI Toxicol. Lett. PD APR PY 1993 VL 67 IS 1-3 BP 201 EP 210 DI 10.1016/0378-4274(93)90056-4 PG 10 WC Toxicology SC Toxicology GA KU597 UT WOS:A1993KU59700016 PM 8451761 ER PT J AU RUNGER, TM SOBOTTA, P DEKANT, B MOLLER, K BAUER, C KRAEMER, KH AF RUNGER, TM SOBOTTA, P DEKANT, B MOLLER, K BAUER, C KRAEMER, KH TI INVIVO ASSESSMENT OF DNA LIGATION EFFICIENCY AND FIDELITY IN CELLS FROM PATIENTS WITH FANCONIS ANEMIA AND OTHER CANCER-PRONE HEREDITARY DISORDERS SO TOXICOLOGY LETTERS LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON APPROACHES FOR THE IDENTIFICATION OF LESIONS RELEVANT IN CARCINOGENESIS CY JUN 18-20, 1992 CL UNIV WURZBURG, INST PHARM & TOXICOL, WURZBURG, GERMANY HO UNIV WURZBURG, INST PHARM & TOXICOL DE HOST CELL DNA LIGATION ASSAY; CHROMOSOME INSTABILITY; FANCONIS ANEMIA; BLOOMS SYNDROME; ATAXIA TELANGIECTASIA; WERNER SYNDROME; DYSPLASTIC NEVUS SYNDROME ID BLOOMS SYNDROME CELLS; DOUBLE-STRAND BREAKS; ATAXIA-TELANGIECTASIA; LIGASE-I; PLASMID DNA; GENE; FIBROBLASTS; MUTAGENESIS; FREQUENCY; MELANOMA AB We developed a host cell DNA ligation assay, in which we transfected linearized plasmid pZ 1 89 into human lymphoblasts or fibroblasts in order to assess the efficiency and accuracy of DNA ligation within these host cells. We used cell lines from patients with Fanconi's anemia and other chromosome breakage or instability syndromes (Bloom's syndrome, ataxia telangiectasia, Werner's syndrome). With the Fanconi's anemia lymphoblast line GM8010 we did not find a reduced, but a slightly hypermutable DNA ligation. Mutation analysis revealed a unique 7.9-12.5-fold increase in insertions or complex mutations. With cells from the other chromosome breakage/instability syndromes we also found a hypermutable and/or reduced DNA ligation. An impaired DNA ligation might be a common molecular mechanism of genetic instability in these disorders. C1 NCI,BETHESDA,MD 20892. RP RUNGER, TM (reprint author), UNIV WURZBURG,HAUTKRANKHEITEN KLINIK & POLIKLIN,JOSEF SCHNEIDER STR 2,W-8700 WURZBURG,GERMANY. FU Intramural NIH HHS [Z01 BC004517-31] NR 46 TC 13 Z9 13 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0378-4274 J9 TOXICOL LETT JI Toxicol. Lett. PD APR PY 1993 VL 67 IS 1-3 BP 309 EP 324 DI 10.1016/0378-4274(93)90064-5 PG 16 WC Toxicology SC Toxicology GA KU597 UT WOS:A1993KU59700024 PM 8451768 ER PT J AU MURPHY, BR AF MURPHY, BR TI IMMUNOGEN-INDUCED ENHANCED PULMONARY HISTOPATHOLOGY IN THE RSV COTTON RAT MODEL - REPLY SO VACCINE LA English DT Letter ID SYNCYTIAL VIRUS RSV; IMMUNIZATION; GLYCOPROTEIN RP MURPHY, BR (reprint author), NIAID,DEPT HLTH & HUMAN SERV,RESP VIRUSES SECT,BETHESDA,MD 20892, USA. NR 6 TC 2 Z9 2 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0264-410X J9 VACCINE JI Vaccine PD APR PY 1993 VL 11 IS 6 BP 690 EP 691 PG 2 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA LA165 UT WOS:A1993LA16500020 ER PT J AU KARACOSTAS, V WOLFFE, EJ NAGASHIMA, K GONDA, MA MOSS, B AF KARACOSTAS, V WOLFFE, EJ NAGASHIMA, K GONDA, MA MOSS, B TI OVEREXPRESSION OF THE HIV-1 GAG-POL POLYPROTEIN RESULTS IN INTRACELLULAR ACTIVATION OF HIV-1 PROTEASE AND INHIBITION OF ASSEMBLY AND BUDDING OF VIRUS-LIKE PARTICLES SO VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; RECOMBINANT VACCINIA VIRUS; MURINE LEUKEMIA-VIRUS; ROUS-SARCOMA VIRUS; EXPRESSION SYSTEM; GENE-PRODUCTS; TYPE-1; PRECURSOR; VECTOR; MATURATION C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,CELL & MOLEC STRUCT LAB & DEV CTR,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74102] NR 40 TC 162 Z9 164 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 APR PY 1993 VL 193 IS 2 BP 661 EP 671 DI 10.1006/viro.1993.1174 PG 11 WC Virology SC Virology GA KT924 UT WOS:A1993KT92400011 PM 7681610 ER PT J AU MORIKAWA, S UEDA, Y AF MORIKAWA, S UEDA, Y TI CHARACTERIZATION OF VACCINIA SURFACE-ANTIGEN EXPRESSED BY RECOMBINANT BACULOVIRUS SO VIROLOGY LA English DT Article ID VIRUS; IDENTIFICATION; SEQUENCE; RECEPTOR; PROTEIN; INTERLEUKIN-1; PURIFICATION; CELLS C1 NIH,DEPT VIROL 1,1-23-1 TOYAMA,SHINJUKU KU,BETHESDA,MD 20892. NIH,DEPT VIROL 2,BETHESDA,MD 20892. NR 29 TC 15 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1993 VL 193 IS 2 BP 753 EP 761 DI 10.1006/viro.1993.1184 PG 9 WC Virology SC Virology GA KT924 UT WOS:A1993KT92400021 PM 8460484 ER PT J AU QUEZADO, ZMN HOFFMAN, WD AF QUEZADO, ZMN HOFFMAN, WD TI THERAPIES DIRECTED AGAINST ENDOTOXIN - HAS THE TIME COME SO WESTERN JOURNAL OF MEDICINE LA English DT Editorial Material ID TUMOR-NECROSIS-FACTOR; HUMAN SEPTIC SHOCK; ANTIBODY; TRIAL RP QUEZADO, ZMN (reprint author), NIH,DIV CRIT CARE MED,BETHESDA,MD 20892, USA. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 14 TC 0 Z9 0 U1 0 U2 0 PU CALIFORNIA PHYSICIAN MAGAZINE PI SAN FRANCISCO PA C/O DONNA TAYLOR, EDITOR, PO BOX 7690, SAN FRANCISCO, CA 94102-7690 SN 0093-0415 J9 WESTERN J MED JI West. J. Med. PD APR PY 1993 VL 158 IS 4 BP 424 EP 425 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KX277 UT WOS:A1993KX27700022 PM 8317138 ER PT J AU YUAN, JH GOEHL, TJ MURRILL, E MOORE, R CLARK, J HONG, L IRWIN, R AF YUAN, JH GOEHL, TJ MURRILL, E MOORE, R CLARK, J HONG, L IRWIN, R TI TOXICOKINETICS OF PENTACHLOROANISOLE IN F344 RATS AND B6C3F1 MICE SO XENOBIOTICA LA English DT Article ID PENTACHLOROPHENOL; METABOLISM AB 1. Toxicokinetics of pentachloroanisole (PCA) were studied in F344 rat and B6C3F1 mouse of both sexes by gavage at doses of 10, 20 and 40 mg/kg and by i.v. at 10 mg/kg. 2. PCA was rapidly demethylated to pentachlorophenol (PCP) in both rat and mouse and the resulting PCP plasma concentrations were much higher than that of parent PCA due to the much smaller apparent volume of distribution of PCP. 3. Peak plasma concentrations of PCA and PCP increased with dose in both rat and mouse. 4. Bioavailability of PCA was low in both rat and mouse and was sex independent. 5. The high plasma concentrations and relatively long biological half-life of PCP in both species after both i.v. and oral dosing with PCA indicate possible bioaccumulation of PCP upon multiple oral administrations of PCA. C1 MIDWEST RES INST,KANSAS CITY,MO 64110. RP YUAN, JH (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 20 TC 5 Z9 5 U1 1 U2 3 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0049-8254 J9 XENOBIOTICA JI Xenobiotica PD APR PY 1993 VL 23 IS 4 BP 427 EP 438 PG 12 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA LF876 UT WOS:A1993LF87600010 PM 8337901 ER PT J AU WEINSTOCK, KG STRATHERN, JN AF WEINSTOCK, KG STRATHERN, JN TI MOLECULAR-GENETICS IN SACCHAROMYCES-KLUYVERI - THE HIS3 HOMOLOG AND ITS USE AS A SELECTABLE MARKER GENE IN S-KLUYVERI AND SACCHAROMYCES-CEREVISIAE SO YEAST LA English DT Article DE SACCHAROMYCES-KLUYVERI; HIS3 ID CELL-CELL RECOGNITION; NUCLEOTIDE-SEQUENCE; CONSTITUTIVE TRANSCRIPTION; MATING PHEROMONES; ESCHERICHIA-COLI; DNA-MOLECULES; ALPHA-FACTOR; YEAST; PROMOTER; STRAINS AB We cloned the Saccharomyces kluyveri HIS3 homolog, k-HIS3, and made a partial deletion of the gene. The k-HIS3 gene complemented a HIS3 deletion in S. cerevisiae. The DNA sequences of the open reading frames (ORFs) of the HIS3 homologs are 70% identical at the DNA level and 83% identical at the deduced amino acid level. The ORF upstream of the k-HIS3 gene is related to the PET56 gene of S. cerevisiae found upstream of the HIS3 gene of S. cerevisiae. The ORF downstream from the k-HIS3 gene is not related to the DED1 gene found downstream of the HIS3 gene in S. cerevisiae. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,EUKARYOTIC GENE EXPRESS LAB,POB B,FREDERICK,MD 21702. NR 47 TC 25 Z9 29 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0749-503X J9 YEAST JI Yeast PD APR PY 1993 VL 9 IS 4 BP 351 EP 361 DI 10.1002/yea.320090405 PG 11 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology GA LA170 UT WOS:A1993LA17000004 PM 8511965 ER PT J AU GONZALEZ, P RAO, PV ZIGLER, JS AF GONZALEZ, P RAO, PV ZIGLER, JS TI MOLECULAR-CLONING AND SEQUENCING OF ZETA-CRYSTALLIN QUINONE REDUCTASE CDNA FROM HUMAN LIVER SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID GUINEA-PIG; LENS; PROTEIN; DEHYDROGENASES RP GONZALEZ, P (reprint author), NEI,MECHANISMS OCULAR DIS LAB,BETHESDA,MD 20892, USA. NR 11 TC 30 Z9 32 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 MAR 31 PY 1993 VL 191 IS 3 BP 902 EP 907 DI 10.1006/bbrc.1993.1302 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KV405 UT WOS:A1993KV40500020 PM 8466529 ER PT J AU LIAO, F SHIN, HS RHEE, SG AF LIAO, F SHIN, HS RHEE, SG TI INVITRO TYROSINE PHOSPHORYLATION OF PLC-GAMMA-1 AND PLC-GAMMA-2 BY SRC-FAMILY PROTEIN TYROSINE KINASES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PHOSPHOLIPASE-C-GAMMA; CELL ANTIGEN RECEPTOR; GROWTH-FACTOR RECEPTOR; LYMPHOCYTES-B; C-GAMMA-1; PDGF; STIMULATION; ASSOCIATION; SUBSTRATE; RESIDUES C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RP LIAO, F (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205, USA. NR 37 TC 84 Z9 84 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 31 PY 1993 VL 191 IS 3 BP 1028 EP 1033 DI 10.1006/bbrc.1993.1320 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KV405 UT WOS:A1993KV40500038 PM 7682059 ER PT J AU BERKOWER, I MURPHY, D AF BERKOWER, I MURPHY, D TI ENZYMATIC LABELING OF BIOLOGICALLY-ACTIVE ENVELOPE GLYCOPROTEIN-GP120 OF HIV-1 SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HUMAN MONOCLONAL-ANTIBODY; NEUTRALIZING EPITOPE; GP120; TYPE-1; BINDING; REGION; INFECTION; CELLS RP BERKOWER, I (reprint author), US FDA,CTR BIOL,DIV ALLERGEN & PARASITOL,IMMUNE RESPONSE LAB,NIH CAMPUS,BETHESDA,MD 20892, USA. NR 31 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 31 PY 1993 VL 191 IS 3 BP 1055 EP 1065 DI 10.1006/bbrc.1993.1324 PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KV405 UT WOS:A1993KV40500042 PM 8466484 ER PT J AU IWANAGA, T FERRIOLA, PC AF IWANAGA, T FERRIOLA, PC TI CELLULAR UPTAKE OF PHOSPHOROTHIOATE OLIGODEOXYNUCLEOTIDES IS NEGATIVELY AFFECTED BY CELL-DENSITY IN A TRANSFORMED RAT TRACHEAL EPITHELIAL-CELL LINE - IMPLICATION FOR ANTISENSE APPROACHES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID GENE-EXPRESSION; INHIBITION; RECEPTORS; RNA C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27707. NR 19 TC 18 Z9 18 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 MAR 31 PY 1993 VL 191 IS 3 BP 1152 EP 1157 DI 10.1006/bbrc.1993.1337 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KV405 UT WOS:A1993KV40500055 PM 8466492 ER PT J AU KAVSAN, V KOVAL, A PETRENKO, O ROBERTS, CT LEROITH, D AF KAVSAN, V KOVAL, A PETRENKO, O ROBERTS, CT LEROITH, D TI 2 INSULIN GENES ARE PRESENT IN THE SALMON GENOME SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PREPROINSULIN GENE; SEQUENCE; EVOLUTION; RNA C1 NIDDK,DIABET BRANCH,BETHESDA,MD 20892. RP KAVSAN, V (reprint author), UKRAINIAN ACAD SCI,INST MOLEC BIOL & GENET,ZABOLOTNOGO STR 150,KIEV 252627,UKRAINE. NR 23 TC 21 Z9 23 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 31 PY 1993 VL 191 IS 3 BP 1373 EP 1378 DI 10.1006/bbrc.1993.1369 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KV405 UT WOS:A1993KV40500087 PM 8466513 ER PT J AU SAFADI, M BINDRA, DS WILLIAMS, T MOSCHEL, RC STELLA, VJ AF SAFADI, M BINDRA, DS WILLIAMS, T MOSCHEL, RC STELLA, VJ TI KINETICS AND MECHANISM OF THE ACID-CATALYZED HYDROLYSIS OF O6-BENZYLGUANINE SO INTERNATIONAL JOURNAL OF PHARMACEUTICS LA English DT Article DE O6-BENZYLGUANINE; HYDROLYSIS; KINETICS; MECHANISM; PH-RATE PROFILE; P-SUBSTITUENT EFFECT; TEMPERATURE EFFECT, NUCLEOPHILE EFFECT; O-18 LABELING ID ALKYLTRANSFERASE ACTIVITY; ALKYLATING-AGENTS; CELLS AB A variety of analytical techniques were used to elucidate the kinetics, reaction pathway and mechanism of hydrolysis of O6-benzylguanine, an O6-alkylguanine-DNA alkyltransferase depleting agent, as a function of pH, buffer concentration, temperature, substituents and halide nucleophiles. The reaction was also carried out in (H2O)-O-18 in order to determine the site of cleavage. The pH-rate profile indicated that the hydrolysis of O6-benzylguanine was acid-catalyzed, with the neutral O6-benzylguanine having greater intrinsic susceptibility to undergo acid catalyzed hydrolysis compared to its protonated form. Alternatively, the kinetics could be described by the kinetically indistinguishable process of spontaneous degradation of fully di- and mono-protonated O6-benzylguanine. In this case, the di-protonated species is more susceptible than the mono-protonated species. Based on the O-18 incorporation data, the site of the bond cleavage for hydrolysis of O6-benzylguanine was unambiguously assigned to the benzylic carbon-oxygen bond leading to the formation of benzyl alcohol and guanine as the predominant products. Benzyl chloride was also detected as a degradation product when the ionic strength of the solution was adjusted with sodium chloride. The rate of hydrolysis of p-substituted O6-benzylguanines increased with increasing electron donating capability of p-substituents, consistent with a mechanism involving positive charge formation on the benzylic carbon in the transition state. An Eyring plot resulted in a value for the observed entropy of activation, DELTAS(not-equal), of -2.4 e.u. which was consistent with a unimolecular, S(N)1, reaction. Although the rate of hydrolysis of O6-benzylguanine was well correlated with the nucleophilicity of various halide nucleophiles, the magnitude of the catalysis was less than anticipated for S(N)2 type reactions. The results suggested that in the presence of bromide and iodide, the transition state had some S(N)2 character. Based on the above observations, a late transition state for this reaction was suggested, where positive charge development at the benzylic carbon atom was quite advanced. C1 UNIV KANSAS,DEPT PHARMACEUT CHEM,LAWRENCE,KS 66045. UNIV KANSAS,CTR DRUG DELIVERY RES,LAWRENCE,KS 66045. UNIV KANSAS,MASS SPECTROMETER LAB,LAWRENCE,KS 66045. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM & CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 10 TC 8 Z9 8 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5173 J9 INT J PHARM JI Int. J. Pharm. PD MAR 31 PY 1993 VL 90 IS 3 BP 239 EP 246 DI 10.1016/0378-5173(93)90196-M PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KX642 UT WOS:A1993KX64200008 ER PT J AU GAWRISCH, K HAN, KH YANG, JS BERGELSON, LD FERRETTI, JA AF GAWRISCH, K HAN, KH YANG, JS BERGELSON, LD FERRETTI, JA TI INTERACTION OF PEPTIDE FRAGMENT-828-848 OF THE ENVELOPE GLYCOPROTEIN OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-I WITH LIPID BILAYERS SO BIOCHEMISTRY LA English DT Article ID TRANSMEMBRANE PROTEIN; MEMBRANES; SEGMENTS; REGION AB The interaction of the peptide fragment 828-848, called P828, from the carboxy-terminal region of the envelope glycoprotein gp41 of HIV-1 with model membranes composed of phosphatidylcholine (PC) and phosphatidylglycerol (PG) was investigated using microelectrophoretic mobility of liposomes, fluorescence polarization of labeled lipids, NMR, and differential scanning calorimetry. The peptide binds to negatively charged lipid surfaces. No interaction between P828 and neutral PC surfaces is observed. The interaction between the peptide and the lipid is exclusively electrostatic with the six positively charged arginines of P828 acting as binding sites for PG. Circular dichroism measurements of P828 indicate that the peptide undergoes a transition from a random coil to an ordered conformation upon binding to negatively charged PG bilayers or SDS micelles, but not in the presence of neutral PC bilayers. The ordered structure has an apparent helical content of 60%. In DOPG/DOPC mixtures containing 20 mol % DOPG, the peptide causes the formation of lipid domains enriched in DOPG, as assessed by measurement of fluorescence energy transfer between labeled PG and PC. The formation of these domains requires energy and therefore reduces the strength of peptide binding to the lipid matrix. Our data support and quantitate the results from antibody binding studies [Haffar, O. K., Dowbenko, D. J., & Berman, P. W. (1988) J. Cell Biol. 107, 1677-1687] that the carboxy-terminal segment of the envelope glycoprotein gp41 interacts with microsomal membranes. C1 MM SHEMYAKIN BIOORGAN CHEM INST,117988 MOSCOW,RUSSIA. RP GAWRISCH, K (reprint author), NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892, USA. NR 23 TC 62 Z9 62 U1 1 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 MAR 30 PY 1993 VL 32 IS 12 BP 3112 EP 3118 DI 10.1021/bi00063a024 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV350 UT WOS:A1993KV35000024 PM 8457572 ER PT J AU SHIMOSATO, K SAITO, T AF SHIMOSATO, K SAITO, T TI SUPPRESSIVE EFFECT OF CYCLOHEXIMIDE ON BEHAVIORAL SENSITIZATION TO METHAMPHETAMINE IN MICE SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE LOCOMOTION; SENSITIZATION; METHAMPHETAMINE; CYCLOHEXIMIDE; (MOUSE) ID AMPHETAMINE PSYCHOSIS; PROTEIN-SYNTHESIS; ENDURING CHANGES; ANIMAL-MODELS; BRAIN; RATS; INHIBITION; TOLERANCE; MEMORY; LONG AB The effect of a protein synthesis inhibitor, cycloheximide, on behavioral sensitization to methamphetamine was investigated in mice. As indicated by the sensitization tests, repeated injection of methamphetamine (2 mg/kg i.p.) at intervals of 3 and 4 days resulted in a progressive augmentation of the locomotor-stimulating effect of methamphetamine. This phenomenon, called locomotor sensitization, was attenuated by simultaneous treatment with cycloheximide (120 mg/kg i.p.) at the time of stimulant injection. In contrast, when mice were treated with cycloheximide 4 h after stimulant injection, locomotor activity was progressively augmented in the same way as observed in mice receiving repeated injections of methamphetamine alone. On challenge, it was noted that locomotor activity was significantly higher in mice injected repeatedly with the stimulant alone and in those mice treated with the inhibitor 4 h after the stimulant injection compared to the saline-treated control mice. However, mice that had been simultaneously treated with cycloheximide and methamphetamine showed almost the same locomotor activity as the saline-treated control mice. These observations indicated that the locomotor sensitization to methamphetamine was possibly suppressed by simultaneous treatment with cycloheximide. We then examined the dose- and time-dependent nature of the effect of cycloheximide on locomotor sensitization. The stimulation of locomotion observed after repeated injection of the stimulant at a dose of 1.5 mg/kg was significantly attenuated by simultaneous treatment with 120 or 240 mg/kg of cycloheximide, but not by treatment with 60 mg/kg of the inhibitor. However, all the treatments failed to suppress the development of locomotor sensitization elicited by 3 mg/kg of methamphetamine. The locomotor stimulation observed after repeated injection of 1.5 mg/kg methamphetamine was effectively suppressed by treatment with 120 mg/kg of cycloheximide given either simultaneously or 2 h after the stimulant injection. Treatment 4 h after methamphetamine did not suppress the stimulation of locomotion. These results suggest that the protein synthesis inhibitor has a.suppressive effect on the development of behavioral sensitization to repeated injections of stimulant drugs in a dose- and time-dependent manner. C1 KAWASAKI MED UNIV,DEPT PHARMACOL,KURASHIKI,OKAYAMA 70101,JAPAN. RP SHIMOSATO, K (reprint author), NIDA,ADDICT RES CTR,PRECLIN PHARMACOL BRANCH,BEHAV PHARMACOL & GENET LAB,POB 5180,BALTIMORE,MD 21224, USA. NR 27 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 MAR 30 PY 1993 VL 234 IS 1 BP 67 EP 75 DI 10.1016/0014-2999(93)90707-O PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KV513 UT WOS:A1993KV51300010 PM 8472762 ER PT J AU VAZQUEZ, A BECERRIL, B MARTIN, BM ZAMUDIO, F BOLIVAR, F POSSANI, LD AF VAZQUEZ, A BECERRIL, B MARTIN, BM ZAMUDIO, F BOLIVAR, F POSSANI, LD TI PRIMARY STRUCTURE DETERMINATION AND CLONING OF THE CDNA-ENCODING TOXIN-4 OF THE SCORPION CENTRUROIDES-NOXIUS HOFFMANN SO FEBS LETTERS LA English DT Article DE SCORPION TOXIN; NA+CHANNEL; CDNA CLONE; NUCLEOTIDE SEQUENCE; PEPTIDE PROCESSING ID VENOM; SEQUENCE AB A peptide (toxin II-10), shown to be a Na+ channel blocker, was purified from the venom of the scorpion Centruroides noxius Hoffmann and sequenced by Edman degradation. It has 66 amino acid residues with the C-terminal residue (asparagine) amidated, as demonstrated by mass spectrometry. In addition, we report the cloning and the nucleotide sequence of the cDNA (CngtV) that codes for this toxin. We discuss the mechanism for processing the precursor peptide to its final form and compare the primary structure to that of other Na+ channel toxins. Two distinct groups of toxins seem to emerge from this comparison, suggesting a structure-function relationship of these peptides towards the recognition of either mammalian or insect tissues. C1 UNIV NACL AUTONOMA MEXICO, INST BIOTECNOL, AV UNIV 2001, APTO POSTAL 5103, CUERNAVACA 62271, MEXICO. NIMH, CLIN NEUROSCI BRANCH, MOLEC NEUROGENET UNIT, BETHESDA, MD 20892 USA. RI Possani, Lourival/J-2397-2013 NR 18 TC 24 Z9 25 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAR 29 PY 1993 VL 320 IS 1 BP 43 EP 46 DI 10.1016/0014-5793(93)81654-I PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA KU541 UT WOS:A1993KU54100011 PM 8462674 ER PT J AU GRAZIOSI, C PANTALEO, G DEMAREST, JF SAAG, MS SHAW, GM FAUCI, AS AF GRAZIOSI, C PANTALEO, G DEMAREST, JF SAAG, MS SHAW, GM FAUCI, AS TI ANALYSIS OF HIV PROVIRAL BURDEN AND VIRAL EXPRESSION DURING PRIMARY HIV-INFECTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35233. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 2 EP 2 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500001 ER PT J AU CLERICI, M BERZOFSKY, JA SHEARER, GM AF CLERICI, M BERZOFSKY, JA SHEARER, GM TI HIV-SPECIFIC T-HELPER CELL RESPONSES IN EXPOSED, SERONEGATIVE, INDIVIDUALS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NCI,METAB BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 5 EP 5 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500011 ER PT J AU GALLO, RC AF GALLO, RC TI ASPECTS OF THE MOLECULAR PATHOGENESIS OF AIDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 5 EP 5 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500010 ER PT J AU FAUCI, AS AF FAUCI, AS TI IMMUNOPATHOGENIC MECHANISMS OF HIV-INFECTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 7 EP 7 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500016 ER PT J AU GAO, F YUE, L BIGGAR, RJ NEEQUAYE, AE HO, DD SHARP, PM SHAW, GM HAHN, BH AF GAO, F YUE, L BIGGAR, RJ NEEQUAYE, AE HO, DD SHARP, PM SHAW, GM HAHN, BH TI GENETIC AND BIOLOGICAL VARIATION OF HIV-2 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. AARON DIAMOND AIDS RES CTR,NEW YORK,NY. UNIV GHANA,DEPT MED,ACCRA,GHANA. UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294. UNIV DUBLIN TRINITY COLL,DEPT GENET,DUBLIN 2,IRELAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 9 EP 9 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500024 ER PT J AU ACHIM, CL MASLIAH, E HEYES, MP WANG, R MINERS, D WILEY, CA AF ACHIM, CL MASLIAH, E HEYES, MP WANG, R MINERS, D WILEY, CA TI NEUROLOGIC DAMAGE AND IMMUNE MEDIATORS IN AIDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,DEPT PATHOL,LA JOLLA,CA 92093. NIMH,LCS,SAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 11 EP 11 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500027 ER PT J AU ANDERSON, BD SHIRASAKA, T MITSUYA, H AF ANDERSON, BD SHIRASAKA, T MITSUYA, H TI IDENTIFICATION OF DRUG-RELATED GENOTYPIC CHANGES IN HIV-1 FROM SERUM USING SELECTIVE POLYMERASE CHAIN-REACTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MED BRANCH,EXPTL RETROVIROL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 11 EP 11 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500029 ER PT J AU DIMITROV, DS WILLEY, RL SATO, H CHANG, LJ BLUMENTHAL, R MARTIN, MA AF DIMITROV, DS WILLEY, RL SATO, H CHANG, LJ BLUMENTHAL, R MARTIN, MA TI QUANTITATION OF HIV-1 INFECTION KINETICS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MEMBRANE STRUCT SECT,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 14 EP 14 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500041 ER PT J AU JURRIAANS, S GOUDSMIT, J COUTINHO, R NARA, P VANSTRIIP, D SCHUKKINK, R LENS, P VANGEMEN, B AF JURRIAANS, S GOUDSMIT, J COUTINHO, R NARA, P VANSTRIIP, D SCHUKKINK, R LENS, P VANGEMEN, B TI HIGH VIRAL-RNA COPY NUMBER AT SEROCONVERSION PERSISTS IN INDIVIDUALS PROGRESSING TO AIDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MUNICIPAL HLTH SERV,AMSTERDAM,NETHERLANDS. ORGANON TEKNIKA NV,BOXTEL,NETHERLANDS. UNIV AMSTERDAM,HUMAN RETROVIRUS LAB,AMSTERDAM,NETHERLANDS. NCI,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 15 EP 15 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500046 ER PT J AU RICE, WG SCHAEFFER, CA MCDOUGAL, JS ORLOFF, SL SUMMERS, MF SOUTH, TL MENDELEVEV, J KUN, E AF RICE, WG SCHAEFFER, CA MCDOUGAL, JS ORLOFF, SL SUMMERS, MF SOUTH, TL MENDELEVEV, J KUN, E TI NOVEL ZINC-EJECTING C-NITROSO COMPOUNDS INHIBIT THE INFECTIOUS AND EXPRESSIVE PHASES OF HIV-1 LIFE-CYCLE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,ANTIVIRAL DRUG MECHANISMS LAB,FREDERICK,MD 21702. OCTAMER RES FDN,TIBURON,CA 94920. CTR DIS CONTROL,NCID,DHA,IMMUNOL BRANCH,ATLANTA,GA 30333. UNIV MARYLAND,DEPT CHEM & BIOCHEM,CATONSVILLE,MD 21228. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 22 EP 22 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500071 ER PT J AU SAVILLE, MW FOLI, A BRODER, S YARCHOAN, R AF SAVILLE, MW FOLI, A BRODER, S YARCHOAN, R TI INVITRO ACTIVITY OF TNP-470, A NOVEL ANGIOGENESIS INHIBITOR IN KAPOSI-SARCOMA (KS)-RELATED SPINDLE CELL-LINES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MED BRANCH,RETROVIRAL DIS SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 22 EP 22 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500074 ER PT J AU SHIRASAKA, T GAO, WY KOJIMA, E MITSUYA, H AF SHIRASAKA, T GAO, WY KOJIMA, E MITSUYA, H TI ANTI-HIV ACTIVITY OF DIDEOXYNUCLEOSIDES IN HUMAN RESTING AND ACTIVATED PERIPHERAL MONONUCLEAR-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MED BRANCH,EXPTL RETROVIROL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 23 EP 23 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500077 ER PT J AU BERGER, EA BRODER, CC NUSSBAUM, O AF BERGER, EA BRODER, CC NUSSBAUM, O TI MEMBRANE-FUSION VIA THE CD4 HIV-1 ENVELOPE GLYCOPROTEIN INTERACTION - A VACCINIA-BASED ASSAY MEASURING SELECTIVE REPORTER GENE-EXPRESSION IN FUSED CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 26 EP 26 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500088 ER PT J AU BLUMENTHAL, R DIMITROV, DS AF BLUMENTHAL, R DIMITROV, DS TI KINETICS OF HIV-1 ENVELOPE GLYCOPROTEIN-MEDIATED FUSION OF INDIVIDUAL CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 26 EP 26 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500089 ER PT J AU LUTHER, DG TODD, WJ SNIDER, R GONDA, MA AF LUTHER, DG TODD, WJ SNIDER, R GONDA, MA TI NERVOUS-TISSUE LESIONS IN CATTLE INFECTED WITH THE BOVINE IMMUNODEFICIENCY VIRUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 LOUISIANA STATE UNIV,SCH VET MED,DEPT PATHOL,LOUISIANA AGR CTR,DEPT VET SCI,BATON ROUGE,LA 70803. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 33 EP 33 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500114 ER PT J AU MANN, DL NALEWAIK, R AF MANN, DL NALEWAIK, R TI MACROPHAGE TO T-CELL TRANSMISSION OF HIV-1 IS REGULATED BY CELL-SURFACE STRUCTURES THAT INTERACT IN THE NORMAL IMMUNE-RESPONSE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDF,VIRAL CARCINOGENESIS LAB,IMMUNOGENET SECT,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 33 EP 33 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500117 ER PT J AU NUSSBAUM, O BRODER, CC BERGER, EA AF NUSSBAUM, O BRODER, CC BERGER, EA TI FACTORS ASSOCIATED WITH SELECTIVE FUSOGENIC ACTIVITIES OF HIV ENVELOPE GLYCOPROTEINS FOR SPECIFIC CD4+ CELL-TYPES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 34 EP 34 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500121 ER PT J AU TRUCKENMILLER, ME SWEETNAM, P COGGIANO, M SNYDER, S WYATT, R KULAGA, H AF TRUCKENMILLER, ME SWEETNAM, P COGGIANO, M SNYDER, S WYATT, R KULAGA, H TI CHARACTERIZATION OF HIV-1 INFECTION IN A HUMAN CORTICAL NEURONAL CELL-LINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. NOVA PHARMACEUT CORP,NOVASCREEN,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 40 EP 40 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500141 ER PT J AU DE, SK MARSH, JW AF DE, SK MARSH, JW TI LOSS OF GROWTH-FACTOR STIMULATED SIGNAL TRANSDUCTION IN NIH-3T3 CELLS EXPRESSING THE HIV-1 NEF GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIMH,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 44 EP 44 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500157 ER PT J AU GORELICK, RJ CHABOT, DJ REIN, AR HENDERSON, LE ARTHUR, LO AF GORELICK, RJ CHABOT, DJ REIN, AR HENDERSON, LE ARTHUR, LO TI REARRANGEMENT OF THE CONSERVED ZINC FINGERS OF THE HIV-1 NUCLEOCAPSID PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYN CORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 47 EP 47 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500168 ER PT J AU HILLER, S VENKATESAN, S AF HILLER, S VENKATESAN, S TI CELL-SURFACE EXPRESSION AS WELL AS INTRACELLULAR PROTEIN-LEVELS OF THE CD4 ANTIGEN ARE DOWN-MODULATED BY THE HIV-1 NEF PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 48 EP 48 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500175 ER PT J AU CONSTANTOULAKIS, P NASIOULAS, G AFONINA, E CAMPBELL, M FELBER, BK PAVLAKIS, GN AF CONSTANTOULAKIS, P NASIOULAS, G AFONINA, E CAMPBELL, M FELBER, BK PAVLAKIS, GN TI AN INTERFERON-INDUCIBLE GENE FAMILY INHIBITING HIV-1 EXPRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,BASIC RES PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 52 EP 52 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500190 ER PT J AU MICHAEL, NL EHRENBERG, PK DARCY, L VAHEY, MT MOSCA, JD RAPPAPORT, J REDFIELD, RR AF MICHAEL, NL EHRENBERG, PK DARCY, L VAHEY, MT MOSCA, JD RAPPAPORT, J REDFIELD, RR TI NEGATIVE-STRAND TRANSCRIPTS ARE PRODUCED IN HIV-1 INFECTED-CELLS AND PATIENTS BY A NOVEL PROMOTER DOWN-REGULATED BY TAT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 WALTER REED ARMY INST RES,DEPT RETROVIRAL RES,WASHINGTON,DC 20307. HENRY M JACKSON FDN,ROCKVILLE,MD 20850. NIDR,ORAL MED LAB,BETHESDA,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 52 EP 52 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500188 ER PT J AU SHARMA, OK MILMAN, G AF SHARMA, OK MILMAN, G TI COLLABORATIVE STUDY OF HIV QUANTITATION IN SEMEN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 56 EP 56 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500207 ER PT J AU DSOUZA, MP MILMAN, G AF DSOUZA, MP MILMAN, G TI INTERNATIONAL COLLABORATIVE STUDY TO COMPARE NEUTRALIZING AND IMMUNOCHEMICAL ASSAYS FOR MONOCLONAL-ANTIBODIES TO HUMAN-IMMUNODEFICIENCY-VIRUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,DIV AIDS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 61 EP 61 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500226 ER PT J AU HENKART, P CLERICI, M SARIN, A SHEARER, GM AF HENKART, P CLERICI, M SARIN, A SHEARER, GM TI PROTEASE INHIBITORS REVERSE TCR MEDIATED PROGRAMMED CELL-DEATH IN A CD4+ MURINE T-CELL HYBRIDOMA AND RESTORE INVITRO T-CELL RESPONSES IN SOME HIV+ INDIVIDUALS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 66 EP 66 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500243 ER PT J AU HYNES, NA GOLDSTEIN, S ELKINS, WR HIRSCH, VM AF HYNES, NA GOLDSTEIN, S ELKINS, WR HIRSCH, VM TI EARLY POST-TRANSMISSION DIVERSIFICATION OF SIV DOES NOT CORRELATE WITH DETECTABLE ANTIBODY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,LID,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 66 EP 66 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500246 ER PT J AU NIGIDA, SM SHOEMAKER, MR ARTHUR, LO AF NIGIDA, SM SHOEMAKER, MR ARTHUR, LO TI CLONING OF A HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 STRAIN MN [HIV-1(MN)] CAPABLE OF EFFICIENT REPLICATION IN PERIPHERAL-BLOOD MONONUCLEAR-CELLS (PBMC) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL DIS & IMMUN SECT,AIDS VACCINE DEV PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 68 EP 68 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500251 ER PT J AU ROSSIO, JL BESS, JW CRESSWELL, P TAUB, DD HENDERSON, LE ARTHUR, LO AF ROSSIO, JL BESS, JW CRESSWELL, P TAUB, DD HENDERSON, LE ARTHUR, LO TI EVALUATION OF HIV-1-ASSOCIATED CLASS-II PROTEIN IN THE INDUCTION OF ANERGY AND APOPTOSIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21701. YALE UNIV,NEW HAVEN,CT 06520. RI Bess, Jr., Julian/B-5343-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 69 EP 69 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500257 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 T-CELL RECEPTOR REPERTOIRE OF HIV-INFECTED SUBJECTS SUGGEST THE PRESENCE OF AN HIV-ASSOCIATED SUPERANTIGEN SO JOURNAL OF CELLULAR BIOCHEMISTRY 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 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0730-2312 EI 1097-4644 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 71 EP 71 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500264 ER PT J AU SINGH, MK TOYOSHIMA, T MARKOWITZ, M KEMPF, DJ NORBECK, DW ERICKSON, J HO, DD AF SINGH, MK TOYOSHIMA, T MARKOWITZ, M KEMPF, DJ NORBECK, DW ERICKSON, J HO, DD TI CHARACTERIZATION OF VIRAL MUTANTS RESISTANT TO A C2-SYMMETRICAL INHIBITOR OF HIV-1 PROTEASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 AARON DIAMOND AIDS RES CTR,NEW YORK,NY. NYU,SCH MED,NEW YORK,NY 10003. ABBOTT LABS,ABBOTT PK,IL. NCI,FREDERICK CANC RES CTR,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 86 EP 86 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500323 ER PT J AU MOFENSON, LM MOYE, J BETHEL, J FLYER, P NUGENT, R AF MOFENSON, LM MOYE, J BETHEL, J FLYER, P NUGENT, R TI CD8+ TRENDS IN HIV-INFECTED CHILDREN IN A TRIAL OF INTRAVENOUS IMMUNOGLOBULIN (IG) - POSSIBLE BEARING ON IMMUNOPATHOGENESIS OF MORE RAPID DISEASE PROGRESSION IN CHILDREN THAN ADULTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,PAMA,NICHD IVIG CLIN TRIAL STUDY GRP,BETHESDA,MD 20892. WESTAT CORP,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 99 EP 99 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500365 ER PT J AU OCHS, HD MORTON, WR KULLER, LD ZHU, QL TSAI, CC AGY, MB BENVENISTE, RE AF OCHS, HD MORTON, WR KULLER, LD ZHU, QL TSAI, CC AGY, MB BENVENISTE, RE TI PRENATAL INOCULATION OF MACAQUE FETUSES WITH SIV HIV SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV WASHINGTON HOSP,REG PRIMATE RES CTR,DEPT PEDIAT,SEATTLE,WA 98195. NCI,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 99 EP 99 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500367 ER PT J AU TUDORWILLIAMS, G MUELLER, B STOCKER, V VENZON, D MARSHALL, D BROUWERS, P BUTLER, K PIZZO, P AF TUDORWILLIAMS, G MUELLER, B STOCKER, V VENZON, D MARSHALL, D BROUWERS, P BUTLER, K PIZZO, P TI SERUM P24-ANTIGEN LEVELS AND DISEASE PROGRESSION IN HIV-1 INFECTED CHILDREN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,BIOSTAT & MANAGEMENT SECT,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 100 EP 100 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500372 ER PT J AU WAHL, SM BRANDES, ME MCCARTNEYFRANCIS, N ALLEN, JB FURCHT, LT MCCARTHY, JB AF WAHL, SM BRANDES, ME MCCARTNEYFRANCIS, N ALLEN, JB FURCHT, LT MCCARTHY, JB TI CYTOKINES AND INFLAMMATION IN THE EARLY STAGES OF WOUND REPAIR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,IMMUNOL LAB,BETHESDA,MD 20892. UNIV MINNESOTA,CTR BIOMED ENGN,MED & PATHOL LAB,MINNEAPOLIS,MN 55455. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 103 EP 103 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500376 ER PT J AU ROBERTS, AB SPORN, MB AF ROBERTS, AB SPORN, MB TI CENTRAL ROLE OF TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) IN HEALING OF SOFT AND HARD TISSUES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 3 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 108 EP 108 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500391 ER PT J AU BONNER, JC AF BONNER, JC TI RECEPTOR-MEDIATED SCAVENGING OF PLATELET-DERIVED GROWTH-FACTOR ALPHA-2-MACROGLOBULIN (PDGF ALPHA-2-M)-PROTEASE COMPLEXES BY MACROPHAGES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 113 EP 113 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500404 ER PT J AU NELSON, K BIDWELL, M ROSS, K EITZMAN, B MCLACHLAN, J AF NELSON, K BIDWELL, M ROSS, K EITZMAN, B MCLACHLAN, J TI THE REGULATION OF PEPTIDE GROWTH-FACTORS INVOLVED IN WOUND-HEALING PLAYS A ROLE IN ESTROGEN MEDIATED UTERINE GROWTH SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709. DUKE UNIV,DURHAM,NC 27706. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 116 EP 116 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500418 ER PT J AU FLANDERS, KC WINOKUR, TS HOLDER, MG SPORN, MB AF FLANDERS, KC WINOKUR, TS HOLDER, MG SPORN, MB TI HYPERTHERMIA INDUCES EXPRESSION OF TGF-BETA-S IN CARDIAC-CELLS INVITRO AND INVIVO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 120 EP 120 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500430 ER PT J AU PADIN, C NELSON, K MCLACHLAN, J WALMER, D AF PADIN, C NELSON, K MCLACHLAN, J WALMER, D TI THE EXPRESSION OF LACTOFERRIN IN THE HUMAN ENDOMETRIUM BY INFLAMMATORY GRANULOCYTES AND GLANDULAR EPITHELIUM - A POSSIBLE ROLE IN GROWTH-REGULATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DURHAM,NC 27710. NIEHS,REPROD & DEV TOXICOL,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 123 EP 123 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500442 ER PT J AU WALMER, D PADIN, C FLANDERS, K KOEHLER, M MCLACHLAN, J NELSON, K AF WALMER, D PADIN, C FLANDERS, K KOEHLER, M MCLACHLAN, J NELSON, K TI TGF-BETA EXPRESSION IN THE CYCLING HUMAN FEMALE REPRODUCTIVE-TRACT - PARALLELS WITH WOUND REPAIR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DURHAM,NC 27710. NCI,BETHESDA,MD 20892. NIEHS,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 124 EP 124 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500446 ER PT J AU WERNER, S WEINBERG, W LIAO, X YUSPA, S WEINER, R WILLIAMS, LT AF WERNER, S WEINBERG, W LIAO, X YUSPA, S WEINER, R WILLIAMS, LT TI ANALYSIS OF FGF FUNCTION IN THE SKIN BY TARGETED EXPRESSION OF A DOMINANT-NEGATIVE FGF RECEPTOR MUTANT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT OBSTET & GYNECOL,SAN FRANCISCO,CA 94143. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 135 EP 135 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500490 ER PT J AU PIEZ, KA AF PIEZ, KA TI COLLAGEN CHAINS, CROSS-LINKS AND TYPES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT BIOCHEM & MOLEC BIOL,PHILADELPHIA,PA 19107. NIH,FOGARTY INT CTR,BETHESDA,MD 20892. NR 4 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 143 EP 143 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500513 ER PT J AU KLEINMAN, HK YAMAMURA, K JUN, SH GRANT, DS AF KLEINMAN, HK YAMAMURA, K JUN, SH GRANT, DS TI ROLE OF THE BASEMENT-MEMBRANE LAMININ IN DEVELOPMENT AND TUMOR-GROWTH SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 146 EP 146 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500520 ER PT J AU HASCALL, VC AF HASCALL, VC TI HYALURONIC-ACID - AN HONORARY PROTEOGLYCAN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 148 EP 148 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500526 ER PT J AU VOGEL, T GUO, NH KRUTZSCH, HC BLAKE, DA HARTMAN, JR MENDELOVITZ, S PANET, A ROBERTS, DD AF VOGEL, T GUO, NH KRUTZSCH, HC BLAKE, DA HARTMAN, JR MENDELOVITZ, S PANET, A ROBERTS, DD TI MODULATION OF ENDOTHELIAL-CELL FUNCTIONS BY RECOMBINANT HEPARIN-BINDING DOMAIN OF THROMBOSPONDIN AND PEPTIDES FROM THE TYPE-I REPEATS CONTAINING TRP-SER-PRO-TRP SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 BIOTECHNOL GEN LTD,REHOVOT,ISRAEL. NCI,PATHOL LAB,BETHESDA,MD 20892. MEHARRY MED COLL,DEPT BIOCHEM,NASHVILLE,TN 37208. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 171 EP 171 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500613 ER PT J AU DAVENPORT, EA GODFREY, VB RANDELL, SH NETTESHEIM, P AF DAVENPORT, EA GODFREY, VB RANDELL, SH NETTESHEIM, P TI THE ROLE OF EXTRACELLULAR-MATRIX (ECM) IN AIRWAY EPITHELIAL-CELL DIFFERENTIATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 173 EP 173 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500619 ER PT J AU LAZOWSKI, KW MERTZ, PM REDMAN, RS KOUSVELARI, E AF LAZOWSKI, KW MERTZ, PM REDMAN, RS KOUSVELARI, E TI LAMININ, COLLAGEN-IV AND INTEGRINS EXPRESSION DURING RAT PAROTID-GLAND DEVELOPMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 VAMC,BETHESDA,MD. NIDR,CIPCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 175 EP 175 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500629 ER PT J AU LUDWICKA, A OHBA, T BINGEL, S HARLEY, R HAMPTON, M MAIZE, J HEYES, M SILVER, R AF LUDWICKA, A OHBA, T BINGEL, S HARLEY, R HAMPTON, M MAIZE, J HEYES, M SILVER, R TI A MURINE MODEL FOR THE EOSINOPHILIA-MYALGIA-SYNDROME (EMS) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,CHARLESTON,SC 29425. NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 176 EP 176 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500630 ER PT J AU CLEMENT, B LEVAVASSEUR, F YAMADA, Y GUILLOUZO, A AF CLEMENT, B LEVAVASSEUR, F YAMADA, Y GUILLOUZO, A TI EARLY CHANGES IN CTC-CONTAINING SITE BINDING COMPLEXES DURING THE RAPID ACTIVATION OF LAMININ-B2 PROMOTER IN CULTURED-HEPATOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HOP PONTCHAILLOU,INSERM,U49,F-35033 RENNES,FRANCE. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 178 EP 178 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500641 ER PT J AU HUGHES, CE CALABRO, A STEVENS, J HASCALL, VC CATERSON, B AF HUGHES, CE CALABRO, A STEVENS, J HASCALL, VC CATERSON, B TI EPITOPE MAPPING OF MONOCLONAL-ANTIBODIES RECOGNIZING HYALURONIC-ACID BINDING PROTEOGLYCANS AND LINK PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNC,CHAPEL HILL,NC 27599. NIH,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 180 EP 180 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500646 ER PT J AU NAKASHIMA, M YAMADA, Y REDDI, AH AF NAKASHIMA, M YAMADA, Y REDDI, AH TI CHANGES IN EXPRESSION OF EXTRACELLULAR-MATRIX AND BONE MORPHOGENETIC PROTEINS IN DENTAL-PULP CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 KYUSHU UNIV,FAC DENT,DEPT CONSERVAT DENT,FUKUOKA 812,JAPAN. NIDR,LDBA,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 180 EP 180 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500649 ER PT J AU BRENNER, MK RILL, DR BUSCHLE, MJ HOLLADAY, MS HESLOP, HE MOEN, RC KRANCE, RA MIRRO, J ANDERSON, WF IHLE, JN AF BRENNER, MK RILL, DR BUSCHLE, MJ HOLLADAY, MS HESLOP, HE MOEN, RC KRANCE, RA MIRRO, J ANDERSON, WF IHLE, JN TI TRANSFERRED GENE-EXPRESSION AFTER AUTOLOGOUS BONE-MARROW TRANSPLANTATION IN MAN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GENET THERAPY INC, CLIN LABS, GAITHERSBURG, MD 20878 USA. ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL ONCOL, MEMPHIS, TN 38101 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT PEDIAT, MEMPHIS, TN 38163 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT MED, MEMPHIS, TN 38163 USA. NHLBI, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 185 EP 185 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500657 ER PT J AU ROSENBERG, SA AF ROSENBERG, SA TI GENE-THERAPY OF CANCER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 2 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 185 EP 185 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500656 ER PT J AU CORNETTA, K MOORE, A SROUR, E MOEN, RC BROUN, ER CUNNINGHAM, I HEDDERMAN, A HROMAS, R MORGAN, RA ANDERSON, WF HOFFMAN, R TRICOT, G AF CORNETTA, K MOORE, A SROUR, E MOEN, RC BROUN, ER CUNNINGHAM, I HEDDERMAN, A HROMAS, R MORGAN, RA ANDERSON, WF HOFFMAN, R TRICOT, G TI RETROVIRAL GENE-TRANSFER IN ADULT AUTOLOGOUS BONE-MARROW TRANSPLANTATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GENET THERAPY INC,GAITHERSBURG,MD. INDIANA UNIV,DEPT MED,INDIANAPOLIS,IN 46202. NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. USC,SCH MED,NORRIS CANC CTR,LOS ANGELES,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 186 EP 186 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500658 ER PT J AU CULVER, KW LINK, CJ AKDEMIR, N MOORMAN, D STANLEY, D BUTLER, D ACKERMANN, M JACOBSON, C SCHNITZER, J BLAESE, RM AF CULVER, KW LINK, CJ AKDEMIR, N MOORMAN, D STANLEY, D BUTLER, D ACKERMANN, M JACOBSON, C SCHNITZER, J BLAESE, RM TI INVIVO GENE-TRANSFER FOR THE TREATMENT OF SOLID TUMORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GENET THERAPY INC,GAITHERSBURG,MD 20878. IOWA METHODIST MED CTR,DES MOINES,IA. NCI,BETHESDA,MD 20892. IOWA STATE UNIV SCI & TECHNOL,AMES,IA 50011. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 186 EP 186 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500660 ER PT J AU CARTER, B FLOTTE, T AFIONE, S SOLOW, R ZEITLIN, P MCGRATH, S AF CARTER, B FLOTTE, T AFIONE, S SOLOW, R ZEITLIN, P MCGRATH, S TI ADENOASSOCIATED VIRUS VECTORS FOR GENE-TRANSFER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 TARGETED GENET CORP,SEATTLE,WA. NIDDK,BETHESDA,MD. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 189 EP 189 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500668 ER PT J AU NECKERS, L CHAVANY, C GESELOWITZ, D FAHMY, B WALBRIDGE, S ALGER, J WHITESELL, L AF NECKERS, L CHAVANY, C GESELOWITZ, D FAHMY, B WALBRIDGE, S ALGER, J WHITESELL, L TI STABILITY, CLEARANCE AND DISPOSITION OF INTRAVENTRICULARLY ADMINISTERED OLIGODEOXYNUCLEOTIDES - IMPLICATIONS FOR THERAPEUTIC APPLICATION WITHIN THE CENTRAL-NERVOUS-SYSTEM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 189 EP 189 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500669 ER PT J AU SUGIYAMA, H SITKOVSKY, MV KIMURA, S SHIMADA, K AF SUGIYAMA, H SITKOVSKY, MV KIMURA, S SHIMADA, K TI ANTISENSE OLIGODEOXYNUCLEOTIDES TO CAMP-DEPENDENT PROTEIN-KINASE (PKA) CATALYTIC SUBUNIT GENE ENHANCE EFFECTOR FUNCTIONS OF CYTOTOXIC T-LYMPHOCYTES (CTL) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. UNIV TOKYO,INST MED SCI,DEPT APPL IMMUNOL & INFECT DIS,TOKYO 113,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 199 EP 199 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500702 ER PT J AU TREPEL, JB HA, MJ KIM, SJ MYERS, CE NECKERS, LM KANG, WK AF TREPEL, JB HA, MJ KIM, SJ MYERS, CE NECKERS, LM KANG, WK TI EVIDENCE THAT THE RETINOBLASTOMA GENE-PRODUCT IS A BIFUNCTIONAL REGULATOR OF CELL-CYCLE PROGRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 199 EP 199 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500701 ER PT J AU KOTANI, H NEWTON, PB CHIANG, YL OTTO, E ROOP, A BLAESE, RM ANDERSON, WF MCGARRITY, GJ AF KOTANI, H NEWTON, PB CHIANG, YL OTTO, E ROOP, A BLAESE, RM ANDERSON, WF MCGARRITY, GJ TI IMPROVED METHODS OF RETROVIRAL VECTOR TRANSDUCTION AND PRODUCTION FOR GENE-THERAPY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GENET THERAPY INC,GAITHERSBURG,MD 20878. NIH,BETHESDA,MD 20892. UNIV SO CALIF,LOS ANGELES,CA 90033. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 201 EP 201 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500708 ER PT J AU MORGAN, RA BRESSLER, P RAGHEB, J SCHNEIDERMAN, R DETTENHOFER, M MARKHAM, R SCHWARTZ, D AF MORGAN, RA BRESSLER, P RAGHEB, J SCHNEIDERMAN, R DETTENHOFER, M MARKHAM, R SCHWARTZ, D TI PROGRESS TOWARD GENE-THERAPY FOR AIDS - CHOICES FOR CLINICAL-APPLICATIONS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. GENET THERAPY INC,GAITHERSBURG,MD 20878. JOHNS HOPKINS SCH HYG & PUBL HLTH,DEPT IMMUNOL & INFECT DIS,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 202 EP 202 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500712 ER PT J AU RAGHEB, JA MORGAN, RA BRESSLER, P ANDERSON, WF AF RAGHEB, JA MORGAN, RA BRESSLER, P ANDERSON, WF TI RETROVIRAL MEDIATED GENE-TRANSFER AS A POLYPHARMACEUTICAL ANTI-HIV AGENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 203 EP 203 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500716 ER PT J AU GESELOWITZ, DA CHAVANY, C FAHMY, B WHITESELL, L NECKERS, L AF GESELOWITZ, DA CHAVANY, C FAHMY, B WHITESELL, L NECKERS, L TI PHARMACOKINETICS AND DISPOSITION OF OLIGONUCLEOTIDES INFUSED INTO THE RAT CENTRAL-NERVOUS-SYSTEM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 207 EP 207 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500731 ER PT J AU BERGAN, RC CONNEL, Y FAHMY, B KYLE, E NECKERS, L AF BERGAN, RC CONNEL, Y FAHMY, B KYLE, E NECKERS, L TI SYNTHETIC OLIGONUCLEOTIDES - POTENT APTAMERIC INHIBITORS OF PROTEIN TYROSINE KINASES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 210 EP 210 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500744 ER PT J AU GOTTESMAN, MM PASTAN, I AF GOTTESMAN, MM PASTAN, I TI MULTIDRUG RESISTANCE AS A SELECTABLE MARKER IN GENE-THERAPY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 221 EP 221 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500779 ER PT J AU SARVER, N AF SARVER, N TI GENE-THERAPY AND RIBOZYME FOR HIV-INFECTION AND IMMUNE RESTORATION STRATEGIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,DIV AIDS,DEV THERAPEUT BRANCH,BASIC RES & DEV PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 221 EP 221 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500778 ER PT J AU BRENNER, MK RILL, DR BUSCHLE, MJ HOLLADAY, MS HESLOP, HE MOEN, RC KRANCE, RA MIRRO, J ANDERSON, WF IHLE, JN AF BRENNER, MK RILL, DR BUSCHLE, MJ HOLLADAY, MS HESLOP, HE MOEN, RC KRANCE, RA MIRRO, J ANDERSON, WF IHLE, JN TI TRANSFERRED GENE-EXPRESSION AFTER AUTOLOGOUS BONE-MARROW TRANSPLANTATION IN MAN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI, BETHESDA, MD 20892 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT MED, MEMPHIS, TN 38163 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT PEDIAT, MEMPHIS, TN 38163 USA. ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL ONCOL, MEMPHIS, TN 38105 USA. GENET THERAPY INC, CLIN LABS, GAITHERSBURG, MD 20878 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 222 EP 222 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500783 ER PT J AU ROSENBERG, SA AF ROSENBERG, SA TI GENE-THERAPY OF CANCER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 222 EP 222 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500781 ER PT J AU RITCHEY, D HALL, E KAUSHAL, S GREENHOUSE, J LARUSSA, V KESSLER, S GARTNER, S LIU, Y SITZ, K PERERA, P KIM, J STLOUIS, D VAHEY, M YU, Z XU, J REDFIELD, R BURKE, D MOSCA, J AF RITCHEY, D HALL, E KAUSHAL, S GREENHOUSE, J LARUSSA, V KESSLER, S GARTNER, S LIU, Y SITZ, K PERERA, P KIM, J STLOUIS, D VAHEY, M YU, Z XU, J REDFIELD, R BURKE, D MOSCA, J TI SURVIVAL AND DIFFERENTIATION OF PRIMITIVE HUMAN CD34+ HEMATOPOIETIC-CELLS IN LIQUID CULTURES AND IN SCID MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NMRI,BETHESDA,MD 20814. NIH,BETHESDA,MD 20894. HENRY M JACKSON FDN,ROCKVILLE,MD 20850. WRAIR,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 233 EP 233 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500821 ER PT J AU SEKHSARIA, S GALLIN, JI MULLIGAN, RC MALECH, HL AF SEKHSARIA, S GALLIN, JI MULLIGAN, RC MALECH, HL TI CORRECTION OF CHRONIC GRANULOMATOUS-DISEASE (CGD) BY GENE-TRANSFER INTO PERIPHERAL-BLOOD HEMATOPOIETIC PROGENITORS (PBHP) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. WHITEHEAD INST,CAMBRIDGE,MA 02142. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 234 EP 234 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500824 ER PT J AU TIBERGHIEN, P REYNOLDS, CW KELLER, JR MURPHY, WJ LYONS, R CHIANG, Y LONGO, DL RUSCETTI, FW AF TIBERGHIEN, P REYNOLDS, CW KELLER, JR MURPHY, WJ LYONS, R CHIANG, Y LONGO, DL RUSCETTI, FW TI ABLATION OF ALLOREACTIVITY INVITRO BY GANCICLOVIR (GCV) TREATMENT OF HERPES-SIMPLEX THYMIDINE KINASE (HS-TK)-TRANSDUCED T-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DYNCORP INC,PRI,BCDP,FREDERICK,MD. NCI,FCRDC,LLB,BRMP,FREDERICK,MD 21702. GTI,GAITHERSBURG,MD 20878. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 234 EP 234 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500826 ER PT J AU HWU, P SHAFER, G TREISMAN, J COWHERD, R ESHHAR, Z ROSENBERG, SA AF HWU, P SHAFER, G TREISMAN, J COWHERD, R ESHHAR, Z ROSENBERG, SA TI LYSIS OF OVARIAN-CANCER CELLS BY HUMAN-LYMPHOCYTES REDIRECTED WITH A CHIMERIC GENE COMPOSED OF AN ANTIBODY VARIABLE REGION AND THE FC-RECEPTOR GAMMA CHAIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 243 EP 243 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500860 ER PT J AU KAUSHAL, S GARTNER, S LARUSSA, S LIU, Y YU, Z RITCHEY, D XU, J PERERA, P AF KAUSHAL, S GARTNER, S LARUSSA, S LIU, Y YU, Z RITCHEY, D XU, J PERERA, P TI HIV-1 EXPRESSION IN HUMAN STROMAL CELLS DOES NOT EFFECT CYTOKINES PRODUCTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 JACKSON FDN,ROCKVILLE,MD 20850. WALTER REED ARMY INST RES,ROCKVILLE,MD 20850. NIH,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 243 EP 243 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500863 ER PT J AU WILLIAMS, LK MULLEN, CA BLAESE, RM AF WILLIAMS, LK MULLEN, CA BLAESE, RM TI A CHIMERIC SUICIDE GENE FORMED BY FUSING RAT GROWTH-HORMONE SIGNAL PEPTIDE SEQUENCE TO THE CYTOSINE DEAMINASE GENE MARKEDLY ENHANCES SECRETION OF ACTIVE ENZYME SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,HOWARD HUGHES MED INST,BETHESDA,MD 20892. NCI,CELLULAR IMMUNOL SECT,METAB BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 248 EP 248 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500882 ER PT J AU MASTRANGELI, A BAJOCCHI, G FELDMAN, SH CRYSTAL, RG AF MASTRANGELI, A BAJOCCHI, G FELDMAN, SH CRYSTAL, RG TI DIRECT INVIVO GENE-TRANSFER TO THE CENTRAL-NERVOUS-SYSTEM USING REPLICATION DEFICIENT RECOMBINANT ADENOVIRUS VECTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 250 EP 250 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500890 ER PT J AU RIVERO, LJ KOZHICH, A NUSSENBLATT, RB JENDOUBI, M AF RIVERO, LJ KOZHICH, A NUSSENBLATT, RB JENDOUBI, M TI RETROVIRUS-MEDIATED GENE-TRANSFER AND EXPRESSION OF HUMAN ORNITHINE DELTA-AMINOTRANSFERASE INTO EMBRYONIC FIBROBLASTS - AN ALTERNATIVE APPROACH TO SOMATIC-CELL GENE-THERAPY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 251 EP 251 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500893 ER PT J AU ROSENFELD, M CHU, CS SETH, P JAFFE, HA BANKS, TC CRYSTAL, RG AF ROSENFELD, M CHU, CS SETH, P JAFFE, HA BANKS, TC CRYSTAL, RG TI E1- E3- REPLICATION DEFICIENT RECOMBINANT ADENOVIRUS VECTOR CONTAINING THE HUMAN CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) CDNA DOES NOT REPLICATE IN HUMAN RESPIRATORY EPITHELIAL-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 251 EP 251 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500892 ER PT J AU SETH, P ROSENFELD, MA HIGGINBOTHAM, JN CRYSTAL, RG AF SETH, P ROSENFELD, MA HIGGINBOTHAM, JN CRYSTAL, RG TI REPLICATION DEFICIENT ADENOVIRUS-MEDIATED DELIVERY OF UNLINKED PLASMID DNAS TO CELLS - AN EFFICIENT AND SIMPLE METHOD OF DNA TRANSFECTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 251 EP 251 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500894 ER PT J AU KIRSCH, IR LOMBARDI, DP FISHBEIN, WN HUONG, T AF KIRSCH, IR LOMBARDI, DP FISHBEIN, WN HUONG, T TI PREDICTION AND STUDY OF LYMPHOID MALIGNANCY MEDIATED BY INTERLOCUS SITE-SPECIFIC RECOMBINATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI, MED ONCOL BRANCH, BETHESDA, MD 20889 USA. ARMED FORCES INST PATHOL, WASHINGTON, DC 20306 USA. CLIN RES INST MONTREAL, MONTREAL H2W 1R7, QUEBEC, CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0730-2312 EI 1097-4644 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 256 EP 256 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500904 ER PT J AU WICKNER, S SKOWYRA, D HOSKINS, J MCKENNEY, K AF WICKNER, S SKOWYRA, D HOSKINS, J MCKENNEY, K TI THE FUNCTION OF ESCHERICHIA-COLI HEAT-SHOCK PROTEINS IN PLASMID P1 DNA-REPLICATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NATL INST STAND & TECHNOL,CTR ADV RES BIOTECHNOL,GAITHERSBURG,MD 20899. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 275 EP 275 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500963 ER PT J AU GOTTESMAN, S CLARK, W DECRECY, V MAURIZI, M AF GOTTESMAN, S CLARK, W DECRECY, V MAURIZI, M TI ENERGY-DEPENDENT PROTEOLYSIS IN ESCHERICHIA-COLI SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 281 EP 281 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500981 ER PT J AU NASH, HA GOODMAN, SD GRANSTON, AE SEGALL, AM AF NASH, HA GOODMAN, SD GRANSTON, AE SEGALL, AM TI SPECIFIC AND NONSPECIFIC COMPONENTS OF A NUCLEOPROTEIN COMPLEX - HU VERSUS IHF SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIMH,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 282 EP 282 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500984 ER PT J AU AUSTIN, SJ ABELES, AL BRENDLER, TG DAVIS, MA HAYES, F RADNEDGE, L YOUNGRENGRIMES, B AF AUSTIN, SJ ABELES, AL BRENDLER, TG DAVIS, MA HAYES, F RADNEDGE, L YOUNGRENGRIMES, B TI REPLICATION AND PARTITIONING - AN ORIGIN SEGREGATION MODEL FOR REPLICATION CONTROL SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 284 EP 284 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500990 ER PT J AU TRUN, NJ CHA, J AF TRUN, NJ CHA, J TI THE GENETICS OF MBR MUTANTS OF ESCHERICHIA-COLI SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 284 EP 284 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500989 ER PT J AU LOBOCKA, M YARMOLINSKY, M AF LOBOCKA, M YARMOLINSKY, M TI ON P1 PLASMID PARTITION - CONTEXT EFFECTS ON CENTROMERE FUNCTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 285 EP 285 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96500992 ER PT J AU BRENDLER, TG ABELES, AL AUSTIN, SJ AF BRENDLER, TG ABELES, AL AUSTIN, SJ TI CONTROL OF P1 ORIR AND HOST ORIC REPLICATION ORIGINS BY DNA ADENINE METHYLATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 290 EP 290 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96501011 ER PT J AU KOZYAVKIN, SA KRAH, R GELLERT, M LAKE, JA STETTER, KO SLESAREV, AI AF KOZYAVKIN, SA KRAH, R GELLERT, M LAKE, JA STETTER, KO SLESAREV, AI TI DNA TOPOISOMERASES FROM HYPERTHERMOPHILIC PROKARYOTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK, MOLEC BIOL LAB, BETHESDA, MD 20892 USA. UNIV REGENSBURG, LEHRSTUHL MIKROBIOL, W-8400 REGENSBURG, GERMANY. UNIV CALIF LOS ANGELES, INST MOLEC BIOL, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 297 EP 297 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96501036 ER PT J AU KRAH, R MENZEL, R GELLERT, M AF KRAH, R MENZEL, R GELLERT, M TI DNA SUPERCOILING AND REGULATION OF TRANSCRIPTION - ANALYSIS OF THE GYRA PROMOTER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,MOLEC BIOL LAB,BETHESDA,MD 20892. BRISTOL MYERS SQUIBB,PRINCETON,NJ 08543. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 297 EP 297 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96501037 ER PT J AU SEGALL, AM NASH, HA AF SEGALL, AM NASH, HA TI JUXTAPOSITION OF DNA-MOLECULES - BIMOLECULAR COMPLEXES IN LAMBDA SITE-SPECIFIC RECOMBINATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIMH,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 304 EP 304 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96501066 ER PT J AU TILLY, K BARBOUR, AG HINNEBUSCH, J AF TILLY, K BARBOUR, AG HINNEBUSCH, J TI GENES, PROTEINS, AND DNA STRUCTURES POTENTIALLY INVOLVED IN LINEAR PLASMID REPLICATION IN BORRELIA-BURGDORFERI, THE LYME-DISEASE AGENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,HAMILTON,MT 59840. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RI Barbour, Alan/B-3160-2009 OI Barbour, Alan/0000-0002-0719-5248 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 29 PY 1993 SU 17E BP 305 EP 305 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KX965 UT WOS:A1993KX96501069 ER PT J AU NASHED, EM PAVLIAK, V KOVAC, P POZSGAY, V GLAUDEMANS, CPJ AF NASHED, EM PAVLIAK, V KOVAC, P POZSGAY, V GLAUDEMANS, CPJ TI INTERACTIONS BETWEEN SH-DYSENTERIAE ANTIGEN AND ANTIBODY SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 7 EP CARB PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98100519 ER PT J AU BAI, X MASCARELLA, SW BOWEN, WD CARROLL, FI AF BAI, X MASCARELLA, SW BOWEN, WD CARROLL, FI TI A NOVEL ASYMMETRIC-SYNTHESIS OF BENZOMORPHANS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. NIH,MED CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 21 EP ORGN PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ983 UT WOS:A1993KQ98300157 ER PT J AU KROEGERKOEPKE, MB SMITH, RH MICHEJDA, CJ AF KROEGERKOEPKE, MB SMITH, RH MICHEJDA, CJ TI DNA ALKYLATION BY 1-HYDROXYETHYL-3-CARBOETHOXY-3-METHYLTRIAZENE AND N-NITROSOMETHYL-(2-HYDROXYETHYL)AMINE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BRP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 22 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98103003 ER PT J AU PETRAKOVA, E GLAUDEMANS, CPJ AF PETRAKOVA, E GLAUDEMANS, CPJ TI SYNTHESES OF METHYL ALPHA-ISOMALTOOLIGOSACCHARIDES SPECIFICALLY DEOXYGENATED AT POSITION-2 SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIDDKD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 37 EP CARB PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98100549 ER PT J AU GARRETT, DS POWERS, R LODI, P GRONENBORN, AM CLORE, GM AF GARRETT, DS POWERS, R LODI, P GRONENBORN, AM CLORE, GM TI AUTOMATED AND INTERACTIVE TOOLS FOR ASSIGNING 3D AND 4D NMR - APPLICATION TO INTERLEUKIN-4 AND HNRNP-A1 SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIDDK,LCP,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 38 EP COMP PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98101690 ER PT J AU MULARD, LA KOVAC, P GLAUDEMANS, CPJ AF MULARD, LA KOVAC, P GLAUDEMANS, CPJ TI SYNTHESIS OF SPECIFICALLY DEOXYGENATED DISACCHARIDES RELATED TO THE O-SPECIFIC ANTIGEN OF SHIGELLA-DYSENTERIAE TYPE-1 SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 38 EP CARB PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98100550 ER PT J AU MOHAN, P VERMA, S TAN, GT WICKRAMASINGHE, A PEZZUTO, JM HUGHES, SH BABA, M AF MOHAN, P VERMA, S TAN, GT WICKRAMASINGHE, A PEZZUTO, JM HUGHES, SH BABA, M TI SULFONIC-ACID POLYMERS - HIGHLY POTENT INHIBITION OF HIV-1 AND HIV-2 REVERSE-TRANSCRIPTASE AND ANTIVIRAL ACTIVITY SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 UNIV ILLINOIS,CHICAGO,IL 60680. NCI,FREDERICK CANC RES & DEV CTR,ABL INC,BASIC RES PROGRAM,FREDERICK,MD 21701. FUKUSHIMA MED SCH,FUKUSHIMA 960,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 45 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98103026 ER PT J AU POMMIER, Y AF POMMIER, Y TI INTERACTION OF ANTHRACYCLINES WITH MAMMALIAN DNA TOPOISOMERASES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,DCT,DTP,LMP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 47 EP CARB PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98100559 ER PT J AU DOMINGUEZ, C DECOSTA, B HE, XS LINDERS, JTM WILLIAMS, W BOWEN, W AF DOMINGUEZ, C DECOSTA, B HE, XS LINDERS, JTM WILLIAMS, W BOWEN, W TI SYNTHESIS AND BIOLOGICAL EVALUATION OF CONFORMATIONALLY RESTRICTED 2-(1-PYRROLIDINYL)-N-[2-(3,4-DICHLOROPHENYL)ETHYL]-N-(METHYL)ETHYLENEDIA MINES AS SIGMA-LIGANDS .2. PIPERAZINES, BRIDGED BICYCLIC AMINES AND MISCELLANEOUS COMPOUNDS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIH,MED CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 70 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98103050 ER PT J AU BURGESS, K HO, KK MALIN, DH LAKE, JR PAYZER, K AF BURGESS, K HO, KK MALIN, DH LAKE, JR PAYZER, K TI CORRELATIONS OF ANTI-OPIATE PEPTIDOMIMETIC SOLUTION STRUCTURES WITH THEIR PHARMACOLOGICAL ACTIVITIES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 TEXAS A&M UNIV SYST, COLL STN, TX 77843 USA. UNIV HOUSTON CLEAR LAKE, HOUSTON, TX 77058 USA. NIMH, WASHINGTON, DC 20032 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 73 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98103053 ER PT J AU CARROLL, FI ABRAHAM, P KUZEMKO, MA GRAY, JL LEWIN, AH BOJA, JW KUHAR, MJ AF CARROLL, FI ABRAHAM, P KUZEMKO, MA GRAY, JL LEWIN, AH BOJA, JW KUHAR, MJ TI SYNTHESIS AND COCAINE RECEPTOR AFFINITIES OF 3-PHENYL-2-(3'-METHYL-1,2,4-OXADIAZOLE-5'-YL)TROPANE ISOMERS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 84 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98103064 ER PT J AU ANANTHAN, S CLAYTON, SD WONG, G SKOLNICK, P AF ANANTHAN, S CLAYTON, SD WONG, G SKOLNICK, P TI SYNTHESIS AND STRUCTURE-ACTIVITY-RELATIONSHIPS FOR 1,2-ANNELLATED AND 1,5-ANNELLATED ETHYL IMIDAZOLE-4-CARBOXYLATES AT BENZODIAZEPINE RECEPTORS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. SO RES INST,BIRMINGHAM,AL 35255. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 88 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98103067 ER PT J AU CASTONGUAY, LA SNOW, PM BRYANT, SH FETROW, JS AF CASTONGUAY, LA SNOW, PM BRYANT, SH FETROW, JS TI A PROPOSED MODEL OF THE CELL-ADHESION MOLECULE, FASCICLIN-III SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 SUNY ALBANY,DEPT ANASTHESIOL,ALBANY,NY 12222. NIH,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20879. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 134 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ981 UT WOS:A1993KQ98103113 ER PT J AU SMITH, RH FARNSWORTH, DW MICHEJDA, CJ AF SMITH, RH FARNSWORTH, DW MICHEJDA, CJ TI ALKYLARYLTRIAZENES AND THEIR MODE OF HYDROLYTIC DECOMPOSITION SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 WESTERN MARYLAND COLL,DEPT CHEM,WESTMINSTER,MD 21157. NCI,FCRDC,BRP,ABL,MSL,MOLEC ASPECTS DRUG DESIGN SECT,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 28 PY 1993 VL 205 BP 275 EP ORGN PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA KQ983 UT WOS:A1993KQ98300411 ER PT J AU HOLLEY, M KACHAR, B AF HOLLEY, M KACHAR, B TI HI-FI CELLS AT THE HEART OF THE EAR SO NEW SCIENTIST LA English DT Article C1 NATL INST DEAFNESS & OTHER COMMUNICAT DIS,WASHINGTON,DC. RP HOLLEY, M (reprint author), UNIV BRISTOL,SCH MED SCI,DEPT PHYSIOL,BRISTOL BS8 1TH,AVON,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NEW SCIENTIST PUBL EXPEDITING INC PI ELMONT PA 200 MEACHAM AVE, ELMONT, NY 11003 SN 0262-4079 J9 NEW SCI JI New Sci. PD MAR 27 PY 1993 VL 137 IS 1866 BP 27 EP 30 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KV301 UT WOS:A1993KV30100030 ER PT J AU CHANDRASEKARAN, K STOLL, J RAPOPORT, SI BRADY, DR AF CHANDRASEKARAN, K STOLL, J RAPOPORT, SI BRADY, DR TI LOCALIZATION OF CYTOCHROME-OXIDASE (COX) ACTIVITY AND COX MESSENGER-RNA IN THE PERIRHINAL AND SUPERIOR TEMPORAL SULCI OF THE MONKEY BRAIN SO BRAIN RESEARCH LA English DT Article DE RHESUS MONKEY; PRORHINAL CORTEX; PERIRHINAL CORTEX; SUPERIOR TEMPORAL SULCUS; CYTOCHROME OXIDASE; INSITU HYBRIDIZATION; CORTICOCORTICAL CONNECTION; ALZHEIMERS DISEASE ID ENTORHINAL AREA 28; ALZHEIMERS-DISEASE; RHESUS-MONKEY; HISTOCHEMICAL-CHANGES; CORTICAL CONNECTIONS; 35 CORTICES; C-OXIDASE; CORTEX; GYRUS; MORPHOLOGY AB Cytochrome oxidase (COX) activity and COX II mRNA expression were localized in the perirhinal and superior temporal sulci of the rhesus monkey brain. In both regions, a laminar distribution of COX activity and COX II mRNA was observed. COX activity was intense in layers I and IV and were localized to the neuropil. In contrast, COX II mRNA was localized to neuronal cell bodies. In the prorhinal region, highest levels of COX II mRNA was detected in cell bodies of layers II and IV, and in the perirhinal region, in cell bodies of layers III and V-VI. In the superior temporal sulcus, COX II mRNA was detected in cell bodies of layers III and V-VI. Thus. COX II mRNA and COX activity are uniquely localized in the cortical layers and to those neurons that support cortico-cortical connections. RP CHANDRASEKARAN, K (reprint author), NIA,NEUROSCI LAB,BLDG 10,RM 6C 103,BETHESDA,MD 20892, USA. NR 33 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 26 PY 1993 VL 606 IS 2 BP 213 EP 219 DI 10.1016/0006-8993(93)90987-X PG 7 WC Neurosciences SC Neurosciences & Neurology GA KU014 UT WOS:A1993KU01400006 PM 8387858 ER PT J AU YAMADA, M KAKITA, A MIZUGUCHI, M RHEE, SG KIM, SU IKUTA, F AF YAMADA, M KAKITA, A MIZUGUCHI, M RHEE, SG KIM, SU IKUTA, F TI SPECIFIC EXPRESSION OF INOSITOL 1,4,5-TRISPHOSPHATE 3-KINASE IN DENDRITIC SPINES SO BRAIN RESEARCH LA English DT Note DE INOSITOL 1,4,5-TRISPHOSPHATE 3-KINASE; INOSITOL 1,3,4,5-TETRAKISPHOSPHATE; INOSITOL 1,4,5-TRISPHOSPHATE; IMMUNOHISTOCHEMISTRY; SPINE; ULTRASTRUCTURE ID CEREBELLAR PURKINJE-CELLS; LONG-TERM POTENTIATION; PROTEIN KINASE-C; RECEPTOR; 1,3,4,5-TETRAKISPHOSPHATE; PHOSPHATES; CA-2+; BRAIN AB Ultrastructural localization of inositol 1,4,5-trisphosphate 3-kinase (IP3K) in the rat cerebral cortex and hippocampus was studied immunohistochemically. In both regions, the major structure expressing a high level of IP3K was the dendritic spines of pyramidal neurons, where immunoreactivity was associated with the spine apparatuses and plasmalemma. The postsynaptic densities showed the most intense labelling. Taking into account the results of our previous observations, which demonstrated the restricted localization of the enzyme in the dendritic spines of Purkinje and basket cells in cerebellum, IP3K may be localized specifically in dendritic spines in various regions of the central nervous system, and involved in synaptic signal transduction at the spines. C1 UNIV TOKYO,FAC MED,DEPT PEDIAT,TOKYO 113,JAPAN. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV BRITISH COLUMBIA,DEPT MED,DIV NEUROL,VANCOUVER V6T 1W5,BC,CANADA. RP YAMADA, M (reprint author), NIIGATA UNIV,BRAIN RES INST,DEPT PATHOL,ASAHIMACHI 1,NIIGATA 951,JAPAN. NR 29 TC 25 Z9 25 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 26 PY 1993 VL 606 IS 2 BP 335 EP 340 DI 10.1016/0006-8993(93)91004-C PG 6 WC Neurosciences SC Neurosciences & Neurology GA KU014 UT WOS:A1993KU01400023 PM 8387863 ER PT J AU MURPHY, PM AF MURPHY, PM TI MOLECULAR MIMICRY AND THE GENERATION OF HOST DEFENSE PROTEIN DIVERSITY SO CELL LA English DT Letter ID TRANSFORMING FELINE RETROVIRUS; GROWTH-FACTOR; RECEPTOR; ENCODES RP MURPHY, PM (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 24 TC 182 Z9 184 U1 1 U2 3 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 26 PY 1993 VL 72 IS 6 BP 823 EP 826 DI 10.1016/0092-8674(93)90571-7 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KU175 UT WOS:A1993KU17500003 PM 8458078 ER PT J AU TOPOL, IA BURT, SK AF TOPOL, IA BURT, SK TI THE CALCULATIONS OF SMALL MOLECULAR-CONFORMATION ENERGY DIFFERENCES BY DENSITY FUNCTIONAL METHOD SO CHEMICAL PHYSICS LETTERS LA English DT Article ID 1,2-DIFLUOROETHANE; ROTATION AB The differences in the conformational energies for the gauche (G) and trans (T) conformers of 1,2-difluoroethane and for myo- and scyllo-conformer of inositol have been calculated by local density functional method (LDF approximation) with geometry optimization using different sets of calculation parameters. It is shown that in contrast to Hartree-Fock methods, density functional calculations reproduce the correct sip and value of the gauche effect for 1,2-difluoroethane and energy difference for both conformers of inositol. The results of normal vibrational analysis for 1,2-difluoroethane showed that harmonic frequencies calculated in LDF approximation agree with experimental data with the accuracy typical for scaled large basis set Hartree-Fock calculations. RP TOPOL, IA (reprint author), DYNCORP,PRI,NCI,FREDERICK CANC RES & DEV CTR,FREDERICK BIOMED SUPERCOMP CTR,FREDERICK,MD 21702, USA. NR 16 TC 14 Z9 14 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0009-2614 J9 CHEM PHYS LETT JI Chem. Phys. Lett. PD MAR 26 PY 1993 VL 204 IS 5-6 BP 611 EP 616 DI 10.1016/0009-2614(93)89213-2 PG 6 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA KU026 UT WOS:A1993KU02600039 ER PT J AU MISCHAK, H GOODNIGHT, J KOLCH, W MARTINYBARON, G SCHAECHTLE, C KAZANIETZ, MG BLUMBERG, PM PIERCE, JH MUSHINSKI, JF AF MISCHAK, H GOODNIGHT, J KOLCH, W MARTINYBARON, G SCHAECHTLE, C KAZANIETZ, MG BLUMBERG, PM PIERCE, JH MUSHINSKI, JF TI OVEREXPRESSION OF PROTEIN KINASE-C-DELTA AND KINASE-EPSILON IN NIH 3T3 CELLS INDUCES OPPOSITE EFFECTS ON GROWTH, MORPHOLOGY, ANCHORAGE DEPENDENCE, AND TUMORIGENICITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HEMATOPOIETIC-CELLS; PHORBOL ESTERS; EXPRESSION; FAMILY; FIBROBLASTS; NPKC; CDNA; PKC; DIFFERENTIATION; PURIFICATION AB We have determined the patterns of mRNA and protein expression of 7 protein kinase C (PKC) isozymes in NIH 3T3 cells. Only PKC-alpha is expressed abundantly in NIH 3T3 cells; endogenous levels of the other 6 PKC isozymes are low or undetectable. We have overexpressed PKC-delta and -epsilon in these cells to observe activation/translocation of these two isozymes and the biological consequences of overexpression. Both PKC-delta and epsilon, but not PKC-alpha, are partially associated with the insoluble fraction even in the absence of phorbol 12-myristate 13-acetate (PMA). Upon PMA stimulation, both PKC-delta and -epsilon translocate to the insoluble fraction of cell homogenates, as can be observed with the endogenous PKC-alpha. Overexpression of PKC-delta induces significant changes in morphology and causes the cells to grow more slowly and to a decreased cell density in confluent cultures. These changes are accentuated by treatment with PMA. Overexpression of PKC-epsilon does not lead to morphological changes, but causes increased growth rates and higher cell densities in monolayers. None of the PKC-delta overexpressers grow in soft agar with or without PMA, but all the cell lines that overexpress PKC-E grow in soft agar in the absence of PMA, but not in its presence. NIH 3T3 cells that overexpress PKC-epsilon also form tumors in nude mice with 100% incidence. This indicates that high expression of PKC-epsilon contributes to neoplastic transformation. C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NCI,GENET LAB,BETHESDA,MD 20892. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. RI Mischak, Harald/E-8685-2011 NR 35 TC 553 Z9 560 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6090 EP 6096 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800006 PM 8454583 ER PT J AU ALI, N CRAXTON, A SHEARS, SB AF ALI, N CRAXTON, A SHEARS, SB TI HEPATIC INS(1,3,4,5)P4 3-PHOSPHATASE IS COMPARTMENTALIZED INSIDE ENDOPLASMIC-RETICULUM SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INOSITOL 1,3,4,5-TETRAKISPHOSPHATE 3-PHOSPHATASE; RAT-LIVER; PORCINE BRAIN; L1210 CELLS; HEXAKISPHOSPHATE; 1,3,4,5,6-PENTAKISPHOSPHATE; 1,4,5-TRISPHOSPHATE; PENTAKISPHOSPHATE; METABOLISM; 1,4,5,6-TETRAKISPHOSPHATE AB In pursuit of the physiological role of inositol 1,3,4,5-tetrakisphosphate 3-phosphatase, which also attacks inositol pentakisphosphate and inositol hexakisphosphate with much higher affinity (Nogimori, K., Hughes, P. J., Glennon, M. C., Hodgson, M. E., Putney, J. W., Jr., and Shears, S. B. (1991) J. Biol. Chem. 266, 16499-16506), we have studied the subcellular distribution of the enzyme in liver. Initially, we had to overcome the problem that potent endogenous inhibitor(s) compromise the detection of this enzyme in vitro (Hodgson, M. E., and Shears, S. B. (1990) Biochem. J. 267, 831-834). We partially purified these inhibitor(s) by anion-exchange chromatography and gel filtration; inhibitory activity co-eluted with standard inositol hexakisphosphate and was depleted by treatment with phytase. Thus, subcellular fractions were pretreated with phytase before assay of 3-phosphatase activity. Our experiments revealed that the hepatic 3-phosphatase was nearly exclusively restricted to the endoplasmic reticulum, and there was little or no activity in either the cytosol, plasma membranes, mitochondria, or nuclei. Detergent treatment of microsomes indicated that there was 93 +/- 2% latency to mannose-6-phosphatase, an intraorganelle enzyme activity (Vanstapel, F., Pua, K., and Blanckaert, N. (1986) Eur. J. Biochem. 156, 73-77). Similar latencies were found for the hydrolysis of inositol 1,3,4,5-tetrakisphosphate (95 +/- 1%), inositol 1,3,4,5,6-pentakisphosphate (94 +/- 1%), and inositol hexakisphosphate (93 +/- 2%). Treatment of microsomes with either sodium carbonate or phosphatidylcholine-specific phospholipase C, to release luminal contents, led to solubilization of approximately 90% of 3-phosphatase activity. Thus, hepatic 3-phosphatase has a highly restricted access to inositol polyphosphates in vivo that needs to be accounted for in the determination of the physiological role of this enzyme. RP ALI, N (reprint author), NIEHS,CELLULAR & MOLEC PHARMACOL LAB,INOSITOL LIPID SECT,RES TRIANGLE PK,NC 27709, USA. NR 50 TC 54 Z9 57 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6161 EP 6167 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800016 PM 8384201 ER PT J AU MOSS, J STANLEY, SJ VAUGHAN, M TSUJI, T AF MOSS, J STANLEY, SJ VAUGHAN, M TSUJI, T TI INTERACTION OF ADP-RIBOSYLATION FACTOR WITH ESCHERICHIA-COLI ENTEROTOXIN THAT CONTAINS AN INACTIVATING LYSINE-112 SUBSTITUTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NUCLEOTIDE-BINDING PROTEIN; CHOLERA-TOXIN; DIPHTHERIA-TOXIN; RIBOSYLTRANSFERASE ACTIVITY; PERTUSSIS TOXIN; NAD; ACTIVATION; SUBUNIT; IDENTIFICATION; EXPRESSION AB Cholera toxin and Escherichia coli heat-labile enterotoxin (LT) exert their effects on cells through ADP-ribosylation of guanine nucleotide-binding proteins. Both toxins consist of one A subunit, which is an ADP-ribosyltransferase, and five B (or binding) subunits. Their enzymatic activities are latent; activation requires reduction and proteolysis, resulting in a catalytically active A1 protein and a much smaller A2 protein. These ADP-ribosyltransferases are activated by GTP-dependent 20-kDa ADP-ribosylation factors or ARFs. To determine if proteolysis plus reduction is required for appearance of the ARF allosteric site as well as for catalytic activity, an inactive mutant of LT, LT(E112K), with replacement of glutamate by lysine at position 112 of its A subunit, was utilized as a competitor in cholera toxin ADP-ribosyltransferase assays containing limiting amounts of ARF. LT(E112K) required trypsinization and reduction to become a potent, concentration-dependent inhibitor. Inhibition was reversed by increasing concentrations of ARF. Reduction or trypsinization alone did not generate an inhibitory form of LT(E112K). These studies are consistent with the conclusion that the ARF site is not expressed in the latent toxin. Both trypsinization and reduction are required for expression of a functional ARF binding site as well as for catalytic activity. C1 FUJITA HLTH UNIV,SCH MED,DEPT MICROBIOL,TOYOAKE,AICHI 47011,JAPAN. RP MOSS, J (reprint author), NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892, USA. NR 32 TC 33 Z9 33 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6383 EP 6387 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800046 PM 8454609 ER PT J AU UCHIDA, K STADTMAN, ER AF UCHIDA, K STADTMAN, ER TI COVALENT ATTACHMENT OF 4-HYDROXYNONENAL TO GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE - A POSSIBLE INVOLVEMENT OF INTRAMOLECULAR AND INTERMOLECULAR CROSS-LINKING REACTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID METAL-CATALYZED OXIDATION; ASCITES TUMOR-CELLS; LIPID-PEROXIDATION; PROTEINS; PRODUCT; CONSEQUENCES; HISTIDINE; RESIDUES AB Cytotoxic action of membrane lipid peroxidation product 4-hydroxynonenal (HNE) is due mainly to its facile reactivity with proteins (Esterbauer, H., Schaur, R. J., and Zollner, H. (1991) Free Radical Biol. Med. 11, 77-80). In the present study, the detailed mechanism of HNE modification of a key enzyme in intermediary metabolism, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), is studied mainly focusing on the formation of HNE-amino acid adducts in the enzyme. When GAPDH (1 mg/ml) was treated with 0-2 mm HNE in sodium phosphate buffer (pH 7.2) for 2 h at 37-degrees-C, the enzyme was inactivated by HNE in a concentration-dependent manner. The loss of enzyme activity was associated with the loss of free sulfhydryl groups. Following its reduction with NaBH4, amino acid analysis of the HNE-modified enzyme demonstrated that histidine and lysine residues were also modified. At concentrations lower than 0.5 mM, HNE reacts preferentially with cysteine and lysine residues. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the HNE-modified enzyme suggested the formation of intra- and intermolecular cross-links of the enzyme subunit. The HNE-dependent loss of amino acid residues was accompanied by the generation of protein-linked carbonyl derivatives as assessed by reduction with NaB[H-3]H-4 and reaction with 2,4-dinitrophenylhydrazine. Thus, the conjugation of all the amino acids appears to involve Michael addition type reactions in which the carbonyl function of HNE would be preserved. The modified histidine residues were quantitatively recovered as the HNE-histidine adduct. However, only 28% of the missing lysine could be accounted for as the HNE-lysine derivative, and only 15.6% of the modified cysteine could be accounted for as the HNE-cysteine thioether derivative. It is proposed that the carbonyl groups of the HNE-derived Michael addition products may undergo secondary reactions with the amino acid groups of lysine residues to yield inter- and intrasubunit cross-links. C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 33 TC 442 Z9 452 U1 2 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6388 EP 6393 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800047 PM 8454610 ER PT J AU CHANG, DY MARAIA, RJ AF CHANG, DY MARAIA, RJ TI A CELLULAR PROTEIN BINDS B1 AND ALU SMALL CYTOPLASMIC RNAS INVITRO SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SIGNAL RECOGNITION PARTICLE; ALPHA-FETOPROTEIN GENE; SRP-RNA; REPETITIVE SEQUENCES; SECONDARY STRUCTURE; 7S RNA; DOMAIN; DNA; TRANSLOCATION; COMPLEMENTARY AB B1 and Alu are sequence-homologous interspersed elements of unknown function that have expanded in the genomes of mice and humans, respectively. A minority of B1 and Alu sequences are expressed as small cytoplasmic RNAs. These RNAs have conserved a secondary structure motif also present in signal recognition particle (SRP) RNA despite substantial sequence divergence, whereas random B1 and Alu sequences have not. This RNA structure has also been conserved by the source sequences that gave rise to successive transpositions during B1 and Alu evolution. In the present work small cytoplasmic B1 and Alu RNAs synthesized in vitro were found to bind a cellular protein by mobility shift and UV cross-linking analyses. The mouse and human proteins demonstrate the same specificity to a panel of competitor RNAs. Results using mutated B1 RNA indicate that a single strand loop in the conserved Alu motif is essential for binding. Previous work by Strub et al. (Stub, K., Moss, J. B., and Walter, P. (1991) Mol. Cell. Biol. 11, 3949-3959) demonstrated that the Alu-specific protein SRP 9/14 does not footprint to this region of SRP RNA. This observation coupled with the failure of anti-SRP/9 antibodies to identify SRP 9/14 in the B1 RNA-protein complex as well as the apparent mass and other characteristics of the protein described here suggest that it is a novel B1-Alu RNA-binding protein. Conservation of primary and secondary structure by B1 and Alu small cytoplasmic RNAs as well as features of their specific expression and ability to interact with the conserved binding protein indicate that these RNAs are more homologous than previously appreciated. C1 NICHHD,MOLEC GROWTH REGULAT LAB,BALTIMORE,MD 21224. NR 33 TC 44 Z9 44 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6423 EP 6428 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800052 PM 7681065 ER PT J AU UEKI, K KINCAID, RL AF UEKI, K KINCAID, RL TI INTERCHANGEABLE ASSOCIATIONS OF CALCINEURIN REGULATORY SUBUNIT ISOFORMS WITH MAMMALIAN AND FUNGAL CATALYTIC SUBUNITS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DEPENDENT PROTEIN PHOSPHATASE; CALMODULIN-BINDING-PROTEIN; CALCIUM-BINDING; IDENTIFICATION; CLONING; CDNA; EXPRESSION; ISOZYMES; SEQUENCE; BRAIN AB Two mammalian genes for the Ca2+-binding regulatory subunit of the calmodulin-dependent protein phosphatase (calcineurin) were identified recently, suggesting unique associations with tissue-specific catalytic subunits. The murine brain (beta1) and testis (beta2) isoforms of the regulatory subunit were expressed with poly-histidine carboxyl termini and purified by Ni2+-chelate chromatography, each exhibiting high affinity Ca2+ binding on nitrocellulose overlays. Using chromatographic methods to assess complex formation, the beta1 and beta2 isoforms appeared indistinguishable in their binding to bacterially expressed forms of the murine brain (alpha1) or testis (alpha3) catalytic subunits; this suggests that multiple heterodimeric forms may be present in some tissues. Furthermore, both beta1 and beta2 formed complexes with the recombinant catalytic subunit from Neurospora crassa. For this catalytically active fungal enzyme, stoichiometric amounts of mammalian regulatory subunit increased calmodulin-dependent activity without affecting that stimulated by Mn2+ alone. Maximal hydrolysis of p-nitrophenyl phosphate by the N. crassa catalytic subunit was stimulated 80-120% with the beta1 isoform and 30-50% by beta2. Significantly, the incubation time at 4-degrees-C required for optimal activation (6-8 h) was much greater than that for association (1 h), indicating that the catalytic subunit undergoes a slow transition to an activated conformation after binding the regulatory subunit. The production of functional heterodimers of mammalian and fungal proteins implies highly conserved interaction domains on the catalytic and regulatory subunits of this phosphatase. RP UEKI, K (reprint author), NIAAA,MOLEC & CELLULAR NEUROBIOL LAB,IMMUNOL SECT,ROCKVILLE,MD 20852, USA. NR 33 TC 22 Z9 22 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6554 EP 6559 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800069 PM 8384215 ER PT J AU YANG, Q CO, D SOMMERCORN, J TONKS, NK AF YANG, Q CO, D SOMMERCORN, J TONKS, NK TI CLONING AND EXPRESSION OF PTP-PEST - A NOVEL, HUMAN, NONTRANSMEMBRANE PROTEIN TYROSINE PHOSPHATASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN-PLACENTA; XENOPUS OOCYTES; SKELETAL-MUSCLE; PURIFICATION; INSULIN; CELLS; SEQUENCE; KINASES; FAMILY; MICROINJECTION AB The polymerase chain reaction was used to amplify protein tyrosine phosphatase (PTPase)-related cDNA from a template of total RNA isolated from human skeletal muscle. A novel PTPase, which we term PTP-PEST, was detected by this method. The polymerase chain reaction fragment was used to screen two different HeLa cell libraries to obtain full length cDNA clones. The cDNA predicts a protein of 510 amino acids, approximately 60 kDa, that does not contain an obvious signal sequence or transmembrane segment suggesting it is a nonreceptor type enzyme. The PTPase domain is located in the N-terminal portion of the molecule and displays approximately 35% identity to other members of this family of enzymes. The C-terminal segment is rich in Pro, Glu, Asp, Ser, and Thr residues, possessing features of PEST motifs which have previously been identified in proteins with very short intracellular half-lives. The protein was expressed in Escherichia coli as a fusion product with glutathione S-transferase. Intrinsic activity was demonstrated in vitro against a variety of phosphotyrosine-containing substrates including BIRK, the autophosphorylated cytoplasmic kinase domain of the insulin receptor beta subunit. It did not dephosphorylate phosphoseryl-phosphorylase a. PTP-PEST mRNA is broadly distributed in a variety of cell lines. Stimulation of human rhabdomyosarcoma A204 cells, a transformed muscle line, with insulin led to an approximately 4-fold induction of PTP-PEST mRNA within 36 h. C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. RP YANG, Q (reprint author), COLD SPRING HARBOR LAB,DEMEREC BLDG,POB 100,COLD SPRING HARBOR,NY 11724, USA. FU NCI NIH HHS [CA53840, CA45508] NR 36 TC 80 Z9 83 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6622 EP 6628 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800079 PM 8454633 ER PT J AU JHON, DY LEE, HH PARK, DG LEE, CW LEE, KH YOO, OJ RHEE, SG AF JHON, DY LEE, HH PARK, DG LEE, CW LEE, KH YOO, OJ RHEE, SG TI CLONING, SEQUENCING, PURIFICATION, AND GQ-DEPENDENT ACTIVATION OF PHOSPHOLIPASE-C-BETA-3 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BOVINE BRAIN; G-PROTEINS; SIGNAL TRANSDUCTION; BETA-1 ISOZYME; COMPLETE CDNA; C ISOZYMES; GENE; DROSOPHILA; DIVERSITY; BINDING AB Six mammalian phospholipase C isozymes (PLC-beta1, PLC-beta2, PLC-gamma1, PLC-gamma2, PLC-delta1, and PLC-delta2) have been identified at both protein and DNA levels. Here, cDNAs corresponding to a previously unidentified PLC isozyme were isolated from a rat thyroid cell FRTL cDNA library. Comparison of the predicted amino acid sequence of this new PLC with other known PLC isozymes revealed a high degree of overall similarity with PLC-beta1 and PLC-beta2. Thus, the new PLC was named PLC-beta3. Comparison with PLC-beta1 and PLC-Beta2 also revealed that the deduced amino-terminal sequence of PLC-beta3 was incomplete by 10-20 amino acids. With the use of antibodies raised against synthetic peptides corresponding to PLC-beta3-specific amino acid sequences, we purified PLC-beta3 from a rat brain particulate fraction. The purified enzyme exhibited an apparent molecular mass of 152 kDa on SDS-polyacrylamide gels, as compared with 150 and 140 kDa for PLC-beta1 and PLC-beta2, respectively. Studies of the activation of PLC-beta isozymes by three alpha subunits of G(q) class G proteins, alpha(q), all, and alpha1 in the presence of guanosine 5-O-(3-thiotriphosphate) (GTPgammaS) revealed that the extent of activation decreased in the order of PLC-beta1 greater-than-or-equal-to PLC-beta3 >> PLC-beta2 for all three alpha subunits, suggesting a certain degree of specificity in the interaction of G(q)alpha subunits with different PLC-beta isozymes. C1 KOREA ADV INST SCI & TECHNOL,DEPT LIFE SCI,DAEDOK 305701,SOUTH KOREA. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RI Yoo, Ook Joon/C-1860-2011 NR 37 TC 190 Z9 195 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6654 EP 6661 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800083 PM 8454637 ER PT J AU KLEMENT, JF CVEKL, A PIATIGORSKY, J AF KLEMENT, JF CVEKL, A PIATIGORSKY, J TI FUNCTIONAL ELEMENTS DE2A, DE2B, AND DE1A AND THE TATA BOX ARE REQUIRED FOR ACTIVITY OF THE CHICKEN ALPHA-A-CRYSTALLIN GENE IN TRANSFECTED LENS EPITHELIAL-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TISSUE-SPECIFIC EXPRESSION; B-CRYSTALLIN; DNA-BINDING; PROMOTER; ENHANCER; PROTEIN; MOUSE; INTERACTS; FEATURES; EXTRACT AB AlphaA-crystallin is an abundant soluble protein of the vertebrate eye lens. In addition to the TATA box, four positive cis-regulatory elements of the chicken alphaA-crystallin gene have been identified by linker scanning mutagenesis, DNase I footprinting, and gel mobility shift experiments. The regulatory elements described here have been named DE2A (at positions -144 to -134), DE2B (at positions -128 to -118), and DE1A (at positions -114 to -103). DE2A and DE2B form a dyad of symmetry between positions -141 and -118 (5'-AGACTGTCAT....AGGTCAGTCT-3'), consistent with the close similarity in the mobility of complexes formed with lens nuclear proteins by these two elements. Mutations in DE2A, DE2B, and DE1A leading to loss of promoter activity using the bacterial chloramphenicol acetyltransferase reporter gene transfected into primary embryonic chicken lens epithelial cells resulted in a corresponding loss in the ability to compete for complex formation with lens nuclear proteins in gel mobility shift assays. Mutation of the alphaA-CRYBP1-like site (-67/-57), necessary for function of the mouse alphaA-crystallin promoter, did not affect the activity of the chicken promoter. The DNase I footprinting and gel mobility shift experiments confirmed the previously noted binding of nuclear proteins to a dyad of symmetry at positions -153 to -140. In contrast to DE2A, DE2B, and DE1A, mutagenesis and gel mobility shift experiments failed to correlate function and protein binding for the -153/-140 dyad. DE2A, DE2B, and DE1A agree well with the regulatory elements alphaCE1 (-162/-134), alphaCE3 (-135/-121), and alphaCE2 (-119/-99) (Matsuo, I., and Yasuda, K. (1992) Nucleic Acids Res. 20, 3701-3712) for this gene. The present results suggest, however, that the lens enhancer activity of alphaCE1 is due to the sequence -141/-134, which forms the upper half of the DE2A/DE2B dyad of symmetry, rather than the -153/-140 dyad as previously suspected. C1 NIH,LMDB,BLDG 6,RM 201,BETHESDA,MD 20892. RI Cvekl, Ales/B-2427-2013 NR 43 TC 17 Z9 18 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6777 EP 6784 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800100 PM 8454650 ER PT J AU REMALEY, AT WONG, AW SCHUMACHER, UK MENG, MS BREWER, HB HOEG, JM AF REMALEY, AT WONG, AW SCHUMACHER, UK MENG, MS BREWER, HB HOEG, JM TI O-LINKED GLYCOSYLATION MODIFIES THE ASSOCIATION OF APOLIPOPROTEIN A-II TO HIGH-DENSITY-LIPOPROTEINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HAMSTER OVARY CELLS; HUMAN-PLASMA; CHOLESTEROL ACYLTRANSFERASE; ACID SEQUENCE; C-III; EXPRESSION; PARTICLES; SECRETION; APOCIII; GENE AB O-Linked glycosylation is a common post-translational modification of apolipoproteins, but no structural or functional role for it has been identified. We examined the biosynthesis of apolipoprotein (apo) A-II in Hep G2 cells and in glycosylation-defective Chinese hamster ovary (CHO) cell mutants transfected with apoA-II cDNA. Three monomeric isoforms of apoA-II with an apparent molecular mass of 8.5, 9.8, and 11.4 kDa were synthesized by Hep G2 cells and transfected wild-type CHO cells. The 9.8- and 11.4-kDa isoforms were sialylated but not the 8.5-kDa isoform. Transfected ldlD cells, which are defective in the biosynthesis of galactose and N-acetylgalactosamine, only produced the 8.5-kDa isoform; however, when grown in media supplemented with these sugars, ldlD cells produced all three isoforms of apoA-II. Pulse-chase analysis of ldlD cells showed that glycosylation was not necessary for secretion of apoA-II. Glycosylation did modify the association of apoA-II with nascent high density lipoprotein (HDL) recreted by Hep G2 cells. The sialylated isoforms were lipid-poor and were present in the lipoprotein-deficient density range, whereas the nonsialylated 8.5-kDa isoform was associated with LpA-I, A-II lipoprotein particles in the HDL density range. ApoA-II from transfected IdlD cells, regardless of glycosylation, were lipid-poor. When preincubated with HDL from serum, however, sialylated apoA-II from both IdlD cells and Hep G2 cells associated with lipoprotein particles within the HDL3 density, whereas nonsialylated apoA-II was found throughout the HDL density range. In summary, O-linked glycosylation is not necessary for the secretion of apoA-II but does modify the association of apoA-II to HDL and may, therefore, play an important role in the metabolism of HDL. RP REMALEY, AT (reprint author), NHLBI,BLDG 10 7N114,BETHESDA,MD 20892, USA. NR 50 TC 26 Z9 26 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1993 VL 268 IS 9 BP 6785 EP 6790 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KT368 UT WOS:A1993KT36800101 PM 8454651 ER PT J AU PANTALEO, G GRAZIOSI, C DEMAREST, JF BUTINI, L MONTRONI, M FOX, CH ORENSTEIN, JM KOTLER, DP FAUCI, AS AF PANTALEO, G GRAZIOSI, C DEMAREST, JF BUTINI, L MONTRONI, M FOX, CH ORENSTEIN, JM KOTLER, DP FAUCI, AS TI HIV-INFECTION IS ACTIVE AND PROGRESSIVE IN LYMPHOID-TISSUE DURING THE CLINICALLY LATENT STAGE OF DISEASE SO NATURE LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; CELLS; AIDS; LYMPHADENOPATHY; AMPLIFICATION; RESERVOIRS; EXPRESSION; NODES; RNA AB PRIMARY infection with the human immunodeficiency virus (HIV) is generally followed by a burst of viraemia with or without clinical symptoms1-3. This in turn is followed by a prolonged period of clinical latency. During this period there is little, if any, detectable viraemia, the numbers of infected cells in the blood are very low, and it is extremely difficult to demonstrate virus expression in these cells4. We have analysed viral burden and levels of virus replication simultaneously in the blood and lymphoid organs of the same individuals at various stages of HIV disease. Here we report that in early-stage disease there is a dichotomy between the levels of viral burden and virus replication in peripheral blood versus lymphoid organs. HIV disease is active in the lymphoid tissue throughout the period of clinical latency, even at times when minimal viral activity is demonstrated in blood. C1 UNIV ANCONA,DEPT INTERNAL MED,I-60020 ANCONA,ITALY. YALE UNIV,SCH MED,DEPT NEUROPATHOL,NEW HAVEN,CT 06510. GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC 20037. ST LUKES ROOSEVELT HOSP,NEW YORK,NY 10025. RP PANTALEO, G (reprint author), NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892, USA. RI Pantaleo, Giuseppe/K-6163-2016 NR 23 TC 1595 Z9 1605 U1 4 U2 44 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 25 PY 1993 VL 362 IS 6418 BP 355 EP 358 DI 10.1038/362355a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KU176 UT WOS:A1993KU17600065 PM 8455722 ER PT J AU POTTER, WZ RUDORFER, MV AF POTTER, WZ RUDORFER, MV TI ELECTROCONVULSIVE-THERAPY - A MODERN MEDICAL PROCEDURE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID ECT RP POTTER, WZ (reprint author), NIMH,BETHESDA,MD 20892, USA. NR 9 TC 44 Z9 44 U1 3 U2 4 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 25 PY 1993 VL 328 IS 12 BP 882 EP 883 DI 10.1056/NEJM199303253281213 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KT814 UT WOS:A1993KT81400013 PM 8441434 ER PT J AU WILLIAMS, AO AF WILLIAMS, AO TI MORE ON VAGINAL INFLAMMATION IN AFRICA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP WILLIAMS, AO (reprint author), NCI,BETHESDA,MD 20892, USA. NR 3 TC 2 Z9 2 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 25 PY 1993 VL 328 IS 12 BP 888 EP 888 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KT814 UT WOS:A1993KT81400026 PM 8441442 ER PT J AU WANG, L PRECHT, P BALAKIR, R HORTON, WE AF WANG, L PRECHT, P BALAKIR, R HORTON, WE TI RAT AND CHICK CDNA CLONES ENCODING HMG-LIKE PROTEINS SO NUCLEIC ACIDS RESEARCH LA English DT Article ID DNA-BINDING MOTIF; HOMOLOGY RP WANG, L (reprint author), NIA,GERONTOL RES CTR,BIOL CHEM LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 7 TC 10 Z9 12 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAR 25 PY 1993 VL 21 IS 6 BP 1493 EP 1493 DI 10.1093/nar/21.6.1493 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW735 UT WOS:A1993KW73500026 PM 8464746 ER PT J AU KOONIN, EV AF KOONIN, EV TI ESCHERICHIA-COLI DING GENE ENCODES A PUTATIVE DNA HELICASE RELATED TO A GROUP OF EUKARYOTIC HELICASES INCLUDING RAD3 PROTEIN SO NUCLEIC ACIDS RESEARCH LA English DT Article ID SACCHAROMYCES-CEREVISIAE; REPLICATION; REPAIR RP NIH, NATL CTR BIOTECHNOL INFORMAT, NATL LIB MED, BLDG 38A, BETHESDA, MD 20892 USA. NR 11 TC 25 Z9 27 U1 1 U2 4 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 EI 1362-4962 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAR 25 PY 1993 VL 21 IS 6 BP 1497 EP 1497 DI 10.1093/nar/21.6.1497 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW735 UT WOS:A1993KW73500030 PM 8385320 ER PT J AU RIVETTI, C MOZZARELLI, A ROSSI, GL HENRY, ER EATON, WA AF RIVETTI, C MOZZARELLI, A ROSSI, GL HENRY, ER EATON, WA TI OXYGEN BINDING BY SINGLE-CRYSTALS OF HEMOGLOBIN SO BIOCHEMISTRY LA English DT Article ID DEOXY QUATERNARY CONFORMATION; STATE HUMAN-HEMOGLOBIN; LIGAND-BINDING; POLYETHYLENE-GLYCOL; T-STATE; ALLOSTERIC INTERPRETATION; MODEL; COOPERATIVITY; MECHANISM; CRYSTALLIZATION AB Reversible oxygen binding curves for single crystals of hemoglobin in the T quaternary structure have been measured using microspectrophotometry. Saturations were determined from complete visible spectra measured with light linearly polarized parallel to the a and c crystal axes. Striking differences were observed between the binding properties of hemoglobin in the crystal and those of hemoglobin in solution. Oxygen binding to the crystal is effectively noncooperative, the Bohr effect is absent, and there is no effect of chloride ion. Also, the oxygen affinity is lower than that of the T quaternary structure in solution. The absence of the Bohr effect supports Perutz's hypothesis on the key role of the salt bridges, which are known from X-ray crystallography to remain intact upon oxygenation. The low affinity and absence of the Bohr effect can be explained by a generalization of the MWC-PSK model (Monod, Wyman, & Changeux, 1965; Perutz, 1970; Szabo & Karplus, 1972) in which both high- and low-affinity tertiary conformations, with broken and unbroken salt bridges, respectively, are populated in the T quaternary structure. Because the alpha and beta hemes make different projections onto the two crystal axes, separate binding curves for the alpha and beta subunits could be calculated from the two measured binding curves. The approximately 5-fold difference between the oxygen affinities of the alpha and beta subunits is much smaller than that predicted from the crystallographic study of Dodson, Liddington, and co-workers, which suggested that oxygen binds only to the alpha hemes. This 5-fold difference is exactly compensated by a small amount of cooperativity to produce the crystal binding curve with a Hill n of 1.0. In terms of free energy, the cooperativity is only about 10% of that observed in solution. It therefore represents only a slight perturbation on the essential feature of an allosteric model that the binding curve for hemoglobin in the T quaternary structure be perfectly noncooperative. If the concentration of the crystallizing agent [poly(ethylene glycol)] and/or the fraction of oxidized hemes are not sufficiently high, oxygen binding is no longer reversible. Under these conditions the crystals crack and undergo a time-dependent increase in their saturation with oxygen. We tentatively assume that this change corresponds to the conversion of the low-affinity T quaternary structure to the high-affinity R quaternary structure, opening up the possibility of carrying out a detailed kinetic study of the quaternary conformational change in the crystal by monitoring the oxygen saturation. C1 UNIV PARMA,INST BIOCHEM SCI,I-43100 PARMA,ITALY. NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. RI Henry, Eric/J-3414-2013; Mozzarelli, Andrea/C-3615-2014; OI Henry, Eric/0000-0002-5648-8696; Mozzarelli, Andrea/0000-0003-3762-0062; Rivetti, Claudio/0000-0003-3775-6779 NR 86 TC 109 Z9 110 U1 2 U2 7 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 23 PY 1993 VL 32 IS 11 BP 2888 EP 2906 DI 10.1021/bi00062a021 PG 19 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KU078 UT WOS:A1993KU07800021 PM 8457555 ER PT J AU NAGAI, K KANBARA, K NAKASHIMA, H YAMAMOTO, N TORRENCE, PF SUHADOLNIK, RJ TAKAKU, H AF NAGAI, K KANBARA, K NAKASHIMA, H YAMAMOTO, N TORRENCE, PF SUHADOLNIK, RJ TAKAKU, H TI CHARACTERIZATION AND BIOLOGICAL-ACTIVITY OF 8-SUBSTITUTED ANALOGS OF 2',5'-OLIGOADENYLATES SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE 2',5'-OLIGOADENYLATE ID RIBONUCLEASE-L BINDING; REVERSE-TRANSCRIPTASE; ACTIVATION ABILITIES; CORDYCEPIN ANALOGS; PURINE NUCLEOSIDES; GLYCOSYL TORSION; CONFORMATION; 8-BROMOADENOSINE; INHIBITION; INFECTION AB Analogues of the 2',5'-linked adenylate trimer 5'-monophosphates (p5'A2'p5'A2'p5'A) containing 8-hydroxyadenosine and 8-mercaptoadenosine in the first, second, and third nucleotide positions were tested for their ability to bind to and activate RNase L of mouse L cells. The ability of p5'A(SH)2'p5'A(SH) 2'p5'A(SH) (pA(SH)3) (1c) to bind 2-5A dependent endonuclease was markedly decreased. On the other hand, an analogue of the 2',5'-linked adenylate trimer monophosphate substituted by 8-hydroxyadenosine in the first, second, and third nucleotide positions bound almost as well as parent 2-5A [pppA(2'p5'A)2] (P3A3) (1d) to RNase L. The 8-substituted analogues of 2-5A were more resistant to the degradation by the (2',5') phosphodiesterase. Of particular interest is monophosphate, pA(SH)3 (1c) which possessed higher anti-HIV activity than pA3 (1a) or pA(OH)3 (1b). C1 NIDDKD,BIOMED CHEM SECT,MED CHEM LAB,BETHESDA,MD. TOKYO MED & DENT UNIV,SCH MED,DEPT MICROBIOL,BUNKYO KU,TOKYO 113,JAPAN. TEMPLE UNIV,HLTH SCI CTR,SCH MED,DEPT BIOCHEM,PHILADELPHIA,PA 19140. NR 25 TC 3 Z9 3 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD MAR 21 PY 1993 VL 1156 IS 3 BP 321 EP 326 DI 10.1016/0304-4165(93)90050-I PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KU097 UT WOS:A1993KU09700014 PM 8461324 ER PT J AU KAGAN, J GELMAN, R WAXDAL, M KIDD, P AF KAGAN, J GELMAN, R WAXDAL, M KIDD, P TI NIAID DIVISION OF AIDS FLOW-CYTOMETRY QUALITY ASSESSMENT PROGRAM SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. FAST SYST INC,GAITHERSBURG,MD 20877. UNIV WASHINGTON,DEPT LAB MED,SEATTLE,WA 98195. RP KAGAN, J (reprint author), NIAID,DIV AIDS,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [N01-AI-95010, N01-AI-95030] NR 0 TC 13 Z9 13 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD MAR 20 PY 1993 VL 677 BP 50 EP 52 DI 10.1111/j.1749-6632.1993.tb38763.x PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX225 UT WOS:A1993KX22500007 PM 8494245 ER PT J AU CHREST, FJ PAULY, RR MONTICONE, R LAKATTA, EG ADLER, WH AF CHREST, FJ PAULY, RR MONTICONE, R LAKATTA, EG ADLER, WH TI TGF-BETA-1 RECEPTOR EXPRESSION AND CELL-CYCLE ANALYSIS OF VASCULAR SMOOTH-MUSCLE CELLS FROM YOUNG AND AGED RATS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article RP CHREST, FJ (reprint author), NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,CLIN IMMUNOL SECT,BALTIMORE,MD 21224, USA. NR 3 TC 2 Z9 2 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD MAR 20 PY 1993 VL 677 BP 396 EP 399 DI 10.1111/j.1749-6632.1993.tb38796.x PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX225 UT WOS:A1993KX22500040 PM 8388181 ER PT J AU KIRBY, MR DONAHUE, RE AF KIRBY, MR DONAHUE, RE TI RARE EVENT SORTING OF CD34+ HEMATOPOIETIC-CELLS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article RP KIRBY, MR (reprint author), NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892, USA. NR 4 TC 3 Z9 3 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD MAR 20 PY 1993 VL 677 BP 413 EP 416 DI 10.1111/j.1749-6632.1993.tb38802.x PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX225 UT WOS:A1993KX22500046 PM 7684209 ER PT J AU PARK, LP MARGOLICK, JB GIORGI, JV FERBAS, J BAUER, K KASLOW, R MUNOZ, A AF PARK, LP MARGOLICK, JB GIORGI, JV FERBAS, J BAUER, K KASLOW, R MUNOZ, A TI INFLUENCE OF HIV-1 INFECTION AND CIGARETTE-SMOKING ON LEUKOCYTE PROFILE IN HOMOSEXUAL MEN SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article C1 JOHNS HOPKINS UNIV,SCH PUBL HLTH,DEPT TOXICOL SCI,BALTIMORE,MD 21205. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT MICROBIOL,PITTSBURGH,PA 15261. NORTHWESTERN UNIV,SCH MED,DEPT PATHOL,CHICAGO,IL 60611. NIAID,EPIDEMIOL & BIOMETRY BRANCH,BETHESDA,MD 20852. RP PARK, LP (reprint author), JOHNS HOPKINS UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD 21205, USA. NR 4 TC 0 Z9 1 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD MAR 20 PY 1993 VL 677 BP 433 EP 436 DI 10.1111/j.1749-6632.1993.tb38809.x PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX225 UT WOS:A1993KX22500053 PM 8494235 ER PT J AU GRASBERGER, BL GRONENBORN, AM CLORE, GM AF GRASBERGER, BL GRONENBORN, AM CLORE, GM TI ANALYSIS OF THE BACKBONE DYNAMICS OF INTERLEUKIN-8 BY N-15 RELAXATION MEASUREMENTS SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE INTERLEUKIN-8; PROTEIN DYNAMICS; HETERONUCLEAR RELAXATION ID HETERONUCLEAR NMR-SPECTROSCOPY; NUCLEAR-MAGNETIC-RESONANCE; MULTIPLE QUANTUM COHERENCE; MODEL-FREE APPROACH; RECEPTOR-BINDING; 3-DIMENSIONAL STRUCTURE; LARGER PROTEINS; MACROMOLECULES; RESIDUES; SPECTRA RP GRASBERGER, BL (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 2,BETHESDA,MD 20892, USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 31 TC 56 Z9 56 U1 0 U2 2 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD MAR 20 PY 1993 VL 230 IS 2 BP 364 EP 372 DI 10.1006/jmbi.1993.1152 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW260 UT WOS:A1993KW26000002 PM 8464050 ER PT J AU PANYUTIN, IG HSIEH, P AF PANYUTIN, IG HSIEH, P TI FORMATION OF A SINGLE BASE MISMATCH IMPEDES SPONTANEOUS DNA BRANCH MIGRATION SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE RECOMBINATION; BRANCH MIGRATION; HOLLIDAY JUNCTION ID SITE-SPECIFIC RECOMBINATION; GENETIC RECOMBINATION; STRAND-EXCHANGE; RECA-PROTEIN; HOLLIDAY JUNCTIONS; MOLECULES; LAMBDA; INSERTIONS; RESOLUTION; DELETIONS RP PANYUTIN, IG (reprint author), NIDDKD, GENET & BIOCHEM BRANCH, BETHESDA, MD 20892 USA. NR 39 TC 111 Z9 112 U1 2 U2 12 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD MAR 20 PY 1993 VL 230 IS 2 BP 413 EP 424 DI 10.1006/jmbi.1993.1159 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW260 UT WOS:A1993KW26000009 PM 8464057 ER PT J AU KANTOROW, M CVEKL, A SAX, CM PIATIGORSKY, J AF KANTOROW, M CVEKL, A SAX, CM PIATIGORSKY, J TI PROTEIN DNA INTERACTIONS OF THE MOUSE ALPHA-A-CRYSTALLIN CONTROL REGIONS - DIFFERENCES BETWEEN EXPRESSING AND NON-EXPRESSING CELLS SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE GENE EXPRESSION; INVIVO FOOTPRINTING; ALPHA-A-CRYSTALLIN ID LENS CRYSTALLINS; TRANSCRIPTION INITIATION; GENE; PROMOTER; TISSUE; DELTA-1-CRYSTALLIN; EPITHELIA; EVOLUTION; ENHANCER; INTRON RP KANTOROW, M (reprint author), NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892, USA. RI Cvekl, Ales/B-2427-2013 NR 32 TC 19 Z9 19 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD MAR 20 PY 1993 VL 230 IS 2 BP 425 EP 435 DI 10.1006/jmbi.1993.1160 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW260 UT WOS:A1993KW26000010 PM 8464058 ER PT J AU STEINERT, PM MAREKOV, LN FRASER, RDB PARRY, DAD AF STEINERT, PM MAREKOV, LN FRASER, RDB PARRY, DAD TI KERATIN INTERMEDIATE FILAMENT STRUCTURE - CROSS-LINKING STUDIES YIELD QUANTITATIVE INFORMATION ON MOLECULAR DIMENSIONS AND MECHANISM OF ASSEMBLY SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE KERATIN; INTERMEDIATE FILAMENTS; 2-DIMENSIONAL SURFACE LATTICE ID EPIDERMOLYSIS-BULLOSA SIMPLEX; TRANSMISSION ELECTRON-MICROSCOPY; BOVINE EPIDERMAL KERATIN; COILED-COIL MOLECULES; ALPHA-KERATIN; VIMENTIN SUBUNITS; NF-L; PROTEINS; INVITRO; EXPRESSION C1 NIH,BETHESDA,MD 20892. MASSEY UNIV,DEPT PHYS & BIOPHYS,PALMERSTON NORTH,NEW ZEALAND. RP STEINERT, PM (reprint author), NIAMSD,SKIN BIOL BRANCH,BLDG 6,ROOM 425,BETHESDA,MD 20892, USA. NR 73 TC 216 Z9 220 U1 4 U2 17 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD MAR 20 PY 1993 VL 230 IS 2 BP 436 EP 452 DI 10.1006/jmbi.1993.1161 PG 17 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KW260 UT WOS:A1993KW26000011 PM 7681879 ER PT J AU MURPHY, EL ENGSTROM, JW MILLER, K SACHER, RA BUSCH, MP HOLLINGSWORTH, CG AF MURPHY, EL ENGSTROM, JW MILLER, K SACHER, RA BUSCH, MP HOLLINGSWORTH, CG TI HTLV-II ASSOCIATED MYELOPATHY IN 43-YEAR-OLD WOMAN SO LANCET LA English DT Letter C1 WESTAT CORP,ROCKVILLE,MD. NHLBI,IRWIN MEM BLOOD CTR,BETHESDA,MD 20892. RP MURPHY, EL (reprint author), UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143, USA. NR 7 TC 54 Z9 54 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD MAR 20 PY 1993 VL 341 IS 8847 BP 757 EP 758 DI 10.1016/0140-6736(93)90529-P PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KT362 UT WOS:A1993KT36200036 PM 8095653 ER PT J AU FEUILLAN, PP MILLAN, MA AGUILERA, G AF FEUILLAN, PP MILLAN, MA AGUILERA, G TI ANGIOTENSIN-II BINDING-SITES IN THE RAT FETUS - CHARACTERIZATION OF RECEPTOR SUBTYPES AND INTERACTION WITH GUANYL NUCLEOTIDES SO REGULATORY PEPTIDES LA English DT Article DE ANGIOTENSIN-II; FETAL RAT; ANGIOTENSIN-II RECEPTOR; CHARACTERIZATION; AUTORADIOGRAPHY ID IDENTIFICATION; EXPRESSION; SYSTEMS AB Angiotensin II (AII) receptor subtypes were studied in the 18-day gestation fetal rat, using two non-peptide All antagonists: (2-n-butyl-4-chloro-5-hydroxymethyl-1-(2'-(1H-tetrazol-5-yl)biphenyl-4-yl)methyl)imidazol (DuP 753; type 1 (AT1) specific), and 1-(4-amino-3-methylpenyl)methyl-5-diphenacetyl-4,5,6,7-tetrahydro-1-H-imidazo[4,5-c]pyridine-6-carboxylic acid (PD 123 177; type 2 (AT2) specific). Autoradiography using I-125-[Sar1,Ile8]AII showed that 10 muM PD 123 177 decreased binding to near-nonspecific levels in skin, skeletal muscle and adrenal medulla, whereas 10 muM DuP 753 blocked binding in the liver and lung. Studies in skin and liver membranes confirmed the autoradiographic data: AT1 receptors were predominant in the liver (95%), and AT2 in the skin (97%). There was no cross-reactivity between receptor subtype and the heterologous antagonist up to a concentration of 10 muM. In both skin and liver, 2 mM dithiothreitol enhanced the binding of AT2 receptors by increasing receptor affinity, but inhibited binding of AT1 by decreasing the receptor number. In the absence of antagonists, guanyl nucleotides, added at equilibrium, caused marked dissociation of I-125-AII binding in liver membranes, but had minimal effect in skin. However, dissociation occurred in the skin when AT2 sites were blocked with 10 muM PD 123 177, and in liver, dissociation was not observed when AT1 sites were blocked with DuP 753. Hence, in contrast to classical AII target tissues, which contain predominantly AT1, most of the sites in fetal skin and skeletal muscle are AT2. The demonstration that the effects of guanyl nucleotides are selective for receptor subtype suggests that the AT1 receptor, but not the AT2, is coupled to cell function via guanyl nucleotide binding proteins. The functional importance of the AT2 receptors and their role in fetal physiology is under current investigation. RP FEUILLAN, PP (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,ENDOCRINE PHYSIOL SECT,BLDG 10,RM 10N262,BETHESDA,MD 20892, USA. NR 25 TC 19 Z9 19 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 MAR 19 PY 1993 VL 44 IS 2 BP 159 EP 169 DI 10.1016/0167-0115(93)90239-5 PG 11 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA KT536 UT WOS:A1993KT53600007 PM 8469771 ER PT J AU GREEN, P LIPMAN, D HILLIER, L WATERSTON, R STATES, D CLAVERIE, JM AF GREEN, P LIPMAN, D HILLIER, L WATERSTON, R STATES, D CLAVERIE, JM TI ANCIENT CONSERVED REGIONS IN NEW GENE-SEQUENCES AND THE PROTEIN DATABASES SO SCIENCE LA English DT Article ID MOTIFS AB Sets of new gene sequences from human, nematode, and yeast were compared with each other and with a set of Escherichia coli genes in order to detect ancient evolutionarily conserved regions (ACRs) in the encoded proteins. Nearly all of the ACRs so identified were found to be homologous to sequences in the protein databases. This suggests that currently known proteins may already include representatives of most ACRs and that new sequences not similar to any database sequence are unlikely to contain ACRs. Preliminary analyses indicate that moderately expressed genes may be more likely to contain ACRs than rarely expressed genes. It is estimated that there are fewer than 900 ACRs in all. C1 NIH, NATL CTR BIOTECHNOL INFORMAT, NATL LIB MED, BETHESDA, MD 20894 USA. RP WASHINGTON UNIV, SCH MED, DEPT GENET, ST LOUIS, MO 63110 USA. NR 31 TC 151 Z9 152 U1 0 U2 5 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 EI 1095-9203 J9 SCIENCE JI Science PD MAR 19 PY 1993 VL 259 IS 5102 BP 1711 EP 1716 DI 10.1126/science.8456298 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KT810 UT WOS:A1993KT81000026 PM 8456298 ER PT J AU ROHAN, PJ DAVIS, P MOSKALUK, CA KEARNS, M KRUTZSCH, H SIEBENLIST, U KELLY, K AF ROHAN, PJ DAVIS, P MOSKALUK, CA KEARNS, M KRUTZSCH, H SIEBENLIST, U KELLY, K TI PAC-1 - A MITOGEN-INDUCED NUCLEAR-PROTEIN TYROSINE PHOSPHATASE SO SCIENCE LA English DT Article ID PURIFICATION; ACTIVATION; RECEPTOR; FAMILY; GENES; CELLS AB Tyrosine phosphorylation of proteins is required for signal transduction in cells and for growth regulation. A mitogen-induced gene (PAC-1) has been cloned from human T cells and encodes a 32-kilodalton protein that contains a sequence that defines the enzymatic site of known protein phosphotyrosine phosphatases (PTPases). Other than this sequence, PAC-1 is different from several other known related PTPases exemplified by PTP-1b. PAC-1 is similar to a phosphatase induced by mitogens or heat shock in fibroblasts, a yeast gene, and a vaccinia virus-encoded serine-tyrosine phosphatase (VH1). PAC-1 was predominantly expressed in hematopoietic tissues and localized to the nucleus in transfected COS-7 cells and in mitogen-stimulated T cells. C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 23 TC 258 Z9 262 U1 0 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 19 PY 1993 VL 259 IS 5102 BP 1763 EP 1766 DI 10.1126/science.7681221 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KT810 UT WOS:A1993KT81000040 PM 7681221 ER PT J AU SMITH, JW LONGO, DL ALVORD, WG JANIK, JE SHARFMAN, WH GAUSE, BL CURTI, BD CREEKMORE, SP HOLMLUND, JT FENTON, RG SZNOL, M MILLER, LL SHIMIZU, M OPPENHEIM, JJ FIEM, SJ HURSEY, JC POWERS, GC URBA, WJ AF SMITH, JW LONGO, DL ALVORD, WG JANIK, JE SHARFMAN, WH GAUSE, BL CURTI, BD CREEKMORE, SP HOLMLUND, JT FENTON, RG SZNOL, M MILLER, LL SHIMIZU, M OPPENHEIM, JJ FIEM, SJ HURSEY, JC POWERS, GC URBA, WJ TI THE EFFECTS OF TREATMENT WITH INTERLEUKIN-1-ALPHA ON PLATELET RECOVERY AFTER HIGH-DOSE CARBOPLATIN SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID RECOMBINANT HUMAN INTERLEUKIN-3; COLONY-STIMULATING FACTOR; ENDOTHELIAL-CELLS; PHASE-I; CANCER; MICE; INVIVO; IL-1; 5-FLUOROURACIL; NEUTROPENIA AB Background. Thrombocytopenia is a frequent side effect of cancer chemotherapy and commonly limits attempts to escalate drug doses. To determine whether interleukin-1alpha could ameliorate carboplatin-induced thrombocytopenia, we combined it with high-dose carboplatin in 43 patients with advanced neoplasms. Methods. High-dose carboplatin (800 mg per square meter of body-surface area) was administered alone to a control group. Subsequent patients were randomly assigned to receive the same dose of carboplatin with interleukin-1alpha, administered either before or after carboplatin. Interleukin-1alpha was given intravenously at a dose of 0.03, 0.1, or 0.3 mug per kilogram of body weight per day for five days. Results. Carboplatin alone consistently produced thrombocytopenia with a median nadir of 19,000 platelets per cubic millimeter and a median of 10 days with less than 1 00,000 platelets per cubic millimeter. All 15 patients receiving interleukin-1alpha before carboplatin had similar findings. In contrast, 5 of the 15 patients given one of the two higher doses of interleukin-1alpha after carboplatin had minimal thrombocytopenia (nadir, 91,000 to 332,000 platelets per cubic millimeter). In the 10 patients given 0.3 mug of interleukin-1alpha per kilogram after carboplatin treatment, the platelet count recovered to 100,000 per cubic millimeter significantly earlier than in either the control group (P = 0.002) or the patients who received interleukin-1alpha before carboplatin (P = 0.003), with the median times to recovery in the three groups being 16, 21, and 23 days, respectively. At the highest dose of interleukin-1alpha, toxicity was substantial (but reversible), requiring inpatient support for hypotension, supraventricular arrhythmias, and pulmonary-capillary leak. Conclusions. Interleukin-1alpha can accelerate the recovery of platelets after high-dose carboplatin therapy and may be clinically useful in preventing or treating thrombocytopenia induced by chemotherapy. C1 NCI,FREDERICK CANC RES & DEV CTR,DATA MANAGEMENT SERV,FREDERICK,MD 21701. FREDERICK MEM HOSP,FREDERICK,MD. PROGRAM RESOURCES INC,DYNCORP,FREDERICK,MD. NCI,CANC TREATMENT EVALUAT PROGRAM,ROCKVILLE,MD. DAINIPPON PHARMACEUT CO LTD,SUITA,OSAKA 564,JAPAN. RP SMITH, JW (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701, USA. FU NCI NIH HHS [N01-CO-74102] NR 42 TC 118 Z9 118 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 18 PY 1993 VL 328 IS 11 BP 756 EP 761 DI 10.1056/NEJM199303183281103 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA KR848 UT WOS:A1993KR84800003 PM 8437596 ER PT J AU LUBIN, JH BLOT, WJ AF LUBIN, JH BLOT, WJ TI LUNG-CANCER AND SMOKING CESSATION - PATTERNS OF RISK SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material RP LUBIN, JH (reprint author), NCI,DIV CANC ETIOL,BIOSTAT BRANCH,6130 EXECUT BLVD,RM 403,ROCKVILLE,MD 20852, USA. NR 8 TC 25 Z9 25 U1 0 U2 1 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 17 PY 1993 VL 85 IS 6 BP 422 EP 423 DI 10.1093/jnci/85.6.422 PG 2 WC Oncology SC Oncology GA KR537 UT WOS:A1993KR53700001 PM 8445662 ER PT J AU PASS, HI AF PASS, HI TI PHOTODYNAMIC THERAPY IN ONCOLOGY - MECHANISMS AND CLINICAL USE SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Review ID CHINESE-HAMSTER CELLS; HEMATOPORPHYRIN DERIVATIVE PHOTORADIATION; MALIGNANT BRAIN-TUMORS; ANTIBODY-TARGETED PHOTOLYSIS; HUMAN BLADDER-CARCINOMA; HUMAN-LUNG-CANCER; RED-BLOOD-CELLS; LASER PHOTORADIATION; PHOTOFRIN-II; BEARING MICE AB In photodynamic therapy (PDT), a sensitizer, light, and oxygen are used to cause photochemically induced cell death. The mechanism of cytotoxicity involves generation of singlet oxygen and other free radicals when the light-excited sensitizer loses or accepts an electron. Although selective retention of sensitizer by malignant tissue is seen in vivo, the mechanisms for this sensitizer targeting remain unclear. The first-generation sensitizers are porphyrin based and vary in lipophilicity and hydrophilicity. Targeting of the vasculature seems to be a prominent feature of the cytotoxic effect of these sensitizers in vivo, with resulting necrosis. Treatment depth varies with the wavelength of light that activates the sensitizer used, and the second-generation sensitizers are activated at longer wavelengths, allowing for a 30% increase in treatment depths. The selectivity of targeting can be increased when the sensitizer is delivered with the use of liposomes or monoclonal antibodies specific for tumor antigens. Studies have demonstrated direct effects of PDT on immune effector cells, specifically those with lineage from macrophages or other monocytes. Clinically, this therapy has been chiefly used for palliation of endobronchial and esophageal obstruction, as well as for treatment of bladder carcinomas, skin malignancies, and brain tumors. The future of PDT rests in defining its use either as an intraoperative adjuvant to marginal surgical procedures or as a primary treatment for superficial malignancies. Phase III trials in esophageal cancer and lung cancer are in progress and will help in evaluation of whether Photofrin II, the most widely used sensitizer, can be added to the oncologic armamentarium, pending approval from the U.S. Food and Drug Administration. RP PASS, HI (reprint author), NCI,SURG BRANCH,THORAC ONCOL SECT,BLDG 10,RM 2B07,BETHESDA,MD 20892, USA. NR 214 TC 582 Z9 598 U1 10 U2 86 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 17 PY 1993 VL 85 IS 6 BP 443 EP 456 DI 10.1093/jnci/85.6.443 PG 14 WC Oncology SC Oncology GA KR537 UT WOS:A1993KR53700014 PM 8445672 ER PT J AU DAY, GL BLOT, WJ AUSTIN, DF BERNSTEIN, L GREENBERG, RS PRESTONMARTIN, S SCHOENBERG, JB WINN, DM MCLAUGHLIN, JK FRAUMENI, JF AF DAY, GL BLOT, WJ AUSTIN, DF BERNSTEIN, L GREENBERG, RS PRESTONMARTIN, S SCHOENBERG, JB WINN, DM MCLAUGHLIN, JK FRAUMENI, JF TI RACIAL-DIFFERENCES IN RISK OF ORAL AND PHARYNGEAL CANCER - ALCOHOL, TOBACCO, AND OTHER DETERMINANTS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID DIET; EPIDEMIOLOGY; ETIOLOGY; SMOKING AB Background: In the United States, Blacks have increasingly higher rates of oral and pharyngeal cancer (oral cancer) than Whites, but determinants of the racial disparity have not been clear. Purpose: The purpose of this study was to explore reasons for the higher incidence of oral cancer among Blacks than Whites. Methods: We used data from a large, population-based case-control study of oral cancer risk factors conducted in four areas of the United States. On the basis of interviews that ascertained characteristics of 1065 oral cancer patients (871 Whites and 194 Blacks) and 1182 controls (979 Whites and 203 Blacks), we examined racial differences in exposure prevalences and relative risks for a number of known etiologic factors, including tobacco and alcohol consumption, diet, and socioeconomic and other variables. To evaluate the extent to which the major risk factors explained the excess risk of oral cancer among Blacks, population-attributable risks were calculated. Results: Differences with respect to alcohol consumption, especially among current smokers, emerged as the most important explanatory variables. After adjusting for smoking, heavy drinking (greater-than-or-equal-to 30 drinks/week) resulted in a 17-fold increased risk among Blacks and a ninefold increase among Whites. Among drinkers, Blacks tended to drink more than Whites. Also, a higher (P = .01) percentage of Blacks (37%) than Whites (28%) were current smokers, although there were little or no racial differences in relative risks or patterns of use for other smoking variables, including number of cigarettes smoked per day, years of smoking, and age started smoking. From population-attributable risk calculations, we estimated that differences in alcohol and tobacco use account for the bulk of the higher incidence of oral cancer among Blacks in the United States and that, in the absence of alcohol and tobacco, the rates of this cancer according to race (Black, White) and gender would be nearly equal. With regard to other potential etiologic factors, protective effects provided by higher dietary intake of fruits and vitamin C were more pronounced for Whites, while Blacks more often tended to be in socio-demographic and medical or dental health categories associated with increased risk. Conclusions: These analyses provide evidence that various environmental or lifestyle determinants of oral cancer may contribute to the higher oral cancer rates in Blacks than in Whites in the United States, but that patterns and risks associated with alcohol consumption, particularly among current smokers, are the most important contributors to the excess risk in Blacks. Implications: These findings suggest that the key to prevention of oral and pharyngeal cancers among both Blacks and Whites is reduced intake of alcoholic beverages and, because of strong interactive effects, the cessation of smoking. C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,EXECUT PLAZA N,RM 431,BETHESDA,MD 20852. CALIF DEPT HLTH SERV,EMERYVILLE,CA. NEW JERSEY DEPT HLTH,TRENTON,NJ. UNIV SO CALIF,LOS ANGELES,CA 90089. EMORY UNIV,SCH PUBL HLTH,ATLANTA,GA 30322. NIDH,BETHESDA,MD. NR 32 TC 143 Z9 148 U1 1 U2 9 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 17 PY 1993 VL 85 IS 6 BP 465 EP 473 DI 10.1093/jnci/85.6.465 PG 9 WC Oncology SC Oncology GA KR537 UT WOS:A1993KR53700016 PM 8445674 ER PT J AU BECKWITH, M URBA, WJ LONGO, DL AF BECKWITH, M URBA, WJ LONGO, DL TI GROWTH-INHIBITION OF HUMAN LYMPHOMA CELL-LINES BY THE MARINE PRODUCTS, DOLASTATIN-10 AND DOLASTATIN-15 SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ANTI-NEOPLASTIC AGENTS; ANTINEOPLASTIC AGENTS; LEUKEMIA-CELLS; TUBULIN; VINBLASTINE; BINDING; VINCRISTINE; DRUGS; POLYMERIZATION; PROLIFERATION AB Background: Dolastatins 10 and 15 are small peptides isolated from the marine sea hare Dolabella auricularia. In vitro studies of these peptides have demonstrated antimitotic and antiproliferative activity and growth inhibition in hematopoietic progenitor cells. Purpose: The purpose of our in vitro study was to determine the biological effects of these marine peptides on growth of human lymphoma cell lines and to investigate mechanisms by which the dolastatins may act. Methods: Cell lines DB, HT, RL, and SR were grown from the ascites or pleural effusion of four patients with lymphoma. The DB, HT, and RL cell lines are of B-cell origin, and the SR cell line appears to be a less differentiated lymphoid cell type. Cells from these lines were cultured in the presence of vincristine or dolastatin 10 or 15. [H-3]Thymidine-uptake assays were used to measure effects on DNA synthesis. Cell cycle analysis using propidium iodide was performed to measure drug-induced cell-cycle arrest. DNA fragmentation was used as an assay for drug-induced apoptosis and was measured by agarose gel electrophoresis. Results: In the three B celt lines, dolastatin 10 was more effective than dolastatin 15. Values for concentrations required for inhibition of proliferation by 50% (lC50) were .00013-.0013 nM for dolastatin 10 in each cell line; values for dolastatin 15 were approximately . 13 nM in DB and HT cells and .0013-.013 nM in RL cells. SR cells were more sensitive to dolastatin 15 than to dolastatin 10 (IC50 = .00013-.0013 nM versus .0013-.013 nM). Both dolastatins arrested more than 70% of cells in mitosis in all cell lines. This effect was reversed if the drug was removed by 4 hours, but by 8 hours of exposure, reversal was not possible. Both dolastatins 10 and 15 produced apoptosis in DB and HT cells but not in the other two cell lines. Conclusions: We have demonstrated that dolastatins 10 and 15 have a profound antiproliferative effect on four different human lymphoma cell lines and that the dolastatins are approximately 3-4 logarithms more effective as antiproliferative compounds, on a molar basis, than vincristine-a clinically useful, antiproliferative agent. These data support the hypothesis that apoptosis, as measured by DNA fragmentation, appears to be a cell-specific response and may not be directly related to the antimitotic effect of the dolostatins. Implications: Our results suggest that these compounds may be good candidates for development as antineoplastic agents. C1 RESOURCES INC DYNCORP INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. PROGRAM RESOURCES INC DYNCORP INC,CLIN SERV PROGRAM,FREDERICK,MD. RP BECKWITH, M (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,BLDG 567,FREDERICK,MD 21702, USA. NR 31 TC 69 Z9 70 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 MAR 17 PY 1993 VL 85 IS 6 BP 483 EP 488 DI 10.1093/jnci/85.6.483 PG 6 WC Oncology SC Oncology GA KR537 UT WOS:A1993KR53700019 PM 8445676 ER PT J AU HORAN, PJ WILD, KD KAZMIERSKI, WM FERGUSON, R HRUBY, VJ WEBER, SJ DAVIS, TP FANG, L KNAPP, RJ YAMAMURA, HI KRAMER, TH BURKS, TF BOWEN, WD TAKEMORI, AE PORRECA, F AF HORAN, PJ WILD, KD KAZMIERSKI, WM FERGUSON, R HRUBY, VJ WEBER, SJ DAVIS, TP FANG, L KNAPP, RJ YAMAMURA, HI KRAMER, TH BURKS, TF BOWEN, WD TAKEMORI, AE PORRECA, F TI UNEXPECTED ANTINOCICEPTIVE POTENCY OF CYCLIC [D-TCA(1)]CTAP - POTENTIAL FOR A NOVEL MECHANISM OF ACTION SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE MU-OPIOID RECEPTORS; DELTA-OPIOID RECEPTORS; ANTINOCICEPTION; OPIOID RECEPTOR ANTAGONISTS; METABOLISM ID MOUSE VAS-DEFERENS; MU-MEDIATED ANTINOCICEPTION; DELTA-RECEPTOR SUBTYPES; KAPPA-OPIOID RECEPTORS; RAT-BRAIN MEMBRANES; GUINEA-PIG ILEUM; BETA-ENDORPHIN; BINDING-SITES; NEUROTRANSMITTER RELEASE; DIFFERENTIAL ANTAGONISM AB This study tested the hypothesis that compounds which may bind simultaneously to delta and mu receptors may be more potent antinociceptive agents than would be predicted from their binding affinities at individual mu and delta opioid receptors. D-Tca-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 ([D-Tca1]CTAP) (where D-Tca is a cyclic D-tryptophan analogue) was synthesized and evaluated in radioligand competition assays, opioid bioassays, and in an antinociceptive assay (the tail-flick test in mice). Additionally, the metabolic stability of [D-Tca1]CTAP was evaluated in striatal and cerebellar tissue slices. In rat brain in vitro, [D-Tca1]CTAP competed weakly for sites labelled by [H-3]D-Phe-Cys-Tyr-D-Trp-Om-Thr-Pen-Thr-NH2 ([H-3]CTOP) (mu-ligand), and [H-3][D-Pen2,pCl-Phe4,D-Pen5]enkephalin (delta-ligand); [D-Pen2,D-Pen5]enkephalin (DPDPE) (delta-agonist) was 6.5-fold less and 230-fold more potent, respectively, against these ligands. Additionally, in mouse isolated vas deferens and guinea pig isolated ileum smooth muscle preparations, [D-Tca1]CTAP proved to be weak as either a delta (IC50 of approximately 2 muM) or mu (IC50 > 8 muM) receptor agonist. Surprisingly, however, i.c.v. [D-Tca1]CTAP produced antinociception with potency similar to DPDPE. The antinociceptive actions of [D-Tca1]CTAP were apparently not due to a metabolite or the release of endogenous opioids, as this compound proved stable in both striatal and cerebellar tissue slices and its antinociceptive actions were not enhanced by the 'enkephalinase' inhibitor thiorphan. The suggestion that [D-Tca1]CTAP might be acting by binding simultaneously to mu and delta receptors to produce its antinociceptive effect is supported by the demonstrated antagonism resulting from mu receptor blockade with either beta-funaltrexamine (beta-FNA) or naloxonazine, or by delta receptor blockade by ICI 174,864 ([N,N-diallyl-Tyr1,Aib2,3,Leu5] enkephalin). Furthermore, the antinociceptive properties of [D-Tca1]CTAP were antagonized by (naltrindole-5'-isothiocyanate) (5'-NTII), an antagonist at the delta2 opioid receptor subtype, but not by the delta1 antagonist [D-Ala2,D-Leu5,Cys6]enkephalin (DALCE). Additionally, no antagonism was produced by nor-binaltorphimine (nor-BNI), a K antagonist. From these data, [D-Tca1]CTAP appears to bind to mu, and 5'-NTII-sensitive delta2, opioid receptors, and may represent the first of a class of compounds which may act at an opioid receptor complex via 'self-potentiation'. C1 UNIV ARIZONA,ARIZONA HLTH SCI CTR,DEPT PHARMACOL,TUCSON,AZ 85724. NIDDK,MED CHEM LAB,RECEPTOR BIOCHEM & PHARMACOL UNIT,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,HOUSTON,TX 77225. UNIV ARIZONA,ARIZONA HLTH SCI CTR,DEPT CHEM,TUCSON,AZ 85724. UNIV MINNESOTA,SCH MED,DEPT PHARMACOL,MINNEAPOLIS,MN 55455. RI davis, thomas/F-3244-2015 OI davis, thomas/0000-0001-8465-4973 FU NIDA NIH HHS [DA 06284] NR 59 TC 16 Z9 16 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD MAR 16 PY 1993 VL 233 IS 1 BP 53 EP 62 DI 10.1016/0014-2999(93)90348-L PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KU394 UT WOS:A1993KU39400008 PM 8386089 ER PT J AU VONLUBITZ, DKJE MCKENZIE, RJ LIN, RCS DEVLIN, TM SKOLNICK, P AF VONLUBITZ, DKJE MCKENZIE, RJ LIN, RCS DEVLIN, TM SKOLNICK, P TI MK-801 IS NEUROPROTECTIVE BUT DOES NOT IMPROVE SURVIVAL IN SEVERE FOREBRAIN ISCHEMIA SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE MK-801; POSTISCHEMIC RECOVERY; POSTISCHEMIC SURVIVAL; ISCHEMIA (FOREBRAIN); (MONGOLIAN GERBIL) ID COMPLETE CEREBRAL-ISCHEMIA; NMDA ANTAGONISTS; NEURONAL DAMAGE; MALEATE MK-801; HYPOTHERMIA; INJURY; BRAIN; PROTECT; GERBILS; HISTOPATHOLOGY AB The effects of MK-801 on postischemic recovery, survival and neuronal preservation in the cortex, hippocampus and striatum were studied in Mongolian gerbils. The drug was administered 30 min prior to 20 of min forebrain ischemia induced by bilateral ligation of the carotids. Neurological recovery and survival were monitored for 7 days. At the end of the monitoring period neuronal damage was analyzed in the brains of the survivors in both groups. Treatment with MK-801 did not improve either neurological recovery or end-point survival. However, significant (P < 0.01) neuronal protection was observed in the hippocampi and striata of the drug treated animals while cortical neurons were not significantly protected. These findings demonstrate that protection against ischemic neuronal damage can be observed without concomitant improvement in either postischemic neurological recovery or survival. Protection of selectively vulnerable brain regions, often used as the predictor of the therapeutic potential of an agent, does not appear to correlate well with postischemic survival in this animal model of ischemia. C1 HAHNEMANN UNIV,DEPT BIOCHEM,PHILADELPHIA,PA 19102. HAHNEMANN UNIV,DEPT PHYSIOL & BIOPHYS,PHILADELPHIA,PA 19102. RP VONLUBITZ, DKJE (reprint author), NIDDK,NEUROSCI LAB,BLDG 8,ROOM 111,BETHESDA,MD 20892, USA. NR 37 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD MAR 16 PY 1993 VL 233 IS 1 BP 95 EP 100 DI 10.1016/0014-2999(93)90353-J PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KU394 UT WOS:A1993KU39400013 PM 8472751 ER PT J AU WINSLOW, JT INSEL, TR AF WINSLOW, JT INSEL, TR TI EFFECTS OF CENTRAL VASOPRESSIN ADMINISTRATION TO INFANT RATS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE VASOPRESSIN; ULTRASONIC VOCALIZATION; ANXIETY; THERMOREGULATION; AFFILIATION; VASOTOCIN ID POSITIVE FEEDBACK; BINDING-SITES; OWN RELEASE; OXYTOCIN; BRAIN; STRESS; VASOTOCIN; NEURONS; RADIOIMMUNOASSAY; AUTORADIOGRAPHY AB The neurohypophyseal peptide hormone arginine-vasopressin functions as a neuropeptide in several brain areas in addition to its role as a posterior pituitary hormone. Several studies indicate that arginine-vasopressin and arginine-vasopressin receptors appear early in the infant rat brain. To determine if arginine-vasopressin receptors in the infant were responsive to exogenous peptides, we compared the behavioral effects of central or peripheral administration of arginine-vasopressin, arginine vasotocin, the oxytocin precursor oxytocin-Gly-Lys-Arg, and arginine-vasopressin receptor antagonists in socially isolated rat pups. Central administration of arginine-vasopressin decreased thc number of rat pup ultrasonic vocalizations, reduced locomotor activity and decreased the latency to express a response to negative geotaxis. Temperature was also reduced at all doses tested. Co-administration of arginine-vasopressin and receptor antagonists suggested that changes in vocal behavior were mediated by the V1 receptor subtype. Changes in core temperature appeared to be mediated by a V2 receptor subtype. Peripheral arginine-vasopressin administration increased calling and decreased core body temperature. Neither effect was blocked by central receptor antagonist administration. The results are consistent with the hypothesis that arginine-vasopressin receptors in the infant rat brain are functional. RP WINSLOW, JT (reprint author), NIHAC,NIMH,DEV BIOPSYCH UNIT,POOLESVILLE,MD 20837, USA. NR 44 TC 69 Z9 69 U1 2 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD MAR 16 PY 1993 VL 233 IS 1 BP 101 EP 107 DI 10.1016/0014-2999(93)90354-K PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KU394 UT WOS:A1993KU39400014 PM 8472738 ER PT J AU CHRAPUSTA, SJ KAROUM, F EGAN, MF WYATT, RJ AF CHRAPUSTA, SJ KAROUM, F EGAN, MF WYATT, RJ TI HALOPERIDOL AND CLOZAPINE INCREASE INTRANEURONAL DOPAMINE METABOLISM, BUT NOT GAMMA-BUTYROLACTONE-RESISTANT DOPAMINE RELEASE SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE NEUROLEPTICS; DOPAMINE RELEASE; DOPAMINE METABOLISM; 3-METHOXYTYRAMINE; STRIATUM; NUCLEUS ACCUMBENS; FRONTAL CORTEX; DEPOLARIZATION BLOCK; (RAT) ID CATECHOL-O-METHYLTRANSFERASE; CENTRALLY ACTING DRUGS; RAT-BRAIN; STRIATAL DOPAMINE; NUCLEUS-ACCUMBENS; CONSCIOUS RATS; NEURONS; INVIVO; 3-METHOXYTYRAMINE; SYSTEM AB In a previous study, two coexisting mechanisms of dopamine release were identified in dopamine neuron terminals. One can be blocked with gamma-butyrolactone, suggesting it is impulse flow-dependent, while the other one cannot and is apparently impulse flow-independent. The goal of this study was to further characterize the gamma-butyrolactone-resistant mechanism and its relation to dopamine metabolism. Following acute and chronic haloperidol or clozapine treatment, gamma-butyrolactone was given to block dopamine neuronal impulse flow. In all groups, 3-methoxytyramine levels after monoamine oxidase inhibition with pargyline (an index of dopamine release) were measured in the frontal cortex, nucleus accumbens and striatum. Regional steady-state levels of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were also measured in the rats treated acutely with neuroleptics. In all three regions, gamma-butyrolactone reduced the 3-methoxytyramine levels by over 50% after chronic neuroleptic treatment. This indicates that dopamine release from the terminals is primarily impulse flow-dependent during chronic neuroleptic treatment, both in the dopamine neurons which do undergo depolarization block, and in those that do not. No neuroleptic effect on the gamma-butyrolactone-resistant dopamine release was observed, while DOPAC and HVA were markedly elevated by the acute treatment, suggesting a predominant production of these metabolites from unreleased dopamine. RP CHRAPUSTA, SJ (reprint author), NIMH,CTR NEUROSCI,NEUROPSYCHIAT BRANCH,BLDG WAW,R531,2700 M L KING JR AVE,WASHINGTON,DC 20032, USA. NR 37 TC 5 Z9 5 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD MAR 16 PY 1993 VL 233 IS 1 BP 135 EP 142 DI 10.1016/0014-2999(93)90359-P PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KU394 UT WOS:A1993KU39400019 PM 8472742 ER PT J AU STANLEY, WS POWELL, CM DEVINE, GC ELLINGHAM, T SAMANGOSPROUSE, CA VAUGHT, DR MURPHY, BA ROSENBAUM, KN AF STANLEY, WS POWELL, CM DEVINE, GC ELLINGHAM, T SAMANGOSPROUSE, CA VAUGHT, DR MURPHY, BA ROSENBAUM, KN TI MOSAIC 5P TETRASOMY SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE 5P SYNDROME; ISOCHROMOSOME; CHROMOSOME-5; SEIZURES; PSYCHOMOTOR RETARDATION; TETRASOMY ID PALLISTER-KILLIAN SYNDROME; PARTIAL TRISOMY; GENETIC MOSAICISM; SHORT ARM; TRANSLOCATION; HYPOMELANOSIS; ITO; CHROMOSOME-5; ASSOCIATION; 12P AB We report on a mildly abnormal 5-year-old girl with seizures, psychomotor retardation, and areas of hyperpigmentation who had a super-numerary marker chromosome in fibroblasts which was identified as an i(5p). To our knowledge, this is the first reported case of tetrasomy 5p. She shares in common some, but not all, manifestations of the dup (5p) syndrome. Cytogenetic analysis of relatives showed that the phenotypically apparently normal mother, maternal grandmother, and a brother of the proband also had a marker chromosome in their lymphocytes which was unrelated to the i(5p). C1 CHILDRENS NATL MED CTR,DEPT MED GENET,WASHINGTON,DC 20010. GEORGE WASHINGTON UNIV,SCH MED,DEPT PEDIAT,WASHINGTON,DC 20052. GEORGE WASHINGTON UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC 20052. NIH,BETHESDA,MD 20892. RP STANLEY, WS (reprint author), CHILDRENS NATL MED CTR,DEPT LAB MED,111 MICHIGAN AVE NW,WASHINGTON,DC 20010, USA. NR 23 TC 24 Z9 24 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD MAR 15 PY 1993 VL 45 IS 6 BP 774 EP 776 DI 10.1002/ajmg.1320450623 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA KN682 UT WOS:A1993KN68200022 PM 8456861 ER PT J AU BECKER, ED AF BECKER, ED TI A BRIEF-HISTORY OF NUCLEAR-MAGNETIC-RESONANCE SO ANALYTICAL CHEMISTRY LA English DT Article ID NMR-SPECTROSCOPY; LARGER PROTEINS; H-1 RP BECKER, ED (reprint author), NIDDKD,BETHESDA,MD 20892, USA. NR 41 TC 12 Z9 12 U1 5 U2 19 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0003-2700 J9 ANAL CHEM JI Anal. Chem. PD MAR 15 PY 1993 VL 65 IS 6 BP A295 EP A302 DI 10.1021/ac00054a001 PG 8 WC Chemistry, Analytical SC Chemistry GA KR445 UT WOS:A1993KR44500001 PM 8460827 ER PT J AU MILLS, JL RAYMOND, E AF MILLS, JL RAYMOND, E TI EFFECTS OF RECENT RESEARCH ON RECOMMENDATIONS FOR PERICONCEPTIONAL FOLATE SUPPLEMENT USE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID NEURAL-TUBE DEFECTS; SERUM ALPHA-FETOPROTEIN; VITAMIN SUPPLEMENTATION; PREVENTION; PREGNANCIES; ABSENCE RP MILLS, JL (reprint author), NICHHD, DESPR,EPIDEMIOL BRANCH,PEDIATR EPIDEMIOL SECT, BLDG 6100, ROOM 7B03, BETHESDA, MD 20892 USA. NR 24 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAR 15 PY 1993 VL 678 BP 137 EP 145 PG 9 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX228 UT WOS:A1993KX22800012 ER PT J AU KOCH, R WENZ, E AZEN, C FRIEDMAN, EG LEVY, H ROHR, F ROUSE, B CASTIGLIONI, L MATALON, R MICHALSMATALON, K HANLEY, W AUSTIN, V DELACRUZ, F ACOSTA, PB AF KOCH, R WENZ, E AZEN, C FRIEDMAN, EG LEVY, H ROHR, F ROUSE, B CASTIGLIONI, L MATALON, R MICHALSMATALON, K HANLEY, W AUSTIN, V DELACRUZ, F ACOSTA, PB TI THE EFFECT OF NUTRIENT INTAKE ON PREGNANCY OUTCOME IN MATERNAL PHENYLKETONURIA SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article C1 CHILDRENS HOSP MED CTR, BOSTON, MA 02115 USA. UNIV TEXAS, MED BRANCH, GALVESTON, TX 77550 USA. MIAMI CHILDRENS HOSP, RES INST, MIAMI, FL 33155 USA. HOSP SICK CHILDREN, TORONTO M5G 1X8, ONTARIO, CANADA. NIH, MENTAL RETARDAT & DEV DISABIL BRANCH, BETHESDA, MD 20892 USA. ROSS LABS, COLUMBUS, OH 43215 USA. RP KOCH, R (reprint author), CHILDRENS HOSP LOS ANGELES, 4650 SUNSET BLVD, MPKU 73, LOS ANGELES, CA 90027 USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAR 15 PY 1993 VL 678 BP 348 EP 349 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX228 UT WOS:A1993KX22800038 ER PT J AU LANDS, WEM AF LANDS, WEM TI EICOSANOIDS AND HEALTH SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID FATTY-ACIDS; PROSTAGLANDIN BIOSYNTHESIS; PLASMA HYDROPEROXIDES; ALCOHOL-CONSUMPTION; NEUTROPHILS; PLATELETS; ASPIRIN; LIPIDS; HUMANS; FISH RP LANDS, WEM (reprint author), NIAAA, DIV BASIC RES, PARKLAWN BLDG, RM 16C-06, 5600 FISHERS LANE, ROCKVILLE, MD 20857 USA. NR 44 TC 3 Z9 3 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAR 15 PY 1993 VL 676 BP 46 EP 59 PG 14 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KX226 UT WOS:A1993KX22600006 ER PT J AU SPALTER, AR GWIRTSMAN, HE DEMITRACK, MA GOLD, PW AF SPALTER, AR GWIRTSMAN, HE DEMITRACK, MA GOLD, PW TI THYROID-FUNCTION IN BULIMIA-NERVOSA SO BIOLOGICAL PSYCHIATRY LA English DT Article DE BULIMIA; METABOLISM; THYROXINE; TRIIADOTHYRONINE; THYROTROPIN; CALORIC INTAKE; HYPOTHALAMIC-PITUITARY AXIS ID RESTING METABOLIC-RATE; ANOREXIA-NERVOSA; PSYCHIATRIC-PATIENTS; SERUM THYROTROPIN; HORMONES; WEIGHT; THYROXINE; TRH; ABNORMALITIES; STARVATION AB Bulimia nervosa is characterized by episodes of binge eating. Bulimic patients have diminished caloric requirements and reduced metabolic rate. Because thyroid function is an important modulator of metabolic rate, we sought to clarify conflicting reports concerning this parameter in bulimic patients. Thyroid indices were examined in 18 bulimics at admission and after 3 weeks of abstinence. Patients had thyroid indices in the normal range at admission but slightly diminished triiodothyronine (T3) compared with control subjects (n = 28). Significant declines in T3 and thyroxine and increases in thyrotropin were noted after 3 weeks of abstinence. At abstinence, T3 was positively correlated with caloric intake, protein, fat, and carbohydrate consumption and inversely correlated with percent ideal body weight. We hypothesize that binge-purge behavior may transiently increase thyroid indices and, consequently, metabolic rate in patients with bulimia nervosa. Furthermore, decreases in T3 following abstinence may be related to diminished caloric consumption or may reflect hypothalamic-pituitary dysregulation in these patients. C1 NIMH,MOOD ANXIETY & PERSONAL DISORDERS BRANCH,5600 FISHER LANE,ROCKVILLE,MD 20857. NIMH,CLIN NEUROENDOCRINOL BRANCH,ROCKVILLE,MD 20857. UNIV MICHIGAN,MED CTR,ANN ARBOR,MI 48109. RI Demitrack, Mark/I-7697-2013 NR 31 TC 13 Z9 13 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6 BP 408 EP 414 DI 10.1016/0006-3223(93)90168-D PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA KZ442 UT WOS:A1993KZ44200003 PM 8490067 ER PT J AU LEONARD, S LOGEL, J LUTHMAN, D CASANOVA, MF KIRCH, D FREEDMAN, R AF LEONARD, S LOGEL, J LUTHMAN, D CASANOVA, MF KIRCH, D FREEDMAN, R TI BIOLOGICAL STABILITY OF MESSENGER-RNA ISOLATED FROM HUMAN POSTMORTEM BRAIN COLLECTIONS SO BIOLOGICAL PSYCHIATRY LA English DT Article DE MESSENGER RNA; POSTMORTEM STABILITY; HUMAN BRAIN COLLECTION; PCR; INVITRO TRANSLATION ID FIBROBLAST GROWTH-FACTOR; NUCLEOTIDE-SEQUENCE; RAT; SCHIZOPHRENIA; CELLS AB RNA isolated from frozen human postmortem brain tissue was evaluated for its utility in molecular biological studies. Samples varying in postmortem interval, delay period before freezing, and long-term freezer storage were analyzed. It was found that storage of human postmortem brain at - 70-degrees-C for more than 5 years may compromise its use for oligo-dT primed library construction and in vitro expression studies. Although biological competency of the messenger RNA may be affected by long-term freezer storage of human brain, enough full-length or partial transcripts remained for amplification by the polymerase chain reaction. We conclude that human postmortem brain collections will continue to be valuable resources for the study of gene expression and isolation of nucleotide sequences. C1 UNIV COLORADO, HLTH SCI CTR, DEPT PSYCHIAT, DENVER, CO 80262 USA. VET ADM MED CTR, GAINESVILLE, FL 32602 USA. NIMH, CLIN BRAIN DISORDERS BRANCH, WASHINGTON, DC 20032 USA. NIMH, DIV CLIN RES, ROCKVILLE, MD 20857 USA. RP LEONARD, S (reprint author), UNIV COLORADO, HLTH SCI CTR, DEPT PHARMACOL, BOX C-268-71, 4200 E 9TH ST, DENVER, CO 80262 USA. FU NIMH NIH HHS [MH44212] NR 27 TC 82 Z9 84 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6 BP 456 EP 466 DI 10.1016/0006-3223(93)90174-C PG 11 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA KZ442 UT WOS:A1993KZ44200009 PM 8098224 ER PT J AU ALTEMUS, M MICHELSON, D GALLIVEN, E GOLD, PW MURPHY, DL AF ALTEMUS, M MICHELSON, D GALLIVEN, E GOLD, PW MURPHY, DL TI REDUCED PERIPHERAL HPA AXIS ACTIVITY IN OCD SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A145 EP A145 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700395 ER PT J AU ANDREASON, PJ ALTEMUS, M ZAMETKIN, A PARVER, D BEMAT, A COHEN, RM AF ANDREASON, PJ ALTEMUS, M ZAMETKIN, A PARVER, D BEMAT, A COHEN, RM TI CSF HVA STRONGLY CORRELATES WITH ANTEROLATERAL PREFRONTAL CORTEX AND GLOBAL CEREBRAL GLUCOSE-METABOLISM IN BULIMIA-NERVOSA SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,ROCKVILLE,MD 20852. NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A161 EP A161 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700449 ER PT J AU BERRETTINI, WH FERRARO, TN GOLDIN, L DETERAWADLEIGH, S CHOI, H HSIEH, WT NURNBERGER, J GERSHON, ES AF BERRETTINI, WH FERRARO, TN GOLDIN, L DETERAWADLEIGH, S CHOI, H HSIEH, WT NURNBERGER, J GERSHON, ES TI A LINKAGE STUDY OF BIPOLAR DISEASE SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107. NIMH,BETHESDA,MD 20892. INST PSYCHIAT RES,INDIANAPOLIS,IN 46202. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A78 EP A78 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700151 ER PT J AU BREWERTON, TD KRAHN, D HARDIN, T WEHR, T ROSENTHAL, N AF BREWERTON, TD KRAHN, D HARDIN, T WEHR, T ROSENTHAL, N TI SEASONAL AFFECTIVE-DISORDER AND EATING DISORDERS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,INST PSYCHIAT,CHARLESTON,SC 29425. UNIV WISCONSIN,DEPT PSYCHIAT,MADISON,WI 53706. NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A56 EP A56 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700072 ER PT J AU CASTELLANOS, FX GULOTTA, CS TANAKA, J RITCHIE, G ELIA, J RAPOPORT, JL AF CASTELLANOS, FX GULOTTA, CS TANAKA, J RITCHIE, G ELIA, J RAPOPORT, JL TI STIMULANT TREATMENT OF PEDIATRIC TOURETTE DISORDER AND ADHD SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. VIRGINIA POLYTECH INST & STATE UNIV,BLACKSBURG,VA 24061. MED COLL PENN,PHILADELPHIA,PA 19129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A42 EP A43 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700022 ER PT J AU COWLEY, DS ROYBYRNE, PP RADANT, A HOMMER, DW GREENBLATT, DJ VITALIANO, PP GODON, C AF COWLEY, DS ROYBYRNE, PP RADANT, A HOMMER, DW GREENBLATT, DJ VITALIANO, PP GODON, C TI SONS OF ALCOHOLIC FATHERS DIFFER FROM MALE CONTROLS IN RESPONSE TO DIAZEPAM SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV WASHINGTON,SEATTLE,WA 98104. NIAAA,BETHESDA,MD 20892. TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA 02111. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A67 EP A67 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700109 ER PT J AU DEBELLIS, MD CHROUSOS, GP DORN, L BURKE, L HELMERS, K KLING, MA TRICKETT, PK PUTNAM, FW AF DEBELLIS, MD CHROUSOS, GP DORN, L BURKE, L HELMERS, K KLING, MA TRICKETT, PK PUTNAM, FW TI BLUNTED PLASMA ACTH RESPONSES TO THE OVINE CORTICOTROPIN-RELEASING HORMONE STIMULATION TEST IN SEXUALLY ABUSED GIRLS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RI Kling, Mitchel/F-4152-2010 OI Kling, Mitchel/0000-0002-2232-1409 NR 0 TC 2 Z9 2 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 MAR 15 PY 1993 VL 33 IS 6A SU S BP A103 EP A103 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700241 ER PT J AU DEBELLIS, MD CHROUSOS, GP DORN, L BURKE, L HELMERS, K KLING, MA TRICKETT, PK PUTNAM, FW AF DEBELLIS, MD CHROUSOS, GP DORN, L BURKE, L HELMERS, K KLING, MA TRICKETT, PK PUTNAM, FW TI BLUNTED PLASMA ACTH RESPONSES TO THE OVINE CORTICOTROPIN-RELEASING HORMONE STIMULATION TEST IN SEXUALLY ABUSED GIRLS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,DEV PSYCHOL LAB,BETHESDA,MD 20892. NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RI Burke, Lillian/A-7334-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A109 EP A109 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700263 ER PT J AU DEUTSCH, SI ROSSE, RB FAYMCCARTHY, M COLLINS, JP ALIM, TN WYATT, RJ AF DEUTSCH, SI ROSSE, RB FAYMCCARTHY, M COLLINS, JP ALIM, TN WYATT, RJ TI DIFFERENCES IN THE PHENOMENOLOGY OF COCAINE-INDUCED PSYCHOSIS AND SCHIZOPHRENIA SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 DEPT VET AFFAIRS MED CTR PSYCHIAT, WASHINGTON, DC 20422 USA. NIMH, NEUROSCI CTR ST ELIZABETHS, NEUROPSYCHIAT BRANCH, WASHINGTON, DC 20032 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A153 EP A153 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700423 ER PT J AU GARCIABORREGUERO, D SCHWARTZ, PJ MOUL, DE SNELBAKER, AJ OREN, DA ROSENTHAL, NE AF GARCIABORREGUERO, D SCHWARTZ, PJ MOUL, DE SNELBAKER, AJ OREN, DA ROSENTHAL, NE TI EFFECTS OF THE SEROTONERGIC AGONIST M-CPP IN PATIENTS WITH SEASONAL AFFECTIVE-DISORDERS AND HEALTHY CONTROLS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A57 EP A57 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700075 ER PT J AU GEORGE, DT LINDQUIST, T ALIM, T ECKARDT, M LINNOILA, M AF GEORGE, DT LINDQUIST, T ALIM, T ECKARDT, M LINNOILA, M TI BEHAVIORAL AND BIOCHEMICAL EFFECTS OF 2-DG IN ALCOHOLICS AND CONTROLS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,CLIN STUDIES LAB,BETHESDA,MD 20892. VET ADM MED CTR,WASHINGTON,DC 20422. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A153 EP A153 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700422 ER PT J AU GEORGE, MS GUIDOTTI, A RUBINOW, D MIKALAUSKAS, K POST, RM AF GEORGE, MS GUIDOTTI, A RUBINOW, D MIKALAUSKAS, K POST, RM TI CSF NEUROSTEROIDS IN AFFECTIVE-DISORDERS - PREGNENOLONE, PROGESTERONE AND DBT SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A67 EP A67 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700111 ER PT J AU GORDON, CT COTELINGAM, M STAGER, S LUDLOW, C RAPOPORT, J AF GORDON, CT COTELINGAM, M STAGER, S LUDLOW, C RAPOPORT, J TI DIFFERENTIAL RESPONSE OF DEVELOPMENTAL STUTTERING TO CLOMIPRAMINE SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NIDOC,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A55 EP A55 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700067 ER PT J AU GREENBERG, BD ANTHONY, BJ MIRSKY, AF AF GREENBERG, BD ANTHONY, BJ MIRSKY, AF TI STARTLE MODULATION IN CHILDREN WITH TOURETTES DISORDER SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. UNIV MARYLAND,BALTIMORE,MD 21201. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A43 EP A43 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700024 ER PT J AU HIGLEY, JD MEHLMAN, PT TAUB, DM FAUCHER, I LILLY, AA SUOMI, SJ LINNOILA, M AF HIGLEY, JD MEHLMAN, PT TAUB, DM FAUCHER, I LILLY, AA SUOMI, SJ LINNOILA, M TI ADOLESCENT MACAQUES WITH LOWER CSF 5-HIAA EXHIBIT INCREASED AGGRESSION AND RISK-TAKING SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,CLIN STUDIES LAB,ROCKVILLE,MD 20852. NICHHD,COMPARAT ETHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A63 EP A63 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700095 ER PT J AU JACOBSEN, FM AF JACOBSEN, FM TI LOW-DOSE VALPROATE TREATMENT OF CYCLOTHYMIA AND BIPOLAR-II DISORDER SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 TRANSCULTURAL MENTAL HLTH INST,WASHINGTON,DC 20036. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A81 EP A82 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700164 ER PT J AU KETTER, TA ANDREASON, PJ GEORGE, MS HERSCOVITCH, P POST, RM AF KETTER, TA ANDREASON, PJ GEORGE, MS HERSCOVITCH, P POST, RM TI PARALIMBIC RCBF INCREASES DURING PROCAINE-INDUCED PSYCHOSENSORY AND EMOTIONAL EXPERIENCES SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NIAAA,BETHESDA,MD 20892. NIHCC,DEPT NUCL MED,BETHESDA,MD 20892. NR 0 TC 8 Z9 8 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 MAR 15 PY 1993 VL 33 IS 6A SU S BP A66 EP A66 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700106 ER PT J AU KRUESI, MJP CASANOVA, M MANNHEIM, G RUMSEY, JM JOHNSON, A HAMBURGER, SD AF KRUESI, MJP CASANOVA, M MANNHEIM, G RUMSEY, JM JOHNSON, A HAMBURGER, SD TI REGIONAL BRAIN VOLUME IN CHILDREN AND ADOLESCENTS WITH CONDUCT DISORDERS AT HIGH-RISK FOR ANTISOCIAL PERSONALITY-DISORDER SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV ILLINOIS,CHICAGO,IL 60680. MED COLL GEORGIA,AUGUSTA,GA 30912. ST ELIZABETH HOSP,WASHINGTON,DC 20032. NIMH,ROCKVILLE,MD 20857. PENN STATE UNIV,MILTON S HERSHEY MED CTR,HERSHEY,PA 17033. NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A114 EP A114 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700284 ER PT J AU LEONARD, HL HYDE, TM RETTEW, DC RICKLER, KC CAROSELLA, N WEINBERGER, D AF LEONARD, HL HYDE, TM RETTEW, DC RICKLER, KC CAROSELLA, N WEINBERGER, D TI COMORBIDITY IN 28 CHILD AND ADULT TOURETTE SYNDROME TWIN PAIRS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. NIMH,CLIN BRAIN DISORDER BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A43 EP A43 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700025 ER PT J AU LITTLE, JT BROOCKS, A MARTIN, A HILL, JL MACK, C CONWAY, A MURPHY, DL SUNDERLAND, T AF LITTLE, JT BROOCKS, A MARTIN, A HILL, JL MACK, C CONWAY, A MURPHY, DL SUNDERLAND, T TI SEROTONERGIC MODULATION OF SCOPOLAMINE IN OLDER NORMAL VOLUNTEERS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NATL INST MENTAL HLTH,LCS,GERIATR PSYCHIAT SECT,BETHESDA,MD 20892. RI martin, alex/B-6176-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A144 EP A144 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700392 ER PT J AU MENTIS, MJ MURPHY, D GRADY, C WEINSTEIN, E AF MENTIS, MJ MURPHY, D GRADY, C WEINSTEIN, E TI PET ANALYSIS OF DELUSIONAL MISIDENTIFICATION SYNDROMES - A NEURAL MECHANISM SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A120 EP A121 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700308 ER PT J AU MURPHY, DGM MENTIS, MJ GRADY, C HAXBY, JV HORWITZ, B RAPOPORT, SI SCHAPIRO, MB AF MURPHY, DGM MENTIS, MJ GRADY, C HAXBY, JV HORWITZ, B RAPOPORT, SI SCHAPIRO, MB TI THE EFFECT OF THE X-CHROMOSOME AND SEX STEROIDS ON HUMAN BRAIN-DEVELOPMENT SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIA,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A107 EP A107 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700255 ER PT J AU NOGA, JT VLADAR, K TORREY, EF WEINBERGER, DR AF NOGA, JT VLADAR, K TORREY, EF WEINBERGER, DR TI BASAL GANGLIA VOLUMES ON MRI OF MZ TWINS DISCORDANT FOR BIPOLAR DISORDER SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CBDB,WASHINGTON,DC 20032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A75 EP A75 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700141 ER PT J AU PAUL, SM AF PAUL, SM TI NEUROACTIVE STEROIDS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,MOLEC PHARMACOL SECT,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A70 EP A70 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700120 ER PT J AU RAPOPORT, JL AF RAPOPORT, JL TI OBSESSIVE-COMPULSIVE SPECTRUM DISORDERS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A71 EP A71 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700124 ER PT J AU RIO, DE MOMENAN, R RAWLINGS, RR ANDREASON, PJ KERRICH, M ECKARDT, MJ AF RIO, DE MOMENAN, R RAWLINGS, RR ANDREASON, PJ KERRICH, M ECKARDT, MJ TI SEMIAUTOMATED ANALYSIS OF PET IMAGES - APPLICATION TO ALCOHOLISM SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,BRAIN ELECTROPHYSIOL & IMAGING SECT,CLIN STUDIES LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A152 EP A152 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700420 ER PT J AU SALZBERG, A RAPPORT, JL HAMBURGER, S AF SALZBERG, A RAPPORT, JL HAMBURGER, S TI CONTAMINATION, DISGUST AND OBSESSIVE-COMPULSIVE DISORDER SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A148 EP A148 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700404 ER PT J AU SU, TP DANACEAU, M SCHMIDT, PJ RUBINOW, DR AF SU, TP DANACEAU, M SCHMIDT, PJ RUBINOW, DR TI FLUOXETINE IN THE TREATMENT OF PATIENTS WITH PREMENSTRUAL-SYNDROME SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892. NIMH,BIOL PSYCHIAT BRANCH,BEHAV ENDOCRINOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A159 EP A160 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700444 ER PT J AU SWEDO, SE ALLEN, AJ GIEDD, J HOFFMAN, C RICHTER, D ROSENTHAL, N AF SWEDO, SE ALLEN, AJ GIEDD, J HOFFMAN, C RICHTER, D ROSENTHAL, N TI PEDIATRIC SEASONAL AFFECTIVE-DISORDER (SAD) SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892. NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015 OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A57 EP A57 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700074 ER PT J AU VLADAR, K KULYNYCH, JJ JONES, DW TORREY, EF WEINBERGER, DR AF VLADAR, K KULYNYCH, JJ JONES, DW TORREY, EF WEINBERGER, DR TI AN MRI STUDY OF THE PLANUM-TEMPORALE IN MONOZYGOTIC TWINS DISCORDANT FOR SCHIZOPHRENIA SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,NEUROSCI CTR ST ELIZABETHS,IRP,CLINICAL BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. NR 0 TC 3 Z9 3 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A123 EP A124 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700318 ER PT J AU YONKERS, K PRATT, L VITALI, A BLUMENTHAL, S WARSHAW, M LAVORI, P KELLER, M AF YONKERS, K PRATT, L VITALI, A BLUMENTHAL, S WARSHAW, M LAVORI, P KELLER, M TI UNIQUE FEATURES OF PANIC DISORDER IN WOMEN SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV TEXAS,SW MED CTR,DALLAS,TX 75230. BROWN UNIV,PROVIDENCE,RI 02912. MCLEAN HOSP,BELMONT,MA 02178. NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1993 VL 33 IS 6A SU S BP A148 EP A148 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LA417 UT WOS:A1993LA41700405 ER PT J AU HEUSEL, JW SCARPATI, EM JENKINS, NA GILBERT, DJ COPELAND, NG SHAPIRO, SD LEY, TJ AF HEUSEL, JW SCARPATI, EM JENKINS, NA GILBERT, DJ COPELAND, NG SHAPIRO, SD LEY, TJ TI MOLECULAR-CLONING, CHROMOSOMAL LOCATION, AND TISSUE-SPECIFIC EXPRESSION OF THE MURINE CATHEPSIN-G GENE SO BLOOD LA English DT Article ID SERINE PROTEASE GENES; TOXIC LYMPHOCYTE-T; AMINO-ACID-SEQUENCE; G-LIKE PROTEINASE; HUMAN MAST-CELLS; V-MYB ONCOGENE; MOUSE CHROMOSOME-14; GRANZYME-B; TRANSCRIPTIONAL ACTIVATION; CYTOTOXIC LYMPHOCYTES C1 WASHINGTON UNIV,MED CTR,JEWISH HOSP,DEPT MED,DIV HEMATOL ONCOL,216 S KINGSHIGHWAY BLVD,ST LOUIS,MO 63110. WASHINGTON UNIV,MED CTR,JEWISH HOSP,DEPT RESP CRIT CARE,ST LOUIS,MO 63110. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. FU NCI NIH HHS [CA 49712, N01-CO-7410]; NIDDK NIH HHS [DK 38682] NR 69 TC 36 Z9 37 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 MAR 15 PY 1993 VL 81 IS 6 BP 1614 EP 1623 PG 10 WC Hematology SC Hematology GA KT363 UT WOS:A1993KT36300028 PM 8453108 ER PT J AU FIBACH, E BURKE, LP SCHECHTER, AN NOGUCHI, CT RODGERS, GP AF FIBACH, E BURKE, LP SCHECHTER, AN NOGUCHI, CT RODGERS, GP TI HYDROXYUREA INCREASES FETAL HEMOGLOBIN IN CULTURED ERYTHROID-CELLS DERIVED FROM NORMAL INDIVIDUALS AND PATIENTS WITH SICKLE-CELL-ANEMIA OR BETA-THALASSEMIA SO BLOOD LA English DT Article ID GAMMA-GLOBIN SYNTHESIS; LIQUID CULTURE; IN-VITRO; 5-AZACYTIDINE; DIFFERENTIATION; PROGENITORS; DISEASE; LINE; ERYTHROPOIETIN; STIMULATION C1 HADASSAH UNIV HOSP,DEPT HEMATOL,JERUSALEM,ISRAEL. RP FIBACH, E (reprint author), NIDDK,CHEM BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Burke, Lillian/A-7334-2008; OI Schechter, Alan N/0000-0002-5235-9408 NR 35 TC 91 Z9 91 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 MAR 15 PY 1993 VL 81 IS 6 BP 1630 EP 1635 PG 6 WC Hematology SC Hematology GA KT363 UT WOS:A1993KT36300030 PM 7680923 ER PT J AU HENSON, DE TARONE, RE AF HENSON, DE TARONE, RE TI ON THE POSSIBLE ROLE OF INVOLUTION IN THE NATURAL-HISTORY OF BREAST-CANCER SO CANCER LA English DT Article; Proceedings Paper CT WORKSHOP ON PROGNOSTIC INDICATORS IN BREAST CANCER CY JAN 17-19, 1992 CL SAN FRANCISCO, CA DE BREAST CANCER; INVOLUTION; MENOPAUSE; PARENCHYMAL PATTERN ID MAMMOGRAPHIC PARENCHYMAL PATTERNS; RISK; AGE; EPIDEMIOLOGY; BIRTH AB Although the importance of the relationship between age and cancer incidence rates is recognized universally, little attention seems to have been paid to the relationship between the physiologic aging process in the breast and breast cancer risk. The natural history of breast cancer was examined in the context of involution of the breast, and it was proposed that the rate and extent of involution might be important determinants of breast cancer risk. It was concluded that additional studies to characterize the process of involution better histopathologically and to examine the associations between the rate and extent of involution and breast cancer risk are warranted. Cancer C1 NCI,BIOSTAT BRANCH,BETHESDA,MD 20892. RP HENSON, DE (reprint author), NCI,EARLY DETECT BRANCH,EPN 407,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 22 TC 16 Z9 16 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1993 VL 71 IS 6 SU S BP 2154 EP 2156 DI 10.1002/1097-0142(19930315)71:6+<2154::AID-CNCR2820711605>3.0.CO;2-# PG 3 WC Oncology SC Oncology GA KQ831 UT WOS:A1993KQ83100004 PM 8443765 ER PT J AU DORR, FA AF DORR, FA TI PROGNOSTIC FACTORS OBSERVED IN CURRENT CLINICAL-TRIALS SO CANCER LA English DT Article; Proceedings Paper CT WORKSHOP ON PROGNOSTIC INDICATORS IN BREAST CANCER CY JAN 17-19, 1992 CL SAN FRANCISCO, CA DE BREAST CANCER; ADJUVANT THERAPY; PROGNOSTIC FACTORS; CLINICAL TRIALS; NODE-NEGATIVE; NODE-POSITIVE ID NEGATIVE BREAST-CANCER; TUMORS AB Adjuvant therapy of breast cancer has evolved over the past 15 years from an interesting clinical experiment to the standard of care for many patients. The toxicities of different treatments vary from those with minimal side effects, such as tamoxifen, to those with potentially life-threatening side effects. Current clinical trials are evaluating increasingly higher risk treatments, such as high-dose chemotherapy autologous bone marrow rescue. Chemotherapy is being used in groups that have previously been treated only with hormonal interventions or who have received no adjuvant therapy. The delineation of risk, such that the risks of treatment can be closely tied to the risk of recurrence is thus a desirable goal for clinical-laboratory research. Prognostic factors identified in treated patients, however, may be measures of treatment resistance versus treatment sensitivity rather than some underlying biologic characteristic defining a tumor's malignant potential. C1 NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,CLIN INVEST BRANCH,MED SECT,BETHESDA,MD 20892. NR 27 TC 18 Z9 19 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1993 VL 71 IS 6 SU S BP 2163 EP 2168 DI 10.1002/1097-0142(19930315)71:6+<2163::AID-CNCR2820711607>3.0.CO;2-W PG 6 WC Oncology SC Oncology GA KQ831 UT WOS:A1993KQ83100006 PM 8443767 ER PT J AU JACOBS, IJ SMITH, SA WISEMAN, RW FUTREAL, PA HARRINGTON, T OSBORNE, RJ LEECH, V MOLYNEUX, A BERCHUCK, A PONDER, BAJ BAST, RC AF JACOBS, IJ SMITH, SA WISEMAN, RW FUTREAL, PA HARRINGTON, T OSBORNE, RJ LEECH, V MOLYNEUX, A BERCHUCK, A PONDER, BAJ BAST, RC TI A DELETION UNIT ON CHROMOSOME-17Q IN EPITHELIAL OVARIAN-TUMORS DISTAL TO THE FAMILIAL BREAST OVARIAN-CANCER LOCUS SO CANCER RESEARCH LA English DT Note ID ALLELE LOSS; OVEREXPRESSION; HETEROZYGOSITY; AMPLIFICATION; CARCINOMAS; HER-2/NEU AB Linkage analysis in familial breast and ovarian cancer and studies of allelic deletion in sporadic ovarian tumors have suggested that chromosome 17q may be the location of a gene of importance in ovarian carcinogenesis. We have examined tumor and normal DNA samples from 120 patients with ovarian tumors for allelic deletion at 12 loci on chromosome 17q. Allelic deletion was observed in 64 cases (53%) of which 56 showed loss of heterozygosity at all loci analyzed on 17q. The pattern of allele loss at metastatic sites was consistent with loss of heterozygosity having occurred prior to metastasis. A common region of deletion, defined by 6 cases of invasive epithelial ovarian cancer and a benign serous cystadenoma, spanned 16 cM and was delimited by nm23 and GH. This region is distal to the region on chromosome 17q to which the familial breast/ovarian cancer susceptibility gene has been mapped. The results suggest that a tumor suppressor gene involved in sporadic ovarian carcinogenesis is located on the distal portion or chromosome 17q and is distinct from the gene linked to familial cases. C1 UNIV CAMBRIDGE,ROSIE MATERN HOSP,DEPT OBSTET & GYNAECOL,CAMBRIDGE CB2 2SW,ENGLAND. NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. UNIV CAMBRIDGE,ADDENBROOKES HOSP,DEPT CLIN ONCOL,CAMBRIDGE CB2 2QQ,ENGLAND. UNIV CAMBRIDGE,ADDENBROOKES HOSP,DEPT PATHOL,CAMBRIDGE CB2 2QQ,ENGLAND. DUKE UNIV,MED CTR,DEPT GYNECOL ONCOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT MICROBIOL & IMMUNOL,DURHAM,NC 27710. DUKE UNIV,CTR COMPREHENS CANC,DURHAM,NC 27710. RP JACOBS, IJ (reprint author), UNIV CAMBRIDGE,CANC RES CAMPAIGN,HUMAN CANC GENET GRP,TENNIS COURT RD,CAMBRIDGE CB2 1QP,ENGLAND. RI Bast, Robert/E-6585-2011; Jacobs, Ian/F-1743-2013 OI Bast, Robert/0000-0003-4621-8462; Jacobs, Ian/0000-0002-8112-4624 NR 25 TC 118 Z9 120 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1993 VL 53 IS 6 BP 1218 EP 1221 PG 4 WC Oncology SC Oncology GA KR297 UT WOS:A1993KR29700002 PM 8095178 ER PT J AU ROSS, H BIGGER, CAH YAGI, H JERINA, DM DIPPLE, A AF ROSS, H BIGGER, CAH YAGI, H JERINA, DM DIPPLE, A TI SEQUENCE SPECIFICITY IN THE INTERACTION OF THE 4 STEREOISOMERIC BENZO[C]PHENANTHRENE DIHYDRODIOL EPOXIDES WITH THE SUPF GENE SO CANCER RESEARCH LA English DT Article ID INVITRO DNA-SYNTHESIS; DEOXYADENOSINE ADDUCTS; ESCHERICHIA-COLI; HUMAN-CELLS; CARCINOGEN; 3,4-DIOL-1,2-EPOXIDES; POLYMERASES; SPECTRUM; ADENINE; GUANINE AB The shuttle vector pS189 was treated with each of the four configurational isomers of benzo[c]phenanthrene 3,4-dihydrodiol 1,2-epoxide, and the modified DNA was used as a template in a polymerase arrest assay examining the supF gene. Sites at which polymerase (Sequenase, version 2.0) progress along the template was blocked were presumed to be at or near sites of adduct formation. The polymerase arrest sites were compared with recently reported mutation hotspots induced by these agents in this gene (Bigger et al., Proc. Natl. Acad. Sci. USA, 89: 368-372, 1992). For 31 of 32 mutation hotspots, a polymerase arrest band was present at or 1 or 2 nucleotides 3'- to that site, indicating that adduct formation tended to be associated with mutation hotspots. However, the arrest bands near mutation hotspots were not particularly prominent in all cases, and there were many sites of substantial polymerase arrest that were not in the vicinity of mutation hotspots. Thus, factors in addition to chemical selectivity must play key roles in determining sites of mutation. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702. NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. FU NCI NIH HHS [N01-CO-74101] NR 25 TC 22 Z9 22 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1993 VL 53 IS 6 BP 1273 EP 1277 PG 5 WC Oncology SC Oncology GA KR297 UT WOS:A1993KR29700013 PM 8443807 ER PT J AU YOU, WC BLOT, WJ LI, JY CHANG, YS JIN, ML KNELLER, R ZHANG, L HAN, ZX ZENG, XR LIU, WD ZHAO, L CORREA, P FRAUMENI, JF XU, GW AF YOU, WC BLOT, WJ LI, JY CHANG, YS JIN, ML KNELLER, R ZHANG, L HAN, ZX ZENG, XR LIU, WD ZHAO, L CORREA, P FRAUMENI, JF XU, GW TI PRECANCEROUS GASTRIC-LESIONS IN A POPULATION AT HIGH-RISK OF STOMACH-CANCER SO CANCER RESEARCH LA English DT Article AB A population-based screening for detection of early cancers evaluated the prevalence of precancerous gastric lesions in an area in Shandong province, China, with one of the world's highest rates of stomach cancer. A total of 3433 residents aged 35 to 64 yr received gastroscopical examinations with biopsies taken from standard locations. Chronic atrophic gastritis was nearly universal; less than 2% of the population had biopsies showing entirely normal mucosa or only superficial gastritis. Intestinal metaplasia was the most advanced lesion for 33% and gastric dysplasia for 20%, although the prevalence of each increased significantly with age. Intestinal metaplasia and gastric dysplasia were detected throughout the stomach, but the lesions were more pronounced along the lesser curvature, especially in the angulus and antrum. There was no sex difference in rates of chronic atrophic gastritis, but males had a slightly higher prevalence of intestinal metaplasia, a 1.6-fold increase in dysplasia, and a 3-fold excess of gastric cancer. The data quantify the extensiveness of gastric lesions likely to be involved in the natural history of stomach cancer in this high-risk population. C1 NCI,BETHESDA,MD 20892. BEIJING INST CANC RES,BEIJING 100034,PEOPLES R CHINA. WEIFANG MED INST,SHANDONG 261041,PEOPLES R CHINA. LINQU PUBL HLTH BUR,SHANDONG 262600,PEOPLES R CHINA. LOUISIANA STATE UNIV,MED CTR,NEW ORLEANS,LA 70112. FU NCI NIH HHS [N01-CP-95660, N01-CP-15620, N01-CP-05631] NR 14 TC 159 Z9 168 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1993 VL 53 IS 6 BP 1317 EP 1321 PG 5 WC Oncology SC Oncology GA KR297 UT WOS:A1993KR29700021 PM 8443811 ER PT J AU KUSAMA, T WANG, TL GUGGINO, WB CUTTING, GR UHL, GR AF KUSAMA, T WANG, TL GUGGINO, WB CUTTING, GR UHL, GR TI GABA RHO-2 RECEPTOR PHARMACOLOGICAL PROFILE - GABA RECOGNITION SITE SIMILARITIES TO RHO-1 SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION LA English DT Note DE GABA (GAMMA-AMINOBUTYRIC ACID); GABA-RHO-2 RECEPTORS; GABA-RHO-1 RECEPTORS; LIGAND-GATED ION CHANNEL; INHIBITORY AMINO ACIDS; RETINA AB The rho2 receptor for gamma-aminobutyric acid (GABA) induces GABA-gated currents when expressed as a homooligomer in Xenopus oocytes. Rho2 responses display pharmacological profiles similar to those of expressed rho1 receptors, although responses were slower, most agonists were more potent at rho2 and I(m) values for the partial agonist imidazole-4-acetic acid were 7-fold higher. Amino acids important for most aspects of GABA agonist ligand recognition may not be among those that differ between rho1 and rho2, including the 20% amino acid difference in the N-terminal region. C1 NIDA,ADDICT RES CTR,BOX 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL & NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,CTR MED GENET,BALTIMORE,MD 21205. NR 7 TC 90 Z9 90 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0922-4106 J9 EUR J PHARM-MOLEC PH JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect. PD MAR 15 PY 1993 VL 245 IS 1 BP 83 EP 84 DI 10.1016/0922-4106(93)90174-8 PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KU357 UT WOS:A1993KU35700013 PM 8386671 ER PT J AU GILMORE, RD AF GILMORE, RD TI COMPARISON OF THE ROMPA GENE REPEAT REGIONS OF RICKETTSIAE REVEALS SPECIES-SPECIFIC ARRANGEMENTS OF INDIVIDUAL REPEATING UNITS SO GENE LA English DT Note DE RICKETTSIA-RICKETTSII; R-CONORII; R-AKARI; GENE REPEAT DOMAINS; PROTECTIVE ANTIGEN ID MOUNTAIN-SPOTTED-FEVER; NEAR-IDENTICAL SEQUENCES; MONOCLONAL-ANTIBODIES; SURFACE-ANTIGEN; GUINEA-PIGS; PROTEIN; DNA; VACCINE AB Genes containing repeating units have been described for several eukaryotic and prokaryotic proteins, although none exhibit the extraordinary length and conservation seen with the Rickettsia rickettsii 190-kDa protein (OmpA) repeat region. The genetic organization of the repeat regions of the ompA gene for R. conorii and R. akari was examined and compared to that of R. rickettsii. Individual repeating units, which constitute the makeup of the repeat regions, share extensive DNA homology among these species. However, differences were observed in the overall numbers and arrangements of repeating units within each species' repeat region. It appears that the distinctive arrangement of repeating units within the gene may represent the basis for encoding a protective species-specific conformational epitope of the protein. RP GILMORE, RD (reprint author), NIAID,ROCKY MT LABS,INTRACELLULAR PARASITES LAB,HAMILTON,MT 59840, USA. NR 21 TC 36 Z9 37 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 MAR 15 PY 1993 VL 125 IS 1 BP 97 EP 102 DI 10.1016/0378-1119(93)90752-O PG 6 WC Genetics & Heredity SC Genetics & Heredity GA KR733 UT WOS:A1993KR73300015 PM 7680636 ER PT J AU AZAR, DT CHAMON, W STARK, W STETTLERSTEVENSON, W AF AZAR, DT CHAMON, W STARK, W STETTLERSTEVENSON, W TI MATRIX METALLOPROTEINASE EXPRESSION IN LASER-ABLATED CORNEAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV HOSP,WILMER OPHTHALMOL INST,BALTIMORE,MD 21205. NCI,BETHESDA,MD 20892. RI Chamon, Wallace/A-5400-2010 OI Chamon, Wallace/0000-0002-2528-0526 NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 704 EP 704 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300009 ER PT J AU IWATA, T HOOG, JO REDDY, VN CARPER, D AF IWATA, T HOOG, JO REDDY, VN CARPER, D TI CLONING OF THE HUMAN SORBITOL DEHYDROGENASE GENE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. KAROLINSKA INST,DEPT CHEM,S-10401 STOCKHOLM 60,SWEDEN. OAKLAND UNIV,EYE RES INST,ROCHESTER,MI 48063. NR 0 TC 3 Z9 3 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 712 EP 712 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300042 ER PT J AU LAVER, NM ROBISON, WG AF LAVER, NM ROBISON, WG TI PROLIFERATIVE RETINOPATHY STAGE IN LONG-TERM GALACTOSE FED RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC. NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 713 EP 713 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300046 ER PT J AU GARDNER, TW KLEIN, R FERRIS, FL REMALEY, N AF GARDNER, TW KLEIN, R FERRIS, FL REMALEY, N TI DIGOXIN DOES NOT ACCELERATE PROGRESSION OF DIABETIC-RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 PENN STATE UNIV,MILTON S HERSHEY MED CTR,COLL MED,DEPT OPHTHALMOL,HERSHEY,PA 17033. UNIV WISCONSIN,MADISON,WI 53706. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 714 EP 714 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300053 ER PT J AU ROBISON, WG LAVER, NM YORK, BM CHANDLER, ML LOU, MF AF ROBISON, WG LAVER, NM YORK, BM CHANDLER, ML LOU, MF TI ARI INTERVENTION STUDIES OF GALACTOSE INDUCED RETINOPATHY BY COMPUTER-ANALYSIS OF RETINAL VESSEL IMAGES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. ALCON LABS INC,FT WORTH,TX 76101. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 718 EP 718 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300072 ER PT J AU MATTHEWS, GP LAVER, N ROBISON, WG AF MATTHEWS, GP LAVER, N ROBISON, WG TI ELECTROPHYSIOLOGICAL AND HISTOLOGICAL-EVALUATION OF INNER RETINA IN GALACTOSEMIC RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV NEW MEXICO,ALBUQUERQUE,NM 87131. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 720 EP 720 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300083 ER PT J AU HAMASAKI, DI SATO, H PEREZ, J SHINOHARA, T AF HAMASAKI, DI SATO, H PEREZ, J SHINOHARA, T TI PHOTORECEPTOR DEGENERATION AND NEGATIVE ERGS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MIAMI,SCH MED,BASCOM PALMER EYE INST,MIAMI,FL 33152. NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 741 EP 741 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300197 ER PT J AU TUMMINIA, SJ QIN, C ZIGLER, JS RUSSELL, P AF TUMMINIA, SJ QIN, C ZIGLER, JS RUSSELL, P TI ASSESSIBILITY OF THE VIABILITY AND INTEGRITY OF MAMMALIAN LENSES IN ORGAN-CULTURE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 756 EP 756 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300272 ER PT J AU FUKASE, S MORI, K SATO, S KADOR, PF AF FUKASE, S MORI, K SATO, S KADOR, PF TI COMPARISON OF NADPH-DEPENDENT REDUCTASES IN DOG LENS AND LEUKOCYTES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 757 EP 757 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300279 ER PT J AU MALIKBARTOSZKO, A SCHAFFHAUSER, M ABDELGHANY, Y MILLER, DD KADOR, PF AF MALIKBARTOSZKO, A SCHAFFHAUSER, M ABDELGHANY, Y MILLER, DD KADOR, PF TI EVALUATION OF NOVEL ALDOSE REDUCTASE INHIBITOR SITE PROBES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. OHIO STATE UNIV,COLL PHARM,COLUMBUS,OH 43210. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 757 EP 757 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300278 ER PT J AU QIN, C RAO, PV TUMMINIA, SJ ZIGLER, JS RUSSELL, P AF QIN, C RAO, PV TUMMINIA, SJ ZIGLER, JS RUSSELL, P TI LOSS OF GLUTATHIONE IN THE ORGAN CULTURED RAT LENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 758 EP 758 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300285 ER PT J AU RAMPALLI, AM ZELENKA, PS AF RAMPALLI, AM ZELENKA, PS TI THE P53 ANTIONCOGENE IS EXPRESSED DURING LENS FIBER CELL-DIFFERENTIATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 759 EP 759 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300291 ER PT J AU TOMAREV, SI ZINOVIEVA, RD CHANG, S PIATIGORSKY, J AF TOMAREV, SI ZINOVIEVA, RD CHANG, S PIATIGORSKY, J TI S-CRYSTALLINS AND GLUTATHIONE-S-TRANSFERASE OF CEPHALOPODS - EVOLUTION OF LENS SPECIFICITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LMDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 759 EP 759 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300286 ER PT J AU SMITH, SB WIGGERT, B HAMASAKI, DI KUTTY, G KUTTY, RK MCCOY, J DUNCAN, T AF SMITH, SB WIGGERT, B HAMASAKI, DI KUTTY, G KUTTY, RK MCCOY, J DUNCAN, T TI RETINAL DEGENERATION IN C57BL/6-VIT/VIT MOUSE - ERGS, DARK-REARING, RETINOIDS AND IRBP SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MED COLL GEORGIA,AUGUSTA,GA 30912. NEI,BETHESDA,MD 20892. BASCOM PALMER EYE INST,MIAMI,FL. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 767 EP 767 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300325 ER PT J AU SCOTT, MH HEITMANCIK, JF WOZENCRAFT, LA REUTER, LM PARKS, MM KAISERKUPFER, MI AF SCOTT, MH HEITMANCIK, JF WOZENCRAFT, LA REUTER, LM PARKS, MM KAISERKUPFER, MI TI AUTOSOMAL DOMINANT CONGENITAL CATARACT - INTRAOCULAR PHENOTYPIC VARIABILITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 796 EP 796 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300467 ER PT J AU RIVERO, JL KOZHICH, A NUSSENBLATT, RB JENDOUBI, M AF RIVERO, JL KOZHICH, A NUSSENBLATT, RB JENDOUBI, M TI RETROVIRUS EXPRESSION OF DELTA-ORNITHINE AMINOTRANSFERASE INVITRO TOWARD GENE-THERAPY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 807 EP 807 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300524 ER PT J AU ABE, T KIKUCHI, T CHANG, T SHINOHARA, T AF ABE, T KIKUCHI, T CHANG, T SHINOHARA, T TI SEVERAL MESSENGER-RNAS ARE EXPRESSED FROM PHOSDUCIN GENE FAMILY IN WIDE-RANGE OF TISSUES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 808 EP 808 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300527 ER PT J AU SINGH, AK KUMAR, G SHINOHARA, T SHICHI, H AF SINGH, AK KUMAR, G SHINOHARA, T SHICHI, H TI CLONING AND STRUCTURAL-ANALYSIS OF CDNA-ENCODING PORCINE S-ANTIGENS(S-AG)-LIKE PROTEIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 WAYNE STATE UNIV,SCH MED,DEPT OPHTHALMOL,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DEPT MOLEC BIOL GENET,DETROIT,MI 48201. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 808 EP 808 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300526 ER PT J AU SUNG, JU MAZURUK, K MCCREA, N CHADER, GJ RODRIGUEZ, IR AF SUNG, JU MAZURUK, K MCCREA, N CHADER, GJ RODRIGUEZ, IR TI CLONING OF A NOVEL CDNA EXPRESSED IN RETINA AND BRAIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 810 EP 810 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300539 ER PT J AU OKAJIMA, TIL WIGGERT, B CHADER, GJ PEPPERBERG, DR AF OKAJIMA, TIL WIGGERT, B CHADER, GJ PEPPERBERG, DR TI FORMATION AND RELEASE OF 11-CIS RETINAL BY THE RETINAL-PIGMENT EPITHELIUM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV ILLINOIS,COLL MED,CHICAGO,IL 60612. NEI,BETHESDA,MD 20892. NR 3 TC 2 Z9 2 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 831 EP 831 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300639 ER PT J AU BUCCI, FA LI, Q LUYO, D TANNER, J CHAN, CC AF BUCCI, FA LI, Q LUYO, D TANNER, J CHAN, CC TI DETECTION OF T-LYMPHOCYTES AND LYMPHOKINES IN PATIENTS WITH ALLERGIC CONJUNCTIVITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. PUGLIESE EYE SPECIALISTS,KINGSTON,PA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 853 EP 853 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300746 ER PT J AU LI, O HIKITA, N WHITCUP, SM NUSSENBLATT, RB CHAN, CC AF LI, O HIKITA, N WHITCUP, SM NUSSENBLATT, RB CHAN, CC TI ALLERGIC CONJUNCTIVITIS INDUCED BY COMPOUND-48/80 IN C57BL/6NCR MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 857 EP 857 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300771 ER PT J AU SHEPPARD, JD BLICK, G CALDWELL, PT DEAN, R ERON, LJ MAZUR, H SNYDER, M AF SHEPPARD, JD BLICK, G CALDWELL, PT DEAN, R ERON, LJ MAZUR, H SNYDER, M TI TREATMENT OF OCULAR TOXOPLASMOSIS WITH ATOVAQUONE, A CYSTICIDAL HYDROXYNAPHOQUINONE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 EASTERN VIRGINIA MED SCH,NORFOLK,VA 23501. NEW YORK MED COLL,VALHALLA,NY 10595. BURROUGHS WELLCOME CO,RES TRIANGLE PK,NC 27709. BROWN UNIV,PROVIDENCE,RI 02912. FAIRFAX HOSP,FALLS CHURCH,VA 22046. NIH,BETHESDA,MD 20892. KAISER PERMANENTE MED CTR,WASHINGTON,DC. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 859 EP 859 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300783 ER PT J AU REMALEY, NA CHEW, EY ZHAO, J TAMBOLI, A KLEBANOFF, M AF REMALEY, NA CHEW, EY ZHAO, J TAMBOLI, A KLEBANOFF, M TI RISK-FACTORS FOR ESOTROPIA AND EXOTROPIA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 862 EP 862 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300797 ER PT J AU LI, A TSAI, L CHADER, G TOMBRANTINK, J AF LI, A TSAI, L CHADER, G TOMBRANTINK, J TI EXPRESSION OF PIGMENT EPITHELIAL-DERIVED FACTOR (PEDF) IN HUMAN NORMAL AND TUMOR-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. HHMI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 870 EP 870 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300841 ER PT J AU TSAI, L LI, A SATCHITHANANDAM, T CHADER, G TOMBRANTINK, J AF TSAI, L LI, A SATCHITHANANDAM, T CHADER, G TOMBRANTINK, J TI LAMININ IS A REGULATOR FOR PIGMENT EPITHELIUM-DERIVED FACTOR (PEDF) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HHMI,BETHESDA,MD. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 870 EP 870 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300840 ER PT J AU ROBERGE, FG JUDDE, JG NUSSENBLATT, RB PFEFFER, BA AF ROBERGE, FG JUDDE, JG NUSSENBLATT, RB PFEFFER, BA TI INHIBITION OF HUMAN RPE AND FIBROBLAST PROLIFERATION BY RAPAMYCIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 872 EP 872 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300849 ER PT J AU FENTON, RM RUBIN, BI DESMET, MD WHITCUP, SM NUSSENBLATT, RB AF FENTON, RM RUBIN, BI DESMET, MD WHITCUP, SM NUSSENBLATT, RB TI A PROSPECTIVE-STUDY OF 5-FU TRABECULECTOMY VS SINGLE PLATE MOLTENO IMPLANT IN PATIENTS WITH PANUVEITIS COMPLICATED BY GLAUCOMA REFRACTORY TO PRIOR THERAPY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. HOWARD UNIV,DEPT OPHTHALMOL,WASHINGTON,DC 20059. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 897 EP 897 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300976 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 THE PATHOGENESIS OF EXPERIMENTAL AUTOIMMUNE UVEORETINITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NIAMS,BETHESDA,MD. VRB,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 902 EP 902 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300996 ER PT J AU MATURI, RK SHIRKEY, BL SASAMOTO, Y KOZHICH, AT CASPI, RR GERY, I AF MATURI, RK SHIRKEY, BL SASAMOTO, Y KOZHICH, AT CASPI, RR GERY, I TI T-LYMPHOCYTE ANERGY TOWARDS A UVEITOGENIC IRBP-DERIVED PEPTIDE IS AN ACTIVE AND REVERSIBLE PROCESS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 902 EP 902 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89300997 ER PT J AU KIKUCHI, T RAJU, K BREITMAN, ML SHINOHARA, T AF KIKUCHI, T RAJU, K BREITMAN, ML SHINOHARA, T TI IDENTIFICATION OF AN EVOLUTIONARILY CONSERVED RETINAL FACTOR BINDING-SITE ASSOCIATED WITH PHOTORECEPTOR-SPECIFIC ACTIVITY OF THE MOUSE ARRESTIN PROMOTER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. UNIV TORONTO,DEPT MMG,TORONTO M5S 1A1,ONTARIO,CANADA. MT SINAI HOSP,SLRI,DIV MDB,TORONTO M5G 1X5,ONTARIO,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 905 EP 905 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301012 ER PT J AU MORI, K CECKLER, TL KADOR, PF BALABAN, RS AF MORI, K CECKLER, TL KADOR, PF BALABAN, RS TI MAGNETIC-RESONANCE-IMAGING OF THE GALACTOSEMIC DOG EYE USING MAGNETIZATION TRANSFER CONTRAST SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NHLBI,CARDIAC ENERGET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 915 EP 915 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301059 ER PT J AU WOEL, V KUSZAK, JR TAKAHASHI, Y WYMAN, M KADOR, PF AF WOEL, V KUSZAK, JR TAKAHASHI, Y WYMAN, M KADOR, PF TI AN ULTRASTRUCTURAL ANALYSIS OF POSTERIOR MIGRATING LENS EPITHELIAL-CELLS IN CATARACTS OF GALACTOSE-FED DOGS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. NEI,BETHESDA,MD 20892. OHIO STATE UNIV,COLL MED,COLUMBUS,OH 43210. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 915 EP 915 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301058 ER PT J AU DELGADO, AM JOSE, NK ARIETA, CE FILHO, DMC MOWERY, RL AF DELGADO, AM JOSE, NK ARIETA, CE FILHO, DMC MOWERY, RL TI DEVELOPMENT OF AN EYE SCREENING-PROGRAM FOR CHILDREN AGED 0 TO 7 YEARS IN THE STATE OF SAO-PAULO, BRAZIL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV ESTADUAL CAMPINAS,BR-13100 CAMPINAS,SP,BRAZIL. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 937 EP 937 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301169 ER PT J AU DATILES, MB MAGNO, B LEFTWOOD, D FRIEDLIN, V VIVINO, M AF DATILES, MB MAGNO, B LEFTWOOD, D FRIEDLIN, V VIVINO, M TI LONGITUDINAL-STUDY OF EYE-RELATED NUCLEAR CATARACTS USING THE NEI SCHEIMPFLUG IMAGING-SYSTEM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 943 EP 943 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301195 ER PT J AU LASA, SM DATILES, MB AF LASA, SM DATILES, MB TI LONGITUDINAL-STUDY OF CORTICAL CATARACTS USING RETROILLUMINATION PHOTOGRAPHS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 943 EP 943 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301194 ER PT J AU LOPEZ, ML DATILES, MB AF LOPEZ, ML DATILES, MB TI LONGITUDINAL-STUDY OF AGE-RELATED POSTERIOR SUBCAPSULAR OPACITIES USING RETROILLUMINATION PHOTOGRAPHS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 943 EP 943 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301196 ER PT J AU MAGNO, BV DATILES, MB FRIEDLIN, V AF MAGNO, BV DATILES, MB FRIEDLIN, V TI REPRODUCIBILITY OF THE NEI SCHEIMPFLUG CATARACT IMAGING-SYSTEM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 943 EP 943 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301193 ER PT J AU DAVIDSON, JK MCLEAN, IW GEORGE, DP KEEFE, KS BURNIER, MN AF DAVIDSON, JK MCLEAN, IW GEORGE, DP KEEFE, KS BURNIER, MN TI PROLIFERATING CELL NUCLEAR ANTIGEN AS AN IMMUNOHISTOCHEMICAL MARKER FOR ATYPIA IN PRIMARY ACQUIRED MELANOSIS OF THE CONJUNCTIVA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 966 EP 966 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301298 ER PT J AU KEEFE, KS MCLEAN, IW GEORGE, DP DAVIDSON, JK GAMEL, JW BURNIER, MN AF KEEFE, KS MCLEAN, IW GEORGE, DP DAVIDSON, JK GAMEL, JW BURNIER, MN TI PROGNOSTIC VALUE OF CLOSED VASCULAR LOOPS IN UVEAL MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. UNIV LOUISVILLE,LOUISVILLE,KY 40292. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 966 EP 966 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301296 ER PT J AU ALBINI, A NOONAN, DM MELCHIORI, A CHADER, GJ GIAVAZZI, R AF ALBINI, A NOONAN, DM MELCHIORI, A CHADER, GJ GIAVAZZI, R TI GROWTH OF RETINOBLASTOMA CELL TUMORS INVIVO USING COINJECTION WITH MATRIGEL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. IST NAZL RIC CANC,GENOA,ITALY. MARIO NEGRI INST PHARMACOL RES,I-20157 MILAN,ITALY. NR 2 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 968 EP 968 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301309 ER PT J AU RAJAGOPALAN, S JONES, K KUTTY, G CHADER, GJ WIGGERT, B RODRIGUES, M AF RAJAGOPALAN, S JONES, K KUTTY, G CHADER, GJ WIGGERT, B RODRIGUES, M TI INTERPHOTORECEPTOR RETINOID-BINDING PROTEIN (IRBP) EXPRESSION IN MEDULLOBLASTOMA ANALYZED BY POLYMERASE CHAIN-REACTION (PCR) AND IMMUNOCYTOCHEMISTRY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MARYLAND,BALTIMORE,MD 21201. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 969 EP 969 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301314 ER PT J AU GEORGE, DP MCLEAN, IW HIDAYAT, A KEEFE, KS DAVIDSON, JK BURNIER, MN AF GEORGE, DP MCLEAN, IW HIDAYAT, A KEEFE, KS DAVIDSON, JK BURNIER, MN TI CLINICOPATHOLOGICAL DIFFERENTIATION OF PRIMARY AND SECONDARY OCULAR LYMPHOMAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 970 EP 970 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301320 ER PT J AU CORCOVAN, KA BARROS, PSM BURNIER, MN AF CORCOVAN, KA BARROS, PSM BURNIER, MN TI THE USE OF IMMUNOHISTOCHEMISTRY IN THE DIAGNOSIS OF BILATERAL INTRAOCULAR TUMORS IN DOGS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 SAO PAULO STATE UNIV,SAO PAULO,BRAZIL. ANIM EYE CLIN,SILVER SPRING,MD. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 971 EP 971 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301326 ER PT J AU REDMOND, TM TSILOU, E PFEFFER, BA DETRICK, B HOOKS, JJ HAMEL, CP AF REDMOND, TM TSILOU, E PFEFFER, BA DETRICK, B HOOKS, JJ HAMEL, CP TI CLONING AND EXPRESSION OF A NOVEL RETINAL-PIGMENT EPITHELIUM-SPECIFIC 65 KDA MICROSOMAL PROTEIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 982 EP 982 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301378 ER PT J AU BETTELHEIM, FA GARLAND, D AF BETTELHEIM, FA GARLAND, D TI WATER BINDING ABILITY OF GAMMA-CRYSTALLINS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. ADELPHI UNIV,GARDEN CITY,NY 11530. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 988 EP 988 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301402 ER PT J AU HUANG, QL DING, LL ZIGLER, JS HORWITZ, J AF HUANG, QL DING, LL ZIGLER, JS HORWITZ, J TI THERMAL-STABILITY OF VARIOUS ENZYMES IN RAT ORGAN-CULTURE SYSTEM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,VISION RES LAB,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,SCH MED,JULES STEIN EYE INST,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 988 EP 988 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301406 ER PT J AU RAO, CM ZIGLER, SJ RAMAN, B AF RAO, CM ZIGLER, SJ RAMAN, B TI DIFFERENTIAL PROTECTIVE ABILITY OF ALPHA-CRYSTALLIN TOWARDS THERMAL AND PHOTOAGGREGATION OF GAMMA CRYSTALLIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LMOD,BETHESDA,MD 20892. CTR CELLULAR & MOLEC BIOL,HYDERABAD 50007,INDIA. NR 1 TC 7 Z9 7 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 988 EP 988 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301405 ER PT J AU RAO, PV HORWITZ, J ZIGLER, JS AF RAO, PV HORWITZ, J ZIGLER, JS TI ALPHA-CRYSTALLIN MEDIATED INHIBITION OF AGGREGATION OF THERMALLY DENATURED ENZYMES - ROLE OF COFACTORS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,SCH MED,JULES STEIN EYE INST,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 989 EP 989 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301407 ER PT J AU HOOKS, JJ BURNIER, MN WANG, Y PERCOPO, C DETRICK, B AF HOOKS, JJ BURNIER, MN WANG, Y PERCOPO, C DETRICK, B TI BIPHASIC RETINAL MANIFESTATIONS OF A MURINE CORONAVIRUS INFECTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 997 EP 997 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301446 ER PT J AU CHAN, CC HIKITA, N DASTGHEIB, K WHITCUP, SM GERY, I NUSSENBLATT, RB AF CHAN, CC HIKITA, N DASTGHEIB, K WHITCUP, SM GERY, I NUSSENBLATT, RB TI IMMUNOPATHOLOGY OF EXPERIMENTAL AUTOIMMUNE ANTERIOR UVEITIS (EAAU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 999 EP 999 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301456 ER PT J AU MASTORAKOS, G BOUZAS, EA BURNIER, MN CHROUSOS, GP CHROUSOS, GA AF MASTORAKOS, G BOUZAS, EA BURNIER, MN CHROUSOS, GP CHROUSOS, GA TI PRESENCE OF IMMUNOREACTIVE CORTICOTROPIN RELEASING HORMONE IN THE OPTIC-NERVE BUT NOT THE INFLAMMATORY INFILTRATE OF ALLERGIC OPTIC NEURITIS ENCEPHALOMYELITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NICHHD,BETHESDA,MD. GEORGETOWN UNIV,WASHINGTON,DC 20057. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1000 EP 1000 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301461 ER PT J AU BREZIN, AP KASNER, L THULLIEZ, P LI, Q DAFFOS, F NUSSENBLATT, RB CHAN, CC AF BREZIN, AP KASNER, L THULLIEZ, P LI, Q DAFFOS, F NUSSENBLATT, RB CHAN, CC TI OCULAR TOXOPLASMOSIS IN THE FETUS - IMMUNOHISTOCHEMISTRY AND DNA AMPLIFICATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. INST PUERICULTURE,TOXOPLASMOSE LAB,F-75014 PARIS,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1001 EP 1001 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301465 ER PT J AU MARTINS, MC BURNIER, MNN GAZZINELLI, R HOOKS, JJ AF MARTINS, MC BURNIER, MNN GAZZINELLI, R HOOKS, JJ TI EXPERIMENTAL-MODEL OF ACQUIRED OCULAR TOXOPLASMOSIS IN MICE USING ME49 AND S2C9 TOXOPLASMA-GONDII STRAINS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIAID,NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1001 EP 1001 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301466 ER PT J AU DOONER, J JOHNSON, M FREUND, J RODRIGUEZ, I HACKETT, S CSAKY, C GROTENDORST, G LAROCHELLE, W CAMPOCHIARO, P AF DOONER, J JOHNSON, M FREUND, J RODRIGUEZ, I HACKETT, S CSAKY, C GROTENDORST, G LAROCHELLE, W CAMPOCHIARO, P TI PLATELET-DERIVED GROWTH FACTOR-LIKE PROTEIN-PRODUCTION BY RPE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV HOSP,WILMER OPHTHALMOL INST,BALTIMORE,MD 21205. NIH,BETHESDA,MD 20892. UNIV MIAMI,MIAMI,FL 33152. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1018 EP 1018 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301554 ER PT J AU NAGINENI, CN DETRICK, B HOOKS, JJ AF NAGINENI, CN DETRICK, B HOOKS, JJ TI INTERFERON-GAMMA ACTS SYNERGISTICALLY WITH INFLAMMATORY MEDIATORS TO INDUCE EXPRESSION OF INTERLEUKIN-6 BY HUMAN RETINAL-PIGMENT EPITHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1020 EP 1020 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301563 ER PT J AU MOSHAYEDI, P GAUDET, SJ JONES, BE SEARCY, G LEROITH, T CHADER, GJ WALDBILLIG, RJ AF MOSHAYEDI, P GAUDET, SJ JONES, BE SEARCY, G LEROITH, T CHADER, GJ WALDBILLIG, RJ TI CHARACTERIZATION OF AN IGFBP-3 PROTEASE IN AQUEOUS AND VITREOUS HUMORS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1023 EP 1023 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301573 ER PT J AU GUERIN, CJ LEWIS, GP FLANDERS, KA FISHER, SK ANDERSON, DH AF GUERIN, CJ LEWIS, GP FLANDERS, KA FISHER, SK ANDERSON, DH TI 3 ISOFORMS OF TRANSFORMING GROWTH-FACTOR-BETA ARE PRESENT IN NORMAL AND DETACHED RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV CALIF SANTA BARBARA,NEUROSCI RES INST,SANTA BARBARA,CA 93106. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1024 EP 1024 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301582 ER PT J AU DETRICK, B RHAME, J WANG, Y NAGINENI, C HOOKS, JJ AF DETRICK, B RHAME, J WANG, Y NAGINENI, C HOOKS, JJ TI CYTOMEGALOVIRUS (CMV) REPLICATION IN HUMAN RETINAL-PIGMENT EPITHELIAL-CELLS IS LIMITED AT THE LEVEL OF IMMEDIATE EARLY (IE) PROTEIN-PRODUCTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1056 EP 1056 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301737 ER PT J AU BOUZAS, EA MASTORAKOS, G CHROUSOS, GP KAISERKUPFER, MI AF BOUZAS, EA MASTORAKOS, G CHROUSOS, GP KAISERKUPFER, MI TI POSTERIOR SUBCAPSULAR CATARACT IS INFREQUENT IN ENDOGENOUS CUSHING SYNDROME SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NICHHD,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1064 EP 1064 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301772 ER PT J AU DREWSBANKIEWICZ, MA CARUSO, RC KAISERKUPFER, MI AF DREWSBANKIEWICZ, MA CARUSO, RC KAISERKUPFER, MI TI THE CLINICAL RELEVANCE OF THE TIME COURSE OF DARK-ADAPTATION IN RETINAL DEGENERATIVE DISEASES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1077 EP 1077 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301830 ER PT J AU JAFFE, MJ FAN, WN BARTKO, JJ VONFRICKEN, MA AF JAFFE, MJ FAN, WN BARTKO, JJ VONFRICKEN, MA TI TEST-RETEST RELIABILITY OF THE GANZFELD ELECTRORETINOGRAM IN NORMAL HUMANS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 FIDIA PHARMACEUT CORP,WASHINGTON,DC. NEI,CLIN BRANCH,BETHESDA,MD 20892. NIMH,NEUROPSYCHIAT BRANCH,BETHESDA,MD 20892. NIMH,MATH & STAT GRP,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,DEPT OPHTHALMOL,WASHINGTON,DC 20052. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1078 EP 1078 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301841 ER PT J AU PARKS, DJ HIKITA, N NAGINENI, C HOOKS, JJ CHAN, CC NUSSENBLATT, RB DESMET, MD AF PARKS, DJ HIKITA, N NAGINENI, C HOOKS, JJ CHAN, CC NUSSENBLATT, RB DESMET, MD TI IMMUNOHISTOCHEMISTRY OF XENOGENEIC RPE TRANSPLANTS IN THE RAT - A MODEL FOR GRAFT-REJECTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1095 EP 1095 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301929 ER PT J AU SEIGEL, GM CASTILLO, B DELCERRO, C CHADER, GJ DILORETO, DA GROVER, DA KOWALEVSKY, G LAZAR, ES BECERRA, P TOMBRANTINK, J WYATT, J DELCERRO, M AF SEIGEL, GM CASTILLO, B DELCERRO, C CHADER, GJ DILORETO, DA GROVER, DA KOWALEVSKY, G LAZAR, ES BECERRA, P TOMBRANTINK, J WYATT, J DELCERRO, M TI TOWARD THE INDUCTION OF NEURONAL DIFFERENTIATION AND ABROGATION OF MALIGNANCY IN TRANSPLANTED Y79 RETINOBLASTOMA CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV ROCHESTER,SCH MED,ROCHESTER,NY 14627. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1097 EP 1097 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301938 ER PT J AU MILLSAP, CM CONWAY, MD DUELAND, AN SROCK, K SOIKE, KF UNGERLEIDER, LG GILDEN, DH PEYMAN, GA AF MILLSAP, CM CONWAY, MD DUELAND, AN SROCK, K SOIKE, KF UNGERLEIDER, LG GILDEN, DH PEYMAN, GA TI VARICELLA ENCEPHALITIS FOLLOWING STEROID TREATMENT OF VARICELLA UVEITIS IN A NONHUMAN PRIMATE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 LSU,CTR EYE,NEW ORLEANS,LA. UNIV COLORADO,SCH MED,DENVER,CO 80202. TULANE UNIV,CTR PRIMATE,COVINGTON,LA 70433. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1107 EP 1107 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89301989 ER PT J AU MUCCIOLI, C BELFORT, R PODGOR, M SAMPAIO, P HAYASHI, S NEVES, R LOTTENBERG, C KIM, MK DESMET, M NUSSENBLATT, R AF MUCCIOLI, C BELFORT, R PODGOR, M SAMPAIO, P HAYASHI, S NEVES, R LOTTENBERG, C KIM, MK DESMET, M NUSSENBLATT, R TI THE DIAGNOSIS OF INTRAOCULAR INFLAMMATION AND CMV RETINITIS IN HIV-INFECTED PATIENTS BY LASER FLARE PHOTOMETRY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 ESCOLA PAULISTA MED SCH,BR-04023 SAO PAULO,BRAZIL. CTR REFERENCIA & TREINAMENTO AIDS,SAO PAULO,BRAZIL. NEI,BETHESDA,MD 20892. RI Belfort Jr, Rubens/E-2252-2012; Muccioli, Cristina/C-3419-2013 OI Belfort Jr, Rubens/0000-0002-8422-3898; NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1110 EP 1110 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302006 ER PT J AU SEDDON, J AJANI, U SPERDUTO, R YANNUZZI, L BURTON, T HALLER, J BLAIR, N FARBER, M MILLER, D GRAGOUDAS, E WILLETT, W AF SEDDON, J AJANI, U SPERDUTO, R YANNUZZI, L BURTON, T HALLER, J BLAIR, N FARBER, M MILLER, D GRAGOUDAS, E WILLETT, W TI DIETARY ANTIOXIDANT STATUS AND AGE-RELATED MACULAR DEGENERATION - A MULTICENTER STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MEETH,BOSTON,MA. CDC,ATLANTA,GA. HARVARD UNIV,SCH MED,MEEI,BOSTON,MA 02115. NEI,BETHESDA,MD 20892. MED COLL WISCONSIN,MILWAUKEE,WI 53226. WILMER EYE INST,BALTIMORE,MD. MEETH,NEW YORK,NY. UNIV ILLINOIS,CHICAGO,IL 60680. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1134 EP 1134 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302120 ER PT J AU DESMET, MD MAINIGI, S NUSSENBLATT, RB AF DESMET, MD MAINIGI, S NUSSENBLATT, RB TI IMMUNOGENICITY AND IMMUNOPATHOGENICITY OF PEPTIDE DETERMINANTS OF HUMAN S-AG IN VARIOUS RAT STRAINS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1143 EP 1143 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302165 ER PT J AU GURU, SC SUNIL, S ETO, K SINGH, VK SHINOHARA, T AF GURU, SC SUNIL, S ETO, K SINGH, VK SHINOHARA, T TI OLIGOPEPTIDES OF 3-5 RESIDUES DERIVED FROM UVEITOPATHOGENIC SITES OF RETINAL S-ANTIGEN INDUCE EXPERIMENTAL AUTOIMMUNE UVEITIS (EAU) IN LEWIS RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. SGPGIMS,DEPT IMMUNOL,LUCKNOW,INDIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1143 EP 1143 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302164 ER PT J AU KOZHICH, AT KAWANO, YI NICKERSON, JM EGWUAGU, CE CASPI, RR GERY, I AF KOZHICH, AT KAWANO, YI NICKERSON, JM EGWUAGU, CE CASPI, RR GERY, I TI THE RAT HOMOLOG OF THE IMMUNODOMINANT PEPTIDE (1181-1191) OF BOVINE IRBP IS TOTALLY INACTIVE IN THE LEWIS RAT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract ID RETINOID-BINDING PROTEIN; DETERMINANT C1 NEI,BETHESDA,MD 20892. SHEMYAKIN INST BIOORGAN CHEM,MOSCOW,RUSSIA. EMORY UNIV,ATLANTA,GA 30322. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1143 EP 1143 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302166 ER PT J AU RIZZO, LV SILVER, PB HAKIM, F CHAN, CC WIGGERT, B CASPI, RR AF RIZZO, LV SILVER, PB HAKIM, F CHAN, CC WIGGERT, B CASPI, RR TI ESTABLISHMENT AND CHARACTERIZATION OF AN IRBP-SPECIFIC T-CELL LINE THAT INDUCES EAU IN B10.A MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1143 EP 1143 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302167 ER PT J AU WHITCUP, SM HIKITA, N SHIRAO, M MOCHIZUKI, M NUSSENBLATT, RB CHAN, CC AF WHITCUP, SM HIKITA, N SHIRAO, M MOCHIZUKI, M NUSSENBLATT, RB CHAN, CC TI EFFECT OF MONOCLONAL-ANTIBODIES AGAINST ICAM-1 (CD54) AND LFA-1-ALPHA (CD11A) IN THE PREVENTION AND TREATMENT OF ENDOTOXIN-INDUCED UVEITIS (EIU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. KURUME UNIV,DEPT OPHTHALMOL,KURUME,FUKUOKA 830,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1143 EP 1143 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302163 ER PT J AU MAHDI, RM CASPI, RR NUSSENBLATT, RB GERY, I EGWUAGU, CE AF MAHDI, RM CASPI, RR NUSSENBLATT, RB GERY, I EGWUAGU, CE TI SELECTIVE ACCUMULATION OF V-BETA-8+ T-LYMPHOCYTES IN EAU SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1144 EP 1144 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302169 ER PT J AU MILLERRIVERO, NE SUH, EDW KOZHICH, AT NUSSENBLATT, RB GERY, I AF MILLERRIVERO, NE SUH, EDW KOZHICH, AT NUSSENBLATT, RB GERY, I TI THE FINE SPECIFICITY OF ORAL TOLERANCE AGAINST A UVEITOGENIC PEPTIDE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1144 EP 1144 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302171 ER PT J AU VISTICA, B GERY, I CHAN, CC NUSSENBLATT, RB WHITCUP, SM AF VISTICA, B GERY, I CHAN, CC NUSSENBLATT, RB WHITCUP, SM TI ANTI-ICAM-1 AND ANTI-LFA-1 MONOCLONAL-ANTIBODIES (MABS) INHIBIT INVITRO PROLIFERATION OF A UVEITOGENIC CELL-LINE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1144 EP 1144 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302168 ER PT J AU ROTH, SI MIDURA, RJ HASCALL, VC OGRADY, RB STOCK, EL AF ROTH, SI MIDURA, RJ HASCALL, VC OGRADY, RB STOCK, EL TI CORNEAL MUCOPOLYSACCHARIDES (MPS) IN HURLER-SCHEIE SYNDROME (HSS) - A COMPARISON WITH MACULAR CORNEAL DYSTROPHY-II (MCD-II) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. LAKESIDE VET ADM MED CTR,CHICAGO,IL 60611. UNIV IOWA,IOWA CITY,IA. NIDR,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1146 EP 1146 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302179 ER PT J AU AYYAGARI, R SMITH, RJH LEE, EC KIMBERLING, WJ DAIGER, SP PELIAS, MZ KEATS, BJB JAY, M BIRD, A REARDON, W GUEST, M HEJTMANCIK, JF AF AYYAGARI, R SMITH, RJH LEE, EC KIMBERLING, WJ DAIGER, SP PELIAS, MZ KEATS, BJB JAY, M BIRD, A REARDON, W GUEST, M HEJTMANCIK, JF TI HETEROGENEITY AND LINKAGE ANALYSIS OF USHER SYNDROME TYPE-I SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1150 EP 1150 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302197 ER PT J AU KOLB, H PFLUG, R DEKORVER, L NELSON, R AF KOLB, H PFLUG, R DEKORVER, L NELSON, R TI SYNAPTIC ORGANIZATION OF HYPERPOLARIZING AMACRINE CELL-A13 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV UTAH,SCH MED,SALT LAKE CITY,UT 84112. UNIV VIENNA,A-1010 VIENNA,AUSTRIA. NIH,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1153 EP 1153 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302212 ER PT J AU HAZARD, ES CROUCH, RK PUTILINA, T WIGGERT, B CHADER, G AF HAZARD, ES CROUCH, RK PUTILINA, T WIGGERT, B CHADER, G TI FLUORESCENCE TRANSFER IN IRBP SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,CHARLESTON,SC 29425. NEI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1197 EP 1197 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302428 ER PT J AU LAI, JC CHAN, CC LI, Q WHITCUP, SM AF LAI, JC CHAN, CC LI, Q WHITCUP, SM TI TREATMENT WITH CORTICOSTEROIDS AND CYCLOSPORINE-A INHIBITS THE EXPRESSION OF CELL-ADHESION MOLECULES IN EXPERIMENTAL AUTOIMMUNE UVEITIS (EAU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1206 EP 1206 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302472 ER PT J AU SCHOEN, TJ WALDBILLIG, RJ BEEBE, D BONDY, C ZHOU, J POTTS, J ARNOLD, D CHADER, G RODRIGUEZ, IR AF SCHOEN, TJ WALDBILLIG, RJ BEEBE, D BONDY, C ZHOU, J POTTS, J ARNOLD, D CHADER, G RODRIGUEZ, IR TI SEQUENCE, DEVELOPMENTAL REGULATION AND INSITU LOCALIZATION OF INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEIN (IGFBP-2) MESSENGER-RNA IN DEVELOPING CHICK OCULAR-TISSUES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NIH,CH DEB,BETHESDA,MD 20892. USUHS,DEPT ANAT & CELL BIOL,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1221 EP 1221 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302541 ER PT J AU CHEPELINSKY, AB OVERBEEK, PA CHAN, CC JAMIESON, S DICKSON, C PARKER, DM ROBINSON, M AF CHEPELINSKY, AB OVERBEEK, PA CHAN, CC JAMIESON, S DICKSON, C PARKER, DM ROBINSON, M TI INT2 ECTOPIC EXPRESSION INDUCES DIFFERENTIATION OF SECRETORY EPITHELIA IN THE EYES OF TRANSGENIC MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. BAYLOR COLL MED,HOUSTON,TX 77030. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1222 EP 1222 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302547 ER PT J AU FISHER, AM MORINELLI, E SVASSAND, LO PARKER, RJ REED, E MURPHREE, AL GOMER, CJ AF FISHER, AM MORINELLI, E SVASSAND, LO PARKER, RJ REED, E MURPHREE, AL GOMER, CJ TI PRECLINICAL ANALYSIS OF DIODE-LASER HYPERTHERMIA AND CARBOPLATIN FOR OCULAR TUMOR TREATMENT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV SO CALIF,CHILDRENS HOSP LOS ANGELES,LOS ANGELES,CA 90089. UNIV TRONDHEIM,TRONDHEIM,NORWAY. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1228 EP 1228 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302573 ER PT J AU JOSEPH, JS OPTICAN, LM AF JOSEPH, JS OPTICAN, LM TI ORIENTATION POP-OUT AS AN EXOGENOUS CUE FOR VISUAL-ATTENTION - TEMPORAL AND SPATIAL PROPERTIES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1235 EP 1235 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302609 ER PT J AU CARUSO, RC REUTER, LM MULLER, SF DREWSBANKIEWICZ, MA KAISERKUPFER, MI AF CARUSO, RC REUTER, LM MULLER, SF DREWSBANKIEWICZ, MA KAISERKUPFER, MI TI ORIGIN OF THE PEAKS OF THE HUMAN TRANSIENT PATTERN REVERSAL VISUAL EVOKED-POTENTIAL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1276 EP 1276 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302826 ER PT J AU REUTER, LM CARUSO, RC MULLER, SF DREWSBANKIEWICZ, MA BOUZAS, EA KAISERKUPFER, MI AF REUTER, LM CARUSO, RC MULLER, SF DREWSBANKIEWICZ, MA BOUZAS, EA KAISERKUPFER, MI TI THE PATTERN REVERSAL VISUAL EVOKED-POTENTIAL - SYMMETRICAL OR ASYMMETRICAL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1276 EP 1276 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302825 ER PT J AU GENTLEMAN, S CHADER, GJ AF GENTLEMAN, S CHADER, GJ TI PURIFICATION OF RETINAL TUBULIN ACETYLTRANSFERASE BY ACETYL-COA AFFINITY-CHROMATOGRAPHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1278 EP 1278 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302835 ER PT J AU RUSSELL, P EPSTEIN, DL AF RUSSELL, P EPSTEIN, DL TI PROTEIN-ANALYSIS OF THE RHESUS-MONKEY AQUEOUS-HUMOR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. DUKE UNIV,DEPT OPHTHALMOL,DURHAM,NC 27706. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1280 EP 1280 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302847 ER PT J AU ARORA, JK LYSZ, TW LIN, C ZELENKA, PS AF ARORA, JK LYSZ, TW LIN, C ZELENKA, PS TI 12HETE REGULATES DNA-SYNTHESIS AND MYC EXPRESSION IN NEONATAL RAT LENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UMDNJ,NEW JERSEY MED SCH,NEWARK,NJ. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1283 EP 1283 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89302865 ER PT J AU CHANG, C CSAKY, KG OBRIEN, TP AF CHANG, C CSAKY, KG OBRIEN, TP TI COMPARATIVE CORNEAL EPITHELIAL HEALING WITH TOPICAL ADJUNCTIVE GROWTH-FACTORS IN AN EXPERIMENTAL-MODEL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,WILMER INST,BALTIMORE,MD 21218. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1314 EP 1314 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303004 ER PT J AU JIAO, XD LI, J GENTLEMAN, S WETZEL, MG OBRIEN, P CHADER, GJ AF JIAO, XD LI, J GENTLEMAN, S WETZEL, MG OBRIEN, P CHADER, GJ TI ISOLATION, CHARACTERIZATION AND COMPLETE PRIMARY STRUCTURE OF FATTY ACID-BINDING PROTEINS FROM ROD OUTER SEGMENT OF RAT RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV KANSAS,MED CTR,KANSAS CITY,KS 66103. HLTH RES ASSOCIATES,ROCKVILLE,MD. NR 0 TC 3 Z9 3 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1328 EP 1328 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303083 ER PT J AU LI, J GENTLEMAN, S JIAO, XD WETZEL, MG OBRIEN, P CHADER, GJ AF LI, J GENTLEMAN, S JIAO, XD WETZEL, MG OBRIEN, P CHADER, GJ TI UPTAKE OF DOCOSAHEXAENOIC ACID (DHA) BY A FATTY ACID-SPECIFIC RECEPTOR IN THE RETINAL PLASMA-MEMBRANE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV KANSAS,MED CTR,KANSAS CITY,KS 66103. HLTH RES ASSOCIATES,ROCKVILLE,MD. NR 0 TC 2 Z9 2 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1329 EP 1329 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303094 ER PT J AU GARLAND, DL TABOR, Y ZIGLER, JS DATILES, MB AF GARLAND, DL TABOR, Y ZIGLER, JS DATILES, MB TI PROTEIN-ANALYSIS OF LENS CORTICAL ASPIRATES OBTAINED AT SURGERY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1335 EP 1335 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303121 ER PT J AU GAO, CY ZELENKA, PS AF GAO, CY ZELENKA, PS TI IDENTIFICATION OF CYCLIN-B IN CHICKEN-EMBRYO LENS FIBER CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1336 EP 1336 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303123 ER PT J AU HEINZMANN, C GONZALEZ, P ZIGLER, JS RAO, PV KLISAK, I KOJIS, TL COMISO, P SPARKES, RS BATEMAN, JB AF HEINZMANN, C GONZALEZ, P ZIGLER, JS RAO, PV KLISAK, I KOJIS, TL COMISO, P SPARKES, RS BATEMAN, JB TI ZETA-CRYSTALLIN MAPS TO HUMAN-CHROMOSOME 1P21-P22 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI, BETHESDA, MD 20892 USA. UNIV CALIF LOS ANGELES, CTR VIS GENET, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, JULES ST STEIN EYE INST, LOS ANGELES, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1336 EP 1336 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303128 ER PT J AU GONZALEZ, P RAO, PV ZIGLER, JS AF GONZALEZ, P RAO, PV ZIGLER, JS TI CLONING OF ZETA-CRYSTALLIN CDNA FROM THE LENS OF LLAMA(LAMA-GUANACOE-F-GLAMA) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1337 EP 1337 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303129 ER PT J AU WEST, JA SIVAK, JG PASTERNAK, J PIATIGORSKY, J AF WEST, JA SIVAK, JG PASTERNAK, J PIATIGORSKY, J TI ONTOGENY OF CEPHALOPOD (LOLIGO-OPALESCENS) LENS CRYSTALLINS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV WATERLOO,DEPT OPTOMETRY,WATERLOO N2L 3G1,ONTARIO,CANADA. UNIV WATERLOO,DEPT BIOL,WATERLOO N2L 3G1,ONTARIO,CANADA. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1338 EP 1338 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303135 ER PT J AU RAFFERTY, NS RAFFERTY, KA ITO, E AF RAFFERTY, NS RAFFERTY, KA ITO, E TI INTRACELLULAR CALCIUM AND ACTIN CYTOSKELETON OF LENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NORTHWESTERN UNIV,CHICAGO,IL 60611. MARINE BIOL LAB,WOODS HOLE,MA 02543. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1339 EP 1339 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303142 ER PT J AU OHTAKAMARUYAMA, C DREW, LR PISANO, MM CHEPELINSKY, AB AF OHTAKAMARUYAMA, C DREW, LR PISANO, MM CHEPELINSKY, AB TI REGULATORY ELEMENTS OF THE MIP GENE PROMOTER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1342 EP 1342 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303161 ER PT J AU WANG, Y BURNIER, MN DETRICK, B HOOKS, JJ AF WANG, Y BURNIER, MN DETRICK, B HOOKS, JJ TI GENETIC PREDISPOSITION TO CORONAVIRUS INDUCED RETINAL DEGENERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1348 EP 1348 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303192 ER PT J AU KIRCH, I CARUSO, R WANG, Y HOOKS, JJ AF KIRCH, I CARUSO, R WANG, Y HOOKS, JJ TI ERG MANIFESTATIONS IN CORONAVIRUS INDUCED RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1370 EP 1370 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303294 ER PT J AU HOLLAND, EJ HARDTEN, DR MURALI, S LUSHINE, K DEMARTELAERE, S OLEVSKY, OM MINDRUP, EA KARLSTAD, R CHAN, CC AF HOLLAND, EJ HARDTEN, DR MURALI, S LUSHINE, K DEMARTELAERE, S OLEVSKY, OM MINDRUP, EA KARLSTAD, R CHAN, CC TI EFFECT OF TOPICALLY ADMINISTERED PLATELET-DERIVED GROWTH-FACTOR ON CORNEAL WOUND STRENGTH IN PENETRATING KERATOPLASTY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MINNESOTA,DEPT OPHTHALMOL,CORNEA SERV,MINNEAPOLIS,MN 55455. NEI,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1375 EP 1375 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303319 ER PT J AU CHEUNG, MK MAGIAKOU, MA MASTORAKOS, G ROBERGE, FG AF CHEUNG, MK MAGIAKOU, MA MASTORAKOS, G ROBERGE, FG TI INDUCTION OF INFLAMMATORY CYTOKINES BY ND-YAG LASER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NICHHD,BETHESDA,MD 20892. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1386 EP 1386 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303373 ER PT J AU BLICE, JP ROBERTSON, TJ ANTOSZYK, AN CHADER, GJ WALDBILLIG, R AF BLICE, JP ROBERTSON, TJ ANTOSZYK, AN CHADER, GJ WALDBILLIG, R TI THE EFFECT OF INTRA-VITREAL LONG ARG IGF-I IN THE RABBIT EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NATL NAVAL MED CTR, BETHESDA, MD 20814 USA. UNIFORMED SERV UNIV HLTH SCI, BETHESDA, MD 20814 USA. NIH, BETHESDA, MD 20892 USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1427 EP 1427 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303586 ER PT J AU PFEFFER, BA FLANDERS, KC GUERIN, CJ DANIELPOUR, D ANDERSON, DH AF PFEFFER, BA FLANDERS, KC GUERIN, CJ DANIELPOUR, D ANDERSON, DH TI TRANSFORMING GROWTH-FACTOR-BETA2 IS THE PREDOMINANT ISOFORM IN THE POSTERIOR POLE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. UCSB,INST NEUROSCI,SANTA BARBARA,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1449 EP 1449 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303688 ER PT J AU KUTTY, RK NAGINENI, CN KUTTY, G HOOKS, JJ CHADER, GJ WIGGERT, B AF KUTTY, RK NAGINENI, CN KUTTY, G HOOKS, JJ CHADER, GJ WIGGERT, B TI TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) INCREASES THE EXPRESSION OF HEME OXYGENASE-1 (HO-1) IN HUMAN RETINAL-PIGMENT EPITHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1451 EP 1451 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303700 ER PT J AU WALDBILLIG, RJ SEARCY, G CHADER, GJ ROMANO, C WAX, MB MOSHAYEDI, P AF WALDBILLIG, RJ SEARCY, G CHADER, GJ ROMANO, C WAX, MB MOSHAYEDI, P TI CULTURED HUMAN NONPIGMENTED CILIARY BODY EPITHELIAL-CELLS SYNTHESIZE INSULIN-LIKE BINDING-PROTEINS (IGFBPS) AND IGFBP PROTEASES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. NR 0 TC 0 Z9 0 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1451 EP 1451 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303698 ER PT J AU EGWUAGU, CE SZTEIN, J CHAN, CC REID, W MAHDI, R NUSSENBLATT, RB CHEPELINSKY, AB AF EGWUAGU, CE SZTEIN, J CHAN, CC REID, W MAHDI, R NUSSENBLATT, RB CHEPELINSKY, AB TI GAMMA-INTERFERON EXPRESSION IN THE EYES OF TRANSGENIC MICE DISRUPTS DIFFERENTIATION OF THE LENS AND RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. RI Sztein, Jorge/B-7165-2012 NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1455 EP 1455 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303718 ER PT J AU GOPALSRIVASTAVA, R PIATIGORSKY, J AF GOPALSRIVASTAVA, R PIATIGORSKY, J TI FUNCTIONAL-ANALYSIS OF MURINE ALPHA-B-CRYSTALLIN ENHANCER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1456 EP 1456 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303721 ER PT J AU LI, X PIATIGORSKY, J AF LI, X PIATIGORSKY, J TI FUNCTIONAL EQUIVALENCE OF THE 2 DELTA-CRYSTALLIN ENHANCERS IN TRANSGENIC MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1456 EP 1456 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303722 ER PT J AU SAX, CM ILAGAN, JG PIATIGORSKY, J AF SAX, CM ILAGAN, JG PIATIGORSKY, J TI FUNCTIONAL REDUNDANCY OF THE DE-1 AND ALPHA-A-CRYBP1 REGULATORY SITES OF THE MOUSE ALPHA-A-CRYSTALLIN PROMOTER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1456 EP 1456 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303720 ER PT J AU WANG, YX LI, J HEJTMANCIK, F KAISERKUPFER, M CHADER, GJ AF WANG, YX LI, J HEJTMANCIK, F KAISERKUPFER, M CHADER, GJ TI THE METABOLISM OF FATTY-ACIDS IN HUMAN BIETTI CRYSTALLINE DYSTROPHY AND WOLMAN-DISEASE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1458 EP 1458 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303731 ER PT J AU WONG, P PINEAULT, J LAKINS, J PUTILINA, T CHADER, G TENNISWOOD, M AF WONG, P PINEAULT, J LAKINS, J PUTILINA, T CHADER, G TENNISWOOD, M TI MOLECULAR CHARACTERIZATION OF THE HUMAN TRPM-2/CLUSTERIN GENE - POSITIONAL EXCLUSION AS A POTENTIAL CANDIDATE GENE FOR RP1 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV OTTAWA,DEPT BIOCHEM,OTTAWA K1N 6N5,ONTARIO,CANADA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1460 EP 1460 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303743 ER PT J AU DANCIGER, M KOZAK, CA APPLEBURY, ML POLANS, A FARBER, DB AF DANCIGER, M KOZAK, CA APPLEBURY, ML POLANS, A FARBER, DB TI CHROMOSOMAL MAPPING IN THE MOUSE OF THE GENES FOR 2 PROTEINS EXPRESSED IN PHOTORECEPTORS - CONE CGMP-PDE-ALPHA' AND RECOVERIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GOOD SAMARITAN HOSP, PORTLAND, OR 97210 USA. UNIV CHICAGO, CHICAGO, IL 60637 USA. NIAID, BETHESDA, MD 20892 USA. UNIV CALIF LOS ANGELES, SCH MED, JULES STEIN EYE INST, LOS ANGELES, CA USA. LOYOLA MARYMOUNT UNIV, LOS ANGELES, CA 90045 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1461 EP 1461 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303750 ER PT J AU MAZURUK, K SUNG, JU MCCREA, N CHADER, GJ RODRIGUEZ, IR AF MAZURUK, K SUNG, JU MCCREA, N CHADER, GJ RODRIGUEZ, IR TI CLONING OF A NOVEL CDNA EXPRESSED IN RETINA AND FETAL TISSUES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1463 EP 1463 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303757 ER PT J AU SHIRKEY, BL SLAVIN, S CHANAUD, NP VISTICA, BP GERY, I AF SHIRKEY, BL SLAVIN, S CHANAUD, NP VISTICA, BP GERY, I TI LINOMIDE, A NOVEL IMMUNOMODULATOR, INHIBITS EXPERIMENTAL AUTOIMMUNE UVEORETINITIS (EAU) IN MICE AND RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. HOWARD HUGHES MED INST,BETHESDA,MD. HADASSAH UNIV HOSP,IL-91120 JERUSALEM,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1475 EP 1475 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303824 ER PT J AU MARTIN, DF DEBARGE, LR NUSSENBLATT, RB CHAN, CC ROBERGE, FG AF MARTIN, DF DEBARGE, LR NUSSENBLATT, RB CHAN, CC ROBERGE, FG TI SYNERGISTIC EFFECT OF RAPAMYCIN AND CYCLOSPORINE-A ON THE INHIBITION OF EXPERIMENTAL AUTOIMMUNE UVEORETINITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1476 EP 1476 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303826 ER PT J AU WESTEREN, AC CHAN, CC DESMET, MD NUSSENBLATT, RB ROBERGE, FG AF WESTEREN, AC CHAN, CC DESMET, MD NUSSENBLATT, RB ROBERGE, FG TI EVALUATION OF THE IMMUNOSUPPRESSANT SK-AND-F-106610 IN THE TREATMENT OF EXPERIMENTAL AUTOIMMUNE UVEORETINITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1477 EP 1477 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303833 ER PT J AU BLOOM, JN NI, M MOORE, TL NICKERSON, JM SHINOHARA, T AF BLOOM, JN NI, M MOORE, TL NICKERSON, JM SHINOHARA, T TI DETECTION OF S-ANTIGEN MESSENGER-RNA AND IRBP MESSENGER-RNA IN HUMAN SYNOVIUM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 EMORY UNIV,ATLANTA,GA 30322. ST LOUIS UNIV,ST LOUIS,MO 63103. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1479 EP 1479 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303848 ER PT J AU GERY, I ALLISON, AC MILLERRIVERO, N VISTICA, BP CHANAUD, NP NUSSENBLATT, RB AF GERY, I ALLISON, AC MILLERRIVERO, N VISTICA, BP CHANAUD, NP NUSSENBLATT, RB TI INHIBITION OF EXPERIMENTAL AUTOIMMUNE UVEORETINITIS (EAU) BY MYCOPHENOLATE MOFETIL (MM) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. SYNTEX INC,PALO ALTO,CA 94304. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1480 EP 1480 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303854 ER PT J AU HIKITA, N CHAN, CC MOCHIZUKI, M MATURI, R NUSSENBLATT, RB WHITCUP, SM AF HIKITA, N CHAN, CC MOCHIZUKI, M MATURI, R NUSSENBLATT, RB WHITCUP, SM TI TOPICAL FK-506 INHIBITS ENDOTOXIN-INDUCED UVEITIS (EIU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. KURUME UNIV,KURUME,FUKUOKA 830,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1480 EP 1480 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303853 ER PT J AU KASNER, L CHAN, CC WHITCUP, SM GERY, I AF KASNER, L CHAN, CC WHITCUP, SM GERY, I TI THE PARADOXICAL ROLE OF TUMOR-NECROSIS-FACTOR-ALPHA IN ENDOTOXIN INDUCED UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1480 EP 1480 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303849 ER PT J AU DEBARGE, LR FENTON, R NUSSENBLATT, RB DESMET, MD AF DEBARGE, LR FENTON, R NUSSENBLATT, RB DESMET, MD TI QUANTITATIVE-DETERMINATION OF THE FLARE IN THE ANTERIOR-CHAMBER OF THE RAT BY A NONINVASIVE METHOD SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV TENNESSEE,KNOXVILLE,TN 37996. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1481 EP 1481 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303857 ER PT J AU RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B AF RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B TI IDENTIFICATION OF A HEAT-SHOCK PROTEIN THAT BINDS TO PEPTIDE 1169-1191 OF IRBP CAUSING AUTOIMMUNE UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1482 EP 1482 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303861 ER PT J AU SILVER, PB RIZZO, LV CHAN, CC DONOSO, LA WIGGERT, B CASPI, RR AF SILVER, PB RIZZO, LV CHAN, CC DONOSO, LA WIGGERT, B CASPI, RR TI IDENTIFICATION OF A PUTATIVE EPITOPE IN THE IRBP MOLECULE THAT IS UVEITOGENIC FOR MICE OF THE H-2(B) HAPLOTYPE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. WILLS EYE HOSP & RES INST,PHILADELPHIA,PA 19107. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1482 EP 1482 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303865 ER PT J AU SINGH, DP ETO, K SUZUKI, S SINGH, VK SHINOHARA, T AF SINGH, DP ETO, K SUZUKI, S SINGH, VK SHINOHARA, T TI IMMUNIZATION WITH RECOMBINANT ESCHERICHIA-COLI EXPRESSING RETINAL S-ANTIGEN INDUCE EXPERIMENTAL AUTOIMMUNE UVEITIS (EAU) IN LEWIS RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. SGPGIMS,DEPT IMMUNOL,LUCKNOW,INDIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1482 EP 1482 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303864 ER PT J AU DASTGHEIB, K HIKITA, N SREDNI, B ALBECK, M NUSSENBLATT, RB CHAN, CC AF DASTGHEIB, K HIKITA, N SREDNI, B ALBECK, M NUSSENBLATT, RB CHAN, CC TI OCULAR INFLAMMATION STIMULATED BY THE IMMUNOMODULATOR AS101 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. BAR ILAN UNIV,DEPT LIFE SCI,INST CAIR,RAMAT GAN,ISRAEL. NR 3 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1483 EP 1483 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303869 ER PT J AU PEARSON, PA JAFFE, GJ MARTIN, DF ASHTON, P AF PEARSON, PA JAFFE, GJ MARTIN, DF ASHTON, P TI SUSTAINED DELIVERY AND CLEARANCE OF INTRAOCULAR CYCLOSPORINE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 DUKE UNIV,DURHAM,NC 27706. NIH,BETHESDA,MD 20892. UNIV KENTUCKY,LEXINGTON,KY 40506. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1492 EP 1492 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303915 ER PT J AU FITZGIBBON, EJ CALVERT, PC ZEE, DS AF FITZGIBBON, EJ CALVERT, PC ZEE, DS TI TORSIONAL NYSTAGMUS DURING VERTICAL PURSUIT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1993 VL 34 IS 4 BP 1500 EP 1500 PG 1 WC Ophthalmology SC Ophthalmology GA KT893 UT WOS:A1993KT89303958 ER PT J AU SHAH, N KLAUSNER, RD AF SHAH, N KLAUSNER, RD TI BREFELDIN-A REVERSIBLY INHIBITS SECRETION IN SACCHAROMYCES-CEREVISIAE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID PERIPHERAL MEMBRANE-PROTEIN; ADP-RIBOSYLATION FACTOR; GOLGI-APPARATUS; COATED VESICLES; BETA-COP; YEAST; TRANSPORT; COMPLEX; BINDING; CELLS AB Brefeldin A has proven to be a useful pharmacologic tool, which, when added to mammalian cells, results in a block in secretion as well as the structural disruption of specific intracellular organelles. In spite of our understanding of some of the biochemistry underlying the action of brefeldin A, the most proximal molecular target(s) of the drug remain elusive. In attempting to address this problem, a genetic approach will undoubtedly prove useful and complementary to the biochemical identification of such a site(s). As a result of the relatively resistant nature of wild-type Saccharomyces cerevisiae to brefeldin A, an approach utilizing yeast genetics has not been possible. We report the selective sensitivity of three drug-sensitive strains of S. cerevisiae (ise-1, ISE-2, and erg6) with enhanced membrane permeability allowing uptake of brefeldin A. Upon addition of the drug, growth is dramatically inhibited and invertase secretion is rapidly, specifically, and reversibly blocked at the level of the endoplasmic reticulum. In addition, only structural analogues of brefeldin A effective in mammalian cells are active in these yeast strains. C1 NICHHD,CELL BIOL & METAB BRANCH,BLDG 18T,RM 101,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 33 TC 43 Z9 44 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1993 VL 268 IS 8 BP 5345 EP 5348 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KR822 UT WOS:A1993KR82200002 PM 8449896 ER PT J AU RON, D REICH, R CHEDID, M LENGEL, C COHEN, OE CHAN, AML NEUFELD, G MIKI, T TRONICK, SR AF RON, D REICH, R CHEDID, M LENGEL, C COHEN, OE CHAN, AML NEUFELD, G MIKI, T TRONICK, SR TI FIBROBLAST GROWTH-FACTOR RECEPTOR-4 IS A HIGH-AFFINITY RECEPTOR FOR BOTH ACIDIC AND BASIC FIBROBLAST GROWTH-FACTOR BUT NOT FOR KERATINOCYTE GROWTH-FACTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ENZYMATIC AMPLIFICATION; MESSENGER-RNA; CELL-GROWTH; DNA; IDENTIFICATION; TRANSFORMATION; FAMILY; EXPRESSION; INDUCTION; MEMBER AB A cDNA predicted to encode a transmembrane tyrosine kinase receptor with sequence features characteristic of known fibroblast growth factor (FGF) receptors was isolated from an expression library constructed from the human mammary epithelial cell line B5/589. This cDNA, designated cl44, encodes a product of 803 amino acid residues and was readily distinguishable from known FGF receptors. During the course of our studies, Partanen et al. (Partanen, J., Makela, T. P., Eerola, E., Korhonen, J., Hirvonen, H., Claesson, W. L., and Alitalo, K. (1991) EMBO J. 10, 1347-1354) isolated a new FGF receptor, designated FGFR4, from the human leukemia cell line, K562. Its amino acid sequence is identical to that of cl44 with the exception of 1 residue. The 5'-untranslated sequences of the two cDNAs diverged far upstream of the initiation codon. A myoblast line, L6E9, which lacks FGF receptors, was utilized to express high levels of FGFR4. We found, in contrast to Partenen et al., who reported only binding of acidic FGF, that FGFR4 bound both acidic and basic FGF with dissociation constants of 10-15 and 120 pM, respectively. No detectable binding of keratinocyte growth factor was observed. In studies aimed to determine whether FGF receptors contribute to the development of human tumors, we screened RNAs prepared from cell lines derived from a variety of solid tumors. High levels of the cl44 transcript were detected in 8 of 14 and 6 of 9 human mammary and kidney carcinomas, respectively, but only infrequently in other types of tumors. In contrast, FGFR1 was found to be frequently expressed in kidney, but not in breast tumor cells, suggesting a possible role for FGFR4 in human mammary cancer. C1 NCI, CELLULAR & MOLEC BIOL LAB, BETHESDA, MD 20892 USA. RP TECHNION ISRAEL INST TECHNOL, DEPT BIOL, IL-32000 HAIFA, ISRAEL. NR 56 TC 90 Z9 93 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 MAR 15 PY 1993 VL 268 IS 8 BP 5388 EP 5394 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KR822 UT WOS:A1993KR82200011 PM 7680645 ER PT J AU LAWTON, MP PHILPOT, RM AF LAWTON, MP PHILPOT, RM TI FUNCTIONAL-CHARACTERIZATION OF FLAVIN-CONTAINING MONOOXYGENASE-1B1 EXPRESSED IN SACCHAROMYCES-CEREVISIAE AND ESCHERICHIA-COLI AND ANALYSIS OF PROPOSED FAD-BINDING AND MEMBRANE-BINDING DOMAINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CATALYTIC ACTIVITY; COVALENT STRUCTURE; MULTIPLE FORMS; RABBIT LIVER; RAT; LUNG; PULMONARY; PROTEINS; DISTINCT; MOUSE AB A cDNA encoding the flavin-containing monooxygenase of rabbit lung (FMO 1B1) was expressed in yeast and Escherichia coli and the recombinant enzymes characterized. A high copy, isopropyl-1-thio-beta-D-galactopyranoside (IPTG)-inducible E. coli expression vector, pKKHC, was used for expression in E. coli strain JM109, and a galactose-inducible vector, YEp53, was used for expression in yeast strain 334. Following transcriptional induction with IPTG or galactose, subcellular fractions were prepared and analyzed immunochemically and catalytically. Antibodies to rabbit FMO 1B1 were used to detect the recombinant proteins in the 100,000 x g pellet prepared from the 10,000 x g supernatant fraction of yeast homogenates and the 2,000 x g supernatant fraction of E. coli homogenates. No FMO 1B1 was detected in cytosol. Mobilities of the recombinant proteins in SDS-polyacrylamide gel electrophoresis appeared identical to that of the native microsomal enzyme. Catalytic similarity to the native FMO 1B1 was demonstrated by the ability of the expressed enzymes to metabolize methimazole, thiourea, dimethylaniline, and cysteamine, but not chlorpromazine or imipramine. In addition, the recombinant enzymes exhibited a number of the unique physical properties associated with FMO 1B1, including stability to elevated temperature and activation by sodium cholate and magnesium chloride. Based on the specific content of FAD, the level of expression was estimated to be approximately 2% of the total protein in the E. coli 100,000 x g particulate fraction and 1% in the fraction from yeast. To demonstrate the utility of the E. coli expression system for studying structure/function relationships of the flavin-containing monooxygenase, two mutant FMOs were expressed and characterized. One mutant, formed by deletion of a putative membrane-anchoring peptide (the 26 carboxyl-terminal amino acids) was tested for membrane association. No difference in the subcellular distribution was found between the truncated and unmodified proteins, suggesting that the 26-residue COOH-terminal peptide is not important in membrane association. Catalytic analysis of the truncated FMO 1B1 established its functional similarity to the full-length protein, indicating that the COOH terminus does not contribute to any of the unique properties of the lung enzyme. A second mutant cDNA was generated by changing the third glycine of the consensus FAD-pyrophosphate-binding site (GxGxxG) to valine. The resulting protein was immunochemically similar to the unmodified form but was catalytically inactive. Total flavin content of the particulate fraction from cells transformed with the glycine-to-valine mutant was similar to that of cells transformed with the vector alone. These results indicate that expression of the flavin-containing monooxygenase in E. coli will be useful in structural analysis of this enzyme. C1 NIEHS,CELLULAR & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. NR 43 TC 52 Z9 52 U1 1 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1993 VL 268 IS 8 BP 5728 EP 5734 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KR822 UT WOS:A1993KR82200056 PM 8449936 ER PT J AU ROHLFF, C CLAIR, T YOON, SCC AF ROHLFF, C CLAIR, T YOON, SCC TI 8-CL-CAMP INDUCES TRUNCATION AND DOWN-REGULATION OF THE RI-ALPHA-SUBUNIT AND UP-REGULATION OF THE RII-BETA-SUBUNIT OF CAMP-DEPENDENT PROTEIN-KINASE LEADING TO TYPE-II HOLOENZYME-DEPENDENT GROWTH-INHIBITION AND DIFFERENTIATION OF HL-60 LEUKEMIA-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BREAST CANCER-CELLS; AMINO-ACID SEQUENCE; CYCLIC-AMP; RECEPTOR PROTEINS; MESSENGER-RNA; HUMAN TESTIS; ANTISENSE OLIGODEOXYNUCLEOTIDE; HORMONAL ACTIVATION; CATALYTIC SUBUNIT; MOLECULAR-CLONING AB 8-Cl-cAMP, a site-selective cAMP analog, induces growth inhibition in a variety of cell types of human cancer cell lines. This inhibitory effect of 8-Cl-cAMP was related to its ability to differentially regulate type I versus type II cAMP-dependent protein kinase. In the present study we demonstrated a unique mechanism of action of 8-Cl-cAMP in the regulation of these kinase isozymes in HL-60 human promyelocytic leukemia cells. High-performance liquid chromatography (HPLC) resolved various isoforms of protein kinase present in HL-60 cells. In control cells, type I protein kinase (PKI) comprised more than 90% and type II protein kinase (PKII) less than 10% of the total cAMP-stimulated kinase activity. Treatment with 8-Cl-cAMP (5 muM, 72 h) decreased PKI to a level below 30% of that in untreated control cells and markedly increased PKII composed of three peaks. Photoaffinity labeling/SDS-polyacrylamide gel electrophoresis of column fractions identified the molecular species of regulatory (R) subunits present in protein kinases. Control cells contained high levels of the 48-kDa protein (RI) that composed PKI and low levels of the 50-kDa RII associated with PKII. 8-Cl-cAMP treatment brought about a decrease in the 48-kDa RI along with an increased formation of the truncated 34-kDa RI associated with PKI and an increase in the 50-54-kDa species of RII associated with PKII. A similar protein kinase profile as that shown by 8-Cl-cAMP treatment was observed in cells infected with the human RII(beta) retroviral vector: the 48-kDa RI of PKI decreased and the 52- and 54-kDa RII associated with PKII increased as compared with uninfected control cells. However, unlike 8-Cl-cAMP treatment, RII(beta) retroviral vector infection brought about no increase in the 34-kDa-truncated RI but exhibited an increase in the free 48-kDa RI subunit. As the 48-kDa RI and the 50-kDa RII were present in control cells, the enhanced expression of the 52- and 54-kDa RII proteins was due to overexpression of the RII(beta) gene. We identified the 48-kDa RI as RI(alpha), the 50-kDa RII as RII(alpha), the 52-kDa RII as RII(beta), and the 54-kDa RII as the phosphorylated form of either the RII(alpha) or RII(beta) subunit. In vivo labeling experiments using [H-3]8-Cl-cAMP demonstrated that 8-Cl-cAMP enters cells and binds to both PKI and PKII. The [H-3]8-Cl-cAMP binding profile of HPLC showed that 8-Cl-cAMP selectively down-regulates PKI and up-regulates PKII, and such an effect of 8-Cl-cAMP is mimicked by exposing cells to RI(alpha) antisense oligodeoxynucleotide, which suppresses RI(alpha) and enhances RII(beta) expression. Dot-blot hybridization analysis demonstrated that both 8-Cl-cAMP treatment (5 muM, 6 h) and RII(beta) retroviral vector infection elicited a marked induction of RII(beta) and C(alpha) mRNA with little or no change in RI(alpha) and RII(alpha) mRNA. These results suggest that the RI(alpha) and RII(beta) regulatory subunits determine the distinct roles of type I and type II cAMP-dependent protein kinase isozymes in the regulation of cell proliferation in HL-60 cells and that the formation of the 34-kDa-truncated RI is an efficient mechanism for type I protein kinase down-regulation. C1 NCI,CELLULAR BIOCHEM SECT,TUMOR IMMUNOL & BIOL LAB,BLDG 10,RM 5B38,BETHESDA,MD 20892. NR 58 TC 123 Z9 124 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1993 VL 268 IS 8 BP 5774 EP 5782 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KR822 UT WOS:A1993KR82200063 PM 8449943 ER PT J AU GOLDSMITH, ME MADDEN, MJ MORROW, CS COWAN, KH AF GOLDSMITH, ME MADDEN, MJ MORROW, CS COWAN, KH TI A Y-BOX CONSENSUS SEQUENCE IS REQUIRED FOR BASAL EXPRESSION OF THE HUMAN MULTIDRUG RESISTANCE (MDR1) GENE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID THYMIDINE KINASE GENE; DNA-BINDING PROTEINS; P-GLYCOPROTEIN; TRANSCRIPTION FACTORS; FUNCTIONAL-ANALYSIS; CP-1/CBF SUBUNITS; CHINESE-HAMSTER; CDNA CLONING; HUMAN-TUMORS; CELL-LINES AB Basal transcription of the human multidrug resistance (mdr1) promoter was studied by chloramphenicol acetyltransferase (CAT) reporter fusion gene analysis in two parental and doxorubicin-resistant human tumor cell lines. Deletion of mdr1 DNA sequences to -89 relative to the start of transcription (at +1) had little effect on expression. Deletion of nucleotide sequences from -89 to -70, however, resulted in a 5-10-fold reduction in mdrCAT expression. DNase I footprint analysis demonstrated that the region from -85 to -70 was protected from nuclease digestion using nuclear extracts from these cell lines. The sequence between -82 and -73 is perfectly homologous with the 10-base pair Y-box consensus sequence found in the promoters of all major histocompatibility complex class-II (MHC II) genes. The Y-box sequence in MHC II genes is required for accurate and efficient transcription and contains the sequence CCAAT in the reverse orientation (Dorn, A., Durand, B., Marfing, C., Le Meur, M., Benoist, C., and Mathis, D. (1987) Proc. Natl. Acad. Sci. U. S. A. 84, 6249-6253). Mutations in the reverse CCAAT sequence of the Y-box consensus substantially reduced expression of an mdrCAT vector and eliminated nucleoprotein binding in an electrophoretic mobility shift assay. These results suggest that proteins which bind to the putative Y-box consensus sequence are critical for basal transcriptional regulation of the human mdr1 gene. RP GOLDSMITH, ME (reprint author), NCI,MED BRANCH,BLDG 10,RM 12N226,BETHESDA,MD 20892, USA. NR 56 TC 104 Z9 108 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1993 VL 268 IS 8 BP 5856 EP 5860 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KR822 UT WOS:A1993KR82200075 PM 8095499 ER PT J AU THEVENIN, C LUCAS, BP KOZLOW, EJ KEHRL, JH AF THEVENIN, C LUCAS, BP KOZLOW, EJ KEHRL, JH TI CELL TYPE-SPECIFIC AND STAGE-SPECIFIC EXPRESSION OF THE CD20/B1 ANTIGEN CORRELATES WITH THE ACTIVITY OF A DIVERGED OCTAMER DNA MOTIF PRESENT IN ITS PROMOTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HEAVY-CHAIN PROMOTER; TRANSCRIPTION FACTOR; STIMULATES TRANSCRIPTION; IMMUNOGLOBULIN GENES; BINDING PROTEINS; LYMPHOCYTES-B; HELA-CELLS; ACTIVATION; DOMAINS; REQUIREMENT AB The CD20(B1) gene encodes a B cell-specific protein involved in the regulation of human B cell proliferation and differentiation. Studies with 5' deletion CD20 promoter-CAT constructs have previously revealed two regions of the promoter between bases -186 and -280 and between bases -280 and -454 which contained positive regulatory elements. In this study we identified a sequence element present in the most proximal region located between bases -214 and -201, TTCTTCTAATTAA, which is important in the high constitutive expression of CD20 in mature B cells and the induction of CD20 in pre-B cells. This sequence element was referred to as the BAT box and its deletion significantly reduced the activity of a CD20 promoter-CAT construct in B cells. Mobility shift assays with various mutant probes and B cell nuclear extracts demonstrated that the core sequence TAAT was essential for binding to this site. Cross competition experiments with an octamer sequence from the Ig heavy chain promoter, the BAT box, and a TA-rich sequence present in the CD21 promoter revealed that all three sequences bound the same nuclear proteins suggesting that the BAT box binding proteins were Oct-1 and Oct-2. Southwestern blotting and UV cross-linking studies confirmed that the BAT box binding proteins were Oct-1 and Oct-2. The affinity of the BAT box binding proteins for the BAT box was approximately 25-fold less than for the octamer sequence and the BAT box binding proteins dissociated from the BAT box 10-fold more rapidly than from the octamer sequence. Despite this lower affinity, a trimer of the BAT box sequence was as efficiently transactivated by an Oct-2 expression vector as was a trimer of the octamer sequence in HeLa cells. The BAT box and Oct-2 were also implicated in the induction of CD20 in the pre-B cell line, PB-697, via phorbol esters. The induction of CD20 mRNA was temporally associated with induction of Oct-2 mRNA and a BAT box-deleted CD20-CAT construct, in contrast to the wild type, was poorly induced by phorbol esters. Together these results suggest that the BAT box binding proteins are important in the B cell specific expression of CD20 and perhaps CD21. C1 NIAID,IMMUNOREGULAT LAB,BLDG 10,RM 11B-13,BETHESDA,MD 20892. NR 32 TC 51 Z9 53 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1993 VL 268 IS 8 BP 5949 EP 5956 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KR822 UT WOS:A1993KR82200088 PM 7680653 ER PT J AU FATHI, Z CORJAY, MH SHAPIRA, H WADA, E BENYA, R JENSEN, R VIALLET, J SAUSVILLE, EA BATTEY, JF AF FATHI, Z CORJAY, MH SHAPIRA, H WADA, E BENYA, R JENSEN, R VIALLET, J SAUSVILLE, EA BATTEY, JF TI BRS-3 - A NOVEL BOMBESIN RECEPTOR SUBTYPE SELECTIVELY EXPRESSED IN TESTIS AND LUNG-CARCINOMA CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GASTRIN-RELEASING PEPTIDE; SWISS 3T3 CELLS; BETA-2-ADRENERGIC RECEPTOR; MOLECULAR-CLONING; FUNCTIONAL-CHARACTERIZATION; PHOSPHORYLATION SITES; PROTEIN-KINASE; GROWTH-FACTOR; CDNA; DESENSITIZATION AB The bombesin (BN)-like peptides mediate a diverse spectrum of biological activities and have been implicated as autocrine growth factors in the pathogenesis and progression of some human small cell lung carcinoma tumors. Previously, two mammalian BN-like peptide receptor subtypes, gastrin-releasing peptide receptor and neuromedin-B receptor, have been cloned and characterized. In this study, we have isolated and characterized human genomic and complementary DNA (cDNA) clones encoding a new BN-like peptide receptor subtype, BN receptor subtype 3 (BRS-3). Expression of BRS-3 cDNA in Xenopus oocytes encodes a functional receptor that is specifically activated by BN-like peptides. Chromosome mapping studies indicate that the BRS-3 gene is located on human chromosome X. BRS-3 mRNA expression in rat tissues is limited to secondary spermatocytes in testis. In contrast, BRS-3 mRNA is widely expressed in a panel of human cell lines from all histological types of lung carcinoma. These results suggest a role for BN-like peptides and their receptors in mammalian reproductive physiology and also indicate that BRS-3 could serve as a potential therapeutic target for human lung carcinoma. C1 NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. MONTREAL GEN HOSP,DIV ONCOL,MONTREAL H3G 1A4,QUEBEC,CANADA. RP FATHI, Z (reprint author), NCI,DEPT CANC TREATMENT,DEV THERAPEUT PROGRAM,BIOL CHEM LAB,BLDG 37,RM 5D02,BETHESDA,MD 20892, USA. NR 28 TC 275 Z9 278 U1 1 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1993 VL 268 IS 8 BP 5979 EP 5984 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KR822 UT WOS:A1993KR82200092 PM 8383682 ER PT J AU KOVACS, JA POWELL, F EDMAN, JC LUNDGREN, B MARTINEZ, A DREW, B ANGUS, CW AF KOVACS, JA POWELL, F EDMAN, JC LUNDGREN, B MARTINEZ, A DREW, B ANGUS, CW TI MULTIPLE GENES ENCODE THE MAJOR SURFACE GLYCOPROTEIN OF PNEUMOCYSTIS-CARINII SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMINO-ACID-SEQUENCE; ANTIGENIC VARIATION; BORRELIA-HERMSII; BINDING-PROTEIN; IDENTIFICATION; EXPRESSION; PNEUMONIA; IMMUNODEFICIENCY; PURIFICATION; RECEPTOR AB The major surface antigen of Pneumocystis carinii, a life-threatening opportunistic pathogen in human immunodeficiency virus-infected patients, is an abundant glycoprotein that functions in host-organism interactions. A monoclonal antibody to this antigen is protective in animals, and thus this antigen is a good candidate for development as a vaccine to prevent or control P. carinii infection. We have cloned and sequenced seven related but unique genes encoding the major surface glycoprotein of rat P. carinii. Partial amino acid sequencing confirmed the identity of these genes. Based on Southern blot studies using chromosomal or restricted DNA, the major surface glycoproteins are the products of a multicopy family of genes. The predicted protein has an M(r) of approximately 123,000, is relatively rich in cysteine residues (5.5%) that are very strongly conserved, and contains a well conserved hydrophobic region at the carboxyl terminus. The presence of multiple related msg genes encoding the major surface glycoprotein of P. carinii suggests that antigenic variation is a possible mechanism for evading host defenses. Further characterization of this family of genes should allow the development of novel approaches to the control of this pathogen. C1 UNIV CALIF SAN FRANCISCO,HORMONE RES INST,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,LAB MED LAB,SAN FRANCISCO,CA 94143. RP KOVACS, JA (reprint author), NIH,CTR CLIN,DEPT CRIT CARE MED,BLDG 10,RM 7D43,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 47 TC 130 Z9 130 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1993 VL 268 IS 8 BP 6034 EP 6040 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KR822 UT WOS:A1993KR82200099 PM 8449961 ER PT J AU GROSS, A BENSASSON, SZ PAUL, WE AF GROSS, A BENSASSON, SZ PAUL, WE TI ANTI-IL-4 DIMINISHES INVIVO PRIMING FOR ANTIGEN-SPECIFIC IL-4 PRODUCTION BY T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID STIMULATORY FACTOR-I; MONOCLONAL-ANTIBODY; MURINE LEISHMANIASIS; INTERFERON-GAMMA; IFN-GAMMA; INTERLEUKIN-4; SUBSETS; PROLIFERATION; SUPPRESSION; PRECURSORS AB Treatment of mice with neutralizing monoclonal anti-IL-4 antibodies at the time of immunization with keyhole limpet hemocyanin causes significant inhibition of priming of T cells for the production of IL-4 upon subsequent in vitro challenge. BALB/c mice received a single injection of anti-IL-4 at the time of immunization. T cells purified from spleen and lymph nodes were obtained at 6 to 7 days and at 30 to 75 days after priming. In the 6- to 7-day group, IL-4 production in response to keyhole limpet hemocyanin among the recipients of anti-IL-4 was reduced by more than twofold in four of four experiments, when low density T cells were challenged. In some, but not all, of these experiments, production of IFN-gamma was enhanced at least twofold. Measurement of frequency of IL-4-producing, keyhole limpet hemocyanin-specific T cells indicated a twofold reduction in the anti-IL-4-treated mice. Among cells obtained between 30 and 75 days after priming, production of IL-4 was diminished in four of four cases in high density cells and three of four cases in low density cells. T cells were also prepared from mice that received a secondary in vivo challenge 90 to 105 days after priming. T cells from boosted donors that had received a single injection of anti-IL-4 at the time of priming showed diminished production of IL-4 in each experiment. By contrast, treatment with anti-IL-4 at the time of secondary challenge did not diminish IL-4-producing capacity of cells from mice that were primed in the absence of anti-IL-4. These results indicate that IL-4 is important in vivo in priming T cells to develop into IL-4-producing cells and indicate an important physiologic role for IL-4 in the establishment of lymphokine-producing phenotype. C1 NIAID,IMMUNOL LAB,BLDG 10,ROOM 11N311,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,HADASSAH MED SCH,LAUTENBERG CTR GEN & TUMOR IMMUNOL,IL-91010 JERUSALEM,ISRAEL. NR 34 TC 73 Z9 73 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 15 PY 1993 VL 150 IS 6 BP 2112 EP 2120 PG 9 WC Immunology SC Immunology GA KR934 UT WOS:A1993KR93400003 PM 7680682 ER PT J AU LITTLE, J ALLING, DW ASOFSKY, R AF LITTLE, J ALLING, DW ASOFSKY, R TI INDUCTION OF DIFFERENTIATION IN A B-LYMPHOMA X-B-LYMPHOCYTE HYBRID LINE .2. INTRACLONAL HETEROGENEITY IN GROWTH, SECRETION OF IGM, AND CYTOKINE PRODUCTION IN RESPONSE TO LIPOPOLYSACCHARIDE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; COLONY-STIMULATING FACTOR; CELL SURFACE-ANTIGENS; HUMAN-MONOCYTES; MONOCLONAL-ANTIBODIES; INVITRO DIFFERENTIATION; THYROID-CELLS; MESSENGER-RNA; EXPRESSION; ENDOTOXIN AB Murine B lymphocyte clones have proven to be useful models to study aspects of B lymphocyte growth and development. It had been previously shown that induction of TH2.2 (B lymphoma X B lymphocyte) with LPS resulted in differentiation into IgM-secreting cells (a feature similar to other B cells lines such as BCL1), and secretion of granulocyte-macrophage-CSF. Many transformed and nontransformed lines (including TH2.2) have been shown to generate progeny heterogenous in size and secretion of product when exposed to mitogen. We extend this study to demonstrate heterogeneity in secretion of IgM, granulocyte-macrophage-CSF, IL-3, and IL-6 in LPS-induced TH2.2. Clones generated by limiting dilution were heterogenous with respect to size, type, and quantity of product secreted. Microscopic clones ranged from 10 to about 1000 cells in size and could not be grown further; the majority secreted one product (mainly IgM). These clones were very efficient secretors of IgM and probably consist mainly of terminal-secreting cells. Microscopic clones secreting cytokine were also efficient producers. Visible clones from LPS-induced cultures grew to the same size as uninduced clones and were often restricted in secretion of products. Although the majority secreted three or four products (52%), many secreted IgM only or IgM and one cytokine. Although there was a strong tendency for clones to secrete multiple products, almost every secretory phenotype could be found. Amounts of different products secreted were not correlated, suggesting an additional level of independent control of this variable. Restriction of secretion was not due to genetic variation because visible clones originally restricted in secretion almost always produced all products when expanded and retested. These findings indicate that cells of TH2.2 were heterogenous with respect to growth and secretion in the presence of LPS and were individually programmed for differentiative responses. The programming of cells was not permanent, but subject to dynamic change. C1 NIAID,OFF DIRECTOR INTRAMURAL RES,BETHESDA,MD 20892. RP LITTLE, J (reprint author), NIAID,IMMUNOL LAB,9000 ROCKVILLE PIKE,BLDG 10,RM IIN3II,BETHESDA,MD 20892, USA. NR 65 TC 6 Z9 6 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 15 PY 1993 VL 150 IS 6 BP 2129 EP 2138 PG 10 WC Immunology SC Immunology GA KR934 UT WOS:A1993KR93400005 PM 8450206 ER PT J AU WU, S YANG, YL SADEGHNASSERI, S ASHWELL, JD AF WU, S YANG, YL SADEGHNASSERI, S ASHWELL, JD TI USE OF BISPECIFIC HETEROCONJUGATED ANTIBODIES (ANTI-T-CELL ANTIGEN RECEPTOR X ANTI-MHC CLASS-II) TO STUDY ACTIVATION OF T-CELLS WITH A FULL LENGTH OR TRUNCATED ANTIGEN RECEPTOR ZETA-CHAIN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID GROWTH-FACTOR RECEPTOR; IMMOBILIZED MONOCLONAL-ANTIBODIES; PRESENTING CELLS; CROSS-LINKING; CYTOCHROME-C; COMPLEX; CD3; CLONES; IA; PROLIFERATION AB Ligand-induced activation of T cells involves recognition of monovalent peptide Ag complexed with a cell surface MHC-encoded molecule. In contrast, antibody-induced activation of T cells typically requires external cross-linking of the TCR. To examine the mechanisms that underlie the ability of these different stimuli to signal, we have created bispecific chimeric antibody molecules (BA) that mimic Ag in several important aspects. Anti-TCR-alpha, -beta, or anti-CD3-epsilon Fab fragments were covalently coupled to an anti-MHC class II Fab fragment. These BA elicited IL-2 production or proliferation from Ag-specific T cell hybridoma cells or splenic T cells, respectively, in the presence, but not the absence, of accessory cells expressing the appropriate MHC class II molecule. This response was prevented by soluble blocking antibodies against the TCR or MHC class II. When ''presented' by MHC class II-bearing accessory cells, anti-TCR X anti-MHC class II BA, like cell surface Ag, elicited IL-2 production from T cell transfectants expressing full length TCR zeta-chain but not from otherwise identical cells expressing truncated zeta; when immobilized on a plastic surface these BA were potent stimulators that induced equal amounts of IL-2 from the same cells. Purified Ag/MHC complexes immobilized on plastic were able to induce IL-2 production from T cells expressing the full length, but not the truncated, form of zeta. We hypothesize that TCR-mediated T cell activation requires stable aggregation of the TCR. In this model, activation by mobile cell surface Ag/MHC or BA occurs in two steps, occupancy-induced TCR clustering followed by stable aggregation facilitated by the presence of a full length zeta-chain. Immobilized high affinity anti-TCR antibodies, but not low affinity Ag/MHC complexes, directly promote stable receptor aggregate, and thus would not require a full length zeta-chain. C1 NCI,IMMUNE CELL BIOL LAB,BIOL RESPONSE MODIFIERS PROGRAM,ROOM 1B-40,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BETHESDA,MD 20892. NR 55 TC 10 Z9 10 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 15 PY 1993 VL 150 IS 6 BP 2211 EP 2221 PG 11 WC Immunology SC Immunology GA KR934 UT WOS:A1993KR93400013 PM 8450208 ER PT J AU VANGURI, P LEE, E HENKART, P SHIN, ML AF VANGURI, P LEE, E HENKART, P SHIN, ML TI HYDROLYSIS OF MYELIN BASIC-PROTEIN IN MYELIN MEMBRANES BY GRANZYMES OF LARGE GRANULAR LYMPHOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; TERMINAL COMPLEMENT COMPLEXES; VASCULAR ENDOTHELIAL-CELLS; CYTOLYTIC LYMPHOCYTES; CYTOPLASMIC GRANULES; SERINE ESTERASES; T-CELLS; INFLAMMATORY DEMYELINATION; MULTIPLE-SCLEROSIS; CYTO-TOXICITY AB Immune-mediated demyelination initially manifests as a separation of myelin lamellae followed by loss of myelin proteins and eventual loss of myelin membranes. Myelin basic protein, one of the major structural proteins of myelin, is highly vulnerable to various proteases derived from diverse cell types. Killer lymphocytes such as CTL, in addition to other immune effectors, have been implicated in inflammatory demyelination. In addition to a pore forming peptide, the granules of CTL and large granular lymphocytes (LGL) contain a number of serine esterases collectively called as granzymes. We studied the effect of these granule enzymes on myelin and found that LGL granule-extracts (LGL-g) hydrolyzed MBP in myelin membranes. LGL-g also cleaved purified MBP at neutral pH in a Ca2+ independent manner and this hydrolysis was inhibited by serine esterase inhibitors. In addition, absorption of LGL-g with antigranzyme A significantly reduced MBP hydrolysis. These findings implicated the granzymes in LGL-g, especially granzyme A, as the agent causing MBP degradation. Inasmuch as activation of CTL in the vicinity of myelinated axons can lead to granule exocytosis, hydrolysis of MBP by granzymes may be a significant event in myelin destruction. C1 UNIV MARYLAND,DEPT PATHOL,600-E,MSTF,10 S PINE,BALTIMORE,MD 21201. NCI,BETHESDA,MD 20814. FU NINDS NIH HHS [P01 NS20022, R01 NS15662] NR 52 TC 22 Z9 22 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 15 PY 1993 VL 150 IS 6 BP 2431 EP 2439 PG 9 WC Immunology SC Immunology GA KR934 UT WOS:A1993KR93400036 PM 7680692 ER PT J AU GOLDING, H DIMITROV, DS BLACKBURN, R MANISCHEWITZ, J BLUMENTHAL, R GOLDING, B AF GOLDING, H DIMITROV, DS BLACKBURN, R MANISCHEWITZ, J BLUMENTHAL, R GOLDING, B TI FUSION OF HUMAN B-CELL LINES WITH HIV-1 ENVELOPE-EXPRESSING T-CELLS IS ENHANCED BY ANTIGEN-SPECIFIC IG RECEPTORS - POSSIBLE MECHANISM FOR ELIMINATION OF GP120-SPECIFIC B-CELLS INVIVO SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; NEUTRALIZING EPITOPE; LYMPHOTROPIC VIRUS; SYNCYTIA FORMATION; AIDS RETROVIRUS; HTLV-III/LAV; CD4 ANTIGEN; INFECTION; BINDING; GLYCOPROTEIN AB The possible contribution of Ag-specific Ig receptors on B cells to syncytium formation with HIV-1 envelope (env)-expressing cells was examined. A unique model system was designed that used anti-TNP/TNP interactions between a panel of TNP-specific human B cell lines and TNP-haptenated HIV-1 env-expressing T cells. The prototype B cell line 1:13 (CD4dull) produced few syncytia with vaccinia gp120/41-infected CD4- T cell effectors. However, TNP-haptenation of the HIV-1 env-expressing cells resulted in a five- to 10-fold increase in syncytium formation. The ''enhanced'' syncytia were blocked by OKT4A mAb, soluble CD4, anti-TNP serum, and TNP-BSA, suggesting a role for both CD4 and Ig receptors. In contrast, the number of syncytia formed between CD4+ CEM T cells and TNP-haptenated effectors was reduced by 30 to 40%, compared with the unhaptenated effectors, suggesting that a fraction of the TNP haptens bound close to the CD4 binding regions on the gp120 envelope, which was confirmed by other experiments. The possibility that B cells specific for the CD4 binding site on HIV-1 gp120 may be involved in syncytium formation with HIV-1 env-expressing cells was tested by screening a panel of five hybrid B cell lines from HIV-1-seropositive individuals. One of these lines produced anti-gp120 antibodies, which bound near the CD4 binding site, and also formed syncytia with HIV-1 env-expressing cells. This study suggests that, in addition to CD4 receptors, certain B cell Ig receptors that bind to gp120 may induce conformational changes leading to cell fusion and their elimination. C1 NCI,LMB,MEMBRANE STRUCT & FUNCT SECT,BETHESDA,MD 20892. RP GOLDING, H (reprint author), US FDA,CBER,DIV VIROL,BLDG 29A,ROOM 2C15,8800 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 37 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 MAR 15 PY 1993 VL 150 IS 6 BP 2506 EP 2516 PG 11 WC Immunology SC Immunology GA KR934 UT WOS:A1993KR93400044 PM 7680694 ER PT J AU KELLER, H DREYER, C MEDIN, J MAHFOUDI, A OZATO, K WAHLI, W AF KELLER, H DREYER, C MEDIN, J MAHFOUDI, A OZATO, K WAHLI, W TI FATTY-ACIDS AND RETINOIDS CONTROL LIPID-METABOLISM THROUGH ACTIVATION OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR RETINOID-X RECEPTOR HETERODIMERS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR RESPONSE ELEMENT; RETINOID-X RECEPTOR RESPONSE ELEMENT; ACYL-COA OXIDASE GENE; NUCLEAR HORMONE RECEPTORS ID BIOCHEMICAL-MECHANISMS; BETA-OXIDATION; RAT-LIVER; CELLS; GENE AB The nuclear hormone receptors called PPARs (peroxisome proliferator-activated receptors alpha, beta, and gamma) regulate the peroxisomal beta-oxidation of fatty acids by induction of the acyl-CoA oxidase gene that encodes the rate-limiting enzyme of the pathway. Gel retardation and cotransfection assays revealed that PPARalpha heterodimerizes with retinoid X receptor beta (RXRbeta; RXR is the receptor for 9-cis-retinoic acid) and that the two receptors cooperate for the activation of the acyl-CoA oxidase gene promoter. The strongest stimulation of this promoter was obtained when both receptors were exposed simultaneously to their cognate activators. Furthermore, we show that natural fatty acids, and especially polyunsaturated fatty acids, activate PPARs as potently as does the hypolipidemic drug Wy 14,643, the most effective activator known so far. Moreover, we discovered that the synthetic arachidonic acid analogue 5,8,11,14 -eicosatetraynoic acid is 100 times more effective than Wy 14,643 in the activation of PPARalpha. In conclusion, our data demonstrate a convergence of the PPAR and RXR signaling pathways in the regulation of the peroxisomal beta-oxidation of fatty acids by fatty acids and retinoids. C1 UNIV LAUSANNE,INST BIOL ANIM,BATIMENT BIOL,CH-1015 LAUSANNE,SWITZERLAND. MAX PLANCK INST ENTWICKLUNGSBIOL,W-7400 TUBINGEN,GERMANY. NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. RI Wahli, Walter/B-1398-2009 OI Wahli, Walter/0000-0002-5966-9089 NR 33 TC 777 Z9 785 U1 1 U2 21 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 MAR 15 PY 1993 VL 90 IS 6 BP 2160 EP 2164 DI 10.1073/pnas.90.6.2160 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KT370 UT WOS:A1993KT37000016 PM 8384714 ER PT J AU HOWARD, OMZ CLOUSE, KA SMITH, C GOODWIN, RG FARRAR, WL AF HOWARD, OMZ CLOUSE, KA SMITH, C GOODWIN, RG FARRAR, WL TI SOLUBLE TUMOR-NECROSIS-FACTOR RECEPTOR - INHIBITION OF HUMAN-IMMUNODEFICIENCY-VIRUS ACTIVATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AIDS ID PROMONOCYTE CELL-LINE; LONG TERMINAL REPEAT; FACTOR-ALPHA; MOLECULAR-CLONING; INTERFERON-ALPHA; BINDING PROTEIN; SERUM LEVELS; KAPPA-B; EXPRESSION; HIV-1 AB The inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) has been shown to stimulate human immunodeficiency virus type 1 (HIV-1) replication in both chronically and acutely infected T lymphocytes and monocytes. Transcriptional activation of the HIV long terminal repeat and subsequent increase in virus production are linked to TNF activation of the cellular transcription factor NF-kappaB. Here we report the use of two forms of soluble recombinant type 1 (p80) TNF receptor to inhibit TNF-induced HIV activation in vitro. One receptor form is a monomer containing the entire 236 residues of the extracellular (ligand-binding) portion of p80. A second receptor form is a chimeric homodimer containing these residues fused to a truncated human IgG1 immunoglobulin heavy chain and, thus, resembles a bivalent antibody without light chains. These recombinant receptor proteins were tested for their ability to inhibit TNF-alpha-induced expression of HIV-1 in chronically infected human cell lines. We also examined the ability of the soluble receptors to limit the activation of the HIV-long terminal repeat transcription. The soluble TNF receptor dimer was most effective at blocking TNF-alpha-induced HIV-1 expression in both monocytoid and lymphoid cells. The molar ratio of TNF-receptor dimer to TNF-alpha found to be most effective was, at least, 5:1. We conclude that at specific TNF/soluble TNF-receptor dimer ratios, TNF-alpha-induced HIV-1 transcription and expression can be limited in vitro. C1 NCI,FREDERICK CANC RES & DEV CTR,MOLEC IMMUNOREGULAT LAB,BIOL RESPONSE MODIFIERS PROGRAM,POB B,FREDERICK,MD 21702. US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,BETHESDA,MD 20014. IMMUNEX RES & DEV CORP,SEATTLE,WA 98101. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RI Howard, O M Zack/B-6117-2012 OI Howard, O M Zack/0000-0002-0505-7052 FU NCI NIH HHS [N01-CO-74102] NR 39 TC 61 Z9 61 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 MAR 15 PY 1993 VL 90 IS 6 BP 2335 EP 2339 DI 10.1073/pnas.90.6.2335 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KT370 UT WOS:A1993KT37000052 PM 7681592 ER PT J AU FESEN, MR KOHN, KW LETEURTRE, F POMMIER, Y AF FESEN, MR KOHN, KW LETEURTRE, F POMMIER, Y TI INHIBITORS OF HUMAN-IMMUNODEFICIENCY-VIRUS INTEGRASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE RETROVIRUS; AIDS; TOPOISOMERASE; ZINC FINGER ID MAMMALIAN TOPOISOMERASE-II; DNA INTEGRATION; RETROVIRAL DNA; VIRAL-DNA; PROTEIN; BINDING; CLEAVAGE; INVITRO; SEQUENCE; TOXICITY AB In an effort to further extend the number of targets for development of antiretroviral agents, we have used an in vitro integrase assay to investigate a variety of chemicals, including topoisomerase inhibitors, antimalarial agents, DNA binders, naphthoquinones, the flavone quercetin, and caffeic acid phenethyl ester as potential human immunodeficiency virus type 1 integrase inhibitors. Our results show that although several topoisomerase inhibitors-including doxorubicin, mitoxantrone, ellipticines, and quercetin-are potent integrase inhibitors, other topoisomerase inhibitors-such as amsacrine, etoposide, teniposide, and camptothecin-are inactive. Other intercalators, such as chloroquine and the bifunctional intercalator ditercalinium, are also active. However, DNA binding does not correlate closely with integrase inhibition. The intercalator 9-aminoacridine and the polyamine DNA minor-groove binders spermine, spermidine, and distamycin have no effect, whereas the non-DNA binders primaquine, 5,8-dihydroxy-1,4-naphthoquinone, and caffeic acid phenethyl ester inhibit the integrase. Caffeic acid phenethyl ester was the only compound that inhibited the integration step to a substantially greater degree than the initial cleavage step of the enzyme. A model of 5,8-dihydroxy-1,4-naphthoquinone interaction with the zinc ringer region of the retroviral integrase protein is proposed. C1 NCI, DIV CANC TREATMENT,MOLEC PHARMACOL LAB, DEV THERAPEUT PROGRAM,BLDG 37, ROOM 5C25, BETHESDA, MD 20892 USA. NR 37 TC 243 Z9 254 U1 0 U2 9 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1993 VL 90 IS 6 BP 2399 EP 2403 DI 10.1073/pnas.90.6.2399 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KT370 UT WOS:A1993KT37000065 PM 8460151 ER PT J AU ROBINSON, MA MITCHELL, MP WEI, S DAY, CE ZHAO, TM CONCANNON, P AF ROBINSON, MA MITCHELL, MP WEI, S DAY, CE ZHAO, TM CONCANNON, P TI ORGANIZATION OF HUMAN T-CELL RECEPTOR BETA-CHAIN GENES - CLUSTERS OF V-BETA GENES ARE PRESENT ON CHROMOSOME-7 AND CHROMOSOME-9 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GENE MAPPING; INTRACHROMOSOMAL TRANSLOCATION; ORPHON GENES; T-CELL ANTIGEN RECEPTOR ID VARIABLE REGION GENES; MULTIPLE-SCLEROSIS; FAMILIES; POLYMORPHISM; COMPLEX; SEGMENTS; ANTIGEN; MURINE; LOCUS AB To ascertain the extent and organization of the germ-line human T-cell receptor (TCR) beta-chain gene repertoire, beta-chain variable region (V(beta)) genes were mapped by pulsed-field gel electrophoresis, cosmid cloning, and in situ hybridization. Probes derived from the 24 known V(beta) families were mapped to a total of six Sfi I fragments in DNA samples from multiple individuals representing all possible haplotypes of TCR V- and C (constant)-region insertion/deletion-related polymorphisms. Four of the Sfi I fragments were linked to one another to develop an extended map of the TCR beta-chain gene complex previously localized to chromosome 7q35. The remaining two Sfi I fragments, containing 6 V(beta) genes, could not be linked to the TCR beta-chain gene complex. Using human-hamster somatic cell hybrids and in situ hybridization, these orphon genes were localized to chromosome 9p. Nucleotide sequences of the orphon V(beta) genes, derived from cosmid clones, were 93-97% identical to V(beta) genes in the TCR beta-chain gene complex. Open reading frames in three of the orphon V(beta) genes were intact as were the recombination signal sequences. As expected, based on their orphon status, none of the V(beta) genes of chromosome 9 was detected in transcripts containing C(beta). These results indicate that the functional germ-line V(beta) repertoire in humans is substantially (10%) smaller than previously estimated. C1 VIRGINIA MASON RES CTR,SEATTLE,WA 98101. UNIV WASHINGTON,SCH MED,DEPT IMMUNOL,SEATTLE,WA 98195. RP ROBINSON, MA (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK 2 FACIL,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. FU NIDDK NIH HHS [DK41347] NR 29 TC 48 Z9 48 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 MAR 15 PY 1993 VL 90 IS 6 BP 2433 EP 2437 DI 10.1073/pnas.90.6.2433 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KT370 UT WOS:A1993KT37000072 PM 8384723 ER PT J AU KEARSE, KP WIEST, DL SINGER, A AF KEARSE, KP WIEST, DL SINGER, A TI SUBCELLULAR-LOCALIZATION OF T-CELL RECEPTOR COMPLEXES CONTAINING TYROSINE-PHOSPHORYLATED ZETA-PROTEINS IN IMMATURE CD4+CD8+ THYMOCYTES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID NATURAL-KILLER CELLS; ANTIGEN RECEPTOR; MONOCLONAL-ANTIBODY; CHAIN; EXPRESSION; ACTIVATION; KINASE; CD4; PURIFICATION; CD3-ZETA AB The T-cell antigen receptor (TCR) is a complex of at least six different proteins (alpha, beta, gamma, delta, epsilon, and zeta) that is assembled in the endoplasmic reticulum (ER) and transported to the cell surface. Unlike mature T cells, most immature CD4+CD8+ thymocytes retain within the ER and degrade greater than 90% of some of the TCR components they synthesize, resulting in low surface expression of TCR complexes. The few surface TCR complexes that most immature CD4+CD8+ thymocytes do express are only marginally capable of transducing signals mobilizing intracellular calcium. The inverse relationship with TCR expression and function suggested that phosphorylated zeta (P-zeta) molecules might function in CD4+CD8+ thymocytes either as an ER retention signal for newly synthesized TCR complexes or as a negative regulatory modification of TCR complexes present on the cell surface. The present study sought to evaluate these two possibilities by determining the subcellular location of TCR complexes containing P-zeta chains. We found that, unlike unmodified zeta chains, all P-zeta chains in CD4+CD8+ thymocytes existed in assembled TCR complexes and that all TCR complexes containing P-zeta molecules had undergone carbohydrate processing events indicative of transit through the Golgi apparatus. These results demonstrate that P-zeta chains are exclusively associated with mature TCR complexes, excluding the possibility that P-zeta serves as an ER retention signal in immature thymocytes. Although we could not directly determine the representation of P-zeta chains among surface TCR complexes, we found that 60-70% of surface TCR complexes on immature CD4+CD8+ thymocytes were associated with tyrosine-phosphorylated protein(s) and that this percentage was inversely correlated with their signaling competence. These results support the concept that tyrosine phosphorylation serves as a negative regulatory modification of certain TCR-associated proteins. RP KEARSE, KP (reprint author), NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892, USA. NR 30 TC 12 Z9 12 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 MAR 15 PY 1993 VL 90 IS 6 BP 2438 EP 2442 DI 10.1073/pnas.90.6.2438 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KT370 UT WOS:A1993KT37000073 PM 7681596 ER PT J AU BROWN, K PARK, S KANNO, T FRANZOSO, G SIEBENLIST, U AF BROWN, K PARK, S KANNO, T FRANZOSO, G SIEBENLIST, U TI MUTUAL REGULATION OF THE TRANSCRIPTIONAL ACTIVATOR NF-KAPPA-B AND ITS INHIBITOR, I-KAPPA-B-ALPHA SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GENE REGULATION; CELL ACTIVATION; HUMAN IMMUNODEFICIENCY VIRUS; TRANSCRIPTION FACTOR; NUCLEAR TRANSLOCATION ID DNA-BINDING SUBUNIT; REL-ASSOCIATED PP40; RETICULOENDOTHELIOSIS VIRUS; 65-KD SUBUNIT; P65 SUBUNIT; PROTO-ONCOGENE; V-REL; C-REL; CLONING; GENE AB The NF-kappaB transcription factor complex is sequestered in the cytoplasm by the inhibitory protein IkappaB-alpha (MAD-3). Various cellular stimuli relieve this inhibition by mechanisms largely unknown, leading to NF-kappaB nuclear localization and transactivation of its target genes. It is demonstrated here with human T lymphocytes and monocytes that different stimuli, including tumor necrosis factor alpha and phorbol 12-myristate 13-acetate, cause rapid degradation of IkappaB-alpha, with concomitant activation of NF-kappaB, followed by a dramatic increase in IkappaB-alpha mRNA and protein synthesis. Transfection studies reveal that the IkappaB-alpha mRNA and the encoded protein are potently induced by NF-kappaB and by homodimers of p65 and of c-Rel. We propose a model in which NF-kappaB and IkappaB-alpha mutually regulate each other in a cycle: saturating amounts of the inhibitory IkappaB-alpha protein are destroyed upon stimulation, allowing rapid activation of NF-kappaB. Subsequently, IkappaB-alpha mRNA and protein levels are quickly induced by the activated NF-kappaB. This resurgence of IkappaB-alpha protein acts to restore an equilibrium in which NF-kappaB is again inhibited. RP BROWN, K (reprint author), NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892, USA. NR 45 TC 567 Z9 573 U1 0 U2 8 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 MAR 15 PY 1993 VL 90 IS 6 BP 2532 EP 2536 DI 10.1073/pnas.90.6.2532 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KT370 UT WOS:A1993KT37000093 PM 8460169 ER PT J AU WEISSMAN, D POLI, G BOUSSEAU, A FAUCI, AS AF WEISSMAN, D POLI, G BOUSSEAU, A FAUCI, AS TI A PLATELET-ACTIVATING-FACTOR ANTAGONIST, RP-55778, INHIBITS CYTOKINE-DEPENDENT INDUCTION OF HUMAN-IMMUNODEFICIENCY-VIRUS EXPRESSION IN CHRONICALLY INFECTED PROMONOCYTIC CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID TUMOR-NECROSIS-FACTOR; LONG TERMINAL REPEAT; FACTOR-ALPHA; PERIPHERAL-BLOOD; FACTOR BINDING; TISSUE-INJURY; LYMPHOCYTES-T; HIV; MECHANISMS; TYPE-1 AB A platelet-activating factor antagonist,. RP 55778, potently suppressed the induction of human immunodeficiency virus (HIV) expression in chronically infected promonocytic U1 cells. RP 55778 inhibited the production of reverse transcriptase activity in U1 cells stimulated with the transcriptionally active inducers of virus production, tumor necrosis factor alpha and phorbol 12-myristate 13-acetate. This effect was correlated only in part with a reduction in the levels of HIV RNA, suggesting that this agent was also affecting posttranscriptional levels of virus production. In this regard, RP 55778 effectively blocked the induction of HIV expression in U1 cells stimulated with interleukin 6 and granulocyte-macrophage colony-stimulating factor, which act predominantly as posttranscriptional activators of HIV expression. Finally, RP 55778 inhibited the production of endogenous tumor necrosis factor a in phorbol 12-myristate 13-acetate-stimulated cells, thereby interfering with an autocrine pathway of virus expression. The suppressive effects of RP 55778 on HIV expression appeared to be independent of the platelet-activating factor cell surface receptor on U1 cells. RP 55778 inhibited acute HIV replication in primary T-cell blasts and the proliferative capacity of these cells. This study suggests that RP 55778 may represent potentially useful compounds in the treatment of HIV infection. C1 RHONE POULENC RORER,CTR RECH VITRY ALFORTVILLE,F-94403 VITRY,FRANCE. RP WEISSMAN, D (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10A,ROOM 6A32,BETHESDA,MD 20892, USA. NR 33 TC 36 Z9 36 U1 1 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 MAR 15 PY 1993 VL 90 IS 6 BP 2537 EP 2541 DI 10.1073/pnas.90.6.2537 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KT370 UT WOS:A1993KT37000094 PM 7681601 ER PT J AU MOSS, B AF MOSS, B TI REGULATION AND FUNCTIONAL-ANALYSIS OF EARLY, INTERMEDIATE, AND LATE GENES OF VACCINIA VIRUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 4 EP 4 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000009 ER PT J AU CHESEBRO, B CAUGHEY, B RAYMOND, G RACE, R AF CHESEBRO, B CAUGHEY, B RAYMOND, G RACE, R TI TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 7 EP 7 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000016 ER PT J AU COLLINS, P DIMOCK, K MINK, M STEC, D KUO, L GROSFELD, H AF COLLINS, P DIMOCK, K MINK, M STEC, D KUO, L GROSFELD, H TI RESCUE OF SYNTHETIC ANALOGS OF GENOMIC RNAS OF RESPIRATORY SYNCYTIAL VIRUS AND PARAINFLUENZA VIRUS TYPE-3 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,INFECT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 10 EP 10 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000026 ER PT J AU CICALA, C AVANTAGGIATI, ML LEVINE, AS RUNDELL, K GRAESSMANN, A CARBONE, M AF CICALA, C AVANTAGGIATI, ML LEVINE, AS RUNDELL, K GRAESSMANN, A CARBONE, M TI SIMIAN VIRUS-40 SMALL-T ANTIGEN ACCELERATES DNA-REPLICATION INVIVO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,VIRUSES & CELLULAR BIOL SECT,BETHESDA,MD. FREE UNIV BERLIN,DEPT BIOCHEM,W-1000 BERLIN 33,GERMANY. NORTHWESTERN UNIV,DEPT MICROBIOL,CHICAGO,IL 60611. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 16 EP 16 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000048 ER PT J AU FIERER, DS CHALLBERG, MD AF FIERER, DS CHALLBERG, MD TI BIOCHEMICAL-CHARACTERIZATION OF THE DNA-BINDING DOMAIN OF HSV-1 UL9 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 16 EP 16 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000050 ER PT J AU GOLDSTEIN, DJ PIERCE, J WANG, LM LI, WQ SCHLEGEL, R AF GOLDSTEIN, DJ PIERCE, J WANG, LM LI, WQ SCHLEGEL, R TI COEXPRESSION OF THE BPV-1 E5 PROTEIN AND THE BETA-TYPE PDGF RECEPTOR IS REQUIRED FOR GROWTH OF A MURINE MYELOID CELL-LINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC 20057. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 16 EP 16 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000051 ER PT J AU GOTTLIEB, J CHALLBERG, MD AF GOTTLIEB, J CHALLBERG, MD TI ROLLING CIRCLE DNA-REPLICATION INVITRO WITH PURIFIED HERPES-SIMPLEX VIRUS TYPE-I REPLICATION PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 17 EP 17 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000052 ER PT J AU MIETZ, JA UNGER, T HUIBREGTSE, JM HOWLEY, PM AF MIETZ, JA UNGER, T HUIBREGTSE, JM HOWLEY, PM TI P53-MEDIATED TRANSCRIPTIONAL ACTIVATION IS INHIBITED BY SV40 LARGE T-ANTIGEN AND BY HPV-16 E6 ONCOPROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 19 EP 19 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000063 ER PT J AU WINOKUR, PL SARAFI, TR MCBRIDE, AA AF WINOKUR, PL SARAFI, TR MCBRIDE, AA TI MAPPING THE DOMAINS OF THE BOVINE PAPILLOMAVIRUS-1 E2-PROTEIN WHICH ARE REQUIRED FOR INTERACTION WITH THE E1-PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 21 EP 21 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000070 ER PT J AU ADACHI, Y COPELAND, TD HATANAKA, M OROSZLAN, S AF ADACHI, Y COPELAND, TD HATANAKA, M OROSZLAN, S TI NUCLEOLAR TARGETING SIGNAL OF HTLV-1 REX PROTEIN SPECIFICALLY BINDS TO NUCLEOLAR SHUTTLE PROTEIN-B-23 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BRP,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD 21702. KYOTO UNIV,INST VIRUS RES,SAKYO KU,KYOTO 606,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 22 EP 22 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000071 ER PT J AU BRADY, JN PIRAS, G RADONOVICH, MF DUVALL, JF FATTAEY, A KASHANCHI, F AF BRADY, JN PIRAS, G RADONOVICH, MF DUVALL, JF FATTAEY, A KASHANCHI, F TI DIRECT INTERACTION OF HUMAN TFIID WITH THE HIV-1 TRANSACTIVATOR TAT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 22 EP 22 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000074 ER PT J AU LEE, MS MIZUUCHI, K CRAIGIE, R AF LEE, MS MIZUUCHI, K CRAIGIE, R TI MOLECULAR-BASIS OF A BARRIER TO AUTOINTEGRATION OF MOLONEY MURINE LEUKEMIA-VIRUS DNA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 24 EP 24 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000082 ER PT J AU PRIOLA, SA CHESEBRO, B AF PRIOLA, SA CHESEBRO, B TI INCREASED EXPRESSION OF PRP PROTEIN DURING DIFFERENTIATION OF MURINE EMBRYONAL CARCINOMA-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,PERSISTENT VIRAL DIS,ROCKY MTN LABS,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 26 EP 26 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000088 ER PT J AU LAUGHLIN, C AF LAUGHLIN, C TI STRATEGIES FOR THE DISCOVERY OF ANTIINFLUENZA AGENTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,ANTIVIRAL RES BRANCH,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 28 EP 28 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000094 ER PT J AU BENNINK, JR BACIK, I LAPHAM, C ARNOLD, D SPIES, T COX, J DENG, YP DAY, P ANDERSON, R RESTIFO, N EISENLOHR, L ESQUIVEL, F YEWDELL, JW AF BENNINK, JR BACIK, I LAPHAM, C ARNOLD, D SPIES, T COX, J DENG, YP DAY, P ANDERSON, R RESTIFO, N EISENLOHR, L ESQUIVEL, F YEWDELL, JW TI PRESENTATION OF VIRAL-ANTIGENS TO CYTOTOXIC T-LYMPHOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NCI,BETHESDA,MD 20892. THOMAS JEFFERSON CANC INST,PHILADELPHIA,PA. RI Restifo, Nicholas/A-5713-2008; yewdell, jyewdell@nih.gov/A-1702-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 32 EP 32 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000100 ER PT J AU RESTIFO, NP YEWDELL, JW BENNINK, JR BACIK, I KAWAKAMI, Y ESQUIVEL, F ROSENBERG, SA AF RESTIFO, NP YEWDELL, JW BENNINK, JR BACIK, I KAWAKAMI, Y ESQUIVEL, F ROSENBERG, SA TI MANIPULATING THE ANTIGEN PROCESSING MACHINERY AND TUMOR IMMUNOLOGY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. RI Restifo, Nicholas/A-5713-2008; yewdell, jyewdell@nih.gov/A-1702-2012; Kawakami, Yutaka /E-7429-2013 OI Kawakami, Yutaka /0000-0003-4836-2855 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 33 EP 33 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000104 ER PT J AU BERZOFSKY, JA AF BERZOFSKY, JA TI SYNTHETIC PEPTIDE STRATEGIES IN THE INDUCTION AND ANALYSIS OF T-CELL RESPONSES TO HIV AND TUMORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 39 EP 39 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000121 ER PT J AU CLERICI, M BERZOFSKY, JA COFFMAN, RL SHEARER, GM AF CLERICI, M BERZOFSKY, JA COFFMAN, RL SHEARER, GM TI TH-1-TYPE AND TH-2-TYPE OF IMMUNE-RESPONSES IN SUSCEPTIBILITY TO HIV-INFECTION AND PROGRESSION TO AIDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NCI,METAB BRANCH,BETHESDA,MD 20892. DNAX RES INST MOLEC & CELLULAR BIOL INC,RES INST,PALO ALTO,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 39 EP 39 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000120 ER PT J AU MORSE, HC HUGIN, A MAKINO, M TANG, Y SELVEY, L HODES, R HARTLEY, JW AF MORSE, HC HUGIN, A MAKINO, M TANG, Y SELVEY, L HODES, R HARTLEY, JW TI PATHOGENESIS OF RETROVIRUS-INDUCED IMMUNODEFICIENCY IN THE MOUSE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 40 EP 40 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000125 ER PT J AU MURPHY, BR KULKARNI, A COLLINS, PL MORSE, H CONNORS, M AF MURPHY, BR KULKARNI, A COLLINS, PL MORSE, H CONNORS, M TI THE IMMUNOBIOLOGY OF RSV INFECTION AND IMMUNIZATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,INFECT DIS LAB,BETHESDA,MD 20892. NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 41 EP 41 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000127 ER PT J AU YUI, K ISHIDA, Y KATSUMATA, M KOMORI, S CHUSED, TM ABE, R AF YUI, K ISHIDA, Y KATSUMATA, M KOMORI, S CHUSED, TM ABE, R TI REVERSIBLE VS IRREVERSIBLE FORMS OF T-CELL UNRESPONSIVENESS TO MIS-1A ARE 2 SEPARATE MECHANISMS OF T-CELL CLONAL ANERGY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV PENN,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. NIAID,IMMUNOL LAB,ROCKVILLE,MD 20852. USN,INST MED,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20889. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 54 EP 54 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000174 ER PT J AU COX, JH BENNINK, JR YEWDELL, JW BULLER, RML KARUPIAH, G AF COX, JH BENNINK, JR YEWDELL, JW BULLER, RML KARUPIAH, G TI THE EFFECT OF THE ADENOVIRUS E3/19K PROTEIN ON ANTIGEN PRESENTATION INVIVO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,VIRAL DIS LAB,BETHESDA,MD 20892. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 55 EP 55 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000176 ER PT J AU KARUPIAH, G BULLER, RML AF KARUPIAH, G BULLER, RML TI INTERFERON-GAMMA IS A POTENT INHIBITOR OF POXVIRUS REPLICATION IN CELLS OF MACROPHAGE MONOCYTIC LINEAGE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 57 EP 57 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000185 ER PT J AU PALUMBO, GJ BULLER, RML HU, F PICKUP, D GLASGOW, W AF PALUMBO, GJ BULLER, RML HU, F PICKUP, D GLASGOW, W TI MULTI-GENIC EVASION OF HOST-DEFENSES BY POXVIRUSES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT MICROBIOL,DURHAM,NC 27710. NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 60 EP 60 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000196 ER PT J AU GOLDING, H DIMITROV, D BLUMENTHAL, R GOLDING, B AF GOLDING, H DIMITROV, D BLUMENTHAL, R GOLDING, B TI FUSION OF HUMAN B-CELLS WITH HIV-1 ENVELOPE EXPRESSING T-CELLS CAN BE INDUCED BY ANTIGEN SPECIFIC IMMUNOGLOBULIN (IG) RECEPTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,LMMB,BETHESDA,MD 20892. US FDA,CBER,DIV VIROL,WASHINGTON,DC 20204. US FDA,CBER,DIV HEMATOL,WASHINGTON,DC 20204. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 73 EP 73 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000247 ER PT J AU JOHNSON, RP TROCHA, A DYNAN, M BERGMANN, CC GAMMON, MC ZWEERINK, HJ BLATTNER, W WALKER, BD AF JOHNSON, RP TROCHA, A DYNAN, M BERGMANN, CC GAMMON, MC ZWEERINK, HJ BLATTNER, W WALKER, BD TI SEQUENCE VARIATION IN THE HUMAN-IMMUNODEFICIENCY-VIRUS AS A MECHANISM OF ESCAPE FROM CYTOTOXIC T-LYMPHOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. UNIV SO CALIF,DEPT NEUROL,LOS ANGELES,CA 90089. MERCK SHARP & DOHME LTD,RAHWAY,NJ 07065. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 74 EP 74 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000251 ER PT J AU REITZ, MS LORI, F MALYKH, A GALLO, RC AF REITZ, MS LORI, F MALYKH, A GALLO, RC TI DETERMINANTS OF HIV-1 MACROPHAGE TROPISM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 75 EP 75 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000256 ER PT J AU ROSENBERG, AS SECHLER, JMG HARTLEY, JW MORSE, HC AF ROSENBERG, AS SECHLER, JMG HARTLEY, JW MORSE, HC TI INDUCTION OF INVIVO T-CELL DYSFUNCTION IN MAIDS DEPENDS ON INFECTION BY DISEASE INDUCING DEFECTIVE GENOME, NOT HELPER VIRUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 US FDA,CBER,DIV HEMATOL PROD,BETHESDA,MD 20892. NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 76 EP 76 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000259 ER EF